3/
4/
05
TABLE
OF
CONTENTS
1.0
EXECUTIVE
SUMMARY
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
2
2.0
OCCUPATIONAL
EXPOSURE
AND
RISK
ASSESSMENT
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
7
A.
Toxicological
Considerations
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
7
(
1)
Criteria
for
Conducting
Exposure
Assessments
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
7
(
2)
Summary
of
Toxicity
Concerns
Relating
to
Occupational
Non­
Dietary
Exposures
.
.
.
.
.
.
.
7
(
a)
Summary
of
Toxicological
Endpoint
Selection
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
8
B.
Occupational
Exposures
and
Risks
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
10
(
1)
Handler
Exposures
and
Risks
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
10
(
a)
Background
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
10
(
b)
Occupational
Handlers
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
11
(
2)
Handler
Risk
Assessment
and
Characterization
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
11
(
a)
Handler
Non­
Cancer
and
Cancer
Risk
Calculations
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
11
(
b)
Handler
Non­
Cancer
Risks
from
Exposures
to
HCB
in
PCP
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
14
(
c)
Handler
Cancer
Risks
from
Absorbed
Doses
of
HCB
in
PCP
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
14
(
3)
Postapplication
Exposures
and
Risks
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
17
(
a)
Occupational
Postapplication
Exposure
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
17
(
4)
Postapplication
Risk
Assessment
and
Characterization
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
18
(
a)
Postapplication
Non­
Cancer
and
Cancer
Risk
Calculations
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
18
(
b)
Postapplication
Non­
Cancer
Risks
from
Exposures
to
HCB
in
PCP
.
.
.
.
.
.
.
.
.
.
.
18
(
c)
Postapplication
Cancer
Risks
from
Absorbed
Doses
of
HCB
in
PCP
.
.
.
.
.
.
.
.
.
.
18
(
5)
Data
Gaps,
Uncertainties
and
Limitations
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
21
3.0
REFERENCES
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
22
1
Manufacturing
monitoring
data
(
i.
e.,
surveillance
sampling
data)
submitted
to
U.
S.
EPA
indicate
that
measured
HCB
microcontaminant
levels
in
PCP
production
batch
samples
may
vary
from
below
50
ppm
to
above
75
ppm.
The
Agency
conducted
a
cursory
review
of
surveillance
data
on
PCP
for
years
2000
and
2001
to
determine
if
monitored
HCB
contaminant
levels
were
consistently
below
the
75
ppm
limit
set
in
the
RPAR
agreement.
Data
showed
that
the
average
batch
from
industry
random
sampling
contained
close
to
60
ppm
HCB.
In
addition,
several
outlier
batches
were
produced
with
HCB
levels
exceeding
75
ppm
which
required
blending
with
other
batches
to
reach
acceptable
levels
(
at
or
below
75
ppm)
for
shipment.
Therefore,
the
Agency
assessment
used
75
ppm
(
75
ng/
mg)
as
a
realistic
maximum
contaminant
level
which
may
be
present
in
PCP
formulations
during
occupational
exposure.

2
1.0
EXECUTIVE
SUMMARY
Preface
As
part
of
the
Pentachlorophenol
(
PCP)
Reregistration
Eligibility
Decision
(
RED)
Document
prepared
by
the
U.
S.
EPA,
the
Occupational
Exposure
Chapter
presented
herein
focuses
on
the
contribution
of
the
hexachlorobenzene
(
HCB)
microcontaminant
contained
in
PCP
to
the
overall
exposure
attributed
to
use
of
PCP
wood
preservative
products.
HCB
is
a
recognized
impurity
in
manufactured
PCP
technical
source
products
from
which
wood
preservatives
are
formulated.
The
maximum
level
of
HCB
that
is
allowed
in
formulations
of
PCP
is
75
ppm.
Therefore,
the
exposure
and
risk
assessments
supporting
this
document
assume
that
HCB
is
present
at
levels
not
exceeding
75
ppm1
(
75
ng/
mg)
in
PCP
wood
preservative
formulations
and
PCP­
treated
wood.

This
HCB
Exposure
Chapter
supplements
the
PCP
RED
Human
Exposure
Chapter
developed
by
the
Agency
(
S.
Mostaghimi,
D246536)
and
is
a
companion
to
the
assessment
also
conducted
on
the
Dioxin/
Furan
microcontaminants
(
CDDs/
CDFs)
of
PCP
(
D.
Aviado,
D272980,
D272983)
for
the
reregistration
eligibility
of
PCP.

This
chapter
utilizes
most
of
the
same
assumptions/
approaches
and
worker
exposure
study
data
(
i.
e.,
biomonitoring
data
from
studies
done
on
pressure
treatment
plant
workers
and
utility
2
Refer
to
the
PCP
RED
Human
Exposure
Chapter,
Section
4.2,
for
a
detailed
overview
of
the
handler
and
postapplication
exposure
study
data
and
assumptions
used
to
develop
the
occupational
scenarios/
assessments.

3
linemen)
found
in
the
PCP
RED
Human
Exposure
Chapter
to
present
exposures
to
HCB
in
occupational
settings.
2
In
addition,
the
occupational
exposure
scenarios
assessed
are
consistent
with
those
detailed
in
the
PCP
RED
and
CDDs/
CDFs
Human
Exposure
Chapters
so
that
a
direct
comparison
can
be
made
between
exposures/
risks
attributed
to
PCP
formulations
and
those
resulting
from
contact
with
the
microcontaminants
of
PCP.

The
HCB
Exposure
Chapter
addresses
potential
exposures
and
risks
to
workers
who
may
be
exposed
occupationally
to
HCB
as
a
microcontaminant
of
PCP.
Occupational
exposure
may
occur
to
pressure
treatment
plant
workers
as:
(
1)
handlers
(
mixers,
loaders,
applicators)
of
PCP
product
concentrates
and
treatment
solutions;
and
(
2)
individuals
who
are
involved
in
postapplication
handling
of
PCP­
treated
wood
products
at
pressure
treatment
sites
or
reentry
activities
requiring
work
in
areas
where
pressure
treatment
occurs
and/
or
work
with
equipment
used
for
pressure
treatment.

Exposures
were
assessed
for
treatment
plant
workers
using
absorbed
PCP
doses
derived
from
biomonitoring
data
from
a
study
submitted
by
the
Pentachlorophenol
Task
Force
entitled
Inhalation
Dosimetry
and
Biomonitoring
Assessment
of
Worker
Exposure
to
Pentachlorophenol
During
Pressure­
Treatment
of
Lumber
(
PTF,
1999).
The
absorbed
doses
were
used
to
characterize
combined
dermal,
inhalation
and
incidental
oral
exposure.

In
addition
to
the
occupational
postapplication
scenarios
developed
for
pressure
treatment
plant
workers,
a
postapplication
scenario
was
included
to
assess
exposures
to
utility
pole
installers
(
electrical
utility
linemen)
involved
with
installation
of
PCP­
treated
poles
and/
or
in
contact
with
inservice
poles.
Biomonitoring
data
from
a
worker
exposure
study
on
utility
linemen
entitled
Occupational
Exposure
of
Electrical
Utility
Linemen
to
Pentachlorophenol
(
Thind
et
al.,
1991)
were
used
to
characterize
chronic
or
long­
term
exposure
from
absorbed
doses
of
HCB
in
PCP
based
on
measured
PCP
residue
levels
in
monitored
worker
urine
samples.
HCB
is
relatively
non­
volatile
(
1.1
x
10­
5
mm
Hg
at
25

C)
and
assumed
to
be
of
negligible
inhalation
concern
from
PCP­
treated
wood
used
in
outdoor
environments.
Therefore,
it
was
assumed
that
the
absorbed
dermal
doses
best
represent
postapplication
dermal
exposure
for
utility
workers.

The
absorbed
PCP
doses
calculated
for
occupational
exposure
scenarios
were
multiplied
by
the
maximum
level
of
HCB
allowed
in
a
given
manufactured
batch
of
PCP
(
i.
e.,
75
ppm
or
75
ng/
mg)
3
Refer
to
the
PCP
RED
Human
Exposure
Chapter
for
full
details
on
scenario
development
and
calculation
of
PCP
absorbed
doses.

4
then
adjusted
by
the
difference
in
dermal
absorption
between
PCP
(
i.
e.,
40%)
and
HCB
(
i.
e.,
26.46%)

(
i.
e.,
.2646/.
40
=.
66)
to
develop
exposure
doses
for
HCB
in
PCP.

It
should
be
noted
that
residential
postapplication
exposure
to
HCB
is
unlikely
to
occur
to
adult
and
child
populations
as
a
result
of
contact
with
PCP­
treated
wood
products
or
through
child
contact
with
PCP­
contaminated
soil
via
the
dermal
and
oral
route
(
i.
e.,
incidental
ingestion
of
HCB
residues
through
hand­
to­
mouth
contact
and
direct
soil
ingestion).
The
Agency
has
not
conducted
an
exposure
and
risk
assessment
for
residential
populations
due
to
the
following
consideration:

°
The
opportunity
for
residential
consumer
contact
is
limited
since
PCP­
treated
wood
is
not
sold
to
the
general
public.
Rather
it
is
predominantly
marketed
for
commercial
installations
as
utility
poles.
Where
utility
poles
are
installed
on
home/
school
or
other
residential
sites,

child
contact
via
the
dermal
or
oral
routes
is
not
anticipated
since
play
activities
with
or
around
these
pole
structures
would
not
normally
occur
and
any
incidental
exposure
would
therefore
be
negligible.

Handlers
Occupational
handler
exposure
scenarios
for
HCB
were
identified
and
developed
as
per
those
developed
for
exposure
to
PCP
in
pressure
treatment
plants.
3
Occupational
handler
scenarios
involve
exposures
to
pressure
treatment
operators
and
assistants
handling
PCP
product
concentrates
and
treatment
solutions
during
the
pressure
treatment
process
and
encompass
related
work
tasks
including
handling
charge
leads,
unwrapping
block
penta,
and
opening
and
closing
cylinder
doors.
Based
on
absorbed
doses
derived
from
the
registrant­
submitted
biomonitoring
study
(
PTF,
1999),
the
maximum
doses
were
used
to
estimate
short­
and
intermediate­
term
PCP
exposures
and
the
average
dose
was
used
to
estimate
long­
term
PCP
exposure.
These
PCP
exposures
were
converted
into
HCB
equivalents
using
the
maximum
level
of
HCB
allowed
in
a
given
batch
of
PCP
and
adjusting
by
the
difference
in
dermal
absorption
between
PCP
and
HCB.
5
Non­
Cancer
Exposure
Risk
The
Agency's
level
of
concern
for
absorbed
short­,
intermediate­
and
long­
term
exposures
for
HCB
are
MOE's
that
are
less
than
100.
MOEs
for
all
scenarios
evaluated
are
presented
in
Table
3
of
this
report.
None
of
the
occupational
handler
scenarios
assessed
exceeded
the
Agency's
level
of
concern
for
non­
cancer
aggregate
risks.

Cancer
Risk
A
carcinogenic
endpoint
related
to
lifetime
average
doses
of
HCB
has
been
identified.
A
cancer
risk
greater
than
E­
6
is
to
be
mitigated
and
risks
greater
than
E­
4
are
generally
considered
to
be
of
concern
(
U.
S.
EPA,
1996a).
The
Agency
will
seeks
ways
to
mitigate
any
risks,
to
the
extent
that
it
is
practical
and
economically
feasible,
to
lower
the
risks
to
E­
6
or
less.
None
of
the
occupational
handler
scenarios
assessed
exceeded
the
Agency's
level
of
concern
(
i.
e.,
E­
4)
for
cancer
risks
and
were
in
the
E­
8
to
E­
7
range
(
See
Table
3).

Postapplication
Occupational
postapplication
exposure
scenarios
for
HCB
were
identified
primarily
for
pressure
treatment
workers.
In
addition,
a
scenario
was
included
for
utility
linemen.
Postapplication
or
reentry
exposures
in
treatment
plants
may
occur
after
the
wood
has
been
pressure
treated.

Individuals
may
be
exposed
to
HCB
through
contact
with
PCP­
treated
wood
products
or
equipment
used
to
pressure
treat
wood.
Exposure
activities
include
sampling
PCP
retort
mixtures,
moving
trams
and
treated
poles,
boring
wood
cores,
and
performing
cleanup
activities
on
drip
pads.
The
industrial
workers
involved
in
postapplication
activities
for
this
assessment
include
the
test
borer,
loader
operator,
and
general
helper
(
as
representative
of
pressure
treatment
plant
workers),
and
the
utility
linemen
involved
with
postapplication
handling
of
PCP­
treated
utility
poles.
The
maximum
doses
for
the
pressure
treatment
operator
and
treatment
assistant
were
used
to
estimate
short­
and
intermediateterm
exposures
to
PCP
and
the
average
dose
was
used
to
estimate
long­
term
exposure
to
PCP.

These
PCP
exposures
were
converted
into
HCB
equivalents
using
the
maximum
level
of
HCB
allowed
in
a
given
batch
of
PCP
and
adjusting
by
the
difference
in
dermal
absorption
between
PCP
and
HCB.
6
Non­
Cancer
Exposure
Risk
The
Agency
has
determined
that
Margins
of
Exposure
(
MOEs)
of
100
or
greater
are
appropriate
for
acceptable
risks
from
absorbed
short­,
intermediate­
and
long­
term
exposures
to
HCB.
MOEs
for
all
scenarios
evaluated
are
presented
in
Table
5
of
this
report.
None
of
the
occupational
postapplication
scenarios
assessed
exceeded
the
Agency's
level
of
concern
for
noncancer
aggregate
risks.

Cancer
Risk
A
carcinogenic
endpoint
related
to
lifetime
average
doses
of
HCB
has
been
identified.
A
cancer
risk
greater
than
E­
6
is
to
be
mitigated
and
risks
greater
than
E­
4
are
generally
considered
to
be
of
concern
(
U.
S.
EPA,
1996a).
The
Agency
will
seeks
ways
to
mitigate
any
risks,
to
the
extent
that
it
is
practical
and
economically
feasible,
to
lower
the
risks
to
E­
6
or
less.
None
of
the
occupational
postapplication
scenarios
assessed
exceeded
the
Agency's
level
of
concern
(
i.
e.,
E­
4)

for
cancer
risks
and
were
within
E­
8
(
See
Table
5).
7
2.0
OCCUPATIONAL
EXPOSURE
AND
RISK
ASSESSMENT
A.
Toxicological
Considerations
(
1)
Criteria
for
Conducting
Exposure
Assessments
An
occupational
exposure
risk
assessment
is
required
for
an
active
ingredient
if
(
1)
certain
toxicological
criteria
are
triggered
and
(
2)
there
is
potential
exposure
to
handlers
(
i.
e.,
mixers,

loaders,
applicators,
etc.)
during
use,
or
to
persons
entering
treated
sites
after
application
is
complete,

or
in
contact
with
the
pesticide­
treated
articles
(
i.
e.,
postapplication
contact
with
treated
wood).
For
the
hexachlorobenzene
(
HCB)
impurity
contained
in
pentachlorophenol,
both
criteria
are
met.

The
toxicological
data
base
for
HCB
is
adequate
and
will
support
the
occupational
exposure
and
risk
assessment
to
be
conducted
as
part
of
the
reregistration
eligibility
of
PCP.
A
detailed
toxicity
profile
and
dose­
response
assessment
for
HCB
is
presented
in
a
hazard
characterization
document
for
this
compound
prepared
in
support
of
the
PCP
RED
(
T.
McMahon,
D272977)
(
U.
S.
EPA,
2003).

(
2)
Summary
of
Toxicity
Concerns
Relating
to
Occupational
Non­
Dietary
Exposures
The
manufacturing
process
of
PCP
produces
several
known
contaminants
of
toxicological
concern
including
HCB.
The
exposure
and
risk
assessment
for
HCB
in
PCP
will
focus
on
the
use
of
PCP
as
a
wood
preservative
pesticide
and
the
potential
occupational
exposure
to
HCB
through
this
use.
This
assessment
includes
only
occupational
non­
dietary
exposures,
as
there
are
no
dietary
or
drinking
water
concerns
based
on
the
use
patterns
for
PCP
as
a
wood
preservative
antimicrobial
pesticide.

The
OPP
has
not
requested
specific
toxicology
studies
on
hexachlorobenzene
as
this
chemical
is
not
under
the
regulatory
authority
of
OPP,
but
exposure
assessments
for
HCB
as
a
microcontaminant
have
been
conducted
by
OPP's
Health
Effects
Division
to
support
certain
REDs.

Also,
there
are
available
scientific
data
in
the
peer
reviewed
literature
which
appear
to
adequately
characterize
the
toxicity
of
HCB,
especially
a
recent
publication
by
the
Agency
for
Toxic
Substances
and
Disease
Registry
(
ATSDR).
In
addition,
the
U.
S.
EPA's
Office
of
Water
(
OW)
has
published
a
health
advisory
document
on
hexachlorobenzene
which
contains
numerous
references
to
the
scientific
literature
and
which
have
been
peer
reviewed
by
OW
prior
to
inclusion
in
the
health
advisory.
Thus,
hazard
characterization
relies
primarily
upon
previous
work
conducted
by
the
OPP's
Health
Effects
Division
as
well
as
work
by
ATSDR
and
OW.
8
The
toxicology
of
hexachlorobenzene
is
discussed
in
detail
within
the
Agency's
1991
publication,
Drinking
Water
Criteria
Document
for
Hexachlorobenzene
(
U.
S.
EPA,
1991)
and
the
ATSDR
Toxicological
Profile
for
Hexachlorobenzene
(
ATSDR,
2002).
Both
assessments
characterize
the
acute
toxicity
of
HCB
as
low,
with
oral
LD50
values
in
the
range
of
3500­
10,000
mg/
kg
in
rats,
and
other
data
citing
1700
mg/
kg
in
rats,
2600
mg/
kg
in
rabbits,
and
4000
mg/
kg
in
mice.

The
Agency
has
classified
HCB
as
a
B2
(
probable
human)
carcinogen,
based
on
data
sets
which
showed
induction
of
tumors
of
the
thyroid,
liver,
and
kidney
in
three
rodent
species
(
U.
S.
EPA,

IRIS,
1996b).
In
the
IRIS
database,
the
oral
cancer
slope
factor
(
CSF)
was
1.6
(
mg/
kg/
day)­
1
calculated
based
on
hepatocellular
carcinomas
in
female
Sprague­
Dawley
rats
using
a
2/
3'
s
animal
to
human
scaling
factor.
The
Office
of
Pesticide
Programs,
Health
Effects
Division,
in
a
memorandum
dated
June
21,
1995
(
memo
from
William
Burnam,
Chief,
Science
Analysis
Branch,
to
Beth
Doyle,

Science
Analysis
Branch)
acknowledged
that
the
Agency's
interspecies
scaling
factor
of
3/
4
should
be
used
to
modify
the
existing
slope
factor
value
for
hexachlorobenzene,
and,
based
on
this
modification,
stated
that
a
CSF
of
1.02
(
mg/
kg/
day)­
1
should
be
used
for
calculation
of
cancer
risk
of
HCB.

(
a)
Summary
of
Toxicological
Endpoint
Selection
The
Antimicrobials
Division,
Office
of
Pesticide
Programs,
has
selected
toxicity
endpoints
for
HCB
for
use
in
exposure
and
risk
assessments.
These
endpoints
were
selected
using
the
available
scientific
literature
on
HCB
(
U.
S.
EPA,
2003).
A
summary
of
these
endpoints
is
shown
below
in
Table
1.
9
Table
1.
Toxicological
Endpoints
Selected
for
Assessing
Occupational
Risks
to
HCB
Exposure
Scenario
Dose
Endpoint
Study
Target
MOE
Incidental
Oral:

Short­
Term
NOAEL=
40
mg/
kg/
day
body
weight
loss,

hyperesthesia,
tremors,

convulsions
in
maternal
rats
at
60
mg/
kg/
day.
Developmental
Toxicity­
Rat
(
Khera,
1974)
100
Incidental
Oral:

Intermediate­
Term
NOAEL=
0.5
mg/
kg/
day
increased
incidence
of
liver
porphyrin
levels
in
female
rats
at
2
mg/
kg/
day
15
Week
Oral
Toxicity­
Rat
(
Kuiper­
Goodman
et
al,
1977)
100
Dermal:

Short­
Term
Oral
NOAEL
=
40
mg/
kg/
day
body
weight
loss,

hyperesthesia,
tremors,

convulsions
in
maternal
rats
at
60
mg/
kg/
day.
Developmental
Toxicity­
Rat
(
Khera,
1974)
100
Dermal:

Intermediate­
Term
Oral
NOAEL
=
0.5
mg/
kg/
day
increased
incidence
of
liver
porphyrin
levels
in
female
rats
at
2
mg/
kg/
day
15
Week
Oral
Toxicity­
Rat
(
Kuiper­
Goodman
et
al,
1977)
100
Dermal:

Long­
Term
Oral
NOAEL
=
0.08
mg/
kg/
day
hepatic
centrilobular
basophilic
chromogenesis
at
0.29
mg/
kg/
day
Chronic
Toxicity
­

Rat
(
Arnold
et
al.,

1985)
100
Inhalation:

Short­,
Intermediate­,

and
Long­
Term
No
route­
specific
endpoints
are
available
for
HCB.
Therefore,
in
accordance
with
Agency
policy,
oral
endpoints
and
route
extrapolation
are
employed
to
estimate
inhalation
risks
as
needed.
1000
Oral
Cancer
Slope
Factor
(
CSF)
Q*=
1.02
(
mg/
kg/
day)­
1
B2
(
probable
human
carcinogen)
based
on
data
showing
significant
increases
in
liver
and
renal
tumor
incidences
in
hamsters
and
rats.

Dermal
Absorption
26.46%
Dermal
absorption
study
in
rats
(
MRID
42651501).
Found
in
the
Agency's
RED
document
for
DCPA,
November
1998,
page
14.

°
Recommended
MOEs
of
100
are
based
on
applied
uncertainty
factors
used
to
account
for
inter­
species
extrapolation
(
10x)
and
intra­
species
variability
(
10x).

°
Since
oral
endpoints
were
selected
for
HCB
risk
assessments,
and
the
occupational
exposures
are
attributed
primarily
to
the
dermal
route,
a
dermal
absorption
value
of
26.46
%
was
recommended
for
use
in
route­

toroute
extrapolations.
A
back
calculation
was
performed
to
convert
absorbed
doses
of
PCP
into
equivalent
HCB
dermal
doses:
Absorbed
short­,
intermediate­,
and
long­
term
PCP
doses
were
multiplied
by
the
maximum
allowed
amount
of
HCB
per
batch
of
PCP
(
75
ppm
or
75
ng/
mg)
then
adjusted
by
multiplying
by
the
difference
in
dermal
absorption
between
PCP
(
i.
e.,
40%)(
U.
S.
EPA,
1997a)
and
HCB
(
i.
e.,
26.46%)
(
i.
e.,

.2646/.
40
=.
66).
10
A.
Occupational
Exposures
and
Risks
(
1)
Handler
Exposures
and
Risks
EPA
has
determined
that
there
are
potential
exposures
to
HCB
for
mixers,
loaders,

applicators,
and
other
handlers
during
typical
pressure
treatment
use­
patterns
associated
with
the
restricted
use
of
PCP
by
certified
applicators
in
industrial
settings.

(
a)
Background
HCB
is
not
currently
manufactured
as
a
commercial
end
use
product
in
the
United
States,
and
evidence
indicates
that
it
has
not
been
commercially
produced
(
ATSDR,
2002).
However,
during
production
of
PCP,
workers
may
become
exposed
to
HCB
contaminants
that
are
formed
as
a
byproduct
or
impurity
during
the
manufacturing
process.
In
addition,
commercially
available
PCP
solutions
used
in
pressure
treatment
operations
may
also
contain
HCB
impurities.
The
conversion
of
PCP
to
HCB
during
manufacturing
is
described
in
the
Product
Chemistry
Chapter
supporting
the
PCP
RED.
The
Agency
is
conducting
a
separate
assessment
for
HCB
due
to
concerns
that
HCB
contaminants
may
trigger
non­
cancer
and
cancer
risks
in
addition
to
those
posed
by
PCP
itself.
(
U.
S.

EPA,
1984).

As
a
result
of
a
settlement
agreement
between
the
EPA
and
chemical
producers
of
PCP,
the
producers
agreed
to
reduce
HCB
contamination
in
pentachlorophenol
to
no
more
than
75
ppm
(
75
ng/
mg)
(
ATSDR,
2002).
Manufacturing
monitoring
data
(
i.
e.,
surveillance
sampling
data)
submitted
to
U.
S.
EPA
indicate
that
measured
HCB
microcontaminant
levels
in
PCP
production
batch
samples
may
vary
from
below
50
ppm
to
above
75
ppm.
The
Agency
conducted
a
cursory
review
of
surveillance
data
on
PCP
for
years
2000
and
2001
to
determine
if
monitored
HCB
contaminant
levels
were
consistently
below
the
75
ppm
limit
set
in
the
RPAR
agreement.
Data
showed
that
the
average
batch
from
industry
random
sampling
contained
close
to
60
ppm
HCB.
In
addition,
several
outlier
batches
were
produced
with
HCB
levels
exceeding
75
ppm
which
required
blending
with
other
batches
to
reach
acceptable
levels
(
at
or
below
75
ppm)
for
shipment.
Therefore,
the
Agency
assessment
used
75
ppm
(
75
ng/
mg)
as
a
realistic
maximum
contaminant
level
which
may
be
present
in
PCP
formulations
during
occupational
exposure.

General
population
and
occupational
information
exists
on
exposure
to
HCB;
however,
there
are
very
limited
data
from
these
studies
that
deal
with
HCB
exposures
associated
directly
from
handling
PCP.
Therefore,
in
lieu
of
data,
the
Antimicrobials
Division
developed
an
approach
for
estimating
HCB
exposure
from
PCP;
Using
PCP
exposures
developed
in
the
existing
11
Pentachlorophenol
RED
Chapter,
HCB
exposures
were
derived
assuming
the
exposure
attributed
to
HCB
was
no
more
than
0.0075%
of
the
PCP
dose
(
i.
e.,
the
maximum
level
of
HCB
contaminant
allowed
in
a
given
manufactured
batch
of
PCP
as
75
ppm
or
75
ng/
mg).
Adjustments
for
the
difference
in
dermal
absorption
between
PCP
and
HCB
were
applied
to
calculate
the
HCB
absorbed
doses.

For
this
HCB
exposure
chapter,
EPA
will
only
assess
handler
and
postapplication
exposure
to
HCB
attributed
to
the
use
of
registered
PCP
wood
preservative
products.
Exposures
to
PCP
during
the
manufacturing
or
production
of
PCP
technical
ingredients
are
currently
regulated
under
the
Occupational
Safety
and
Health
Administration
(
OSHA).

(
b)
Occupational
Handlers
Handler
exposure
to
PCP
wood
preservatives,
as
product
concentrates
and
treatment
solutions,
results
in
potential
exposure
to
HCB
during
handler
operations
in
pressure
treatment
plants.
The
following
handler
scenarios
for
pressure
treatment
uses
have
been
identified
from
the
PCP
biomonitoring
and
inhalation
study
submitted
by
the
Pentachlorophenol
Task
Force
entitled
Inhalation
Dosimetry
and
Biomonitoring
Assessment
of
Worker
Exposure
to
Pentachlorophenol
During
Pressure­
Treatment
of
Lumber
(
PTF,
1999),
further
detailed
in
the
PCP
RED
Human
Exposure
Chapter:

(
1a)
Applying
crystalline
technical
grade
product­
Pressure
Treatment
Operator;

(
1b)
Applying
liquid
formulation­
Pressure
Treatment
Operator;

(
2a)
Applying
crystalline
technical
grade
product­
Pressure
Treatment
Assistant;
and
(
2b)
Applying
liquid
formulation­
Pressure
Treatment
Assistant.

(
2)
Handler
Risk
Assessment
and
Characterization
(
a)
Handler
Non­
Cancer
and
Cancer
Risk
Calculations
Table
2
provides
the
non­
cancer
absorbed
short­,
intermediate­,
and
long­
term
dose
estimates
as
well
as
the
lifetime
average
daily
dose
(
LADD)
estimates
used
for
the
cancer
assessment,
for
the
occupational
handler
scenarios
for
which
data
are
available
(
e.
g.
liquid
or
solid
block
penta).

(
i)
Total
Aggregated
Non­
Cancer
Dose
Calculations
12
HCB
Absorbed
Dose

PCP
Absorbed
Dose
mg
ai
kg/
day
x
PCP/
HCB
Factor
75
ng/
mg
x
1E

6
CF
mg
ng
x
HCB
ABS
Factor
PCP
ABS
Factor
MOE

NOAEL
(
mg/
kg/
day)
HCB
Absorbed
Dose
(
mg/
kg/
day)
Dermal
dosimetry
data
were
not
available
from
the
registrant;
therefore,
absorbed
doses
were
derived
from
the
biomonitoring
study
data
(
PTF,
1999).
Biomonitoring
absorbed
doses
were
used
to
represent
a
total
aggregated
exposure
for
dermal,
inhalation,
and
incidental
ingestion
for
pressure
treatment
workers.
It
is
assumed
that
exposure
is
primarily
attributed
to
the
dermal
route
(
i.
e.,

concurrent
inhalation
sampling
showed
nearly
all
non­
detects
on
inhalation
dosimeters).
Details
on
how
PCP
doses
were
calculated
are
presented
in
the
PCP
RED
Human
Exposure
Chapter,
Section
4.2.

Since
derived
HCB
doses
used
in
the
assessment
are
assumed
to
represent
dermal
exposure,

a
back
calculation
was
performed
to
convert
absorbed
doses
of
PCP
from
the
biomonitoring
study
into
equivalent
HCB
dermal
doses.
Absorbed
short­,
intermediate­,
and
long­
term
PCP
doses
were
multiplied
by
the
maximum
level
of
HCB
allowed
in
a
given
manufactured
batch
of
PCP
(
i.
e.,
75
ng/
mg)
then
adjusted
by
the
difference
in
dermal
absorption
(
ABS)
between
PCP
(
i.
e.,
40%)
and
HCB
(
i.
e.,
26.46%)
(
i.
e.,
.2646/.
40
=.
66)
to
develop
exposure
doses
for
HCB
in
PCP:

The
HCB
doses
are
presented
in
bold
face
under
non­
cancer
aggregate
doses
in
Table
2.

These
doses
are
then
used
to
calculate
MOEs
presented
in
Table
3.
The
short­
term
MOE
is
calculated
using
a
short­
term
oral
NOAEL
of
40
mg/
kg/
day;
the
intermediate­
term
MOE
is
derived
using
an
intermediate­
term
oral
NOAEL
of
0.5
mg/
kg/
day;
and
the
long­
term
MOE
is
based
on
a
long­
term
oral
NOAEL
of
0.08
mg/
kg/
day.

The
following
formula
was
used
to
calculate
the
MOEs
(
ii)
Cancer
Risk
Calculations
The
LADDs
for
the
HCB
cancer
risk
assessment
are
derived
from
the
absorbed
long­
term
doses
for
PCP
adjusted
by
the
75
ng/
mg
PCB/
HCB
factor
to
yield
absorbed
long­
term
doses
for
HCB,
which
are
then
amortized
over
a
lifetime.
Exposure
frequency
is
assumed
to
be
250
working
days
per
year
(
i.
e.,
five
days
per
week,
50
days
per
year).
This
is
a
standard
Agency
assumption
for
13
PCP
Absorbed
LongTerm
Dose
mg
ai
kg/
day

PCP
Urinary
Conc.
µ
g
L
x
CF
mg
µ
g
x
Urinary
Volume
(
L)
x
1
Body
Weight
(
kg)

HCB
Absorbed
LongTerm
Dose

PCP
Absorbed
LongTerm
Dose
mg
ai
kg/
day
x
PCP/
HCB
Factor
75
ng/
mg
x
1E

6
CF
mg
ng
x
HCB
ABS
Factor
PCP
ABS
Factor
HCB
LADD
mg
ai
kg/
day

HCB
Absorbed
LongTerm
Dose
(
mg/
kg/
day)
x
Exposure
Frequency
(
days/
yr)
x
Exposure
Duration
(
yrs)
365
days/
yr
x
Lifetime
(
yrs)

Risk

HCB
LADD
mg
ai
kg/
day
x
Cancer
Slope
Factor
1
(
mg/
kg/
day)
days
worked
per
year.
Exposure
duration
was
assumed
to
be
40
years
and
is
a
conservative
standard
value
used
by
OPP
to
represent
a
working
lifetime.
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
(
U.
S.

EPA,
1997b)
and
typically
used
in
OPP
assessments
as
a
standard
value.

The
following
formula
was
used
to
calculate
the
PCP
absorbed
long­
term
dose
as
presented
in
the
PCP
RED
Human
Exposure
Chapter:

The
PCP
absorbed
long­
term
dose
was
then
multiplied
by
the
PCP/
HCB
factor
of
75
ng/
mg,

and
adjusted
by
the
difference
in
dermal
absorption
between
PCP
(
i.
e.,
40%)
and
HCB
(
i.
e.,
26.46%)

(
i.
e.,
.2646/.
40
=.
66)
to
develop
an
HCB
absorbed
long­
term
dose:

The
HCB
LADD
is
then
calculated
from
the
absorbed
long­
term
dose
which
is
amortized
over
a
lifetime,
as
follows:

Cancer
risk
was
calculated
by
multiplying
the
HCB
LADD
by
the
cancer
slope
factor
of
1.02
(
mg/
kg/
day)
­
1
using
the
following
formula:

(
b)
Handler
Non­
Cancer
Risks
from
Exposures
to
HCB
in
PCP
14
Short­
term,
intermediate­
term,
and
long­
term
exposures
have
been
identified.
The
Agency's
level
of
concern
for
short­,
intermediate­
and
long­
term
exposures
to
HCB
are
MOE's
that
are
less
than
100.
MOEs
for
all
scenarios
evaluated
are
presented
in
Table
3
of
this
report.
All
the
occupational
handler
scenarios
assessed
did
not
exceed
the
Agency's
level
of
concern
for
non­
cancer
aggregate
exposures.

(
c)
Handler
Cancer
Risks
from
Absorbed
Doses
of
HCB
in
PCP
A
carcinogenic
endpoint
related
to
lifetime
average
absorbed
doses
of
HCB
has
been
identified.
A
cancer
risk
greater
than
E­
6
is
to
be
mitigated
and
risks
greater
than
E­
4
are
generally
considered
to
be
of
concern
(
U.
S.
EPA,
1996a).
The
Agency
will
seeks
ways
to
mitigate
any
risks,

to
the
extent
that
it
is
practical
and
economically
feasible,
to
lower
the
risks
to
E­
6
or
less.
None
of
the
occupational
handler
scenarios
assessed
exceeded
the
Agency's
level
of
concern
(
i.
e.,
E­
4)
for
cancer
aggregate
risks
and
were
in
the
E­
8
to
E­
7
range
(
See
Table
3).
15
Table
2.
Occupational
Handler­
Calculation
of
Non­
cancer
and
Cancer
Exposure
Doses
for
HCB
in
PCP
Exposure
Scenarios
PCP/
HCB
Factor
a
(
ng/
mg)
NON­
CANCER
AGGREGATE
EXPOSURE
DOSES
CANCER
AGGREGATE
EXPOSURE
DOSES
PCP
Adjusted
Absorbed
Short­
Term
Dose
b
(
mg/
kg/
day)
HCB
Absorbed
Short­
Term
Dose
c
(
ng/
kg/
day)
PCP
Absorbed
Intermediate­

Term
Dose
d
(
mg/
kg/
day)
HCB
Absorbed
Intermediate­

Term
Dose
c
(
ng/
kg/
day)
PCP
Absorbed
Long­
Term
Dose
e
(
mg/
kg/
day)
HCB
Absorbed
Long­
Term
Dose
c
(
ng/
kg/
day)
HCB
Lifetime
Average
Daily
Dose
f
(
ng/
kg/
day)

(
1a)
Mixing/
Loading/
Applying
Crystalline
Grade
Product
­

Pressure
Treatment
Operator
75
0.021
1.04
0.007
0.35
0.0031
0.15
0.055
(
1b)
Mixing/
Loading/
Applying
Liquid
Formulation
­

Pressure
Treatment
Operator
75
0.036
1.78
0.012
0.59
0.0065
0.32
0.12
(
2a)
Mixing/
Loading/
Applying
Crystalline
Grade
Product
­

Pressure
Treatment
Assistant
75
0.054
2.67
0.018
0.89
0.012
0.59
0.22
(
2b)
Mixing/
Loading/
Applying
Liquid
Formulation
­

Pressure
Treatment
Assistant
75
0.075
3.71
0.025
1.24
0.019
0.94
0.34
a
PCP/
HCB
Factor
­
HCB
concentration
in
PCP
is
75
ng
per
mg
PCP
based
on
the
allowed
concentration
limit
of
75
ppm
HCB
per
batch.

b
Adjusted
maximum
PCP
dose
by
a
factor
of
3
to
correct
for
the
cumulative
effects
of
an
8­
day
steady­
state
excretion
in
a
3­
day
PCP
study.

c
HCB
dose
=
PCP/
HCB
Factor
(
ng/
mg)
x
[
HCB
ABS
Factor
(.
2646)/
PCP
ABS
Factor
(.
40)]
x
PCP
dose
(
mg/
kg/
day).

d
Based
on
maximum
absorbed
doses
over
3
days.
Based
on
PCP
biomonitoring
data,
absorbed
doses
(
i.
e.,
representing
combined
dermal,
inhalation
and
incidental
oral
exposure)
were
assumed
to
be
attributed
primarily
to
exposure
via
the
dermal
route
since
the
majority
of
the
inhalation
monitoring
data
were
below
the
limit
of
quantitation.

e
Based
on
average
absorbed
doses
over
3
days.
Based
on
PCP
biomonitoring
data,
absorbed
doses
(
i.
e.,
representing
combined
dermal,
inhalation
and
incidental
oral
exposure)
were
assumed
to
be
attributed
primarily
to
exposure
via
the
dermal
route
since
the
majority
of
the
inhalation
monitoring
data
were
below
the
limit
of
quantitation..

f
HCB
Lifetime
Average
Daily
Dose
(
LADD)
=
[
HCB
absorbed
long­
term
dose
(
as
representing
long­
term
dermal
dose)
x
exposure
frequency
(
i.
e.,
250
working
days)
x
exposure
duration
(
i.
e.,
40
working
years
in
a
lifetime)]
/
[(
365
days/
yr
x
lifetime
(
i.
e.,
75
yrs)].
16
Table
3.
Occupational
Handler­
Non­
cancer
and
Cancer
Exposure
Doses/
Risks
for
HCB
in
PCP
Exposure
Scenarios
NON­
CANCER
AGGREGATE
EXPOSURE
DOSES
&
MOEs
CANCER
AGGREGATE
EXPOSURE
DOSES/
RISKS
HCB
Absorbed
Short­
Term
Dosea
(
mg/
kg/
day)
Short­
Term
MOEb
HCB
Absorbed
Intermediate­

Term
Dosea
(
mg/
kg/
day)
Intermediate­

Term
MOEc
HCB
Absorbed
Long­
Term
Dosea
(
mg/
kg/
day)
Long­
Term
MOEd
HCB
Lifetime
Average
Daily
Dosea
(
mg/
kg/
day)
Cancer
Risk
e
(
1a)
Mixing/
Loading/
Applying
Crystalline
Grade
Product
­
Pressure
Treatment
Operator
1.04E­
06
3.8E+
07
3.5E­
07
1.4E+
06
1.5E­
07
5.3E+
05
5.5E­
08
5.6E­
08
(
1b)
Mixing/
Loading/
Applying
Liquid
Formulation
­
Pressure
Treatment
Operator
1.78E­
06
2.2E+
07
5.9E­
07
8.5E+
05
3.2E­
07
2.5E+
05
1.2E­
07
1.2E­
07
(
2a)
Mixing/
Loading/
Applying
Crystalline
Grade
Product
­
Pressure
Treatment
Assistant
2.67E­
06
1.5E+
07
8.9E­
07
5.6E+
05
5.9E­
07
1.4E+
05
2.2E­
07
2.2E­
07
(
2b)
Mixing/
Loading/
Applying
Liquid
Formulation
­
Pressure
Treatment
Assistant
3.71E­
06
1.1E+
07
1.24E­
06
4.0E+
05
9.4E­
07
8.5E+
04
3.4E­
07
3.5E­
07
a
HCB
Doses
presented
above
have
been
converted
to
mg/
kg/
day
in
order
to
calculate
MOEs.
[
Doses
from
Table
2
in
ng/
kg/
day
x
1E­
6
(.
000001)
mg/
ng
=
mg/
kg/
day].

NON­
CANCER
AGGREGATE:

b
Short­
term
MOE=
Short­
term
oral
NOAEL
(
HCB=
40
mg/
kg/
day)/
Absorbed
Short­
term
daily
dose
(
mg/
kg/
day).
Target
MOE
=
100.

c
Intermediate­
term
MOE=
Intermediate­
term
oral
NOAEL(
HCB=
0.5
mg/
kg/
day)/
Absorbed
Intermediate­
term
daily
dose
(
mg/
kg/
day).
Target
MOE
=
100.

d
Long­
term
MOE=
Long­
term
oral
NOAEL(
HCB=
0.08
mg/
kg/
day)/
Absorbed
Long­
term
daily
dose
(
mg/
kg/
day).
Target
MOE
=
100.

CANCER
AGGREGATE:

e
Cancer
Risk=
HCB
LADD
(
mg/
kg/
day)
x
Cancer
Slope
Factor
(
Q*
=
1.02
mg/
kg/
day­
1).
17
(
3)
Postapplication
Exposures
and
Risks
The
Agency
is
concerned
about
potential
postapplication
exposures
to
HCB
impurities
in
PCP.
The
Agency
has
determined
that
there
are
potential
exposure
concerns
relating
to
postapplication
exposure
to
individuals
following
pentachlorophenol
applications
in
pressure
treatment
plants
and
for
utility
linemen
engaged
in
such
work
tasks
as
installation
of
PCP­
treated
utility
poles.
The
potential
individual
postapplication
exposures
are
outlined
below.

(
a)
Occupational
Postapplication
Exposure
(
i)
Pressure
Treatment
Plant
Workers
In
the
pressure
treatment
industry,
postapplication
exposure
may
result
from
typical
work
tasks
associated
with
removing
wet
treated
wood
from
treatment
cylinders,
reentry
activities
in
treatment
areas
including
maintenance
of
treatment
equipment
and
cleanup,
handling
freshly­
treated
wood
to
bore
test
core
samples,
stacking/
loading
wet
wood
onto
drip
pads,
and
handling
dry
wood
for
storage
or
transport.
The
following
postapplication
exposure
scenarios
for
pressure
treatment
uses
have
been
identified
from
the
PCP
biomonitoring
and
inhalation
study
entitled
Inhalation
Dosimetry
and
Biomonitoring
Assessment
of
Worker
Exposure
to
Pentachlorophenol
During
Pressure­
Treatment
of
Lumber
(
PTF,
1999)
further
detailed
in
the
PCP
RED
Human
Exposure
Chapter:

(
1)
Pressure
Treatment
Loader
Operator;

(
2)
Pressure
Treatment
Test
Borer;
and,

(
3)
Pressure
Treatment
General
Helpers.

(
ii)
Electrical
Utility
Workers
In
addition,
potential
occupational
postapplication
exposures
exist
for
electrical
utility
linemen
in
dermal
contact
with
PCP­
treated
utility
poles
during
installation
and/
or
while
working
on
in­
service
poles.
Biomonitoring
data
from
a
worker
exposure
study
on
utility
linemen
entitled
Occupational
Exposure
of
Electrical
Utility
Linemen
to
Pentachlorophenol.
(
Thind
et
al.,
1991)
were
used
to
characterize
chronic
or
long­
term
exposure
from
absorbed
doses
of
HCB
microcontaminant
in
PCP
based
on
measured
PCP
residue
levels
in
monitored
worker
urine
samples.
The
work
activities
of
the
linemen
include
frequent
climbing
of
new
or
in­
service
PCP­
treated
poles,
which
require
significant
skin
contact
to
PCP­
containing
oils
which
run
down
the
surface
of
the
telephone
poles
(
Thind
et
al.,

1991).
The
following
postapplication
exposure
scenario
represents
electrical
utility
workers:
18
(
4)
Pole
Installers
(
Electrical
Utility
Linemen).

(
4)
Postapplication
Risk
Assessment
and
Characterization
(
a)
Postapplication
Non­
Cancer
and
Cancer
Risk
Calculations
For
both
postapplication
pressure
treatment
and
electrical
utility
linemen
scenarios,

noncancer
aggregate
short­,
intermediate­,
and
long­
term
doses
and
lifetime
average
daily
doses
(
LADDs)
for
the
cancer
risk
assessment
are
based
on
the
absorbed
doses
derived
from
the
data
on
PCP
residues
in
worker
urine
samples
from
both
biomonitoring
studies
detailed
in
the
PCP
RED
Human
Exposure
Chapter
(
PTF,
1999
and
Thind
et
al.,
1991).
Total
aggregated
non­
cancer
dose
and
cancer
risk
calculations
were
conducted
as
described
previously
in
the
handler
risk
assessment
and
characterization
section
(
2)(
a).
The
HCB
exposure
doses
are
presented
in
bold
face
under
noncancer
cancer
aggregate
exposure
doses
in
Table
4.
These
doses
are
then
used
to
calculate
the
short­,

intermediate­,
and
long­
term
MOEs
and
cancer
risks
presented
in
Table
5.

(
b)
Postapplication
Non­
Cancer
Risks
from
Exposures
to
HCB
in
PCP
The
Agency
has
determined
that
Margins
of
Exposure
(
MOEs)
of
100
or
greater
are
appropriate
for
acceptable
risks
from
short­,
intermediate­
and
long­
term
exposures
to
HCB.
MOEs
for
all
scenarios
evaluated
are
presented
in
Table
5
of
this
report.
None
of
the
occupational
postapplication
scenarios
assessed
exceeded
the
Agency's
level
of
concern
for
non­
cancer
aggregate
risks.

(
c)
Postapplication
Cancer
Risks
from
Absorbed
Doses
of
HCB
in
PCP
A
carcinogenic
endpoint
related
to
lifetime
average
absorbed
doses
of
HCB
has
been
identified.
A
cancer
risk
greater
than
E­
6
is
to
be
mitigated
and
risks
greater
than
E­
4
are
generally
considered
to
be
of
concern
(
U.
S.
EPA,
1996a).
The
Agency
will
seeks
ways
to
mitigate
any
risks,

to
the
extent
that
it
is
practical
and
economically
feasible,
to
lower
the
risks
to
E­
6
or
less.
None
of
the
occupational
postapplication
scenarios
assessed
exceeded
the
Agency's
level
of
concern
(
i.
e.,
E­
4)

for
cancer
aggregate
risks
and
were
within
E­
8
(
See
Table
5).

Table
4.
Occupational
Postapplication­
Calculation
of
Non­
cancer
and
Cancer
Exposure
Doses
for
HCB
in
PCP
19
Exposure
Scenarios
PCP/
HCB
Factor
a
(
ng/
mg)
NON­
CANCER
AGGREGATE
EXPOSURE
DOSES
CANCER
AGGREGATE
EXPOSURE
DOSES
PCP
Adjusted
Absorbed
Short­
Term
Doseb
(
mg/
kg/
day)
HCB
Absorbed
Short­
Term
Dose
c
(
ng/
kg/
day)
PCP
Absorbed
Intermediate­

Term
Dosed
(
mg/
kg/
day)
HCB
Absorbed
Intermediate­

Term
Dose
c
(
ng/
kg/
day)
PCP
Absorbed
Long­
Term
Dose
e
(
mg/
kg/
day)
HCB
Absorbed
Long­
Term
Dose
c
(
ng/
kg/
day)
HCB
Lifetime
Average
Daily
Dose
f
(
ng/
kg/
day)

(
1)
Pressure
Treatment
Loader
Operator
75
0.025
1.24
0.0084
0.42
0.0027
0.13
0.048
(
2)
Pressure
Treatment
Test
Borer
75
0.016
0.79
0.0053
0.26
0.0024
0.12
0.044
(
3)
Pressure
Treatment
General
Helpers
75
0.0066
0.33
0.0022
0.11
0.0014
0.069
0.025
(
4)
Pole
Installers
(
Electrical
Utility
Linemen)
75
0.0019
0.094
0.0019
0.094
0.00098
0.048
0.018
a
PCP/
HCB
Factor
­
HCB
concentration
in
PCP
is
75
ng
per
mg
PCP
based
on
the
allowed
concentration
limit
of
75
ppm
HCB
per
batch.

b
Adjusted
based
on
increasing
the
maximum
absorbed
dose
reported
in
the
PCP
biodosimetry
study
by
3
times
to
correct
for
the
cumulative
effects
of
an
8­
day
steady­
state
excretion.

c
HCB
dose
=
PCP/
HCB
Factor
(
ng/
mg)
x
[
HCB
ABS
Factor
(.
2646)/
PCP
ABS
Factor
(.
40)]
x
PCP
dose
(
mg/
kg/
day).

d
Based
on
maximum
absorbed
doses.
Based
on
PCP
biomonitoring
data,
absorbed
doses
(
i.
e.,
representing
combined
dermal,
inhalation
and
incidental
oral
exposure)
were
assumed
to
be
attributed
primarily
to
exposure
via
the
dermal
route
since
the
majority
of
the
inhalation
monitoring
data
were
below
the
limit
of
quantitation.

e
Based
on
average
absorbed
doses.
Based
on
PCP
biomonitoring
data,
absorbed
doses
(
i.
e.,
representing
combined
dermal,
inhalation
and
incidental
oral
exposure)
were
assumed
to
be
attributed
primarily
to
exposure
via
the
dermal
route
since
the
majority
of
the
inhalation
monitoring
data
were
below
the
limit
of
quantitation.

f
HCB
Lifetime
Average
Daily
Dose
(
LADD)
=
[
HCB
absorbed
long­
term
dose
(
as
representing
long­
term
dermal
dose)
x
exposure
frequency
(
e.
g.,
250
working
days)
x
exposure
duration
(
e.
g.,
40
working
years
in
a
lifetime)]
/
[(
365
days/
yr
x
lifetime
(
e.
g.,
75
yrs)].

Table
5.
Occupational
Postapplication
­
Non­
cancer
and
Cancer
Exposure
Doses/
Risks
for
HCB
in
PCP
20
Exposure
Scenarios
NON­
CANCER
AGGREGATE
EXPOSURE
DOSES/
MOEs
CANCER
AGGREGATE
EXPOSURE
DOSES/
RISKS
HCB
Absorbed
Short­
Term
Dosea
(
mg/
kg/
day)
Short­
Term
MOE
b
HCB
Absorbed
Intermediate­
Term
Dosea
(
mg/
kg/
day)
Intermediate­

Term
MOE
c
HCB
Absorbed
Long­
Term
Dosea
(
mg/
kg/
day)
Long­
Term
MOE
d
HCB
Lifetime
Average
Daily
Dosea
(
mg/
kg/
day)
Cancer
Risk
e
(
1)
Pressure
Treatment
Loader
Operator
1.24E­
06
3.2E+
07
4.2E­
07
1.2E+
06
1.3E­
07
6.1E+
05
4.8E­
08
4.9E­
08
(
2)
Pressure
Treatment
Test
Borer
7.9E­
07
5.1E+
07
2.6E­
07
1.9E+
06
1.2E­
07
6.7E+
05
4.4E­
08
4.5E­
08
(
3)
Pressure
Treatment
General
Helpers
3.3E­
07
1.2E+
08
1.1E­
07
4.5E+
06
6.9E­
08
1.2E+
06
2.5E­
08
2.6E­
08
(
4)
Pole
Installers
(
Electrical
Utility
Linemen)
9.4E­
08
4.2E+
08
9.4E­
08
5.3E+
06
4.8E­
08
1.7E+
06
1.8E­
08
1.8E­
08
a
HCB
Doses
presented
above
have
been
converted
to
mg/
kg/
day
in
order
to
calculate
MOEs.
[
Doses
from
Table
4
in
ng/
kg/
day
x
1E­
6
(.
000001)
mg/
ng
=
mg/
kg/
day].

NON­
CANCER
AGGREGATE:

b
Short­
term
MOE=
Short­
term
oral
NOAEL
(
HCB=
40
mg/
kg/
day)/
Absorbed
Short­
term
daily
dose
(
mg/
kg/
day).

c
Intermediate­
term
MOE=
Intermediate­
term
oral
NOAEL(
HCB=
0.5
mg/
kg/
day)/
Absorbed
Intermediate­
term
daily
dose
(
mg/
kg/
day).

d
Long­
term
MOE=
Long­
term
oral
NOAEL(
HCB=
0.08
mg/
kg/
day)/
Absorbed
Long­
term
daily
dose
(
mg/
kg/
day).

CANCER
AGGREGATE:

e
Cancer
Risk=
HCB
LADD
(
mg/
kg/
day)
x
Cancer
Slope
Factor
(
Q*
=
1.02
mg/
kg/
day­
1).

(
5)
Data
Gaps,
Uncertainties
and
Limitations
21
There
are
several
data
gaps
pertaining
to
the
lack
of
actual
human
exposure
data
on
the
HCB
microcontaminant
of
PCP
wood
preservatives.
The
data
used
to
develop
the
occupational
scenarios
and
estimates
of
exposure
to
HCB
in
PCP
were
from
limited
available
study
data
on
PCP.
The
handler/
postapplication
assessments
for
pressure
treatment
plant
workers
were
based
on
data
for
PCP
in
the
study
entitled
Inhalation
Dosimetry
and
Biomonitoring
of
Worker
Exposure
to
Pentachlorophenol
During
Pressure­
Treatment
of
Lumber
(
PTF,
1999).
The
postapplication
assessment
for
pole
installers
utilized
published
biomonitoring
data
in
the
industrial
hygiene
study
entitled
Occupational
Exposure
of
Electrical
Utility
Linemen
to
Pentachlorophenol
(
Thind
et
al.,

1991)
to
estimate
potential
worker
dermal
exposure.
Specific
limitations
related
to
these
studies
are
noted
in
the
PCP
RED
Human
Exposure
Chapter.

Occupational
postapplication
scenarios
were
developed
for
workers
engaged
in
posttreatment
handling
of
wood
in
a
pressure
treatment
plant,
and
for
electrical
utility
linemen
involved
in
utility
pole
installation.
Other
PCP
exposures
not
addressed
in
this
study
include
postapplication
exposure
to
workers
engaged
in
construction
fabrication
of
PCP­
treated
timbers/
lumber.
Activities
involving
cutting
and
sanding
of
PCP­
treated
wood
may
cause
dermal,
inhalation
or
oral
ingestion
exposure
concerns
for
HCB
in
PCP.

3.0
REFERENCES
22
Agency
for
Toxic
Substances
and
Disease
Registry
(
ATSDR).
2002.
Toxicological
Profile
for
Hexachlorobenzene.
Prepared
for
U.
S.
Department
of
Health
and
Human
Services.
Public
Health
Service.
Agency
for
Toxic
Substances
and
Disease
Registry.
September,
2002.

Pentachlorophenol
Task
Force
(
PTF).
1999.
Inhalation
Dosimetry
and
Biomonitoring
Assessment
of
Worker
Exposure
to
Pentachlorophenol
During
Pressure
Treatment
of
Lumber.
Sponsor
Vulcan
Chemicals,
Washington,
DC.
AASI
Study
No.
AA980307.
(
MRID
No.
448137­
01).

Thind,
K.
S.,
Karmali,
S.,
and
House,
R.
A.,
1991.
Occupational
Exposure
of
Electrical
Utility
Linemen
to
Pentachlorophenol.
American
Industrial
Hygiene
Association
Journal
52:
547­
552.

U.
S.
EPA.
1984.
Wood
Preservative
Pesticides:
Creosote,
Pentachlorophenol,
Inorganic
Arsenicals:

Position
Document
4.
Washington,
DC:
Office
of
Pesticides
and
Toxic
Substances.

U.
S.
EPA.
1991.
Drinking
Water
Criteria
Document
for
Hexachlorobenzene.
Prepared
by
the
Office
of
Water
(
OW),
U.
S.
EPA,
Cincinnati,
OH.
ECAO­
CIN
424.

U.
S.
EPA.
1996a.
Non­
Dietary
Cancer
Risk
Policy.
Guidance
Memorandum
from
Daniel
M.
Barolo,

Director,
Office
of
Pesticide
Programs
to
OPP
Division
Directors.
August
14,
1996.

U.
S.
EPA.
1996b.
Integrated
Risk
Information
System
(
IRIS).
Hexachlorobenzene.

U.
S.
EPA.
1997a.
Pentachlorophenol­
Report
of
the
Hazard
Identification
Assessment
Review
Committee.
December
8,
1997.

U.
S.
EPA.
1997b.
Exposure
Factors
Handbook.
Volume
1.
Office
of
Research
and
Development.

Washington
DC.
EPA/
600/
P­
95/
002Fa.

U.
S.
EPA.
2003.
Hexachlorobenzene
Microcontaminant
of
Pentachlorophenol
(
PCP):
AD
Hazard
Identification
and
Risk
Assessment
Chapter
(
DP
Barcode:
D272977).
Transmittal
Memorandum
from
Timothy
F.
McMahon,
Ph.
D.,
Senior
Toxicologist
and
Jonathan
Chen,
Ph.
D.,
Toxicologist
to
Bonaventure
Akinlosotu,
Reregistration
Team
36.
February
10,
2003.
