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EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR PESTICIDE
PETITIONS PUBLISHED IN THE FEDERAL REGISTER

EPA Registration Division contact: Kathryn Montague,<PHONE_NUMBER>

BASF

5F8421

	EPA has received a pesticide petition (5F8421) from BASF Corporation,
26 Davis Drive, P.O. Box 13528, Research Triangle Park, NC 27709
requesting, 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

	1. By establishing a tolerance for residues of

	3-(4,5-Dihydro-isoxazol-3-yl)-4-methanesulfonyl-2-methylphenyl]-(5-hydr
oxyl-1-methyl-1H-pyrazol-4-yl)methanone in or on the raw agricultural
commodity sugarcane, cane at 0.01 parts per million (ppm).  EPA has
determined that the petition contains data or information regarding the
elements set forth in section 408 (d)(2) of  FDDCA; 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. The metabolism of Topramezone was determined in
corn forage, stover and grain using 14C labeled materials applied to
young corn plants at an exaggerated application rate of 0.134 lb
ai/acre. Topramezone and one significant metabolite, M670H05, were found
in low levels in the plant matrices with the majority of the radioactive
residues incorporated into natural products. M670H05 resulted from
oxidation of the carbonyl bridge to a carboxylic acid with concomitant
loss and breakdown of the pyrazole ring. The significant metabolite
M670H05 was found in the rat metabolism study.

	2. Analytical method. Suitable independently validated analytical
methods (for animal matrices) are submitted for detecting and measuring
Topramezone levels in or on food with a limit of detection that is
satisfactory for enforcing the requested tolerances. Residues are first
extracted from the matrices by aqueous solvent then cleaned up by acid
partitioning into organic solvent, then base partitioned, and quantified
with application to high performance liquid chromatography with dual
mass selective detectors (LC/MS/MS).

	3. Magnitude of residues. A total of eight (8) sugarcane residue trials
were conducted in NAFTA growing regions 3, 4, 6 and 13.  Topramezone in
the form of Armezon herbicide (2.8 pounds topramezone per gallon) was
applied late postemergence to sugarcane, just prior to canopy closure.
A single application was made at a targeted rate of 4.0 fluid ounces per
acre (0.0875 pounds topramezone per acre).

All samples were analyzed for residues of topramezone (BAS 670 H), and
its metabolite, M670H05, using BASF Method D1302, which quantifies
residues by LC-MS/MS. Mean recoveries for all analytes were within the
acceptable range of 70-120%. Fortification levels for each analyte were
adequate to bracket residue levels found in treated samples. The method
limit of detection (LOD) and limit of quantitation (LOQ) for both
analytes were 0.002 and 0.01 ppm, respectively.

No residues above the LOD of topramezone and its metabolite were found
in any of the control samples (n=8) analyzed. After one broadcast
application of topramezone, totaling 0.087 lb ai/A to 0.094 lb ai/A per
season for sugarcane, maximum residues were <LOD ppm for topramezone and
M670H05 in/on all sugarcane samples (n=16) harvested at crop maturity
(97 to 255 DALA). Mean residues were 0.002 ppm for topramezone and
M670H05 in/on all treated sugarcane samples (n=16) harvested at crop
maturity (97 to 255 DALA).

B. Toxicological Profile

	1. Acute toxicity.

a. Oral (rat): LD50 = >2000 mg/kg b.w. (male/female) = Category III

b. Dermal (rat): LD50 = >2000 mg/kg b.w. (male/female) = Category III

c. Inhalation (rat): LC50 = >5.8 mg/L (male/female) = Category IV

d. Primary eye irritation (rabbit): slightly irritating = Category III

e. Primary dermal irritation (rabbit): slightly irritating = Category
III

f. Dermal sensitization (guinea pig): not a sensitizer

g. Oral neurotoxicity (rat): NOAEL = 2000mg/kg b.w.(male/female)

	2. Genotoxicty. Topramezone was tested for its genotoxic potential in a
battery of five in vitro or in vivo studies covering all required
end-points (gene mutations, chromosomal and chromosome aberrations, and
DNA damage and repair) several batches of Topramezone have been tested
over the time, from early laboratory produced material to current
manufacturing process material. Topramezone did not demonstrate any
genotoxic effects in vivo. In vitro, either batches tested for
chromosomal aberrations caused a slight, significant clastogenic effect
in the presence of S-9 mix, but the in vivo test for the equivalent
end-point was negative.  Three of the four batches tested in the
bacterial reverse mutation assay were not mutagenic, but the batch with
the least purity displayed a weak mutagenic effect at the highest dose
in Salmonella typhimurium TA98 in the absence of S-9 mix, most likely
caused by impurities, which are not present in the current production
batch. Overall, the weight of the evidence is that Topramezone is not
genotoxic.

	3. Reproductive and developmental toxicity. The reproductive and
developmental toxicity of Topramezone was investigated in a 2-generation
rat reproduction study as well as in rat, mouse and several rabbit
teratology studies (with different batches of Topramezone) and a rat
developmental neurotoxicity study.  There were no adverse effects on
fertility of both genders and no effect on the reproductive performance
of males in the two-generation study at any dose tested. There was,
however, a high litter loss in F0 and F1 associated with insufficient
maternal care at higher dose levels with clear maternal toxicity.
General parental toxicity included eye- and kidney effects, caused by
elevated tyrosine levels due to HPPD (hydroxyphenylpyruvate dioxygenase)
inhibition. The same organs were affected in subchronic and chronic
feeding studies with rats. Pup effects were observed in the F1 and F2
generation including perinatal pup mortality and impaired body weight
gain, the lower body weight effects were considered to lead to brain and
spleen weight changes and delays in preputial separation. As observed in
the parental animals, effects on eyes and kidneys were observed in the
pups. Renal pelvis dilation was observed at lower doses, although there
was no overt maternal toxicity, significantly elevated tyrosine levels
were observed in the dams and pups. The NOAEL for fertility (F0 and F1,
both genders) was 4,000 ppm (about 450 mg/kg b.w./day); the NOAEL for
reproductive performance was 40 ppm (about 4 mg/kg body weight/day) for
the F1 females. The NOAEL for general toxicity was 4 ppm (about 0.4
mg/kg b.w./day). The NOAEL for developmental toxicity (growth and
development of the offspring) was 4 ppm (about 0.4 mg/kg body
weight/day) for the F1 pups, but was lower than 4 ppm for the F2 pups
due to renal pelvis dilations at all dose levels.

Developmental neurotoxicity was not observed at any dose in the
developmental neurotoxicity study. At all dose levels, eye effects due
to elevated tyrosine levels were found in dams and pups. Additionally
there were decreased body weights in the dams at the high and mid dose,
but there were no indications of adverse effects on reproductive
performance of the parental females. In pups of both genders, decreased
pre and post weaning body weight gains and body weights were observed at
the low dose level and above. This is an indicator of a retardation of
the general physical development, which is considered to be responsible
for a slight delay of maturation. The NOAEL for developmental
neurotoxicity was 800 mg/kg b.w./day (highest dose tested). There is no
NOAEL for the eye lesions and reduced body weight gain of the pups.
NOAELs for these effects were determined in prenatal development studies
in rats, rabbits and mice.

No developmental toxicity was noted in the mouse prenatal development
study. In the prenatal development study in rats no teratogenic effect
was observed, but there was maternal toxicity together with skeletal
variations in the pups. The same skeletal variation (i.e. supernumerary
ribs) was also found in rabbit prenatal development studies. This effect
is associated with the family of HPPD inhibiting substances. In
addition, several rabbits had pups with a soft tissue malformation:
unilateral kidney agenesis. The NOAEL for the skeletal variations and
the kidney agenesis was 0.5 mg/kg b.w./day, the NOAEL for overt maternal
toxicity was 50 mg/kg b.w./day. The developmental effects in rabbits
occurred at dose-levels below overt maternal toxicity, however measured
tyrosine blood levels in the dams were substantially elevated at these
dose levels. Elevated tyrosine levels are known to cause kidney
toxicity.

	4. Subchronic toxicity. The subchronic toxicity of Topramezone was
investigated in 90-day feeding studies in rats, mice and dogs, and in a
28-day dermal administration study in rats. Several supplemental
short-term mechanistic studies in rats and mice were performed to
elucidate the mode of action. Generally, very mild toxicity was observed
in mice and dogs at high doses. In a combined neurotoxicity 90-day
feeding study in rats, no signs of neurotoxicity were observed. Effects
were seen in the pancreas, eye, kidney, liver and thyroid gland. The
target organs are identical with those in the chronic feeding studies
with rats. Two modes of action have been elucidated for Topramezone by
short-term mechanistic studies, one leading to effects on eyes, kidney
and liver, and a second leading to effects at the thyroid: Topramezone
causes elevated tyrosine levels by HPPD inhibition accounting for
effects on eye, liver and kidney. The mouse is the accepted model for
this tyrosine level elevations, and a NOAEL of 1.2 mg/kg b.w./day was
established for tyrosine elevation in mice. Other mechanistic studies
demonstrated an impairment of pituitary-thyroid hormone levels by
enhancing the hepatic clearance of thyroid hormones. The NOAEL for
interference with thyroid hormones was 0.4 mg/kg b.w./day. The NOAEL for
effects on the exocrine pancreas in rats was 1.1 mg/kg b.w./day. Similar
effects were seen in the 28-day dermal study with rats; the NOAEL was
100 mg/kg b.w./day.

	5. Chronic toxicity. The chronic toxicity and oncogenicity studies with
Topramezone include two 12-month feeding studies with dogs, an 18-month
mouse feeding study, a 12-month rat chronic feeding study and a 24-month
rat oncogenicity study. In the chronic dog study mild reductions of the
body weight were observed at high doses. The NOAEL was 100 ppm (2.9 and
3.1 mg/kg b.w./day in males and females respectively).

In the 18-month chronic feeding study in mice increased liver weights
were seen at high doses. The NOAEL was 80 ppm (19 and 26 mg/kg b.w./day
in males and females respectively). Topramezone was not carcinogenic to
mice. In the chronic feeding studies in rats the main target organs were
eye, liver, kidney, thyroid gland and pancreas. The same organs were
affected in the subchronic studies. Short-term mechanistic studies
demonstrated that Topramezone causes elevated tyrosine levels by HPPD
inhibition accounting for effects on eye, liver and kidney. The mouse is
the accepted model for this tyrosine level elevation, and a NOAEL of 1.2
mg/kg b.w./day was established for tyrosine elevation in mice. The NOAEL
for effects on the exocrine pancreas in rats 6 ppm in both genders (0.4
and 0.5 mg/kg b.w./day in males and females respectively). At the end of
the 24-month oncogenicity study, there was a slight but significant
increase in benign thyroid adenomas in both genders. The thyroid was the
only organ affected and the increase of the adenomas was significant
only at the highest dose tested, while considerable general toxicity was
already seen at 20-times lower doses. The mechanism of thyroid tumor
formation by Topramezone was thoroughly investigated in short-term
mechanistic studies. An enhanced hepatic clearance of thyroid hormones
impairs pituitary-thyroid hormone levels leading to hypertrophy,
hyperplasia and ultimately neoplasia. There is general agreement that
this mechanism is well-understood in rodents and is of minor relevance
to humans. A clear NOAEL of 0.4 mg/kg b.w./day was demonstrated for
effects on thyroid hormone levels. A threshold (non-linear) cancer
assessment is proposed and a cancer classification as “not likely to
be a human carcinogen”.

	6. Animal metabolism. In the rat metabolism studies the majority of the
residue was excreted within 48 hours from both males and females. In all
matrices investigated unchanged parent is the main component.
Degradation starts with hydroxylation of the oxazole ring. The
identified metabolites from both pyrazole ring label and phenyl ring
label studies are reported. Goat and hen metabolism studies were
conducted with feeding levels of about 10 ppm. In the goat, the majority
of the applied dose was excreted. Non-metabolized BAS 670H was the major
radioactive residue, and M670H02, formed from hydroxylation at the
4-position of the isoxazole ring, was the only significant metabolite
formed. In poultry BAS 670 F was also rapidly excreted. Residues in
liver consisted mainly of BAS 670H and the only significant metabolite
in poultry was again M670H02. The significant metabolite M670H02 was
found in the rat metabolism study.

	7. Metabolite toxicology. Toxicity of the metabolites of Topramezone
with potential exposure to humans was concurrently evaluated during
toxicity testing of the parent, because both plant and animal
metabolites are formed during the course of toxicity testing. Both plant
and animal metabolites are considered not of toxicological concern. Some
testing was conducted on the anaerobic aquatic metabolite, 670M10. The
results as given below show no toxicological concern:

Bacterial reverse mutation test (Ames): no effect = negative

Mammalian somatic cell gene mutation test (MNT): no effect = negative

Cytogenetic study in vivo (mouse – HPRT): no effect = negative

28 day feeding study (rat): NOAEL 1197 mg/kg b.w./da and 1304 mg/kg
b.w./day (male and female, respectively).

	8. Endocrine disruption. Topramezone has been shown to alter thyroid
hormone levels in rats as also observed with other
4-hydroxyphenylpyruvate dioxygenase (HPPD) enzyme inhibitor active
ingredients.  However, there have been no effects noted on sexual or
other hormones in numerous subchronic and chronic toxicity studies with
multiple species.

C. Aggregate Exposure

	1. Dietary exposure. Exposure assessments were conducted to evaluate
the potential risk due to acute and chronic dietary exposure of the U.S.
population to residues of Topramezone. The current tolerance values are
listed in the U.S. 40 CFR § 180.612. This analysis includes all
commodities with established tolerances values and proposed new
tolerances for sugarcane, cane = 0.01 ppm.

Food.

Acute Dietary Exposure Assessment

The US EPA has determined that an acute dietary assessment is required
for all sub-populations.

An acute dietary exposure estimate (food and drinking water) was
conducted for all populations using the currently established tolerances
for topramezone (40 CFR 180.612) and currently proposed tolerances for
sugarcane, cane. The assessment was conducted using tolerance values,
default process factors, and 100% crop treatment factors.  The
consumption data was from the USDA Continuing Survey of Food Intake by
Individuals (CSFII 1994 - 1996, 1998) and the EPA Food Commodity
Ingredient Database (FCID) using Exponent's Dietary Exposure Evaluation
Module (DEEM-FCID) software.  The water concentration used in the acute
dietary assessment was 40 ppb based on the aquatic application rate.

The resulting exposure estimates were compared against the topramezone
acute Population Adjusted Dose (aPAD) of 0.008 mg/kg b.w/day for all
populations except females 13-49 years of age.  The topramezone acute
Population Adjusted Dose (aPAD) for females 13 – 49 years of age is
0.005 mg/kg b.w/day. The endpoint of 0.008 mg/kg bw/day is based on the
NOAEL of 8.0 mg/kg/day with the standard inter- and intra-species
uncertainty factors of 100X and an FQPA safety factor of 10.  The
endpoint of 0.005 mg/kg bw/day is based on the NOAEL of 0.5 mg/kg/day
with the standard inter- and intra-species uncertainty factors of 100X
and an FQPA safety factor of 1.   The most highly exposed population
subgroup was all infants (< 1 year) which utilized 93.9 % of the aPAD.

The results of the analysis show that the estimated exposure is below
the Agency's level of concern (< 100% aPAD).  Additional refinements in
the dietary risk assessment (i.e. utilizing anticipated residue values,
percent crop treated values) would further reduce the estimated exposure
value.

Chronic Dietary Exposure Assessment

Chronic dietary exposure (food and drinking water) were conducted using
the currently established tolerances for topramezone (40 CFR 180.612)
and currently proposed tolerances for sugarcane, cane. The assessment
was conducted using tolerance values, default process factors, and 100%
crop treatment factors.  The consumption data was from the USDA
Continuing Survey of Food Intake by Individuals (CSFII 1994 - 1996,
1998) and the EPA Food Commodity Ingredient Database (FCID) using
Exponent's Dietary Exposure Evaluation Module (DEEM-FCID) software.  The
water concentration used in the chronic dietary assessment was 40 ppb
based on the aquatic application rate and not taking into account
degradation in water body.

The chronic Population Adjusted Dose (cPAD) used for U.S. population and
all sub-populations is 0.004 mg/kg bw/day. This endpoint is based on the
NOAEL value of 0.4 using the standard inter- and intra-species
uncertainty factors of 100X and with a FQPA safety factor of 1.  The
most highly exposed population sub-group was infants (<1year old) which
utilized 76.8 % cPAD.  The results of the chronic dietary assessment are
presented in Table 1.

Table 1. Results for Topramezone Chronic Dietary Exposure Analysis
Considering all Current and Proposed Tolerances using DEEM-FCID, food
and drinking water.

Population	Exposure Estimate	%cPAD

Subgroups	(mg/kg b.w./day)

U.S. Population	0.000859	21.48

All Infants (< 1 year old)	0.003073	76.83

Children (1-2 years old)	0.001230	30.75

Children (3-5 years old)	0.001016	25.40

Children (6-12 years old)	0.000753	18.83

Youth (13-19 years old)	0.000616	15.40

Adults (20-49 years old)	0.000847	21.18

Adults (50+ years old)	0.000820	20.50

Females (13-49 years old)	0.000828	20.70

The results of the analysis show that for all populations, the exposures
are below the US EPA level of concern (< 100% cPAD).  Additional
refinements in the chronic dietary risk assessment (i.e. utilizing
anticipated residue values and percent crop treated values) would
further reduce the estimated exposure values.

Acute Aggregate Exposure and Risk (food and water)

The aggregate acute risk includes exposure of topramezone from food and
water. The results demonstrate that there are no risk concerns for any
subpopulation based on the proposed uses and the results meet the FQPA
standard of reasonable certainty of no harm.

Short- and Intermediate-Term Aggregate Exposure and Risk (food, water,
and residential)

Short- and intermediate-term aggregate risk assessments include exposure
from food, water, and residential uses.  Topramezone is registered for
use on turfgrass and golf courses. The US EPA has conducted a risk
assessment for this use of Topramezone (Topramezone: Human Health Risk
Assessment for Proposed Uses on Golf Courses, Sod Farms, and Residential
Turfgrass).  For this assessment, the US EPA used a dermal absorption
value of 13%, the correct value for dermal absorption is 2.6% and it is
noted in the document.  But, the calculations for exposure were done
with 13%. The residential exposure calculations were repeated using a
dermal absorption value of .6%.   The short-term aggregate MOE was
determined for the General population and Children 1-2 years of age.
The aggregate MOE for the General population is 321 and the aggregate
MOE for children 1-2 years of age is 220.  The aggregate MOE limit of
concern for both of these populations is 100.  So an MOE greater than
100 indicates that there is no risk concern from the aggregate exposures
for Topramezone.

Chronic Aggregate Exposure and Risk (food and water)

The aggregate chronic risk includes exposure of Topramezone from food
and water (Table 1). The results demonstrate there are no risk concerns
for any subpopulation based on the proposed uses and the results meet
the FQPA standard of reasonable certainty of no harm.

Drinking water. The concentration of topramezone in water is based on
the aquatic use pattern with an application rate of 40 ppb.   The acute
surface water concentration used in the dietary assessment was 40 ppb
based on the application rate.   The chronic surface water concentration
used in the assessment was also 40 ppb, which assumes no degradation in
the water body.  This is a very conservative water value and
over-estimates the actual chronic drinking water exposure.

	2. Non-dietary exposure. Topramezone is registered for use on turfgrass
and golf courses. The US EPA has conducted a risk assessment for this
use of Topramezone (Topramezone: Human Health Risk Assessment for
Proposed Uses on Golf Courses, Sod Farms, and Residential Turfgrass).
For this assessment, the US EPA used a dermal absorption value of 13%,
the correct value for dermal absorption is 2.6% and it is noted in the
document.  But, the calculations for exposure were done with 13%. The
calculations were repeated using a dermal absorption value of 2.6%.  For
adults, the exposure includes handler and dermal exposure from turf.
The MOE for adults was 1033.  For children 1-2 years of age, the
exposure includes dermal exposure from turf and exposure from
hand-to-mouth activities.  The MOE for children 1-2 years of age is 678.
   The MOE values are greater the limit of concern of 100.  The MOE
values greater than 100 indicates that there is no risk concern from the
non-dietary uses of topramezone.

D. Cumulative Effects

	At this time, there is no available information to indicate that
Topramezone or its metabolites have a common mechanism of toxicity with
other substances. Therefore, there is no reason to include this
pesticide or its metabolites in a cumulative risk assessment. For the
purposes of this tolerance action EPA has not assumed that Topramezone
and its metabolites have a common mechanism of toxicity with other
substances.

E. Safety Determination

	1. U.S. population. Based on the current risk assessments, the US EPA
can conclude that there is a reasonable certainty that no harm will
result to the general population from aggregate exposure to tompramezone
residues from the proposed uses.

	2. Infants and children. Based on the current risk assessments, the US
EPA can conclude that there is a reasonable certainty that no harm will
result to infants and children from aggregate exposure to topramezone
residues from the proposed uses.

F. International Tolerances

	No maximum residue levels (MRLs) have been established for Topramezone
by the Codex Alimentarius Commission (CODEX) or in Mexico.

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 PAGE   2


[Federal Register: January 28, 2008 (Volume 73, Number 18)]
[Notices]
[Page 4929-4931]
[DOCID:fr28ja08-123]

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SECURITIES AND EXCHANGE COMMISSION

[Release No. 34-57176; File No. SR-NYSE-2008-04]

Self-Regulatory Organizations; New York Stock Exchange LLC;
Notice of Filing and Immediate Effectiveness of Proposed Rule Change To
Implement a Four-Month Pilot Program To Offer Liquidity Takers a
Reduced Transaction Fee Structure for Certain Bond Trades Executed on
the NYSE Bonds\SM\ System

January 18, 2008.
    Pursuant to Section 19(b)(1) of the Securities Exchange Act of 1934
(``Act'') \1\ and Rule 19b-4 thereunder,\2\ notice is hereby given that
on January 11, 2008, the New York Stock Exchange LLC ( ``NYSE'' or the
``Exchange'') filed with the Securities and Exchange Commission
(``Commission'') the proposed rule change as described in Items I, II,
and III below, which Items have been substantially prepared by NYSE.
The Exchange has designated this proposal as one establishing or

changing a due, fee, or other charge imposed by the Exchange under
Section 19(b)(3)(A)(ii) of the Act \3\ and Rule 19b-4(f)(2)
thereunder,\4\ which renders the proposal effective upon filing with
the Commission. The Commission is publishing this notice to solicit
comments on the proposed rule change from interested persons.
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    \1\ 15 U.S.C. 78s(b)(1).
    \2\ 17 CFR 240.19b-4.
    \3\ 15 U.S.C. 78s(b)(3)(A)(ii).
    \4\ 17 CFR 240.19b-4(f)(2).
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I. Self-Regulatory Organization's Statement of the Terms of Substance
of the Proposed Rule Change

    The Exchange proposes to implement a four-month pilot program that
will offer liquidity takers a reduced transaction fee structure for
certain bond trades executed on the NYSE Bonds\SM\ system. This pilot
program will terminate on the close of business May 15, 2008 and will
apply to all orders. The text of the proposed rule change is available
at the Exchange's principal office, in the Commission's Public
Reference Room, and at http://www.nyse.com.

II. Self-Regulatory Organization's Statement of the Purpose of, and
Statutory Basis for, the Proposed Rule Change

    In its filing with the Commission, NYSE included statements
concerning the purpose of, and basis for, the proposed rule change and
discussed any comments it received on the proposed rule change. The
text of these statements may be examined at the places specified in
Item IV below. NYSE has prepared summaries, set forth in Sections A, B,
and C below, of the most significant aspects of such statements.

A. Self-Regulatory Organization's Statement of the Purpose of, and
Statutory Basis for, the Proposed Rule Change

1. Purpose
    The Exchange proposes to implement a four-month pilot program that
will offer liquidity takers a reduced transaction fee structure for
transaction fees for certain bond trades executed on NYSE Bonds. This
pilot program will commence on January 15, 2008 and will terminate at
the close of business May 15, 2008.
    The Exchange proposes to reduce transaction fees charged to
liquidity takers for transactions executed on NYSE Bonds with a
staggered transaction fee schedule based on the number of bonds
purchased in excess of ten bonds. Currently, the transaction fee for
orders that take liquidity from the market is $0.50 per bond. This fee
remains unchanged for orders up to ten bonds. The proposed fee filing
provides for the following transaction fee schedule: (1) When the
liquidity taker purchases between one to ten bonds, the Exchange will
charge an execution fee of $0.50 per bond; (2) when the liquidity taker
purchases between 11 and 25 bonds, the Exchange will charge an
execution fee of $0.20 per bond; and (3) when the liquidity taker
purchases 26 bonds or more, the Exchange will charge an execution fee
of $0.10 per bond. The Exchange will impose a $100 fee cap per
transaction.
2. Statutory Basis
    The Exchange believes that the proposed rule change is consistent
with the provisions of Section 6 of the Act \5\ in general and furthers
the objectives of Section 6(b)(4) of the Act \6\ in particular, in that
it is designed to provide for the equitable allocation of reasonable
dues, fees, and other charges among its members and other persons using
its facilities.
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    \5\ 15 U.S.C. 78f.
    \6\ 15 U.S.C. 78f(b)(4).
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B. Self-Regulatory Organization's Statement on Burden on Competition

    The Exchange does not believe that the proposed rule change will
impose any burden on competition that is not necessary or appropriate
in furtherance of purposes of the Act.

C. Self-Regulatory Organization's Statement on Comments on the Proposed
Rule Change Received From Members, Participants or Others

    The Exchange has neither solicited nor received written comments on
the proposed rule change.

III. Date of Effectiveness of the Proposed Rule Change and Timing for
Commission Action

    Because the foregoing rule change establishes or changes a due,
fee, or other charge imposed by the Exchange, it has become effective
pursuant to Section 19(b)(3)(A) of the Act \7\ and subparagraph (f)(2)
of Rule 19b-4 thereunder.\8\ At any time within 60 days of the filing
of the proposed rule change, the Commission may summarily abrogate such
rule change if it appears to the Commission that such action is
necessary or appropriate in the public interest, for the protection of
investors, or otherwise in furtherance of the purposes of the Act.
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    \7\ 15 U.S.C. 78s(b)(3)(A).
    \8\ 17 CFR 240.19b-4(f)(2).
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IV. Solicitation of Comments

    Interested persons are invited to submit written data, views, and
arguments concerning the foregoing, including whether the proposed rule
change is consistent with the Act. Comments may be submitted by any of
the following methods:

Electronic Comments

     Use the Commission's Internet comment form (http://
www.sec.gov/rules/sro.shtml); or
     Send an e-mail to<EMAIL_ADDRESS>Please include
File Number SR-NYSE-2008-04 on the subject line.

Paper Comments

     Send paper comments in triplicate to Nancy M. Morris,
Secretary, Securities and Exchange Commission, 100 F Street, NE.,
Washington, DC 20549-1090.

All submissions should refer to File Number SR-NYSE-2008-04. This file
number should be included on the subject line if e-mail is used. To
help the Commission process and review your comments more efficiently,
please use only one method. The Commission will post all comments on
the Commission's Internet Web site (http://www.sec.gov/rules/
sro.shtml). Copies of the submission, all subsequent amendments, all
written statements with respect to the proposed rule change that are
filed with the Commission, and all written communications relating to
the proposed rule change between the Commission and any person, other
than those that may be withheld from the public in accordance with the
provisions of 5 U.S.C. 552, will be available for inspection and
copying in the Commission's Public Reference Room, 100 F Street, NE.,
Washington, DC 20549, on official business days between the hours of 10
a.m. and 3 p.m. Copies of such filing also will be available for
inspection and copying at the principal office of NYSE. All comments
received will be posted without change; the Commission does not edit
personal identifying information from submissions. You should submit
only information that you wish to make available publicly. All
submissions should refer to File Number SR-4-NYSE-2008-04 and should be
submitted on or before February 19, 2008.

    For the Commission, by the Division of Trading and Markets,
pursuant to delegated authority.\9\
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    \9\ 17 CFR 200.30-3(a)(12).
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Florence E. Harmon,
Deputy Secretary.
[FR Doc. E8-1374 Filed 1-25-08; 8:45 am]

BILLING CODE 8011-01-P