Document ID: EPA-HQ-OAR-2003-0048-0116
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2004-02-26T05:00Z

UNITED
STATES
ENVIRONMENTAL
PROTECTION
AGENCY
OFFICE
OF
AIR
QUALITY
PLANNING
AND
STANDARDS
EMISSION
STANDARDS
DIVISION
RESEARCH
TRIANGLE
PARK,
NC
27711
February
18,
2004
MEMORANDUM
SUBJECT:
Risk
Assessment
for
the
Final
Maximum
Achievable
Control
Technology
(
MACT)
Rule
for
the
Plywood
and
Composite
Wood
Products
(
PCWP)
Source
Category
FROM:
Scott
Jenkins,
Maria
Pimentel,
Dennis
Pagano
Risk
and
Exposure
Assessment
Group
(
C404­
01)

TO:
David
E.
Guinnup,
Leader
Risk
and
Exposure
Assessment
Group
(
C­
404­
01)

Introduction
The
purpose
of
this
memo
is
to
describe
the
methodology
and
results
of
a
risk
assessment
performed
for
the
plywood
and
composite
wood
products
(
PCWP)
source
category.

This
assessment
was
performed
in
order
to
determine
the
magnitude
of
potential
cancer
and
noncancer
chronic
human
health
risks,
acute
human
health
risks,
and
ecological
risks
associated
with
the
sources
in
this
source
category.
In
addition,
this
assessment
was
used
to
evaluate
the
potential
development
of
a
low­
risk
subcategory
which
could
be
delisted
and
thereby
exempted
from
regulation.

Background
on
Source
Category
Delisting
The
U.
S.
Environmental
Protection
Agency
has
proposed
the
national
emission
standards
for
hazardous
air
pollutant
(
NESHAP)
for
the
plywood
and
composite
wood
products
(
PCWP)
source
category.
Section
112(
c)(
9)(
B)
allows
for
the
removal
of
a
source
category
from
consideration
in
EPA's
program
to
promulgate
MACT
standards.
EPA
interprets
these
provisions
to
apply
to
each
listed
subcategory
as
well.

To
commence
a
proceeding
to
delete
a
category
or
subcategory
on
the
Administrator's
own
motion,
the
Administrator
must
make
an
initial
determination
that
no
source
in
the
category
emits
carcinogens
in
amounts
that
may
result
in
a
lifetime
cancer
risk
exceeding
one
in
one
million
to
the
individual
most
exposed;
emits
noncarcinogens
in
amounts
that
exceed
a
level
protective
of
public
health
with
an
ample
margin
of
safety;
or
emits
any
HAP
in
amounts
that
will
result
in
adverse
environmental
effects.
2
1Baseline
Emissions
Estimates
for
the
Plywood
and
Composite
Wood
Products
Industry.
Memorandum
to
Mary
Tom
Kissell,
from
Katie
Hanks
and
David
Bullock,
Midwest
Research
Institute.
June
9,
2000.
Assessment
Methodology
1.
Scope
The
first
step
in
conducting
a
risk
assessment
is
to
plan
and
scope
the
assessment.
EPA
provides
guidance
on
this
step
in
the
Risk
Characterization
Handbook
(
EPA,
2000)
and
Framework
for
Cumulative
Risk
Assessment
(
EPA,
2003).
The
process
of
planning
and
scoping
includes
defining
the
range
of
factors
that
are
to
be
considered
in
the
assessment.
In
designing
this
assessment,
we
considered
several
factors,
including,
statutory
requirements
of
the
CAA
section
112
(
c),
the
available
data
for
the
source
category,
and
available
methods
and
models.

Based
on
these
factors,
the
risk
assessment
for
the
plywood
and
composite
wood
products
source
category
was
designed
to
evaluate
potential
human
cancer
and
noncancer
chronic
risks
due
to
inhalation
and
ingestion
exposures,
acute
risks
to
human
health
due
to
inhalation
exposures,
and
ecological
risks.
Since
data
for
individual
sources
in
the
category
were
limited,
a
combination
of
data,
methods,
models
and
assumptions
were
considered
in
developing
an
approach
that
would
be
protective
of
human
health
and
the
environment.
Thus,
while
some
of
the
assumptions
and
modeling
choices
used
in
this
analysis
tend
to
overestimate
the
risk
estimates,
not
all
factors
will
do
so
(
e.
g.,
use
of
site­
specific
information
represents
a
"
best
guess"
of
these
parameters).
Overall,
we
consider
the
predicted
results
of
this
assessment
to
be
conservative;
that
is,
the
risks
estimated
are
likely
higher
than
those
which
would
be
expected
to
occur
in
the
actual
exposed
population.

2.
Source
Category
Characterization
The
analysis
included
emissions
associated
with
the
production
of
medium
density
fiberboard
(
MDF),
particleboard,
hardboard,
fiberboard,
oriented
strand
board
(
OSB),
softwood
plywood
and
veneer,
and
engineered
wood
products
(
EWP).
Estimates
of
emissions
were
generated
to
represent
the
level
of
pollution
control
that
is
actually
used
in
facilities
across
the
nation
(
baseline
emissions).
A
detailed
explanation
of
the
methodology
utilized
to
identify
and
characterize
the
HAP
emission
sources
and
to
calculate
these
emissions
can
be
found
in
the
Baseline
Emissions
Estimates
for
the
Plywood
and
Composite
Wood
Products
Industry
Memorandum1.
While
emissions
from
some
of
these
sources
may
vary
temporally
(
over
hours
or
days),
we
do
not
include
this
variation
when
evaluating
effects
associated
with
long­
term
exposures.
We
do
include
this
variation
when
evaluating
effects
associated
with
short­
term
exposures.

The
emissions
data
were
based
on
site­
specific
annual
emission
rates
by
HAP
and
known
map
coordinates.
Some
latitude
and
longitude
coordinates
were
available
for
223
facilities.
The
facility
coordinates
were
evaluated
using
geographic
information
systems
software,
ArcGIS
(
version
8).
Facilities
where
location
data
were
ambiguous
or
where
information
was
declared
confidential
were
excluded
from
the
analysis,
leaving
a
total
of
181
facilities
in
the
assessment.
Summaries
of
the
site­
specific
emissions
data
included
in
the
assessment
are
documented
in
Printout
of
Risk
3
2
Printout
of
Risk
Analysis
Input
Spreadsheets.
Memorandum
to
Plywood
and
Composite
Wood
Products
(
PCWP)
Docket
File
from
Katie
Hanks,
Research
Triangle
Institute.
July
29,2002.

3
Documentation
of
Stack
Parameters
Provided
in
2002
Submittal
of
National
Emission
Inventory
(
NEI)
Data
and
as
Inputs
for
Risk
Assessment.
Memorandum
to
Project
file
110168.1.003:
Plywood
and
Composite
Wood
Products
(
PCWP)
NESHAP
from
Melissa
Icenhour,
Midwest
Research
Institute.
February
20,
2002.
Analysis
Input
Spreadsheets;
Memorandum
to
Plywood
and
Composite
Wood
Products
(
PCWP)
Docket
File2
and
appendix
B.

Additional
data
regarding
source
release
characteristics
(
e.
g.,
stack
heights
and
diameters,
exit
velocities,
stack
gas
temperatures)
are
documented
elsewhere3.
Based
on
these
characteristics,
we
developed
one
model
facility
consisting
of
two
emission
points
for
the
chronic
assessments.
Two
thirds
(
66%)
of
the
model
facility's
emissions
were
assigned
to
a
taller
stack
(
stack
1,
dryer
stack);
the
remaining
emissions
(
34%)
were
assigned
to
the
shorter
stack
(
stack
2,
press
stack).
Although
each
stack
was
individually
modeled,
both
were
placed
at
the
latitude
and
longitude
of
the
center
of
the
model
facility.
The
release
parameters
for
each
stack
are
summarized
as
follows:

Stack
1
Stack
2
Stack
height
(
meters)
21.3
12.3
Stack
diameter
(
meters)
1.5
1.8
Stack
gas
exit
velocity
(
meters/
sec)
18.46
12.3
Stack
gas
temperature
(
kelvin)
360.9
316.5
Building
cross­
sectional
area
(
meters2)
100
100
Regulatory
default
dispersion
modeling
options
were
used
for
this
analysis.
All
plants
were
assumed
to
be
located
in
rural
areas
and
no
terrain
elevation
for
sources
or
receptors
was
considered.
The
rural
option
is
consistent
with
engineering
judgement
for
the
PCWP
industry
and
represents
a
conservative
assumption.

3.
Selection
of
HAPs
and
Dose­
Response
Information
The
analysis
for
this
source
category
included
all
HAP
that
were
reported
as
emitted
by
any
of
the
facilities.
These
HAP
are
listed
in
Table
1
with
their
respective
cancer,
chronic
noncancer,
and
acute
noncancer
dose­
response
values.
These
values
are
described
in
more
detail
in
the
EPA's
Air
Toxics
Website
at
http://
www.
epa.
gov/
ttn/
atw/
toxsource/
summary.
html
The
EPA
is
constantly
evaluating
new
dose­
response
values
and
updating
the
recommended
values
accordingly.
HAP
were
not
considered
in
the
cancer
risk
analysis
if
there
was
either
no
available
weight
of
evidence
conclusion
on
potential
human
carcinogenicity
or
there
was
no
adequate
quantitative
potency
estimate.
The
dose­
response
values
used
in
the
analyses
and
shown
in
Table
1
were
current
as
of
October
1,
2003
except
for
formaldehyde.
The
formaldehyde
dose­
response
value
as
of
October,
2003
is
from
IRIS
and
is
based
on
a
1987
study
that
no
longer
represents
the
best
available
science
in
the
peer­
reviewed
literature.
Since
that
time,
significant
new
data
and
analyses
have
become
available
leading
to
the
development
of
a
revised
dose­
response
value.
We
used
this
revised
value
for
the
PCWP
assessment
although
it
was
incorporated
into
the
EPA's
Air
Toxics
Website
after
October
1,
2004.
4
4:
Unit
risk
estimate
(
URE):
The
upper­
bound
excess
lifetime
cancer
risk
estimated
to
result
from
continuous
exposure
to
an
agent
at
a
concentration
of
1
µ
g/
m3
in
air.
The
interpretation
of
unit
risk
would
be
as
follows:
if
URE
=
1.5
x
10­
6
(
µ
g/
m3)­
1,
1.5
excess
tumors
are
expected
to
develop
per
1,000,000
people
if
exposed
daily
for
a
lifetime
to
1
µ
g
of
the
chemical
in
1
m3
of
inhaled
air.
"
Upper­
bound"
in
this
context
is
defined
as
a
plausible
upper
limit
to
the
true
probability.
An
appropriate
interpretation
of
upper­
bound
unit
risk
estimates
is
that
the
true
value
is
probably
less,
and
unlikely
to
be
greater.

5:
Reference
Concentration
(
RfC):
An
estimate
(
with
uncertainty
spanning
perhaps
an
order
of
magnitude)
of
a
continuous
inhalation
exposure
to
the
human
population
(
including
sensitive
subgroups)
that
is
likely
to
be
without
an
appreciable
risk
of
deleterious
effects
during
a
lifetime.
Dose­
response
values
and
sources
can
be
found
at
http://
www.
epa.
gov/
ttn/
atw/
toxsource/
summary.
html.
The
values
presented
in
Table
1
are
current
as
of
the
time
of
the
analysis.
If
there
was
either
no
available
weight
of
evidence
conclusion
on
potential
human
carcinogenicity,
or
there
was
no
adequate
quantitative
potency
estimate
for
a
particular
HAP,
it
was
not
considered
in
the
cancer
risk
analysis
and
thedore­
response
value
was
left
blank.

6:
Acute
reference
level
(
ARL):
A
short­
term
(
e.
g.,
1­
hour)
inhalation
exposure
to
the
human
population
estimated
to
cause
only
mild,
reversible
adverse
effects,
or
no
adverse
effects.
Because
EPA
has
not
developed
either
ARLs
or
guidelines
for
their
derivation,
ARLs
were
selected
from
a
number
of
publically­
available
health
effects
reference
values
to
assess
"
routine"
acute
or
subchronic
environmental
exposures.
These
values
were
developed
for
slightly
different
purposes
by
different
organizations,
e.
g.,
AEGLs,
EPRGs
and
IDLH/
10
address
emergency
situations
often
associated
with
industrial
accidents
while
the
more
stringent
RELs
and
MRLs
address
exposures
of
a
non­
emergency
nature.
Therefore,
the
intended
uses
and
derivations
of
the
reference
values
are
not
always
directly
comparable
and
may
provide
varying
degrees
of
protection.
For
this
reason,
the
ARLs
should
be
regarded
as
less
certain
than
either
UREs
or
RfCs.
Table
1.
Unit
risk
estimates1,
reference
concentrations2
(
or
similar
values),
and
acute
reference
levels3
used
in
the
risk
assessment
for
PCWP
source
category
HAP
URE
1/(

g/
m3)
RfC
or
similar
value
(

g/
m3)
ARL
(

g/
m3)

Acetaldehyde
2.2E­
06
9.0E+
00
1.8E+
04
Acrolein
 
2.0E­
02
6.9E+
01
Antimony
compounds
 
2.0E­
01
 
Arsenic
compounds
4.3E­
03
3.0E­
02
1.9E­
01
Benzene
7.8E­
06
3.0E+
01
1.3E+
03
Beryllium
compounds
2.4E­
03
2.0E­
02
2.5E+
01
Cadmium
compounds
1.8E­
03
2.0E­
02
9.0E+
03
Chromium
(
Cr+
6)
1.2E­
02
1.0E­
01
1.5E+
03
Cobalt
compounds
 
1.0E­
01
2.0E+
03
Cumene
 
4.0E+
02
4.4E+
05
Ethylbenzene
 
1.0E+
03
3.5E+
05
Formaldehyde
5.5E­
09
9.8E+
00
9.4E+
01
Lead
compounds
 
1.5E+
00
1.0E+
04
Manganese
compounds
 
5.0E­
02
5.0E+
04
Mercury
compounds
 
9.0E­
02
1.8E+
00
Methanol
 
4.0E+
03
2.8E+
04
Methyl
ethyl
ketone
 
5.0E+
03
1.3E+
04
Methyl
isobutyl
ketone
 
3.0E+
03
 
5
HAP
URE
1/(

g/
m3)
RfC
or
similar
value
(

g/
m3)
ARL
(

g/
m3)

Methylene
chloride
4.7E­
07
1.0E+
03
1.4E+
04
Methylene
diphenyl
diisocyanate
 
6.0E­
01
2.0E+
02
Nickel
compounds
*
4.8E­
04
 
6.0E+
00
Phenol
 
2.0E+
02
5.8E+
03
Selenium
compounds
 
2.0E+
01
1.0E+
02
Styrene
 
1.0E+
03
2.1E+
04
Toluene
 
4.0E+
02
3.7E+
04
Xylenes
(
mixed
isomers)
 
1.0E+
02
2.2E+
04
*
Due
to
lack
of
speciation
data
we
used
the
URE
of
nickel
subsulfide
and
assumed
that
65%
of
nickel
emissions
are
nickel
subsulfide
as
done
in
the
1996
National
Air
Toxics
Assessment
(
NATA).

4.
Dispersion
Modeling
for
Chronic
Exposures.

The
EPA
Human
Exposure
Model
(
HEM,
2000
Version)
was
used
for
the
chronic
portion
of
the
assessment.
A
description
of
that
model
and
how
it
is
used
in
this
type
of
assessment
can
be
found
in
Using
the
Human
Exposure
Model
(
Version
2000)
for
Residual
Risk
Tests
and
Other
Risk
Screening
Assessments
Memorandum.
A
copy
of
this
memorandum
is
found
in
Appendix
A.

5.
Dispersion
Modeling
for
Acute
Exposures
For
the
acute
assessment,
we
utilized
the
SCREEN3
atmospheric
dispersion
model
to
predict
maximum
1­
hour
exposures
from
a
slightly
modified
model
facility,
which
consisted
of
a
single
stack
with
conservative
stack
parameters
(
stack
height
=
17
m,
stack
diameter
=
1.1
m,
exit
gas
velocity
=
9.0
m/
sec,
exit
gas
temperature
=
293k).
Hourly
emission
rates
for
the
acute
analysis
were
40%
higher
than
those
used
for
the
chronic
analysis.
This
is
based
on
an
engineering
examination
of
emissions
data
from
the
industry
as
a
whole
(
across
all
HAP
and
all
process
units
tested)
that
demonstrated
the
maximum
1­
hour
emissions
test
result
typically
exceeds
the
average
emissions
test
result
by
approximately
40%.

The
acute
analysis
included
all
PCWP
facilities
for
which
we
had
emissions
data.
This
assessment
assumed
worst­
case
meteorology
defaults,
local
flat
terrain,
and
that
an
individual
could
be
exposed
for
an
hour
at
the
point
of
highest
predicted
HAP
concentration.

The
acute
hazard
quotient
(
HQ)
for
each
HAP
was
calculated
by
dividing
the
maximum
predicted
concentration
by
the
appropriate
acute
benchmark
values.
Benchmark
values
were
obtained
from
the
air
toxics
website
cited
elsewhere,
and
are
listed
as
Acute
Reference
Levels
(
ARL)
in
Table
1.

6.
Multipathway
Risk
Analysis
6
To
evaluate
the
potential
for
HAP
emitted
from
PCWP
facilities
to
cause
cancer
or
noncancer
risks
to
humans
via
ingestion,
a
conservative
screening
level
multipathway
analysis
was
conducted.

The
multipathway
analysis
considered
exposures
from
ingestion
from
two
of
the
emitted
HAP:
cadmium
and
mercury.
These
HAP
were
the
only
ones
included
in
the
multipathway
analysis
because
they
are
the
only
ones
considered
to
be
persistent,
bioaccumulative,
and
toxic
(
PBT)
substances
under
any
EPA
programs
(
e.
g.,
the
Pollution
Prevention
Program,
the
Great
Waters
program,
the
Toxics
Release
Inventory).
All
other
HAP
emitted
by
this
source
category
are
considered
to
have
insignificant
non­
inhalation
risks.
Lead
was
not
included
in
the
multipathway
analysis
because
predicted
air
concentrations
from
PCWP
emissions
were
well
below
the
National
Ambient
Air
Quality
Standard
of
1.5
µ
g/
m3.
Derivation
of
this
standard
incorporates
multipathay
effects,
therefore,
emissions
below
this
level
are
not
expected
to
pose
a
significant
multipathway
risk.

Very
limited
site­
specific
data
were
available
to
allow
us
to
predict
potential
multipathway
impacts.
To
account
for
this
uncertainty
we
developed
a
model
facility,
with
stack
parameters
the
same
as
those
used
for
the
chronic
assessment,
which
emitted
the
maximum
amounts
of
cadmium
and
mercury
seen
across
the
entire
source
category.
We
created
a
worst­
case
farmer
exposure
scenario
with
this
facility
by
placing
it
near
a
working
homestead.
The
resulting
impact
of
the
facility
was
then
evaluated
on
livestock,
produce,
and
aquatic
life
by
coupling
the
Industrial
Source
Complex
Short­
Term
(
ISCST3)
air
dispersion
model
with
the
Indirect
Exposure
Model
(
IEM­
2M)
multipathway
model.
These
impacts
were
compared
to
dose­
response
values
to
estimate
human
health
and
ecological
risks.

To
simulate
meteorological
variability,
the
farmer
scenario
was
evaluated
using
meteorological
data
from
six
locations
across
the
country:
Montgomery,
AL;
Baton
Rouge
LA;
Minneapolis,
MN;
Raleigh,
NC;
Salem,
OR;
and
Allentown,
PA.

The
maximum
air
concentrations
and
deposition
rate
estimates
at
or
beyond
the
facility
fenceline
of
200
meters
were
combined
to
estimate
the
impacts
at
the
farm.
The
environmental
fate
and
transport
of
the
deposited
HAP
were
then
simulated
using
central
tendency
exposure
factors
for
the
subsistence
farmer
scenario
for
the
following
exposure
pathways:
inhalation,
soil
ingestion,
produce
ingestion,
animal
product
ingestion
(
including
beef,
dairy
products,
and
pork),
fish
ingestion,
and
drinking
water
ingestion.
This
subsistence
farmer
scenario
was
evaluated
because
it
is
considered
to
be
a
reasonable
worst­
case
multimedia
exposure
scenario.
A
summary
of
the
modeling
inputs
to
the
ISCST3
and
IEM­
2M
models
are
presented
in
Appendix
E,
along
with
a
detailed
explanation
of
the
methodology
used
for
the
exposure
assessment.

7.
Ecological
Risk
Assessment
A
conservative
screening­
level
ecological
risk
assessment
was
performed
according
to
the
EPA's
Guidelines
for
Ecological
Risks
Assessment
(
ISAPI
1998a,
1999)
and
using
the
methods
and
toxicological
dose
response
screening
values
identified
in
the
draft
secondary
lead
smelters
analysis
(
EPA,
2003).
The
screening­
level
risk
assessment
identifies
HAP
posing
potential
risks
to
7
ecological
receptors
and
the
relative
magnitude
of
those
potential
risks.
To
account
for
uncertainties
due
to
limited
site­
specific
data,
the
worst­
case
media
concentrations
from
the
chronic
multipathway
human
health
analysis
were
used
to
perform
the
ecological
analysis.

For
screening
endpoints,
we
use
the
structure
and
function
of
generic
aquatic
and
terrestrial
populations
and
communities,
including
threatened
and
endangered
species,
that
might
be
exposed
to
HAP
emissions
from
the
model
facility
via
contaminated
soil
or
water.
The
HAP
included
in
the
quantitative
ecological
assessment
are
the
same
evaluated
in
the
multipathway
human
health
analysis:
cadmium
and
mercury.
The
exposure
pathways
were
selected
to
mimic
the
potential
routes
of
exposure
through
sediment,
soil,
water
and
air.
Within
these
environments
the
receptors
evaluated
consisted
of
two
main
groups:
terrestrial
and
aquatic
(
i.
e.,
including
aquatic,
benthic
and
soil
organisms;
terrestrial
plants
and
wildlife;
and
herbivorous
and
carnivorous
wildlife).

The
chronic
ecological
toxicity
values
used
in
the
assessment
were
estimates
of
the
maximum
concentrations
that
would
not
be
expected
to
affect
survival,
growth,
or
reproduction
of
sensitive
species
after
long­
term
exposure
(
more
than
30
days)
to
the
HAP.
Individual
HAP,
pathways
and
receptors
were
screened
using
the
ecological
HQ
method,
which
calculates
the
ratio
of
the
estimated
environmental
concentrations
to
the
selected
ecological
screening
values.

Inputs
and
chronic
ecological
toxicity
values
used
in
the
ecological
analysis
are
described
in
Appendix
D.

Results
and
Discussion
Summary
of
Chronic
Cancer
Inhalation
Risk
Assessment
The
individual
cancer
risk
results
for
the
most­
exposed
census
blocks
for
each
facility
are
summarized
in
table
2.
The
cancer
risks
represent
upper­
bound
estimates
for
lifetime
residents
in
the
most
impacted
areas.
For
cancer
risk,
Table
2
shows
24
facilities
with
maximum
individual
cancer
risks
potentially
greater
than
or
equal
to
1
in
one
million.
None
of
the
facilities
showed
maximum
individual
risks
in
excess
of
10
in
one
million.
On
the
other
hand,
a
total
of
157
facilities
were
estimated
to
pose
maximum
individual
lifetime
cancer
risks
lower
than
1
in
one
million.
(
See
Appendix
C
for
HEM
Output
files).

The
cancer
risk
estimates
were
dominated
by
contributions
from
acetaldehyde,
benzene,
arsenic,
beryllium,
cadmium,
hexavalent
chromium,
lead,
nickel
subsulfide
and
formaldehyde.
These
HAPs
contributed
to
at
least
95%
of
cancer
risk
in
all
the
facilities.
Among
them,
acetaldehyde
and
arsenic
the
accounted
for
approximately
80%
of
this
risk.
8
Table
2.
Summary
of
results
of
cancer
risk
estimates
for
the
plywood
and
composite
wood
products
source
category
Cancer
Risk
Estimates
Number
of
Facilities
Greater
than
or
equal
to
1
in
1
million
24
Greater
than
or
equal
to
0.1
in
1
million
117
Greater
than
or
equal
to
0.01
in
1
million
179
Summary
of
Chronic
Noncancer
Inhalation
Assessment
The
individual
noncancer
target­
organ
specific
HI
results
for
the
most
exposed
census
blocks
for
each
facility
are
summarized
in
Table
3.
The
noncancer
impacts
were
dominated
primarily
by
impacts
to
the
respiratory
system,
and
secondarily
by
impacts
to
the
central
nervous
system
(
CNS).
Other
target
organ
systems
were
found
to
be
negligibly
impacted.
The
HAP
affecting
the
respiratory
system
included
acetaldehyde,
acrolein,
formaldehyde,
and
methylene
diphenyl
diisocyanate.
The
HAP
affecting
the
central
nervous
system
included
phenol,
lead,
and
manganese.
Most
of
the
facilities
showed
maximum
offsite
HI
values
below
1.0,
with
about
half
of
the
modeled
facilities
showing
maximum
HI
values
below
0.2.

Table
3.
Summary
of
results
of
noncancer
risk
estimates
for
the
plywood
and
composite
wood
products
source
category
Chronic
Noncancer
Estimates
Number
of
Facilities
Maximum
respiratory
and
CNS
HI
less
than
10
179
Maximum
respiratory
and
CNS
HI
less
than
1.0
156
Maximum
respiratory
and
CNS
HI
less
than
0.5
137
Maximum
respiratory
and
CNS
HI
less
than
0.2
103
9
Summary
of
Acute
Assessment
Two
HAP
were
identified
as
having
the
potential
to
cause
risks
due
to
acute
exposures:
acrolein
and
formaldehyde.
The
maximum
acute
HQ
for
acrolein
was
1.4,
and
the
maximum
acute
HQ
for
formaldehyde
was
6.3.

Summary
of
Multipathway
and
Ecological
Results
The
maximum
multipathway
cancer
risks
were
considerably
lower
than
predicted
maximum
inhalation
cancer
risks
from
the
PCWP
source
category.
The
highest
cancer
and
noncancer
multipathway
impacts
were
seen
from
the
scenarios
using
meteorological
data
from
Oregon
and
Minnesota,
respectively.
The
maximum
individual
cancer
risk
from
ingestion
was
0.02
in
one
million
due
to
cadmium.
The
highest
noncancer
ingestion
hazard
index
was
0.0058,
and
it
was
also
dominated
by
cadmium
exposure.

The
ecological
hazard
quotients
were
also
estimated
to
be
significantly
less
than
one.
The
maximum
estimate
was
0.043
for
cadmium
exposure
to
aquatic
life
through
surface
water.
We
conclude
that
it
is
unlikely
that
any
of
the
PCWP
facilities
would
pose
a
significant
ecological
risk
to
any
actual
ecosystem.
We
also
conclude,
given
these
low
impacts
from
the
hypothetical
worstcase
scenario,
that
it
is
unlikely
that
any
potentially­
exposed
threatened
or
endangered
species
would
be
affected
by
HAP
emissions
from
these
facilities.

Detailed
results
of
the
multipathway
human
health
and
ecological
assessments
are
presented
in
Appendix
D.

Documentation
utilized
in
this
risk
assessment
is
included
in
the
following
attachments:

Appendix
A
Using
the
Human
Exposure
Model
(
Version
2000)
for
Residual
Risk
Tests
and
Other
Risk
Screening
Assessments.
Memorandum
to
Maria
Pimentel,
U.
S.
Environmental
Protection
Agency,
from
Darcie
Smith
and
Phil
Norwood,
EC/
R
Incorporated.
September
29,
2003.

Appendix
B
HEM
Inputs
Appendix
C
HEM
Outputs
Appendix
D
Draft
Multipathway
and
Ecological
Risks
from
Model
PCWP
Facilities.
Memorandum
to
Dennis
Pagan
and
Maria
Pimentel,
U.
S.
Environmental
Protection
Agency,
from
Nancy
Jones
and
Lesley
Stobert,
EC/
R
Incorporated.
January
28,
2004.

Appendix
E
Human
Health
Effects
of
HAPs
Considered
in
this
Assessment
10
References:

USEPA
2003:
Framework
for
Commutative
Risk
Assessment,
EPA/
630/
P­
02/
001F,
Office
of
Science
Policy,
Washington,
D.
C.,
May
2003.

USEPA
2003:
Draft
Secondary
Lead
Smelter
Residual
Risk
Assessment,
EPA
68­
D­
01­
071.

USEPA
2000:
Risk
Characterization
handbook,
EPA
100­
B­
00­
02,
Office
of
Science
Policy,
Washington,
D.
C.,
December
2000.

USEPA
1998a:
Guidelines
for
Ecological
Risk
Assessment,
EPA
630/
R­
95/
002F.

USEPA
1999:
Draft
Screening
Methodology
for
Ecological
Risk
Assessment,
Manuscript.

OAQPS:
ESD:
REAG:
SJenkins:
bmiles:
x5648:
2­
18­
04