Document ID: EPA-HQ-OPP-2005-0321-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2007-02-27T05:00Z

1
EPA
Registration
Division
contact:
Bipin
Gandhi
(
703
305­
8380)

ExxonMobil
Chemical
Company
[
4E6937]

EPA
has
received
a
pesticide
petition
[
4E6937]
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
(
Aromatic
200
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid,
there
is
little
likelihood
of
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
remaining
intact
in
any
crop
matrix.

B.
Toxicological
Profile
1.
Acute
toxicity.
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
(
Aromatic
200
Fluid)
has
a
low
order
of
acute
toxicity
based
on
studies
conducted
in
rats
via
oral
and
inhalation
exposure,
in
mice
via
inhalation
exposure,
and
in
rabbits
via
dermal
exposure.
In
an
acute
oral
rat
study,
the
animals
were
dosed
at
0.5,
1.5
and
5.0
g/
kg
(
EMBSI
1991a).
All
animals
in
the
low
and
mid­
dose
groups
survived
to
study
termination,
while
3
females
and
2
males
(
of
a
total
of
10
animals)
died
in
the
high
dose
group.
All
deaths
occurred
between
days
2
and
4
following
test
material
administration.
Based
on
the
results
of
this
study,
the
LD50
for
female
rats
is
5.0
g/
kg;
the
LD50
for
male
rats
is
calculated
at
10.65
g/
kg
and
the
LD50
for
both
sexes
combined
is
calculated
at
7.05
g/
kg
for
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid.
The
rabbit
dermal
LD50
is
greater
than
3.16
g/
kg
for
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
(
EMBSI
1990).
In
the
acute
dermal
study,
rabbits
were
dosed
at
3.16
g/
kg.
All
animals
survived
to
study
termination
and
there
were
no
treatment­
related
clinical
signs,
indicating
that
the
dermal
LD50
for
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
exceeds
3.16
g/
kg.
In
an
acute
rat
inhalation
study,
animals
were
dosed
at
the
maximum
attainable
vapor
concentration
of
169
mg/
m3
(
0.2
mg/
liter
or
26
ppm)
(
EMBSI
1993).
All
animals
survived
to
study
termination,
indicating
that
the
rat
inhalation
LC50
for
2
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
is
greater
than
169
mg/
m3.
Inhalation
studies
were
also
performed
using
combined
vapor
and
aerosol
generation.
In
rats,
the
LC50
was
greater
than
4778
mg/
m3
(
4.8
mg/
liter
or
726
ppm)
(
4618
mg/
m
aerosol,
160
mg/
m3
vapor)
(
EMBSI
1997c).
In
mice,
the
LC50
was
greater
than
1073
mg/
m3
(
1.1
mg/
liter
or
163
ppm)
(
961
mg/
m3
aerosol,
112
mg/
m3
vapor)
(
EMBSI
1997a).
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
is
a
mild
skin
and
eye
irritant
in
rabbits.

2.
Genotoxicity.
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
(
Aromatic
200
Fluid),
showed
no
evidence
of
causing
mutagenic
effects
in
in
vitro
and
in
vivo
genotoxicity
assays.
In
an
Ames
assay,
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
was
not
mutagenic
in
Salmonella
strains
tested
in
the
presence
or
absence
of
metabolic
activation
(
EMBSI
1991c).
It
was
also
non­
mutagenic
when
tested
in
an
in
vivo
mouse
bone
marrow
micronucleus
assay
using
oral
gavage
doses
of
0.25,
0.5,
and
1.0
g/
kg
(
EMBSI
1991b).

3.
Reproductive
and
developmental
toxicity.
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
showed
no
evidence
of
causing
developmental
toxicity
and
is
unlikely
to
be
a
selective
developmental
toxicant.
In
a
Sprague
Dawley
rat
developmental
study
(
EMBSI
1992),
pregnant
dams
were
dosed
by
oral
gavage
with
75,
150
or
450
mg/
kg/
day
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
during
gestational
days
6
through
15.
At
450
mg/
kg/
day,
maternal
body
weight
gain
and
food
consumption
were
significantly
decreased
during
the
first
three
days
of
treatment.
Mean
body
weight
change
was
comparable
between
treated
animals
and
controls
during
the
overall
study
period,
and
there
were
no
statistically
significant
differences
in
organ
weights
and
uterine
implantation
data
between
treated
groups
and
controls.
There
were
no
differences
in
mean
fetal
body
weight,
nor
were
there
any
significant
differences
in
the
incidences
of
fetal
variations
or
malformations
in
treated
groups
as
compared
to
controls,
either
on
a
per
fetus
or
a
per
litter
basis.
Based
on
the
study
results,
the
maternal
No
Observed
Adverse
Effect
Level
(
NOAEL)
is
150
mg/
kg/
day
and
the
developmental
NOAEL
is
greater
than
450
mg/
kg/
day.

C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
has
not
been
tested
for
reproductive
toxicity.
However,
OECD
SIDS
guidelines
expressly
provide
that
chemicals
such
as
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
need
not
be
tested
for
reproductive
toxicity
to
conclude
that
they
are
not
likely
to
be
reproductive
toxicants:

"
For
health
effects
testing
the
reproductive
toxicity
requirements
may
be
satisfied
through
the
use
of
data
from
several
studies.
.
.
.
Requirements
are
met
when
a
developmental
toxicity
study
is
available
together
with
a
90­
day
repeated
dose
study
that
sufficiently
documents
that
reproductive
organs
were
examined
histologically
and
indicate
no
effects."

OECD,
Manual
for
Investigation
of
HPV
Chemicals,
Chapter
2:
SIDS,
The
SIDS
Plan
and
the
SIDS
Dossier,
p.
11
(
2002).
For
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid,
a
developmental
toxicity
study
was
conducted
(
EMBSI
1992),
which
was
also
tested
in
a
90­
day
subchronic
study
3
(
EMBSI
1991)
and
histopathology
of
reproductive
organs
showed
no
effects.
Together,
these
studies
demonstrate
that
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
is
a
low
concern
for
reproductive
toxicity.

4.
Subchronic
toxicity.
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
has
low
order
of
subchronic
toxicity
by
the
oral
route
of
exposure.
In
a
subchronic
oral
gavage
study,
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
was
administered
to
Sprague­
Dawley
rats
at
concentrations
of
300,
600
or
1000
mg/
kg/
day,
7
days/
week
for
13
weeks
(
EMBSI
1991).
A
satellite
group
received
1000
mg/
kg/
day
for
13
weeks,
followed
by
a
4­
week
recovery
period.
Body
weights
and
food
consumption
were
significantly
decreased
in
male
rats
at
1000
mg/
kg/
day;
this
effect
was
not
seen
in
female
rats.
Hematologic
and
serum
chemistry
changes
were
observed
in
both
male
and
female
rats
at
600
and
1000
mg/
kg/
day
dose
levels
and
correlated
with
effects
seen
in
the
liver
and
spleen.
Kidney
and
liver
weights
increased
in
both
sexes
at
all
dose
levels,
but
the
organ
weights
for
animals
in
the
recovery
group
were
similar
to
those
of
control
animals,
indicating
that
this
was
a
reversible
effect.
No
treatment
related
histopathological
effects
were
observed
in
the
kidney.

Treatment­
related
microscopic
changes
were
observed
in
the
liver,
thyroid,
stomach,
spleen
and
urinary
bladder
of
rats.
Histopathologic
evaluation
showed
that
these
effects
were
decreased
and/
or
reversed
in
the
recovery
group,
and/
or
also
observed
in
control
animals.
Inflammation
and
necrosis
of
the
stomach
were
observed
in
some
treated
animals
and
were
attributed
to
the
effects
of
intubation
of
a
bolus
dose
of
a
locally
irritating
substance
on
the
gastrointestinal
tract.
The
effects
had
reversed
completely
after
the
4­
week
recovery
period.
The
NOAEL
for
this
study
is
600
mg/
kg/
day
and
that
the
minor
effects
seen
in
the
study
were
the
result
of
the
gavage
dosing
mechanism,
and
the
inherent
irritating
effect
of
large
bolus
dosing,
rather
than
toxicity
of
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid.
Nonetheless,
to
maximize
conservatism
in
the
analysis,
and
for
purposes
of
this
risk
assessment,
a
NOAEL
of
300
mg/
kg/
day
was
assumed.
Based
on
the
results
from
this
study,
repeated
exposure
to
very
high
oral
doses
of
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
can
result
in
reversible
effects
to
the
liver,
thyroid,
stomach,
spleen,
and
urinary
bladder.

The
neurotoxicity
of
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
was
assessed
as
part
of
a
neurobehavioral
testing
program
on
aliphatic,
cycloaliphatic
and
aromatic
hydrocarbon
solvents.
This
study
suggests
that
C11­
12
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
C11­
12
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
(
HSPA)
(
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
C11­
12
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
4
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
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.
C11­
12
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
is
not
likely
to
have
carcinogenic
properties.
C11­
12
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
indicate
that
this
compound
is
not
genotoxic
and
also
does
not
produce
significant
cumulative
toxicity.
Therefore,
C11­
12
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.

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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid.
However,
sufficient
data
on
other
aromatic
solvents
 
such
as
alkylbenzenes
and
alkylnaphthalenes
 
exist
to
describe
the
absorption,
distribution,
metabolism
and
excretion
of
C11­
12
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
well­
absorbed
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
C11­
12
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
may
also
occur.
This
conjugation
typically
serves
to
detoxify
the
heavy
aromatic
hydrocarbon
solvent
metabolites,
and
the
conjugates
often
can
be
found
excreted
in
the
urine.
5
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
 
may
also
be
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
produces
effects
characteristic
of
the
disruption
of
endocrine
function.
In
addition,
the
absence
of
any
endocrinerelated
structural
alerts
suggest
that
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
is
not
likely
to
have
endocrine­
distrupting
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
C11­
C12
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
represent
a
conservative
assessment.
Physicochemical
properties
of
the
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid,
e.
g.,
volatility,
which
directly
impacts
bioavailability,
was
considered
using
a
tiered
approach
to
assess
potential
dietary
exposure.
Evaporative
loss
experiments
were
conducted
using
ASTM
Method
D3539
(
Section
16.2)
with
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
(
Aromatic
200
Fluid)
to
show
that
there
was
significant
potential
for
evaporative
loss
from
treated
agricultural
surfaces.
These
studies
showed
that
the
evaporative
loss
rate
for
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
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
C11­
12
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
or
equal
to
that
of
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
and
6
associated
"
relative
diffusion"
or
loss
to
air
that
are
generally
much
lower
than
those
for
C11­
12
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
in
maternal
animals
in
the
developmental
toxicity
study
with
a
NOAEL
of
150
mg/
kg/
day
and
a
NOAEL
for
developmental
effects
of
greater
than
450
mg/
kg/
day.
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
300
mg/
kg/
day
was
applied
based
on
the
subchronic
toxicity
study
on
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid.
In
addition,
to
ensure
a
highly
conservative
risk
assessment,
an
additional
10­
fold
safety
factor
to
the
usual
100­
fold
safety
factor
was
applied,
resulting
in
a
chronic
safety
factor
of
1000.
No
additional
database
uncertainty
factors
were
warranted
since
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
has
been
tested
for
all
major
toxicological
endpoints
with
the
exception
of
reproductive
toxicity
and
carcinogenicity,
and
the
available
data
show
that
neither
of
these
endpoints
is
likely
to
be
of
concern.

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,
as
experimentally
demonstrated
for
neat
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid,
resulted
in
acceptable
acute
and
chronic
MOEs.
When
a
conservative
evaporative
loss
rate
of
98%
was
adopted,
while
retaining
all
other
conservative
assumptions
in
the
exposure
assessment,
the
calculated
MOE
far
exceeded
the
acceptable
MOE
of
100.
Chronic
dietary
MOEs,
even
with
no
evaporative
loss,
far
exceeded
the
acceptable
MOE
of
1000.
In
sum,
these
data
support
a
conclusion
that
any
dietary
exposures
to
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
satisfy
the
statute's
"
reasonable
certainty
of
no
harm"
standard,
based
on
worst­
case
exposure
assumptions
about
how
C11­
12
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.
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
is
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
in
7
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
C11­
12
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
C11­
12
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
allowable
in
the
product
formulation
and
with
no
evaporative
loss.
Calculated
MOEs
for
female
adults
and
for
children
far
exceeded
the
acceptable
MOE
of
100.
No
further
analysis
was
warranted.
Thus,
the
results
of
this
conservative
risk
assessments
support
the
conclusion
that
typical
residential
exposures
to
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
satisfy
the
statute's
"
reasonable
certainty
of
no
harm"
standard,
based
on
worst­
case
exposure
assumptions
about
how
C11­
12
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
would
be
cumulative
with
those
of
other
chemical
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,
C11­
12
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
was
considered
from
dietary
and
non­
dietary
exposure
routes
to
infants
and
children
and
based
on
this
risk
assessment,
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
C11­
12
Rich
Aromatic
Hydrocarbon
Fluid
in
food
or
animal
feed.