1
Richard_
Canady@
om
b.
eop.
gov
To:
Larry
Sorrels/
RTP/
USEPA/
US@
EPA
cc:
Edmond_
Toy@
omb.
eop.
gov
02/
23/
2004
06:
06
PM
Subject:
plywood
Ch6
Larry,

suggested
edits
as
discussed
in
call
today
on
plywood
ch
6
(
See
attached
file:
pcwcria­
ch6finalomb204
rac.
doc)
2
6
QUALITATIVE
ASSESSMENT
OF
BENEFITS
OF
EMISSION
REDUCTIONS
The
emission
reductions
achieved
by
this
environmental
regulation
will
provide
benefits
to
society
by
improving
environmental
quality.
This
chapter
provides
information
on
the
types
and
levels
of
social
benefits
anticipated
from
the
plywood
and
composite
wood
products
(
PCWP)
NESHAP,
including
the
health
and
welfare
effects
associated
with
the
HAPs
and
other
pollutants
emitted
by
affected
sources.

In
general,
the
reduction
of
HAP
emissions
resulting
from
the
regulation
will
reduce
human
and
environmental
exposure
to
these
pollutants
and
thus,
reduce
potential
adverse
health
and
welfare
effects.
This
chapter
provides
a
general
discussion
of
the
various
components
of
total
benefits
that
may
be
gained
from
a
reduction
in
HAPs
through
this
NESHAP.
The
rule
will
also
achieve
reductions
of
coarse
particulate
matter
(
PM10),
volatile
organic
compounds
(
VOC),
and
carbon
monoxide
(
CO).
There
will
also
be
emissions
increases
in
nitrogen
oxides
(
NOx)
and
sulfur
dioxide
(
SO2)
associated
with
the
use
of
incineration­
based
controls.
The
benefits
and
disbenefits
of
the
PM,
NOx,
and
SO2
emissions
reductions
and
increases
are
presented
separately
from
the
benefits
associated
with
HAPs
and
CO.
The
benefits
and
disbenefits
associated
with
PM,
NOx,
and
SO2,
along
with
the
benefits
associated
with
HAPs
and
CO
are
presented
in
this
chapter.

6.1
Identification
Of
Potential
Benefit
Categories
The
benefit
categories
associated
with
the
emission
reductions
predicted
for
this
regulation
can
be
broadly
categorized
as
those
benefits
which
are
attributable
to
reduced
exposure
to
HAPs,
which
are
also
VOCs,
and
those
attributable
to
reduced
exposure
to
other
pollutants.
Some
of
the
HAPs
associated
with
this
regulation
have
been
classified
as
probable
or
possible
human
carcinogens.
As
a
result,
one
of
the
benefits
of
the
regulation
is
a
reduction
in
the
risk
of
cancer.
Other
benefit
categories
include:
reduced
incidence
of
neurological
effects
and
irritants
associated
with
exposure
to
noncarcinogenic
HAPs,
reduced
incidence
of
cardiovascular
and
central
nervous
system
problems
associated
with
CO.
In
addition
to
health
impacts
occurring
as
a
result
of
reductions
in
HAP
and
CO
emissions,
there
are
welfare
impacts
which
can
also
be
identified.
In
general,
welfare
impacts
include
effects
on
crops
and
other
plant
life,
materials
damage,
soiling,
and
acidification
of
estuaries.
Each
category
is
discussed
separately
in
the
following
section.

6.2
Qualitative
Description
Of
Air
Related
Benefits
­
HAPs
and
CO
The
operation
of
plywood
and
composite
wood
product
sources
produces
emissions
of
acrolein,
formaldehyde,
acetaldehyde,
and
phenol,
among
other
HAPs.
[
why
not
list
all
of
them
as
in
6.4?
acetaldehyde,
acrolein,
benzene,
formaldehyde,
manganese,
methanol,
methylene
chloride,
and
phenol?]
The
qualitative
health
and
welfare
benefits
of
these
HAPs,
and
CO
reductions
are
summarized
separately
in
the
discussions
below.
6.2.1
Benefits
of
Reducing
HAP
Emissions
According
to
emission
estimates,
the
regulation
will
reduce
approximately
11,000
tons
of
emissions
of
HAPs
such
as
acrolein,

formaldehyde,
acetaldehyde,
phenol,
and
methanol
at
all
affected
plywood
and
composite
wood
products
sources.

Human
exposure
to
these
HAPs
may
occur
directly
through
inhalation
or
indirectly
through
ingestion
of
food
or
water
contaminated
by
HAPs
or
through
dermal
exposure.
HAPs
may
also
enter
terrestrial
and
aquatic
ecosystems
through
atmospheric
deposition.
HAPs
can
be
deposited
on
vegetation
and
soil
through
wet
or
dry
deposition.
HAPs
may
also
enter
the
aquatic
environment
from
the
atmosphere
via
gas
exchange
between
surface
water
and
the
ambient
air,
wet
or
dry
deposition
of
particulate
HAPs
and
particles
to
which
HAPs
adsorb,
and
wet
or
dry
deposition
to
watersheds
with
subsequent
leaching
or
runoff
to
bodies
of
water.
1
This
analysis
is
focused
only
on
the
air
quality
benefits
of
HAP
reduction.
6.2.1.1
Health
Benefits
of
Reduction
in
HAP
Emissions.

The
HAP
emission
reductions
achieved
by
this
rule
are
expected
to
reduce
exposure
to
ambient
concentrations
of
acrolein,
formaldehyde,

acetaldehyde,
and
phenol,
[
why
not
list
all
used
in
6.4
­
acetaldehyde,
acrolein,
benzene,
formaldehyde,
manganese,
methanol,
methylene
chloride,

and
phenol
?]
which
will
reduce
a
variety
of
adverse
health
effects
considering
both
cancer
and
noncancer
endpoints.
Acrolein
is
classified
as
a
possible
human
carcinogen,
according
to
the
Integrated
Risk
Information
System
(
IRIS)
13,
an
EPA
system
for
classifying
chemicals
by
cancer
risk.

This
means
that
there
is
some
evidence
to
indicate
that
exposure
to
this
chemical
could
cause
an
increased
risk
of
cancer
in
humans.
Acrolein
may
also
cause
general
respiratory
congestion
and
upper
respiratory
tract
irritation.
Formaldehyde
and
acetaldehyde
are
classified
as
probable
human
carcinogens,
according
to
IRIS.
Therefore,
a
reduction
in
human
exposure
to
acrolein,
formaldehyde,
and
acetaldehyde
could
lead
to
a
decrease
in
cancer
risk
and
ultimately
to
a
decrease
in
cancer
mortality.

The
remaining
HAP
emitted
by
plywood
and
composite
wood
products
sources,
phenol
and
methanol,
have
not
been
shown
to
cause
cancer.
However,
exposure
to
these
pollutants
may
still
result
in
adverse
health
impacts
to
human
and
non­
human
populations.
In
particular,

methanol
has
been
shown
to
be
an
irritant
causing
dizziness,
headaches,
and
slight
visual
impairment.

For
the
HAPs
covered
by
the
NESHAP,
evidence
on
the
potential
toxicity
of
the
pollutants
varies.
However,
given
sufficient
exposure
conditions,
each
of
these
HAPs
has
the
potential
to
elicit
adverse
health
or
environmental
effects
in
the
exposed
populations.
It
can
be
expected
that
emission
reductions
achieved
through
the
NESHAP
will
decrease
the
incidence
of
these
adverse
health
effects.

6.2.1.2
Welfare
Benefits
of
Reduction
in
HAP
Emissions.

The
welfare
effects
of
exposure
to
HAPs
have
received
less
attention
from
analysts
than
the
health
effects.
However,
this
situation
is
changing,
especially
with
respect
to
the
effects
of
toxic
substances
on
ecosystems.
Over
the
past
ten
years,
ecotoxicologists
have
started
to
build
models
of
ecological
systems
which
focus
on
interrelationships
in
function,
the
dynamics
of
stress,
and
the
adaptive
potential
for
recovery.
This
is
consistent
with
the
observation
that
chronic
sub­
lethal
exposures
may
affect
the
normal
functioning
of
individual
species
in
ways
that
make
it
less
than
competitive
and
therefore
more
susceptible
to
a
variety
of
factors
including
disease,
insect
attack,
and
decreases
in
habitat
quality.
15
All
of
these
factors
may
contribute
to
an
overall
change
in
the
structure
(
i.
e.,
composition)
and
function
of
the
ecosystem.
5
The
adverse,
non­
human
biological
effects
of
HAP
emissions
include
ecosystem
and
recreational
and
commercial
fishery
impacts.
Atmospheric
deposition
of
HAPs
directly
to
land
may
affect
terrestrial
ecosystems.
Atmospheric
deposition
of
HAPs
also
contributes
to
adverse
aquatic
ecosystem
effects.
This
not
only
has
adverse
implications
for
individual
wildlife
species
and
ecosystems
as
a
whole,
but
also
the
humans
who
may
ingest
contaminated
fish
and
waterfowl.
In
general,
HAP
emission
reductions
achieved
through
the
NESHAP
should
reduce
the
associated
adverse
environmental
impacts.

6.2.2
Benefits
of
Reduced
CO
Emissions
Due
to
HAP
Controls
As
is
mentioned
above,
controls
that
will
be
required
on
plywood
and
composite
wood
products
sources
to
reduce
HAPs
will
also
reduce
emissions
of
CO.
The
EPA
Staff
Paper
for
CO
provides
a
summary
of
the
health
effects
information
pertinent
to
the
NAAQS
for
CO16.
This
information
is
a
summary
of
information
from
the
CO
Criteria
Document
(
CD)
17,
which
provides
a
critical
review
of
a
wide
variety
of
health
effects
studies,
including
a
limited
number
of
newer
health
effects
studies,
as
well
as
older
studies.
Some
were
conducted
at
extremely
high
levels
of
CO
(
i.
e.
much
higher
than
typically
found
in
ambient
air);
however,
the
focus
of
this
Staff
Paper
is
on
those
key
controlled­
exposure
laboratory
studies
and
newer
epidemiology
studies,
which
were
conducted
with
human
subjects
at
COHb
levels
that
are
most
relevant
to
regulatory
decision
making.

Based
on
the
CD,
staff
concludes
that
human
health
effects
associated
with
exposure
to
CO
include
cardiovascular
system
and
central
nervous
system
(
CNS)
effects.
In
addition,
consideration
is
given
in
the
CD
to
combined
exposure
to
CO,
other
pollutants,
drugs,
and
the
influence
of
environmental
factors.
Cardiovascular
effects
of
CO
are
directly
related
to
reduced
oxygen
content
of
blood
caused
by
combination
of
CO
with
Hb
to
form
COHb,
resulting
in
tissue
hypoxia.
Most
healthy
individuals
have
mechanisms
(
e.
g.
increased
blood
flow,
blood
vessel
dilation)
which
compensate
for
this
reduction
in
tissue
O2,
although
the
effect
of
reduced
maximal
exercise
capacity
has
been
reported
in
healthy
persons
at
low
COHb
levels.
Several
other
medical
conditions
such
as
occlusive
vascular
disease,
chronic
obstructive
lung
disease,
and
anemia
can
increase
susceptibility
to
potential
adverse
effects
of
CO
during
exercise.

Effects
of
CO
on
the
CNS
involve
both
behavioral
and
physiological
changes.
These
include
modification
of
visual
perception,
hearing,
motor
and
sensorimotor
performance,
vigilance,
and
cognitive
ability.
Developmental
toxicity
effects
of
low­
level
ambient
CO
exposures,
though
not
well
studied
in
humans,
may
pose
a
threat
to
the
fetus.
Finally,
environmental
factors
(
e.
g.
altitude,
temperature),
drug
interaction,
and
pollutant
interaction
also
can
play
a
role
in
the
public
health
impact
of
ambient
CO
exposure.
There
is
little
new
information
on
these
effects.

Exhibit
6­
2
is
a
summary
of
key
health
effects
and
studies
which
have
been
identified
as
being
most
pertinent
to
a
regulatory
decision
on
the
NAAQS
for
CO18.
Each
of
the
key
studies
is
considered
in
light
of
limitations
discussed
in
the
CD
and
the
Staff
Paper.
For
example,
epidemiological
studies
are
limited
by
factors
such
as
exposure
uncertainties
and
confounding
variables,
and
many
of
the
controlled
exposure
studies
of
CO
health
effects
have
been
hampered
by
uncertainties
regarding
COHb
measurements,
relatively
small
sample
sizes,
and
lack
of
"
real
world"
exposure
conditions.
Exhibit
"
6­
2
Key
Health
Effects
of
Exposure
to
Ambient
Carbon
Monoxide
Target
Organ
Health
Effectsa,
b
Tested
Populationc
References
Lungs
Reduced
maximal
exercise
duration
with
1­
h
peak
CO
exposures
resulting
in

2.3%
COHb
(
GC)
Healthy
individuals
Drinkwater
et
al.
(
1974)

Raven
et
al.
(
1974b)

Horvath
et
al.
(
1975)

Heart
Reduced
time
to
ST
segment
change
of
the
ECG
(
earlier
onset
of
myocardial
ischemia)
with
peak
CO
exposures
resulting
in

2.4%
COHb
(
GC)
Individuals
with
coronary
artery
disease
Allred
et
al.
(
1989a,
b;

1991)

Heart
Reduced
exercise
duration
because
of
increased
chest
pain
(
angina)
with
peak
CO
exposures
resulting
in

3%
COHb
(
CO­
Ox)
Individuals
with
coronary
artery
disease
Anderson
et
al.
(
1973)

Sheps
et
al.
(
1987)

Adams
et
al.
(
1988)

Kleinman
et
al.
(
1989,

1998*)

Allred
et
al.
(
1989a,
b;

1991)

Heart
Increased
number
and
complexity
of
arrhythmia
(
abnormal
heart
rhythm)
with
peak
CO
exposures
resulting
in

6%
COHb
(
CO­
Ox)
Individuals
with
coronary
artery
disease
and
high
baseline
ectopy
(
chronic
arrhythmia)
Sheps
et
al.
(
1990)

Heart
Increased
hospital
admissions
associated
with
ambient
pollutant
exposures
Individuals
>
65
years
old
with
cardiovascular
disease
Schwartz
and
Morris
(
1995*)

Morris
et
al.
(
1995*)

Schwartz
(
1997*)

Burnett
et
al.
(
1997*)

Brain
Central
nervous
system
effects,
such
as
decrements
in
hand­
eye
coordination
(
driving
or
tracking)
and
in
attention
or
vigilance
(
detection
of
infrequent
events),
with
1­
h
peak
CO
exposures
(

5
to
20%
COHb)
Healthy
individuals
Horvath
et
al.
(
1971)

Fodor
and
Winneke
(
1972)

Putz
et
al.
(
1976,
1979)

Benignus
et
al.
(
1987)
aThe
EPA
has
set
significant
harm
levels
of
50
ppm
(
8­
h
average),
75
ppm
(
4­
h
average),
and
125
ppm
(
1­
h
average).
Exposure
under
these
conditions
could
result
in
COHb
levels
of
5
to
10%
and
cause
significant
health
effects
in
sensitive
individuals.

bMeasured
blood
COHb
level
after
CO
exposure.

cFetuses,
infants,
pregnant
women,
elderly
people,
and
people
with
anemia
or
with
a
history
of
cardiac
or
respiratory
disease
may
be
particularly
sensitive
to
CO.

dThis
table
is
a
reproduction
of
Table
6­
7
of
the
CD
(
p.
6­
36,
U.
S.
EPA,
1999a).

*
Newer
studies,
published
since
completion
of
the
last
CO
NAAQS
review.
Although
acute
poisoning
induced
by
CO
can
be
lethal
and
is
probably
the
best
known
health
endpoint
of
CO,
this
only
occurs
at
very
high
concentrations
of
CO
(
greater
than
100
ppm,
hourly
average),
which
are
not
pertinent
to
the
setting
of
the
NAAQS.
In
the
ambient
air,

exposures
to
lower­
levels
of
CO
predominate.
[
these
are
the
occupational
limits
 
why
are
they
being
presented
as
ambient?]
Very
little
data
are
available
demonstrating
human
health
effects
in
healthy
individuals
caused
by
or
associated
with
exposures
to
low
CO
concentrations.

Decrements
in
maximal
exercise
duration
and
performance
in
healthy
individuals
have
been
reported
at
COHb
levels
of
>
2.3%
an
d
>
4.3%
(
GC),

respectively;
however,
these
decrements
are
small
and
likely
to
affect
only
athletes
in
competition.
No
effects
were
seen
in
healthy
individuals
during
submaximal
exercise,
representing
more
typical
daily
activities,
at
levels
as
high
as
15
to
20
%
COHb20.
Most
recent
evidence
of
CNS
effects
induced
by
exposure
to
CO
indicates
that
behavioral
impairments
in
healthy
individuals
should
not
be
expected
until
COHb
levels
exceed
20%
(
CO­
Ox),
well
above
what
would
be
caused
by
typical
ambient
air
levels
of
CO21.
Evidence
of
CO­
induced
fetal
toxicity
or
of
interactions
with
high
altitudes,
drugs,
other
pollutants,
or
other
environmental
stresses
remains
uncertain
or
suggests
that
effects
of
concern
will
occur
in
healthy
individuals
only
with
exposure
to
much
higher
levels
of
CO
than
are
likely
for
offsite
receptors
for
these
facilities22.

6.3
Qualitative
Description
of
Effects
from
Reductions
and
Increases
in
Emissions
from
Other
Pollutants
Due
to
HAP
Controls
As
is
mentioned
above,
controls
that
will
be
required
on
PCWP
sources
to
reduce
HAPs
will
also
reduce
emissions
of
other
pollutants,

namely:
PM10,
PM2.5,
and
increase
NOx
and
SO2
emissions.
For
more
information
on
these
non­
HAP
emissions
and
emission
reductions,
please
refer
to
Chapter
3
of
this
RIA,
the
preamble
for
this
rule,
and
the
docket.
The
effects
associated
with
exposure
to
PM
(
both
coarse
and
fine),
NOx,

and
SO2
emissions
are
presented
below.
9
6.3.1
Effects
of
NOx
Emissions.

Emissions
of
NOx
produce
a
wide
variety
of
health
and
welfare
effects.
Nitrogen
dioxide
can
irritate
the
lungs
at
high
occupational
levels
and
may
lower
resistance
to
respiratory
infection,
although
the
research
has
been
equivocal.
NOx
emissions
are
an
important
precursor
to
acid
rain
and
may
affect
both
terrestrial
and
aquatic
ecosystems.
Atmospheric
deposition
of
nitrogen
leads
to
excess
nutrient
enrichment
problems
("
eutrophication")
in
the
Chesapeake
Bay
and
several
nationally
important
estuaries
along
the
East
and
Gulf
Coasts.
Eutrophication
can
produce
multiple
adverse
effects
on
water
quality
and
the
aquatic
environment,
including
increased
algal
blooms,
excessive
phytoplankton
growth,
and
low
or
no
dissolved
oxygen
in
bottom
waters.
Eutrophication
also
reduces
sunlight,
causing
losses
in
submerged
aquatic
vegetation
critical
for
healthy
estuarine
ecosystems.
Deposition
of
nitrogen­
containing
compounds
also
affects
terrestrial
ecosystems.
Nitrogen
fertilization
can
alter
growth
patterns
and
change
the
balance
of
species
in
an
ecosystem.

Nitrogen
dioxide
and
airborne
nitrate
also
contribute
to
pollutant
haze
(
often
brown
in
color),
which
impairs
visibility
and
can
reduce
residential
property
values
and
the
value
placed
on
scenic
views.

NOx
in
combination
with
volatile
organic
compounds
(
VOC)
also
serves
as
a
precursor
to
ozone.
Based
on
a
large
number
of
recent
studies,
EPA
has
identified
several
key
health
effects
that
may
be
associated
with
exposure
to
elevated
levels
of
ozone.
Exposures
to
ambient
ozone
concentrations
have
been
linked
to
increased
hospital
admissions
and
emergency
room
visits
for
respiratory
problems.
Repeated
exposure
to
ozone
may
increase
susceptibility
to
respiratory
infection
and
lung
inflammation
and
can
aggravate
preexisting
respiratory
disease,
such
as
asthma.
Repeated
prolonged
exposures
(
i.
e.,
6
to
8
hours)
to
ozone
at
levels
between
0.08
and
0.12
ppb,
over
months
to
years
may
lead
to
repeated
inflammation
of
the
lung,
impairment
of
lung
defense
mechanisms,
and
irreversible
changes
in
lung
structure,
which
could
in
turn
lead
to
premature
aging
of
the
lungs
and/
or
chronic
respiratory
illnesses
such
as
emphysema,
chronic
bronchitis,
and
asthma.

Children
have
the
highest
exposures
to
ozone
because
they
typically
are
active
outside
playing
and
exercising,
during
the
summer
when
ozone
levels
are
highest.
Further,
children
are
more
at
risk
than
adults
from
the
effects
of
ozone
exposure
because
their
respiratory
systems
are
still
developing.
Adults
who
are
outdoors
and
moderately
active
during
the
summer
months,
such
as
construction
workers
and
other
outdoor
workers,
also
are
among
those
with
the
highest
exposures.
These
individuals,
as
well
as
people
with
respiratory
illnesses
such
as
asthma,
especially
children
with
asthma,
may
experience
reduced
lung
function
and
increased
respiratory
symptoms,
such
as
chest
pain
and
cough,
when
exposed
to
relatively
low
ozone
levels
during
periods
of
moderate
exertion.
In
addition
to
human
health
effects,
ozone
adversely
affects
crop
yield,
vegetation
and
forest
growth,
and
the
durability
of
materials.
Ozone
causes
noticeable
foliar
damage
in
many
crops,
trees,
and
ornamental
plants
(
i.
e.,
grass,
flowers,
shrubs,
and
trees)
and
causes
reduced
growth
in
plants.

Particulate
matter
(
PM)
can
also
be
formed
from
NOx
emissions.
Secondary
PM
is
formed
in
the
atmosphere
through
a
number
of
physical
and
chemical
processes
that
transform
gases
such
as
NOx,
SO2,
and
VOC
into
particles.
A
discussion
of
the
effects
of
PM
on
human
health
and
the
environment
are
discussed
further
below.
Overall,
emissions
of
NOx
from
PCWP
sources
can
lead
to
some
of
the
effects
discussed
in
this
section
­
either
those
directly
related
to
NOx
emissions,
or
the
effects
of
ozone
and
PM
10
resulting
from
the
combination
of
NOx
with
other
pollutants.

6.3.2
Benefits
of
PM
Reductions.

Scientific
studies
have
linked
PM
(
alone
or
in
combination
with
other
air
pollutants)
with
a
series
of
health
effects
(
EPA,
1996).
Fine
particles
(
PM2.5)
can
penetrate
deep
into
the
lungs
to
contribute
to
a
number
of
the
health
effects.
These
health
effects
include
decreased
lung
function
and
alterations
in
lung
tissue
and
structure
and
in
respiratory
tract
defense
mechanisms
which
may
be
manifest
in
increased
respiratory
symptoms
and
disease
or
in
more
severe
cases,
increased
hospital
admissions
and
emergency
room
visits
or
premature
death.
Children,
the
elderly,
and
people
with
cardiopulmonary
disease,
such
as
asthma,
are
most
at
risk
from
these
health
effects.

PM
also
causes
a
number
of
adverse
effects
on
the
environment.
Fine
PM
is
the
major
cause
of
reduced
visibility
in
parts
of
the
U.
S.,
including
many
of
our
national
parks
and
wilderness
areas.
Other
environmental
impacts
occur
when
particles
deposit
onto
soil,
plants,
water,
or
materials.
For
example,
particles
containing
nitrogen
and
sulfur
that
deposit
onto
land
or
water
bodies
may
change
the
nutrient
balance
and
acidity
of
those
environments,
leading
to
changes
in
species
composition
and
buffering
capacity.
Particles
that
are
deposited
directly
onto
leaves
of
plants
can,
depending
on
their
chemical
composition,
corrode
leaf
surfaces
or
interfere
with
plant
metabolism.
Finally,
PM
causes
soiling
and
erosion
damage
to
materials.

Thus,
reducing
the
emissions
of
PM
and
PM
precursors
from
PCWP
sources
can
help
to
improve
some
of
the
effects
mentioned
above
­
either
those
related
to
primary
PM
emissions,
or
the
effects
of
secondary
PM
generated
by
the
combination
of
NOx
or
SO2
with
other
pollutants
in
the
atmosphere.

6.3.3
Effects
of
SO2
Emissions.

Very
high
concentrations
of
sulfur
dioxide
(
SO2)
affect
breathing
and
ambient
levels
have
been
hypothesized
to
aggravate
existing
respiratory
and
cardiovascular
disease.
Potentially
sensitive
populations
include
asthmatics,
individuals
with
bronchitis
or
emphysema,
children
and
the
elderly.
SO2
is
also
a
primary
contributor
to
acid
deposition,
or
acid
rain,
which
causes
acidification
of
lakes
and
streams
and
can
damage
trees,
crops,
historic
buildings
and
statues.
In
addition,
sulfur
compounds
in
the
air
contribute
to
visibility
impairment
in
large
parts
of
the
country.
This
is
especially
noticeable
in
national
parks.

PM
can
also
be
formed
from
SO2
emissions.
Secondary
PM
is
formed
in
the
atmosphere
through
a
number
of
physical
and
chemical
processes
that
transform
gases,
such
as
SO2,
into
particles.
Overall,
emissions
of
SO2
can
lead
to
some
of
the
effects
discussed
in
this
section
­
either
those
directly
related
to
SO2
emissions,
or
the
effects
of
ozone
and
PM
resulting
from
the
combination
of
SO2
with
other
pollutants.

6.4
Lack
Of
Approved
Methods
To
Quantify
HAP
Benefits
11
The
most
significant
effect
associated
with
the
HAPs
that
are
controlled
with
the
rule
is
the
potential
incidence
of
cancer.
In
previous
analyses
of
the
benefits
of
reductions
in
HAPs,
EPA
has
quantified
and
monetized
the
benefits
of
potential
reductions
in
the
incidences
of
cancer
23,
24.
In
some
cases,
EPA
has
also
quantified
(
but
not
monetized)
reductions
in
the
number
of
people
exposed
to
noncancer
HAP
risks
above
no­
effect
levels25.

Monetization
of
the
benefits
of
reductions
in
cancer
incidences
requires
several
important
inputs,
including
central
estimates
of
cancer
risks,
estimates
of
exposure
to
carcinogenic
HAPs,
and
estimates
of
the
value
of
an
avoided
case
of
cancer
(
fatal
and
non­
fatal).
In
the
above
referenced
analyses,
EPA
relied
on
unit
risk
factors
(
URF)
developed
through
risk
assessment
procedures.
The
unit
risk
factor
is
a
quantitative
estimate
of
the
carcinogenic
potency
of
a
pollutant,
often
expressed
as
the
probability
of
contracting
cancer
from
a
70
year
lifetime
continuous
exposure
to
a
concentration
of
one

g/
m3
of
a
pollutant.
These
URFs
are
designed
to
be
conservative,
and
as
such,
are
more
likely
to
represent
the
high
end
of
the
distribution
of
risk
rather
than
a
best
or
most
likely
estimate
of
risk.

In
a
typical
analysis
of
the
expected
health
benefits
of
a
regulation
(
e.
g.,
the
Heavy­
Duty
Engine
/
Diesel
Fuel
Regulatory
Impact
Analysis),
health
effects
are
estimated
by
applying
changes
in
pollutant
concentrations
to
best
estimates
of
risk
obtained
from
epidemiological
studies.
As
the
purpose
of
a
benefit
analysis
is
to
describe
the
benefits
most
likely
to
occur
from
a
reduction
in
pollution,
use
of
highend
conservative
risk
estimates
will
over­
estimate
the
expected
benefits
of
the
regulation.
For
this
reason,
we
will
not
attempt
to
quantify
the
health
benefits
of
reductions
in
HAPs
unless
best
estimates
of
risks
are
available.
While
we
used
high­
end
risk
estimates
in
past
analyses,
recent
advice
from
the
EPA
Science
Advisory
Board
(
SAB)
and
internal
methods
reviews
have
suggested
that
we
avoid
using
highend
estimates
in
current
analyses.
EPA
is
working
with
the
SAB
to
develop
better
methods
for
analyzing
the
benefits
of
reductions
in
HAPs.

While
not
appropriate
for
inclusion
in
our
primary
quantified
benefits
analysis,
to
estimate
the
potential
baseline
risks
posed
by
the
PCWP
source
category
and
the
potential
impact
of
applicability
cutoffs,
EPA
performed
a
"
rough"
risk
assessment
for
185
of
the
223
facilities
in
the
PCWP
source
category.
There
are
large
uncertainties
regarding
all
components
of
the
risk
quantification
step,
including
location
of
emission
reductions,
emission
estimates,
air
concentrations,
exposure
levels
and
dose­
response
relationships.
However,
if
these
uncertainties
are
properly
identified
and
characterized,
it
is
possible
to
provide
upper
bound
estimates
of
the
potential
reduction
in
inhalation
cancer
incidence
associated
with
this
rule.
It
is
important
to
keep
in
mind
that
these
estimates
will
not
cover
non­
inhalation
based
cancer
risks
and
non­
cancer
health
effects.

The
HAP
included
in
this
"
rough"
risk
assessment
were
acetaldehyde,
acrolein,
benzene,
formaldehyde,
manganese,
methanol,
methylene
chloride,
and
phenol.
Of
these
HAP,
four
are
presently
not
considered
to
have
thresholds:
acetaldehyde,
benzene,
formaldehyde,
and
methylene
chloride.

Of
the
185
facilities
assessed,
148
facilities
were
found
to
pose
cancer
risks
equal
to
or
greater
than
1
in
1,000,000
to
their
surrounding
population.
Forty­
six
facilities
were
predicted
to
pose
cancer
risks
of
1
in
100,000
or
greater,
and
two
PCWP
facilities
were
found
to
pose
cancer
risks
equal
to
or
greater
than
1
in
10,000.

If
this
rule
is
implemented
at
all
PCWP
facilities,
annual
cancer
incidence
would
be
reduced
from
12
about
0.09
cases/
year
to
about
0.02
cases/
year,
while
the
number
of
people
at
or
above
a
cancer
risk
level
of
1
in
a
million
would
be
reduced
from
about
900,000
to
150,000.
The
HAP
contributing
the
greatest
to
this
estimate
were .
In
addition,
the
number
of
people
exposed
to
hazard
index
(
HI)
values
equal
to
or
greater
than
1
was
estimated
to
be
reduced
from
about
270,000
to
about
30,000.
The
HAP
contributing
the
greatest
to
this
estimate
were .
(
Details
of
these
analyses
are
available
in
the
docket).
EPA
has
not
tried
to
monetize
this
reduced
incidence
of
inhalation
cancer
for
several
important
technical
reasons.
The
primary
reasons
include
the
lack
of
information
on
the
latency
period
for
the
onset
of
the
disease
and
the
fact
that
we
have
no
information
on
the
proportion
of
fatal
versus
nonfatal
cancers
which
may
occur.
These
factors
prevent
us
from
providing
monetized
estimates.

For
non­
cancer
health
effects,
previous
analyses
have
estimated
changes
in
populations
exposed
above
the
reference
concentration
level
(
RfC).
However,
this
requires
estimates
of
populations
exposed
to
HAPs
from
controlled
sources.
Due
to
data
limitations,
we
do
not
have
sufficient
information
on
emissions
from
specific
sources
and
thus
are
unable
to
model
changes
in
population
exposures
to
ambient
concentrations
of
HAPs
above
the
RfC.
As
a
result,
we
are
unable
to
place
a
monetary
value
of
the
HAP
related
benefits
associated
with
this
rule.

6.5
Summary
The
HAPs
that
are
reduced
as
a
result
of
implementing
the
plywood
and
composite
wood
products
NESHAP
will
produce
a
variety
of
benefits,
some
of
which
include:
a
possible
reduction
in
the
incidence
of
cancer
to
exposed
populations,
neurotoxicity,
irritation,
and
crop
or
plant
damage.
The
rule
will
also
produce
benefits
associated
with
reductions
in
CO.
Human
health
effects
associated
with
exposure
to
CO
include
cardiovascular
system
and
central
nervous
system
(
CNS)
effects.
Although
we
are
unable
to
place
a
monetary
value
on
these
benefits,
the
information
on
the
variety
of
effects
associated
with
these
pollutants
and
the
level
of
reductions
anticipated
from
the
NESHAP
indicate
that
the
benefits
of
the
rule
will
be
substantial.
13
6.6
REFERENCES
1.
U.
S.
Environmental
Protection
Agency.
Regulatory
Impact
Analysis
for
the
National
Emissions
Standards
for
Hazardous
Air
Pollutants
for
Source
Categories:
Organic
Hazardous
Air
Pollutants
from
the
Synthetic
Organic
Chemical
Manufacturing
Industry
and
Seven
Other
Processes.
Draft
Report.
Office
of
Air
Quality
Planning
and
Standards.
Research
Triangle
Park,
NC.
EPA­
450/
3­
92­
009.
December
1992.

2.
Mathtech,
Inc.
Benefit
Analysis
Issues
for
Section
112
Regulations.
Final
report
prepared
for
U.
S.
Environmental
Protection
Agency.
Office
of
Air
Quality
Planning
and
Standards.
Contract
No.
68­
D8­
0094.
Research
Triangle
Park,
NC.
May
1992.

3.
U.
S.
Environmental
Protection
Agency.
Cancer
Risk
from
Outdoor
Exposure
to
Air
Toxics.
Volume
I.
EPA­
450/
1­
90­
004a.
Office
of
Air
Quality
Planning
and
Standards.
Research
Triangle
Park,
NC.
September
1990.

4.
Graham,
John
D.,
D.
R.
Holtgrave,
and
M.
J.
Sawery.
"
The
Potential
Health
Benefits
of
Controlling
Hazardous
Air
Pollutants."
In:
Health
Benefits
of
Air
Pollution
Control:
A
Discussion.
Blodgett,
J.
(
ed).
Congressional
Research
Service
report
to
Congress.
CR589­
161.
Washington,
DC.
February
1989.

5.
Reference
4.

6.
Voorhees,
A.,
B.
Hassett,
and
I.
Cote.
Analysis
of
the
Potential
for
Non­
Cancer
Health
Risks
Associated
with
Exposure
to
Toxic
Air
Pollutants.
Paper
presented
at
the
82nd
Annual
Meeting
of
the
Air
and
Waste
Management
Association.
1989.

7.
Reference
4.

8.
Reference
6.

9.
Cote,
I.,
L.
Cupitt
and
B.
Hassett.
Toxic
Air
Pollutants
and
Non­
Cancer
Health
Risks.
Unpublished
paper
provided
by
B.
Hassett.
1988.

10.
NAS.
Chlorine
and
Hydrogen
Chloride.
National
Academy
of
Sciences,
National
Research
Council.
Chapter
7.
1975.

11.
Stern,
A.
et
al.
Fundamentals
of
Air
Pollution.
Academic
Press,
New
York.
1973.

12.
Weinstein,
D.
and
E.
Birk.
The
Effects
of
Chemicals
on
the
Structure
of
Terrestrial
Ecosystems:
Mechanisms
and
Patterns
of
Change.
In:
Levin,
S.
et
al.
(
eds).
Ecotoxicology:
Problems
and
Approaches.
Chapter
7.
pp.
181­
209.
Springer­
Verlag,
New
York.
1989.

13.
U.
S.
Environmental
Protection
Agency.
Integrated
Risk
Information
System;
website
access
available
at
www.
epa.
gov/
ngispgm3/
iris.
14.
Reference
1.
p.
3­
5.

14.
Reference
1.
pp.
8­
4
to
8­
5.

15.
U.
S.
Environmental
Protection
Agency.
Ecological
Exposure
and
Effects
of
Airborne
Toxic
Chemicals:
An
Overview.
EPA/
6003­
91/
001.
Environmental
Research
Laboratory.
Corvallis,
OR.
1991.

16.
U.
S.
Environmental
Protection
Agency;
Staff
Paper
for
the
Carbon
Monoxide
NAAQS;
Office
of
Air
Quality
Planning
and
Standards,
Research
Triangle
Park,
N.
C.;
2000.

17.
U.
S.
Environmental
Protection
Agency;
Criteria
Document
for
Carbon
Monoxide;
Office
of
Air
Quality
Planning
and
Standards,
Research
Triangle
Park,
N.
C.;
1999.

18.
Reference
17
at
Section
6.9.

19.
Reference
18.

20.
Reference
18.

21.
Reference
18.

22.
Reference
18.

23.
U.
S.
Environmental
Protection
Agency.
1992.
Draft
Regulatory
Impact
Analysis
of
National
Emissions
Standards
for
Hazardous
Air
Pollutants
for
By
Product
Coke
Oven
Charging,
Door
Leaks,
and
Topside
Leaks.
Office
of
Air
Quality
Planning
and
Standards,
Research
Triangle
Park,
NC.

24.
U.
S.
Environmental
Protection
Agency.
1995.
Regulatory
Impact
Analysis
for
the
Petroleum
Refinery
NESHAP.
Revised
Draft
for
Promulgation.
Office
of
Air
Quality
Planning
and
Standards,
Research
Triangle
Park,
NC.

25.
Reference
24.
