1
EPA
Registration
Division
contact:
Bipin
Gandhi
(
703
308­
8380)

ExxonMobil
Chemical
Company
[
4E6935]

EPA
has
received
a
pesticide
petition
[
4E6935]
from
ExxonMobil
Chemical
Company
(
ExxonMobil),
division
of
Exxon
Mobil
Corporation,
13501
Katy
Freeway,
Houston,
TX
77079
proposing,
pursuant
to
section
408(
d)
of
the
Federal
Food,
Drug,
and
Cosmetic
Act
(
FFDCA),
21
U.
S.
C.
346a(
d),
to
amend
40
CFR
part
180
to
establish
an
exemption
from
the
requirement
of
a
tolerance
for
C9
Rich
Aromatic
Hydrocarbon
Fluid,
(
Aromatic
100
Fluid),
in
or
on
the
raw
agricultural
commodities.
EPA
has
determined
that
the
petition
contains
data
or
information
regarding
the
elements
set
forth
in
section
408(
d)(
2)
of
the
FFDCA;
however,
EPA
has
not
fully
evaluated
the
sufficiency
of
the
submitted
data
at
this
time
or
whether
the
data
supports
granting
of
the
petition.
Additional
data
may
be
needed
before
EPA
rules
on
the
petition.

A.
Residue
Chemistry
1.
Plant
metabolism.
Due
to
the
inherent
physicochemical
properties
(
volatility)
of
C9
Rich
Aromatic
Hydrocarbon
Fluid,
there
is
little
likelihood
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
remaining
intact
in
any
crop
matrix.

B.
Toxicological
Profile
2
1.
Acute
toxicity.
C9
Rich
Aromatic
Hydrocarbon
Fluid
has
a
low
order
of
acute
toxicity
based
on
studies
conducted
in
rats
via
oral
and
inhalation
exposure,
and
in
rabbits
via
dermal
exposure.
The
oral
LD50
of
1,2,4­
trimethylbenzene,
a
structurally
similar
analog,
was
3.4
and
6.0
g/
kg
in
rats
(
US
EPA
1976).
A
four­
hour
acute
inhalation
study
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
(
Aromatic
100
Fluid)
showed
no
mortality
at
the
maximum
attainable
vapor
concentration
(
6193
mg/
m3
or
1192
ppm)
(
EMBSI
1996).
Some
animals
exhibited
decreased
motor
activity
during
exposure,
but
all
animals
appeared
normal
following
removal
from
the
chamber
and
no
clinical
signs
were
observed
during
the
14­
day
postexposure
observation
period.
There
were
no
abnormalities
observed
following
gross
post­
mortem
examination.
Based
on
this
study,
inhalation
exposure
to
C9
Rich
Aromatic
Hydrocarbon
Fluid
up
to
the
maximum
attainable
vapor
concentrations
does
not
result
in
mortality
or
gross
systemic
toxicity.
The
acute
dermal
study
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
in
rabbits
exceeds
3.1
g/
kg.
All
animals
survived
to
study
termination
and
clinical
signs
of
skin
irritation
were
minimal,
indicating
that
the
dermal
LD50
exceeds
3.1
g/
kg
(
EMBSI
1984).
These
data
demonstrate
that
C9
Rich
Aromatic
Hydrocarbon
Fluid
has
low
acute
toxicity
by
all
routes
of
exposure.
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
a
moderate
skin
irritant
in
rabbits.
Also,
an
eye
irritation
study
in
rabbits
showed
that
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
a
mild
to
moderate
eye
irritant.

2.
Genotoxicity.
Aromatic
fluids
containing
primarily
C9
Aromatic
Hydrocarbon
Material
(
C9AHM)
have
been
tested
in
several
mutagencity
assays,
all
showing
no
evidence
of
mutagenic
activity.
C9AHM
showed
no
evidence
of
causing
mutagenic
effects
when
tested
for
mutagenic
activity
in
the
following
in
vitro
tests:
bacterial
reverse
mutation
assay;
CHO
gene
mutation
assay;
CHO
sister
chromatid
exchange
assay;
and
CHO/
HGPRT
forward
mutation
suspension
assay
(
Schreiner
et
al
1989).
In
addition,
C9AHM
was
tested
in
an
in
vivo
bone
marrow
chromosomal
3
aberration
test
(
Schreiner
et
al.
1989).
There
was
no
indication
of
mutagenic
activity
in
any
of
the
assays,
providing
evidence
that
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
not
mutagenic.

3.
Reproductive
and
developmental
toxicity.
C9
Rich
Aromatic
Hydrocarbon
Fluid
showed
no
evidence
of
causing
developmental
toxicity
and
is
unlikely
to
be
a
selective
developmental
toxicant.
Based
on
the
data
from
C9AHM,
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
unlikely
to
be
a
reproductive
toxicant.
C9AHM
has
been
tested
for
both
reproductive
and
developmental
toxicity.
In
a
mouse
inhalation
developmental
toxicity
test,
there
was
evidence
of
developmental
delays
at
maternally
toxic
levels,
but
there
was
no
evidence
of
selective
developmental
toxicity
(
McKee
et
al.
1990).
Pregnant
mice
were
exposed
to
100,
500,
or
1500
ppm
for
6
hr/
day
from
days
6­
15
of
gestation.
Exposure
to
1500
ppm
produced
severe
maternal
toxicity
and
fetal
effects
including
mortality,
reduced
body
weight,
delayed
ossification
and
an
increased
incidence
of
cleft
palate.
Exposure
to
500
ppm
resulted
in
a
significant
reduction
in
fetal
weight
gain,
but
no
other
evidence
of
developmental
effects,
nor
any
adverse
effects
in
the
maternal
animals.
The
lowest
dose
level
(
100
ppm)
did
not
cause
any
developmental
toxicity.
C9AHM
was
evaluated
in
a
three­
generation
reproduction
study
by
inhalation
in
rats
at
0,
100,
500,
or
1500
ppm
(
McKee
et
al.
1990).
1
The
only
adverse
reproductive
effect
among
parental
animals
was
reduced
fertility
in
high
dose
F1
males.
However,
comparable
effects
were
not
seen
in
FO
or
F2
males,
or
among
females
of
any
generation.
The
500
ppm
dose
level
was
identified
as
the
NOAEL
with
respect
to
reproductive
effects
across
all
three
generations;
further
analysis
of
the
data,
however,
support
the
conclusion
that
even
the
1500
ppm
dose
level
displayed
a
lack
of
adverse
reproductive
effects.
Exposure
at
the
mid­
and
high­
dose
1
Actual
exposures
were
0,
103,
495
and
1480
ppm.
4
levels
resulted
in
reduced
parental
weight
gain
in
both
the
F0
and
F1
generations,
resulting
in
a
NOAEL
for
parental
systemic
toxicity
of
100
ppm.
For
F2
rats,
this
effect
was
seen
at
100
ppm
as
well.
Thus,
there
was
no
consistent
evidence
of
reproductive
toxicity
even
at
exposure
levels
that
resulted
in
significantly
reduced
parental
weight
gain.
Based
on
these
data,
the
NOAEL
for
reproductive
effects
is
either
500
or
1500
ppm.
The
NOAEL
for
parental
system
toxicity
is
100
ppm
in
the
F0
and
F1
generations,
and
the
LOAEL
is
100
ppm
in
the
F2
generation.
The
NOAEL
for
offspring
toxicity
is
500
ppm
in
the
F1
and
F2
generations,
and
100
ppm
in
the
F3
generation.

4.
Subchronic
toxicity.
The
available
data
show
that
C9
Rich
Aromatic
Hydrocarbon
Fluid
has
low
order
of
subchronic
toxicity
by
the
inhalation
and
oral
routes
of
exposure.
In
one
study,
rats
were
exposed
via
inhalation
to
a
50/
50
mixture
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
at
450,
900,
and
1800
mg/
m3
for
6
hours/
day,
5
days/
week
for
twelve
months
(
Clark
et
al.
1989).
Transient
changes
in
hematologic
and
plasma
clinical
chemical
parameters
and
increased
liver
and
kidney
weights
were
observed
at
the
highest
dose
only.
No
corresponding
histopathological
differences
or
evidence
of
exposure­
related
kidney
dysfunction
were
observed,
leading
the
study
researchers
to
conclude
that
the
observed
effects
were
physiological
adaptive
responses
and
not
biologically
significant.
The
study
NOAEL
was
greater
than
1800
mg/
m3.
In
a
90­
day
oral
gavage
subchronic
toxicity
study
on
a
structurally
related
analog,
1,3,5­
trimethylbenzene,
(
IIT
Research
Institute
1995),
Sprague
Dawley
rats
were
dosed
at
levels
of
0,
50,
200
and
600
mg/
kg/
day.
A
satellite
groups
received
600
mg/
kg/
day
and
was
held
for
a
28­
day
recovery
period.
There
were
no
treatment­
related
deaths
during
the
study.
There
was
a
statistically
significant
decrease
in
body
weight
gain
in
the
high
dose
males
at
the
end
of
Week
5;
although
weight
gain
in
the
high
dose
males
was
still
decreased
compared
to
controls
at
the
end
of
the
treatment
period,
cumulative
body
weight
gain
was
not
significantly
5
different
in
treatment
versus
control
animals.
In
addition,
cumulative
body
weight
gain
in
the
recovery
animals
at
the
end
of
the
28­
day
recovery
period
was
similar
to
control
animals.
The
only
significant
changes
observed
were
increased
phosphorous
levels
and
alterations
in
liver
and
kidney
weights
in
high
dose
animals.
At
the
end
of
the
28­
day
recovery
period,
these
effects
were
no
longer
observed,
indicating
that
these
effects
are
reversible.
These
effects
were
considered
an
adaptive
response
and
therefore
not
an
adverse
effect
from
exposure
to
the
test
material.
Based
on
the
results
of
this
study,
the
NOAEL
was
600
mg/
kg/
day.
The
neurotoxicity
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
was
assessed
as
part
of
a
neurobehavioral
testing
program
on
aliphatic,
cycloaliphatic
and
aromatic
hydrocarbon
solvents.
This
study
suggests
that
C9
Rich
Aromatic
Hydrocarbon
Fluid
can
cause
slight,
transient
central
nervous
system
depression
 
with
related,
minor
neurobehavioral
effects
which
are
known
to
occur
under
conditions
of
very
high
exposures
to
hydrocarbon
solvents 
but
that
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
not
expected
to
cause
any
nervous
system
damage.
This
test
program
was
jointly
sponsored
by
the
Dutch
government
and
the
CEFIC
Hydrocarbon
Solvent
Producers
Association
(
Nessel
et
al.
2000;
TNO
Nutrition
and
Food
Research
Institute
2001).
The
purpose
of
this
testing
program
was
to
develop
data
on
the
neurobehavioral
effects
of
hydrocarbon
solvent
constituents
on
the
central
nervous
system.
Most
representative
for
purposes
of
evaluating
the
toxicity
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
was
the
test
on
C10­
C11
Aromatics.
Male
rats
were
exposed
by
inhalation,
8
hours
per
day
for
3
consecutive
days
to
0,
35,
110
or
365
ppm
(
0,
0.2,
0.6
and
2.0
g/
m3).
Animals
were
tested
for
effects
on
motor
activity,
functional
observation
measures
(
FOB),
and
learned
performance
of
a
visual
discrimination
task.
No
remarkable
clinical
signs
were
observed
during
the
testing
period.
Some
low
to
moderate
gait
abnormalities
were
observed
during
the
3­
day
exposure
period
in
rats
exposed
at
the
maximum
concentration
level.
In
the
learned
performance
test,
the
high
dose
rats
had
increased
latencies
to
make
a
6
correct
choice
and
latencies
to
obtain
water
reinforcement,
as
well
as
increases
in
the
variability
of
the
speed
of
responding.
A
small,
but
statistically
significant,
decrease
in
the
number
of
collected
reinforcements
also
was
observed
in
the
high
dose
group.
Effects
of
exposure
were
most
clearly
observed
after
the
first
eight­
hour
exposure
period.
The
LOAEL
for
this
test
was
365
ppm
(
2.0
g/
m3),
and
the
NOAEL
was
110
ppm
(
0.6
g/
m3).

5.
Chronic
toxicity.
C9
Rich
Aromatic
Hydrocarbon
Fluid
has
not
been
tested
specifically
for
carcinogenicity
because
data
on
its
structure
and
metabolism,
subchronic
health
effects,
and
genotoxicity
indicate
that
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
not
likely
to
have
carcinogenic
properties.
C9
Rich
Aromatic
Hydrocarbon
Fluid
does
not
belong
to
a
class
of
chemicals
known
to
react
with
DNA,
nor
is
it
metabolized
to
materials
that
are
likely
to
react
with
DNA.
The
data
available
for
C9
Rich
Aromatic
Hydrocarbon
Fluid
indicate
that
this
compound
is
not
genotoxic
and
also
does
not
produce
significant
cumulative
toxicity.
Therefore,
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
unlikely
to
be
carcinogenic
either
by
genetic
or
epigenetic
mechanisms
and
is
unlikely
to
be
either
an
inducer
or
promoter
of
carcinogenicity.
In
addition,
when
C9AHM
was
evaluated
as
part
of
a
TSCA
Section
4
Test
Rule,
EPA
concluded
based
on
the
negative
mutagenicity
studies
and
other
available
data
that
no
further
mutagenicity
or
carcinogenicity
testing
of
these
compounds
was
required.

6.
Animal
metabolism.
Due
to
the
complex,
multi­
constituent
nature
of
these
types
of
aromatic
hydrocarbon
solvents,
absorption,
metabolism,
distribution
and
excretion
studies
are
not
conducted
specifically
on
C9
Rich
Aromatic
Hydrocarbon
Fluid.
However,
sufficient
data
on
other
aromatic
solvents
 
such
as
alkylbenzenes
and
alkylnaphthalenes
 
exist
to
describe
the
absorption,
distribution,
7
metabolism
and
excretion
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
(
Hissink,
et
al.
1999;
Snyder
1987;
Patty's
Toxicology
2001;
European
Union,
1999).
Typically,
aromatic
hydrocarbons
are
well
absorbed,
widely
distributed
between
tissues,
extensively
metabolized
and
rapidly
excreted.
Heavy
aromatic
hydrocarbon
solvents
are
generally
wellabsorbed
by
most
routes
of
exposure.
They
are
rapidly
absorbed
into
the
blood
from
oral,
dermal
or
inhalation
routes
of
exposure,
although
the
efficiency
of
dermal
absorption
varies
depending
on
the
molecular
weight
and
structure
of
the
compounds.
Following
absorption,
heavy
aromatic
hydrocarbon
solvents
distribute
throughout
the
body
and
are
extensively
metabolized
and
eliminated.
Typically,
these
solvents
will
be
found
at
higher
levels
in
the
organs
of
metabolism
and
excretion,
although
they
can
distribute
to
other
tissues
as
well,
particularly
those
with
high
lipid
content.
The
most
common
metabolic
pathway
for
heavy
aromatic
hydrocarbon
solvents
is
oxidation
followed
by
conjugation.
Cytochrome
P450
catalyzes
the
oxidation
of
the
solvents
to
alcohol
or
acidic
forms.
For
compounds
with
side
chains
 
including
many
constituents
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
 
side
chain
oxidation
is
the
first
step
in
metabolism.
Glucuronidation
and
sulfation
are
both
common
Phase
II
reactions
in
the
metabolism
of
heavy
aromatic
hydrocarbon
solvents,
and
these
reactions
typically
occur
in
the
liver.
Other
conjugation
reactions
also
may
occur.
This
conjugation
typically
serves
to
detoxify
the
heavy
aromatic
hydrocarbon
solvent
metabolites,
and
the
conjugates
often
can
be
found
excreted
in
the
urine.
Heavy
aromatic
hydrocarbon
solvents
are
rapidly
excreted.
Both
rodents
and
humans
show
similar
clearance
kinetics
of
hydrocarbons
from
blood.
Typically,
they
are
excreted
as
various
metabolites
in
the
urine,
although
some
parent
compound
may
still
be
present.
Urine
is
the
primary
route
of
excretion
for
hydrophilic
conjugates
from
both
oral
and
inhalation
exposure
to
heavy
aromatic
hydrocarbon
solvents,
although
a
much
smaller
fraction
of
metabolite
excretion
can
also
occur
through
the
feces.
Some
lower
molecular
weight
components
of
heavy
aromatic
hydrocarbon
solvents
 
including
a
few
of
the
constituents
in
C9
Rich
Aromatic
Hydrocarbon
Fluid
 
may
also
be
8
excreted
through
the
lung.
In
radiotracer
experiments,
most
heavy
aromatic
hydrocarbon
solvents
are
almost
completely
eliminated
from
the
body
within
48
hours,
although
small
amounts
may
reside
in
organs
with
high
lipid
content
for
slightly
longer
periods
of
time.

7.
Metabolite
toxicology.
There
are
no
known
metabolites
of
toxicological
concern.

8.
Endocrine
disruption.
There
are
no
significant
findings
in
other
relevant
toxicity
tests,
i.
e.,
developmental
toxicity,
which
would
suggest
that
C9
Rich
Aromatic
Hydrocarbon
Fluid
produces
effects
characteristic
of
the
disruption
of
endocrine
function.
In
addition,
the
absence
of
any
endocrine­
related
structural
alerts
suggest
that
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
not
likely
to
have
endocrine­
disrupting
properties.

C.
Aggregate
Exposure
1.
Dietary
exposure.
For
Tier
1
"
generic
inert"
acute
and
chronic
estimates,
a
conservative
approach
was
taken
which
did
not
account
for
considerations
of
inert
ingredient­
specific
weight
fractions
and
effective
application
rates,
or
for
evaporative
loss,
an
important
physical
property
of
the
C9
Rich
Aromatic
Hydrocarbon
Fluid.
In
addition,
actual
application
rates
are
lower
than
the
tolerance­
based
residue
data
used
in
the
Tier
1
assessment.
Therefore,
Tier
1
estimates
on
C9
Rich
Aromatic
Hydrocarbon
Fluid
represent
a
conservative
assessment.
Physicochemical
properties
of
C9
Rich
Aromatic
Hydrocarbon
Fluid,
e.
g.,
volatility,
which
directly
impacts
bioavailability,
were
considered
in
assessing
potential
dietary
exposure.
Evaporative
loss
experiments
were
conducted
using
ASTM
Method
D3539
(
Section
16.2)
on
structurally
related
analogs
to
show
that
there
was
significant
potential
for
evaporative
9
loss
from
treated
agricultural
surfaces.
These
studies
showed
that
the
evaporative
loss
rate
for
C9
Rich
Aromatic
Hydrocarbon
Fluid
was
rapid
and
far
exceeded
the
realistic
application
rate.
These
data
represent
a
conservative
evaporative
loss
rate
estimates
since
environmental
conditions,
e.
g.,
air
movement
and
variable
temperature,
were
not
taken
into
consideration.
To
further
explore
the
potential
for
evaporative
loss
and
the
impact
on
dietary
exposure
to
C9
Rich
Aromatic
Hydrocarbon
Fluid,
a
refined
Tier
2
and
3
dietary
exposure
analysis
was
developed
based
on
selection
of
publicly
available
surrogate
food
residue
data
for
volatile
pesticide
active
ingredients.
These
volatile
active
ingredients,
which
have
vapor
pressures
less
than
that
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
and
associated
"
relative
diffusion"
or
loss
to
air
that
are
generally
much
lower
than
those
for
C9
Rich
Aromatic
Hydrocarbon
Fluid,
have
extensive
food
residue
data
reported
in
the
USDA
Pesticide
Data
Program
(
PDP).
The
extensive,
multiyear
PDP
data
for
these
two
volatile
surrogates
were
all
below
the
detection
limit
therefore,
these
data
clearly
demonstrate
the
low
potential
for
food
residues
associated
with
relatively
volatile
chemicals
used
on
a
variety
of
fruits
and
vegetables.
For
the
health
benchmark,
a
review
of
the
dataset
suggested
that
the
most
sensitive
acute
endpoint
is
the
reduced
weight
gain
for
both
maternal
animals
and
offspring
in
the
developmental
study,
with
a
NOAEL
of
100
ppm
for
offspring
and
500
ppm
for
maternal
animals.
Because
the
majority
of
exposure
to
C9
Rich
Aromatic
Hydrocarbon
Fluid
as
a
pesticide
inert
will
occur
through
the
oral
route,
these
inhalation
NOAELs
wer
converted
to
oral
NOAELs
of
182
mg/
kg/
day
(
offspring)
and
909
mg/
kg/
day
(
maternal
animals).
Consistent
with
EPA
practice,
a
100­
fold
safety
factor
(
or
Margin
of
Exposure,
MOE)
was
applied
to
these
NOAELs
to
determine
the
level
at
which
adverse
effects
would
not
be
anticipated.
For
the
chronic
endpoint,
a
NOAEL
of
600
mg/
kg/
day
was
applied
based
on
the
subchronic
toxicity
study
on
1,3,5
trimethylbenzene,
which
showed
reversible
increased
phosphorous
levels
and
alterations
in
liver
and
kidney
weights.
In
addition
the
NOAEL
in
the
12­
month
inhalation
study
in
rats
on
C9
Rich
Aromatic
Hydrocarbon
Fluid
showed
10
NOAEL
of
1,800
mg/
m3,
equivalent
to
169
mg/
kg/
day.
To
ensure
a
highly
conservative
risk
assessment,
an
additional
10­
fold
safety
factor
was
applied
to
the
usual
100­
fold
safety
factor,
resulting
in
a
chronic
safety
factor
of
1000.
No
additional
database
uncertainty
factors
were
warranted
since
C9
Rich
Aromatic
Hydrocarbon
Fluid
has
been
assessed
for
all
major
toxicological
endpoints.

i.
Food.
A
conservative
tiered
dietary
exposure
assessment
was
conducted.
Exposure
values
were
expressed
in
terms
of
margin
of
exposure
(
MOE)
which
was
calculated
by
dividing
the
NOAEL
by
the
exposure
for
each
population
subgroup.
The
acute
MOEs
focused
on
the
lowest
NOAELs
developmental/
maternal
toxicity,
and
therefore,
are
based
on
upper­
percentile
(
99.9th)
exposures
for
the
subpopulations
of
females
in
reproductive
age,
i.
e.,
13
to
49
years,
and
children
1
to
2
years
(
the
highest
exposed
subgroup).
Tier
I
screening
level
analysis
for
a
generic
inert,
adjusted
for
evaporative
loss,
resulted
in
acceptable
acute
and
chronic
MOEs.
When
a
conservative
evaporative
loss
rate
of
98%
is
adopted,
while
retaining
all
other
conservative
assumptions
in
the
exposure
assessment,
the
MOE
far
exceeded
the
acceptable
level
of
100.
Chronic
dietary
MOEs,
even
with
no
consideration
for
evaporative
loss,
far
exceeded
the
acceptable
MOE
of
1000.
In
sum,
these
data
support
a
conclusion
that
any
dietary
exposures
to
C9
Rich
Aromatic
Hydrocarbon
Fluid
satisfy
the
statute's
"
reasonable
certainty
of
no
harm"
standard,
based
on
worst­
case
exposure
assumptions
about
how
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
used
and
conservative
health
benchmarks.

ii.
Drinking
water.
An
exposure
assessment
for
drinking
water
is
not
necessary
due
to
the
volatile
nature
of
this
product,
lack
of
water
solubility,
and
the
proposed
use
patterns.

2.
Non­
dietary
exposure.
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
11
not
typically
suitable
for
indoor
use
in
consumer
products
due
to
its
inherent
characteristic
odor
which
cannot
be
masked
by
fragrances.
Three
outdoor
residential
application
scenarios
with
the
greatest
potential
for
human
exposure
were
modeled
to
determine
whether
these
uses
also
satisfy
the
statue's
"
reasonable
certainty
of
no
harm"
standard.
Maximum
weight
percentages
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
in
residential
use
products
were
assumed
based
on
federal
and
state
Volatile
Organic
Compound
(
VOC)
limits
for
consumer
product
formulations.
OPP
recommended
values
for
applicator
dermal
and
inhalation
unit
exposure
values,
specific
to
method
of
application,
were
used
for
estimating
potential
exposures
during
application.
And
based
on
a
weight
of
empirical
evidence,
an
upper
bound
dermal
absorption
value
was
assumed
for
C9
Rich
Aromatic
Hydrocarbon
Fluid.
Chronic
residential
exposures
were
not
considered
plausible
given
the
seasonal
and
intermittent
application
events
,
and
the
rapid
evaporative
loss
of
the
relatively
volatile
C9
Rich
Aromatic
Hydrocarbon
Fluid.
Based
on
the
health
benchmarks
and
foregoing
exposure
analysis
described
for
the
dietary
exposure,
non­
dietary
exposure
showed
that
in
all
cases,
the
calculated
MOEs
were
met
even
using
the
most
conservative
Tier
1
exposure
assessment,
with
maximum
possible
concentrations
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
allowable
in
the
product
formulation
and
with
no
evaporative
loss.
No
further
analysis
was
warranted.
Thus,
the
results
of
this
conservative
risk
assessments
support
the
conclusion
that
typical
residential
exposures
to
C9
Rich
Aromatic
Hydrocarbon
Fluid
satisfy
the
statute's
"
reasonable
certainty
of
no
harm"
standard,
based
on
worst­
case
exposure
assumptions
about
how
C9
Rich
Aromatic
Hydrocarbon
Fluid
is
used.

D.
Cumulative
Effects
There
are
currently
no
available
data
or
other
reliable
information
to
indicate
that
any
toxic
effects
produced
by
C9
Rich
Aromatic
Hydrocarbon
Fluid
would
be
cumulative
with
those
of
other
chemical
12
compounds.

E.
Safety
Determination
1.
U.
S.
population.
Based
on
the
inherent
characteristic
odor
property,
low
toxicity,
high
volatility
resulting
in
rapid
evaporative
loss,
lack
of
water
solubility,
and
the
conservatism
applied
in
the
dietary
and
non­
dietary
(
residential)
risk
assessments,
C9
Rich
Aromatic
Hydrocarbon
Fluid
meets
the
statute's
"
reasonable
certainty
of
no
harm"
standard
and
a
tolerance
exemption
should
be
granted.

2.
Infants
and
children.
The
potential
aggregate
exposure
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
from
dietary
and
non­
dietary
exposure
routes
to
infants
and
children
and
based
on
this
risk
assessment,
concluded
that
aggregate
exposure
is
not
expected
to
exceed
the
acceptable
MOEs,
even
when
infants
and
children
are
considered.

F.
International
Tolerances
There
are
no
known
international
tolerances
for
residues
of
C9
Rich
Aromatic
Hydrocarbon
Fluid
in
food
or
animal
feed.
