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174. Mangano K.M., Hutchins-Wiese H.L., Kenny A.M., Walsh S.J.,
Abourizk R.H., Bruno R.S., Lipcius R., Fall P., Kleppinger A.,
Kenyon-Pesce L., Prestwood K.M., Kerstetter J.E. ``Soy Proteins and
Isoflavones Reduce Interleukin-6 but Not Serum Lipids in Older
Women: A Randomized Controlled Trial''. Nutrition Research.
2013;33:1026-1033.
175. Steinberg F.M., Guthrie N.L., Villablanca A.C., Kumar K.,
Murray M.J. ``Soy Protein with Isoflavones Has Favorable Effects on
Endothelial Function That Are Independent of Lipid and Antioxidant
Effects in Healthy Postmenopausal Women''. American Journal of
Clinical Nutrition. 2003;78:123-130.
176. Bakhit R.M., Klein B.P., Essex-Sorlie D., Ham J.O., Erdman
J.W., Jr., Potter S.M. ``Intake of 25 G of Soybean Protein with or
without Soybean Fiber Alters Plasma Lipids in Men with Elevated
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177. van Raaij J.M., Katan M.B., Hautvast J.G., Hermus R.J.
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Clinical Nutrition. 1981;34:1261-1271.
178. Takatsuka N., Nagata C., Kurisu Y., Inaba S., Kawakami N.,
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Preventive Medicine. 2000;31:308-314.
179. Mitchell J.H., Collins A.R. ``Effects of a Soy Milk Supplement
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180. Murkies A.L., Lombard C., Strauss B.J., Wilcox G., Burger H.G.,
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181. Matthan N.R., Jalbert S.M., Ausman L.M., Kuvin J.T., Karas
R.H., Lichtenstein A.H. ``Effect of Soy Protein from Differently
Processed Products on Cardiovascular Disease Risk Factors and
Vascular Endothelial Function in Hypercholesterolemic Subjects''.
American Journal of Clinical Nutrition. 2007;85:960-966.
182. Jenkins D.J., Wolever T.M., Spiller G., Buckley G., Lam Y.,
Jenkins A.L., Josse R.G. ``Hypocholesterolemic Effect of Vegetable
Protein in a Hypocaloric Diet''. Atherosclerosis. 1989;78:99-107.
183. Bosello O., Cominacini L., Zocca I., Garbin U., Compri R.,
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Apoproteins of Obese Subjects''. Annals of Nutrition and Metabolism.
1988;32:206-214.
184. Greany K.A., Nettleton J.A., Wangen K.E., Thomas W., Kurzer
M.S. ``Probiotic Consumption Does Not Enhance the Cholesterol-
Lowering Effect of Soy in Postmenopausal Women''. Journal of
Nutrition. 2004;134:3277-3283.
185. Wong W.W., Smith E.O., Stuff J.E., Hachey D.L., Heird W.C.,
Pownell H.J. ``Cholesterol-Lowering Effect of Soy Protein in
Normocholesterolemic and Hypercholesterolemic Men''. American
Journal of Clinical Nutrition. 1998;68:1385S-1389S.
186. Goldberg A.P., Lim A., Kolar J.B., Grundhauser J.J., Steinke
F.H., Schonfeld G. ``Soybean Protein Independently Lowers Plasma
Cholesterol Levels in Primary Hypercholesterolemia''.
Atherosclerosis. 1982;43:355-368.
187. Hoie L.H., Guldstrand M., Sjoholm A., Graubaum H.J., Gruenwald
J., Zunft H.J., Lueder W. ``Cholesterol-Lowering Effects of a New
Isolated Soy Protein with High Levels of Nondenaturated Protein in
Hypercholesterolemic Patients''. Advances in Therapy. 2007;24:439-
447.
188. Hoie L.H., Sjoholm A., Guldstrand M., Zunft H.J., Lueder W.,
Graubaum H.J., Gruenwald J. ``Ultra Heat Treatment Destroys
Cholesterol-Lowering Effect of Soy Protein''. International Journal
of Food Sciences and Nutrition. 2006;57:512-519.
189. Hoie L.H., Morgenstern E.C., Gruenwald J., Graubaum H.J., Busch
R., Luder W., Zunft H.J. ``A Double-Blind Placebo-Controlled
Clinical Trial Compares the Cholesterol-Lowering Effects of Two
Different Soy Protein Preparations in Hypercholesterolemic
Subjects''. European Journal of Nutrition. 2005;44:65-71.
190. Hoie L.H., Graubaum H.J., Harde A., Gruenwald J., Wernecke K.D.
``Lipid-Lowering Effect of 2 Dosages of a Soy Protein Supplement in
Hypercholesterolemia''. Advances in Therapy. 2005;22:175-186.
191. Teede H.J., Dalais F.S., Kotsopoulos D., McGrath B.P., Malan
E., Gan T.E., Peverill R.E. ``Dietary Soy Containing Phytoestrogens
Does Not Activate the Hemostatic System in Postmenopausal Women''.
Journal of Clinical Endocrinology and Metabolism. 2005;90:1936-1941.
192. Harrison R.A., Sagara M., Rajpura A., Armitage L., Birt N.,
Birt C.A., Yamori Y. ``Can Foods with Added Soya-Protein or Fish-Oil
Reduce Risk Factors for Coronary Disease? A Factorial Randomised
Controlled Trial''. Nutrition, Metabolism and Cardiovascular
Diseases. 2004;14:344-350.

193. Blum A., Lang N., Vigder F., Israeli P., Gumanovsky M.,
Lupovitz S., Elgazi A., Peleg A., Ben-Ami M. ``Effects of Soy
Protein on Endothelium-Dependent Vasodilatation and Lipid Profile in
Postmenopausal Women with Mild Hypercholesterolemia''. Clinical
Investigative Medicine. 2003;26:20-26.
194. Cuevas A.M., Irribarra V.L., Castillo O.A., Yanez M.D., Germain
A.M. ``Isolated Soy Protein Improves Endothelial Function in
Postmenopausal Hypercholesterolemic Women''. European Journal of
Clinical Nutrition. 2003;57:889-894.
195. Gardner C.D., Newell K.A., Cherin R., Haskell W.L. ``The Effect
of Soy Protein with or without Isoflavones Relative to Milk Protein
on Plasma Lipids in Hypercholesterolemic Postmenopausal Women''.
American Journal of Clinical Nutrition. 2001;73:728-735.
196. Hori G., Wang M.F., Chan Y.C., Komatsu T., Wong Y., Chen T.H.,
Yamamoto K., Nagaoka S., Yamamoto S. ``Soy Protein Hydrolyzate with
Bound Phospholipids Reduces Serum Cholesterol Levels in
Hypercholesterolemic Adult Male Volunteers''. Bioscience,
Biotechnology, and Biochemistry. 2001;65:72-78.
197. Chen S.T., Chen J.R., Yang C.S., Peng S.J., Ferng S.H. ``Effect
of Soya Protein on Serum Lipid Profile and Lipoprotein
Concentrations in Patients Undergoing Hypercholesterolaemic
Haemodialysis''. British Journal of Nutrition. 2006;95:366-371.
198. Ma Y., Chiriboga D., Olendzki B.C., Nicolosi R., Merriam P.A.,
Ockene I.S. ``Effect of Soy Protein Containing Isoflavones on Blood
Lipids in Moderately Hypercholesterolemic Adults: A Randomized
Controlled Trial''. Journal of the American College of Nutrition.
2005;24:275-285.
199. West S.G., Hilpert K.F., Juturu V., Bordi P.L., Lampe J.W.,
Mousa S.A., Kris-Etherton P.M. ``Effects of Including Soy Protein in
a Blood Cholesterol-Lowering Diet on Markers of Cardiac Risk in Men
and in Postmenopausal Women with and without Hormone Replacement
Therapy''. Journal of Womens Health. 2005;14:253-262.
200. Hilpert K.F., Kris-Etherton P.M., West S.G. ``Lipid Response to
a Low-Fat Diet with or without Soy Is Modified by C-Reactive Protein
Status in Moderately Hypercholesterolemic Adults''. Journal of
Nutrition. 2005;135:1075-1079.
201. Jenkins D.J., Kendall C.W., Jackson C.J., Connelly P.W., Parker
T., Faulkner D., Vidgen E., Cunnane S.C., Leiter L.A., Josse R.G.
``Effects of High- and Low-Isoflavone Soyfoods on Blood Lipids,
Oxidized Ldl, Homocysteine, and Blood Pressure in Hyperlipidemic Men
and Women''. American Journal of Clinical Nutrition. 2002;76:365-
372.
202. Jenkins D.J., Kendall C.W., Connelly P.W., Jackson C.J., Parker
T., Faulkner D., Vidgen E. ``Effects of High- and Low-Isoflavone
(Phytoestrogen) Soy Foods on Inflammatory Biomarkers and
Proinflammatory Cytokines in Middle-Aged Men and Women''.
Metabolism. 2002;51:919-924.
203. Lichtenstein A.H., Jalbert S.M., Adlercreutz H., Goldin B.R.,
Rasmussen H., Schaefer E.J., Ausman L.M. ``Lipoprotein Response to
Diets High in Soy or Animal Protein with and without Isoflavones in
Moderately Hypercholesterolemic Subjects''. Arteriosclerosis,
Thrombosis, and Vascular Biology. 2002;22:1852-1858.
204. Wang Y., Jones P.J., Ausman L.M., Lichtenstein A.H. ``Soy
Protein Reduces Triglyceride Levels and Triglyceride Fatty Acid
Fractional Synthesis Rate in Hypercholesterolemic Subjects''.
Atherosclerosis. 2004;173:269-275.
205. Desroches S., Mauger J.F., Ausman L.M., Lichtenstein A.H.,
Lamarche B. ``Soy Protein Favorably Affects Ldl Size Independently
of Isoflavones in Hypercholesterolemic Men and Women''. Journal of
Nutrition. 2004;134:574-579.
206. Van H.L., Liu K., Gerber J., Garside D., Schiffer L., Gernhofer
N., Greenland P. ``Oats and Soy in Lipid-Lowering Diets for Women
with Hypercholesterolemia: Is There Synergy?''. Journal of the
American Dietetic Association. 2001;101:1319-1325.
207. Gardner C.D., Messina M., Kiazand A., Morris J.L., Franke A.A.
``Effect of Two Types of Soy Milk and Dairy Milk on Plasma Lipids in
Hypercholesterolemic Adults: A Randomized Trial''. Journal of the
American College of Nutrition. 2007;26:669-677.
208. Jenkins D.J., Kendall C.W., Vidgen E., Vuksan V., Jackson C.J.,
Augustin L.S., Lee B., Garsetti M., Agarwal S., Rao A.V., Cagampang
G.B., Fulgoni V., III. ``Effect of Soy-Based Breakfast Cereal on
Blood Lipids and Oxidized Low-Density Lipoprotein''. Metabolism.
2000;49:1496-1500.
209. Teede H.J., Giannopoulos D., Dalais F.S., Hodgson J., McGrath
B.P. ``Randomised, Controlled, Cross-over Trial of Soy Protein with
Isoflavones on Blood Pressure and Arterial Function in Hypertensive
Subjects''. Journal of the American College of Nutrition.
2006;25:533-540.
210. Burke V., Hodgson J.M., Beilin L.J., Giangiulioi N., Rogers P.,
Puddey I.B. ``Dietary Protein and Soluble Fiber Reduce Ambulatory
Blood Pressure in Treated Hypertensives''. Hypertension.
2001;38:821-826.
211. Jenkins D.J., Kendall C.W., Faulkner D.A., Kemp T., Marchie A.,
Nguyen T.H., Wong J.M., de Souza R., Emam A., Vidgen E., Trautwein
E.A., Lapsley K.G., Josse R.G., Leiter L.A., Singer W. ``Long-Term
Effects of a Plant-Based Dietary Portfolio of Cholesterol-Lowering
Foods on Blood Pressure''. European Journal of Clinical Nutrition.
2008;62:781-788.
212. He J., Gu D., Wu X., Chen J., Duan X., Chen J., Whelton P.K.
``Effect of Soybean Protein on Blood Pressure: A Randomized,
Controlled Trial''. Annals of Internal Medicine. 2005;143:1-9.
213. Rivas M., Garay R.P., Escanero J.F., Cia P., Jr., Cia P., Alda
J.O. ``Soy Milk Lowers Blood Pressure in Men and Women with Mild to
Moderate Essential Hypertension''. Journal of Nutrition.
2002;132:1900-1902.
214. Chan Y.H., Lau K.K., Yiu K.H., Li S.W., Chan H.T., Tam S., Shu
X.O., Lau C.P., Tse H.F. ``Isoflavone Intake in Persons at High Risk
of Cardiovascular Events: Implications for Vascular Endothelial
Function and the Carotid Atherosclerotic Burden''. American Journal
of Clinical Nutrition. 2007;86:938-945.
215. Ho S.C., Woo J.L., Leung S.S., Sham A.L., Lam T.H., Janus E.D.
``Intake of Soy Products Is Associated with Better Plasma Lipid
Profiles in the Hong Kong Chinese Population''. Journal of
Nutrition. 2000;130:2590-2593.
216. Ho S.Y., Schooling M., Hui L.L., McGhee S.M., Mak K.H., Lam
T.H. ``Soy Consumption and Mortality in Hong Kong: Proxy-Reported
Case-Control Study of All Older Adult Deaths in 1998''. Preventive
Medicine. 2006;43:20-26.
217. Kokubo Y., Iso H., Ishihara J., Okada K., Inoue M., Tsugane S.,
Group J.S. ``Association of Dietary Intake of Soy, Beans, and
Isoflavones with Risk of Cerebral and Myocardial Infarctions in
Japanese Populations: The Japan Public Health Center-Based (Jphc)
Study Cohort I''. Circulation. 2007;116:2553-2562.
218. Nagata C., Shimizu H., Takami R., Hayashi M., Takeda N., Yasuda
K. ``Soy Product Intake Is Inversely Associated with Serum
Homocysteine Level in Premenopausal Japanese Women''. Journal of
Nutrition. 2003;133:797-800.
219. Nagata C., Takatsuka N., Kurisu Y., Shimizu H. ``Decreased
Serum Total Cholesterol Concentration Is Associated with High Intake
of Soy Products in Japanese Men and Women''. Journal of Nutrition.
1998;128:209-213.
220. Rosell M.S., Appleby P.N., Spencer E.A., Key T.J. ``Soy Intake
and Blood Cholesterol Concentrations: A Cross-Sectional Study of
1033 Pre- and Postmenopausal Women in the Oxford Arm of the European
Prospective Investigation into Cancer and Nutrition''. American
Journal of Clinical Nutrition. 2004;80:1391-1396.
221. Sasazuki S., Fukuoka Heart Study G. ``Case-Control Study of
Nonfatal Myocardial Infarction in Relation to Selected Foods in
Japanese Men and Women''. Jpn Circ J. 2001;65:200-206.
222. Yang G., Shu X.O., Jin F., Zhang X., Li H.L., Li Q., Gao Y.T.,
Zheng W. ``Longitudinal Study of Soy Food Intake and Blood Pressure
among Middle-Aged and Elderly Chinese Women''. American Journal of
Clinical Nutrition. 2005;81:1012-1017.
223. Zhang B., Chen Y.M., Huang L.L., Zhou X.X., Chen C.G., Ye Y.B.,
Su Y.X. ``Greater Habitual Soyfood Consumption Is Associated with
Decreased Carotid Intima-Media Thickness and Better Plasma Lipids in
Chinese Middle-Aged Adults''. Atherosclerosis. 2008;198:403-411.
224. Zhang X., Shu X.O., Gao Y.T., Yang G., Li Q., Li H., Jin F.,
Zheng W. ``Soy Food Consumption Is Associated with Lower Risk of
Coronary Heart Disease in

Chinese Women''. Journal of Nutrition. 2003;133:2874-2878.
225. Flegal K.M. ``Evaluating Epidemiologic Evidence of the Effects
of Food and Nutrient Exposures''. American Journal of Clinical
Nutrition. 1999;69:1339S-1344S.
226. Lichtenstein A.H., Russell R.M. ``Essential Nutrients: Food or
Supplements? Where Should the Emphasis Be?''. Journal of the
American Medical Association. 2005;294:351-358.
227. Peto R., Doll R., Buckley J.D., Sporn M.B. ``Can Dietary Beta-
Carotene Materially Reduce Human Cancer Rates?''. Nature.
1981;290:201-208.
228. ``The Effect of Vitamin E and Beta Carotene on the Incidence of
Lung Cancer and Other Cancers in Male Smokers. The Alpha-Tocopherol,
Beta Carotene Cancer Prevention Study Group''. New England Journal
of Medicine. 1994;330:1029-1035.
229. Omenn G.S., Goodman G.E., Thornquist M.D., Balmes J., Cullen
M.R., Glass A., Keogh J.P., Meyskens F.L., Valanis B., Williams
J.H., Barnhart S., Hammar S. ``Effects of a Combination of Beta
Carotene and Vitamin a on Lung Cancer and Cardiovascular Disease''.
New England Journal of Medicine. 1996;334:1150-1155.
230. Food and Drug Administration, ``Tables of Scientific Evidence
Regarding the Relationship Between Soy Protein and CHD''

List of Subjects in 21 CFR Part 101

    Food labeling, Nutrition, Reporting and recordkeeping requirements.

    Therefore, under the Federal Food, Drug, and Cosmetic Act and under
authority delegated to the Commissioner of Food and Drugs, it is
proposed that 21 CFR part 101 be amended as follows:

PART 101--FOOD LABELING

0
1. The authority citation for part 101 continues to read as follows:

    Authority: 15 U.S.C. 1453, 1454, 1455; 21 U.S.C. 321, 331, 342,
343, 348, 371; 42 U.S.C. 243, 264, 271.

Sec.  101.82  [Removed]

0
2. Remove Sec.  101.82.

    Dated: October 26, 2017.
Anna K. Abram,
Deputy Commissioner for Policy, Planning, Legislation, and Analysis.
[FR Doc. 2017-23629 Filed 10-30-17; 8:45 am]
 BILLING CODE 4164-01-P


[Federal Register Volume 77, Number 70 (Wednesday, April 11, 2012)]
[Notices]
[Pages 21833-21834]
[FR Doc No: 2012-8711]

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SECURITIES AND EXCHANGE COMMISSION

[Release No. 34-66746; File No. SR-ISE-2012-28]

Self-Regulatory Organizations; International Securities Exchange,
LLC; Notice of Filing and Immediate Effectiveness of Proposed Rule
Change To Increase the Route-Out Fee for Priority Customer Orders and
Modify the Rebate for Primary Market Makers That Send Intermarket Sweep
Orders

April 5, 2012.
    Pursuant to Section 19(b)(1) of the Securities Exchange Act of 1934
(the ``Exchange Act'') \1\ and Rule 19b-4 thereunder,\2\ notice is
hereby given that on March 30, 2012, the International Securities
Exchange, LLC (the ``Exchange'' or the ``ISE'') filed with the
Securities and Exchange Commission (the ``Commission'') the proposed
rule change as described in Items I and II below, which Items have been
prepared by the Exchange. The Commission is publishing this notice to
solicit comments on the proposed rule change from interested persons.
---------------------------------------------------------------------------

    \1\ 15 U.S.C. 78s(b)(1).
    \2\ 17 CFR 240.19b-4.
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I. Self-Regulatory Organization's Statement of the Terms of Substance
of the Proposed Rule Change

    The ISE is proposing to raise a fee related to the execution of
Priority Customer orders subject to linkage handling. The text of the
proposed rule change is available on the Exchange's Web site (http://www.ise.com), at the principal office of the Exchange, and at the
Commission's Public Reference Room.

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

    In its filing with the Commission, the self-regulatory organization
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. The self-regulatory organization
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 purpose of this proposed rule change is to raise a fee related
to the execution of Priority Customer \3\ orders subject to linkage
handling (``Linkage Fee'').
---------------------------------------------------------------------------

    \3\ Pursuant to ISE Rule 100(37A), a Priority Customer is a
person or entity that is not a broker or dealer in securities, and
does not place more than 390 orders in listed options per day on
average during a calendar month for its own beneficial account.
---------------------------------------------------------------------------

    On August 31, 2009, the Exchange implemented the new Options Order
Protection and Locked/Crossed Market Plan (``Distributive Linkage'')
and the use of Intermarket Sweep Orders (``ISOs''). Consistent with
Distributive Linkage and pursuant to ISE rules, the Exchange's Primary
Market Makers (``PMMs'') have an obligation to address customer \4\
orders when there is a better market displayed on another exchange.
ISE's PMMs meet this obligation via the use of ISOs. In meeting their
obligations, PMMs may incur fees when they send ISOs, especially when
sending ISOs to exchanges that charge ``taker'' fees. To minimize the
PMM's financial burden and help offset such fees, the ISE amended its
schedule of fees on October 1, 2009 to adopt a rebate for the PMM of
$0.20 per contract on all ISO orders sent to an away exchange
(regardless of the fee charged by the exchange where the ISO order sent
away was executed).\5\ With the costs associated with servicing
Priority Customer orders that must be executed at another exchange
coupled with the cost of funding the existing fee credit, the Exchange
recently adopted the Linkage Fee, at a rate of $0.25 per contract, for
executions that result from the PMM routing ISOs to another exchange in
a limited number of symbols.\6\ The Linkage Fee is only charged for
Priority Customer orders that are routed to an away exchange in symbols
that are subject to the Exchange's modified maker/taker pricing model.
These symbols, which currently number 101, are identified on the
Exchange's Schedule of Fees as Select Symbols. Priority Customer orders
that are routed out to another exchange are charged the Linkage Fee at
the current rate instead of the standard taker fee applicable to the
Select Symbols.
---------------------------------------------------------------------------

    \4\ Pursuant to ISE Rule 1900(f) of the Distributive Linkage
rules, a customer is an individual or organization that is not a
broker-dealer.
    \5\ See Securities and Exchange Act Release No. 60791 (October
5, 2009), 74 FR 52521 (October 13, 2009) (SR-ISE-2009-74).
    \6\ See Securities and Exchange Act Release No. 66589 (March 14,
2012), 76 [sic] FR 16311 (March 20, 2012) (SR-ISE-2012-13).
---------------------------------------------------------------------------

    The Linkage Fee allows the Exchange to equitably assess reasonable
fees incurred for processing such orders, and permit the Exchange to
recoup administrative and other costs. However, because the fees
assessed by other exchanges vary considerably, the Exchange has
determined that instead of providing PMMs with a rebate of $0.20 per
contract, it will now simply rebate to PMMs the actual transaction fee
assessed by the exchange to which the order is routed, while requiring
the PMM to make every effort, all things being equal, to route the
order to the lowest cost away market. Furthermore, as a result of
recent fee changes, notably the taker fee increases adopted by NASDAQ
OMX PHLX, Inc.,\7\ the overall cost to PMMs has risen significantly and
will likely cause the overall rebate level to the PMMs incurred by the
Exchange to rise also. To offset this increased rebate, the Exchange
also proposes to increase the Linkage Fee from $0.25 per contract to
$0.35 per contract.
---------------------------------------------------------------------------

    \7\ See Securities and Exchange Act Release No. 66367 (February
9, 2012), 77 FR 8934 (February 15, 2012) (SR-Phlx-2012-15).
---------------------------------------------------------------------------

    The Exchange notes that it currently has a similar fee and credit
for Customer (Professional) orders. Specifically, the Exchange
currently charges PMMs a fee of $0.45 per contract for executions of
Customer (Professional) orders that are routed to one or more exchanges
in connection with Distributive Linkage, and also provides PMMs with a
credit equal to the fee charged by the destination exchange for such
Customer (Professional) orders, but not more than

$0.45 per contract.\8\ This routing fee and credit applies to all the
symbols that are traded on the Exchange.
---------------------------------------------------------------------------

    \8\ See Securities and Exchange Act Release No. 61855 (April 6,
2010), 75 FR 19441 (April 14, 2010) (SR-ISE-2010-26).
---------------------------------------------------------------------------

    The Exchange has designated this proposal to be operative on April
2, 2012.
2. Statutory Basis
    The basis under the Securities Exchange Act of 1934 (the ``Exchange
Act'') for this proposed rule change is the requirement under Section
6(b)(4) that an exchange have an equitable allocation of reasonable
dues, fees and other charges among its members and other persons using
its facilities. In particular, the Exchange believes charging a route-
out fee for Priority Customer orders is reasonable if doing so provides
the Exchange the ability to recover the costs of funding a credit the
Exchange provides to its PMMs, who, in the course of meeting their
obligation, are incurring a financial burden. The Exchange further
believes it is equitable and reasonable to assess the proposed fee to
recoup costs associated with routing Priority Customer orders to away
markets. The Exchange also believes that the proposed fees are
equitable and not unfairly discriminatory because the fees would be
uniformly applied to all Priority Customer orders. ISE notes that a
number of other exchanges currently charge a variety of routing related
fees associated with customer and non-customer orders that are subject
to linkage handling. The Exchange further notes that the fees proposed
herein are substantially lower than the level of fees charged by some
of the Exchange's competitors.\9\ And, as noted above, the Exchange
already provides a credit equal to the fee charged by a destination
exchange for Customer (Professional) orders, although that credit is
currently capped at $0.45 per contract.
---------------------------------------------------------------------------

    \9\ See NASDAQ OMX PHLX Fee Schedule, Section V.
---------------------------------------------------------------------------

B. Self-Regulatory Organization's Statement on Burden on Competition

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

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

    The Exchange has not solicited, and does not intend to solicit,
comments on this proposed rule change. The Exchange has not received
any unsolicited written comments from members or other interested
parties.

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

    The foregoing rule change has become effective pursuant to Section
19(b)(3)(A)(ii) of the Exchange Act.\10\ At any time within 60 days of
the filing of such proposed rule change, the Commission summarily may
temporarily suspend 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 Exchange Act. If the Commission takes such action, the
Commission shall institute proceedings to determine whether the
proposed rule should be approved or disapproved.
---------------------------------------------------------------------------

    \10\ 15 U.S.C. 78s(b)(3)(A)(ii).
---------------------------------------------------------------------------

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 Exchange 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 email to<EMAIL_ADDRESS>Please include
File Number SR-ISE-2012-28 on the subject line.

Paper Comments

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

All submissions should refer to File Number SR-ISE-2012-28. This file
number should be included on the subject line if email 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 Web site viewing and
printing 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 the filing also will be available for
inspection and copying at the principal office of the Exchange. 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-ISE-2012-28 and should be
submitted on or before May 2, 2012.

    For the Commission, by the Division of Trading and Markets,
pursuant to delegated authority.\11\
---------------------------------------------------------------------------

    \11\ 17 CFR 200.30-3(a)(12).
---------------------------------------------------------------------------

Kevin M. O'Neill,
Deputy Secretary.
[FR Doc. 2012-8711 Filed 4-10-12; 8:45 am]
BILLING CODE 8011-01-P


[Federal Register Volume 78, Number 87 (Monday, May 6, 2013)]
[Notices]
[Pages 26356-26357]
[FR Doc No: 2013-10641]

-----------------------------------------------------------------------

DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

 Notice of Environmental Site Review

York Haven Power Company, LLC.............  Project No. 1888-030.
Exelon Generation Company, LLC............  Project No. 405-106.
Exelon Generation Company, LLC............  Project No. 2355-018.

    On May 21, 22, and 23, 2013, Commission staff will hold an
environmental site review for the Susquehanna River Projects, including
the York Haven Project (FERC No. 1888-030), the Conowingo Hydroelectric
Project (FERC No. 405-106), and the Muddy Run Pumped Storage Project
(FERC No. 2355-018). The projects are located on the Susquehanna River
in York, Dauphin, and Lancaster counties, Pennsylvania, and Cecil and
Hartford counties, Maryland. The purpose of the site review is to
introduce the Commission's contractor team to the project. All
participants should be prepared to provide their own transportation.

Schedule for the York Haven Hydroelectric Project Site Review

    Date and Time: Tuesday, May 21, 2013, 9:00 a.m.
    Location: York Haven Project, 1 Hydro Park Drive & Locust Street,
York Haven, Pennsylvania 17370.
    All participants planning to attend the site visit should RSVP to
Dave David at<PHONE_NUMBER> or<EMAIL_ADDRESS>
Schedule for the Conowingo Hydroelectric Project Site Review

    Date and Time: Wednesday, May 22, 2013, 10:00 a.m.
    Location: Conowingo Project, Conowingo Pavilion (next to Conowingo
dam), 2569 Shures Landing Road, Darlington, Maryland 21034.

    All participants planning to attend the Conowingo Project site
review should RSVP to Robert Judge at<PHONE_NUMBER> or
<EMAIL_ADDRESS>
Schedule for the Muddy Run Pumped Storage Project Site Review

    Date and Time: Thursday, May 23, 2013, 9:00 a.m.
    Location: Visitor's Center at Muddy Run Recreation Park, Muddy Run
Pumped Storage Project, 172 Bethesda Church Rd W, Holtwood,
Pennsylvania.
    All participants planning to attend the Muddy Run Project site
review should RSVP to Robert Judge at<PHONE_NUMBER> or
<EMAIL_ADDRESS>    If you have any questions please contact Emily Carter at (202) 502-
6512 or<EMAIL_ADDRESS>
    Dated: April 30, 2013.
Kimberly D. Bose,
 Secretary.
[FR Doc. 2013-10641 Filed 5-3-13; 8:45 am]
BILLING CODE 6717-01-P


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

<EPA Registration Division contact: Tony Kish,<PHONE_NUMBER>>

<INSTRUCTIONS:  Please utilize this outline in preparing the pesticide
petition.  In cases where the outline element does not apply, please
insert “NA-Remove” and maintain the outline. Please do not change
the margins, font, or format in your pesticide petition. Simply replace
the instructions that appear in green, i.e., “[insert company
name],” with the information specific to your action.>

<TEMPLATE:>

<  SEQ CHAPTER \h \r 1 Interregional Research Project Number 4 (IR-4)>

<2F7977>

<	EPA has received a pesticide petition <2F7977> from ISK Biosciences
Corporation, 7470 Auburn Road, Suite A, Concord, Ohio 44077, 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 by establishing a
tolerance for residues of fluazinam  in or on the raw agricultural
commodity soybean, seed at 0.01 parts per million (ppm) and soybean,
hulls at 0.02 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>

<Plant metabolism.   SEQ CHAPTER \h \r 1 The residue of concern is best
defined as the parent, fluazinam in most crops and as the parent,
fluazinam and its metabolite, AMGT, in fruit crops (grape and
blueberry).    SEQ CHAPTER \h \r 1 The metabolism of fluazinam in plants
(potatoes, peanuts, apples and wine grapes) is adequately understood for
the purposes of these tolerances.  The metabolism of fluazinam in peanut
and potato involves initial reduction of the nitro groups, hydrolysis of
the trifluoromethyl group as well as replacement of chlorine by
glutathione with subsequent reactions along the glutathione pathway.
Following replacement of the deactivating NO2 and Cl groups with
activating groups such as OH, NH2 and sulfhydryl, ring cleavage occurs.
Parent fluazinam is then rapidly degraded to form CO2 and carbon
fragments which are incorporated into natural products such as glucose,
fructose, sucrose, oils and protein.  Thus, parent fluazinam is either
not found or barely detectable in peanuts and potatoes.  Fluazinam
parent was the major identifiable residue in both the grape and apple
metabolism studies.  However, minor levels of AMGT (less than 5% of the
total radioactive residue) were also formed in grapes and apples.  In
grape and apple metabolism studies, following reduction of the nitro
groups and replacement of chlorine with a sulfur containing side-chain
such as glutathione (as occurred in peanuts and potatoes), glucose is
attached to the thiolactic acid conjugate of AMPA to form the metabolite
known as AMGT.  This metabolite was not found in   SEQ CHAPTER \h \r 1
the peanut or potatoes metabolism studies.  It is analogous to the
cysteine conjugate of AMPA found in rats.  Identifiable residues in
plant metabolism studies either closely resemble fluazinam in structure
or are the result of re-incorporation of the fluazinam carbon pool into
natural products.

    Ruminant and poultry metabolism studies demonstrated that the
transmittal of residues from the feed of goats and hens through to meat,
milk, and eggs was low.  Total 14C residues were below 1 ppm in all
tissues, milk and eggs.  Identifiable residues were less than 2% of the
administered dose in all matrices, except for chicken fat and liver.
The major metabolite found in animal tissues and milk were DAPA, AMPA,
and their sulfamate conjugates.  Parent Fluazinam was only detected in
very small amounts.>

<	2. Analytical method. An analytical method using LC-MS/MS for the
determination of fluazinam and AMGT residues on soybeans has been
developed and validated.  The method involves solvent extraction
followed by liquid-liquid partitioning and concentration prior to a
final purification.  The method has been successfully validated by an
independent laboratory using peanut nutmeat as the matrix.  The limit of
quantitation (LOQ) of the method is 0.01 ppm for both fluazinam and AMGT
in both crops.>

<	3. Magnitude of residues. A total of 16 field trials were conducted on
soybeans.  Treatment 2 of each field site consisted of two (2) foliar
applications at the target rate of approximately 0.50 lb a.i./A, applied
at 9-16 day intervals.  Two decline trials were included with sampling
at 10, 20 and 40 days after the last application.  Forage was harvested
at each site at 29-35 days after the last application.  Fluazinam
residues ranged from 0.072 ppm to 11.978 ppm, while AMGT was not
detected in any forage sample.  Hay samples were cut and allowed to dry
resulting in pre-harvest intervals (PHI’s) of 31-72 days.  Fluazinam
residues ranged from 0.024 ppm to 7.264 ppm in hay and again no
detectable AMGT was observed.  A feeding restriction will be place on
the label for these items.  Soybean seed samples had PHI’s from 56 to
94 days excluding the decline trials.  The results show that no
detectable residues of Fluazinam or AMGT at the LOD (0.003 ppm) were
found in soybean seed, even at PHI’s as short as 36 days.  Fluazinam
residues were below the LOQ in the aspirated grain fraction.  A
processing study was conducted at a 10X rate that resulted in no
concentration of residues in soybean meal or refined oil.  Residues of
Fluazinam did concentrate at a 5X level in the hulls.  No residues of
AMGT were observed in any sample, even at the 10X rate.

>

<B. Toxicological Profile>

<	1. Acute toxicity.  A battery of acute toxicity studies was conducted
which placed technical fluazinam in Toxicity Category IV for acute oral
LD50 and dermal irritation, and Category III for dermal LD50, inhalation
LC50 and eye irritation.  Technical fluazinam showed potential for
dermal sensitization.  In an acute neurotoxicity study, the NOAEL for
neurotoxicity was 2000 mg/kg bw (the highest dose tested) and the NOAEL
for systemic effects was 50 mg/kg bw.>

<	2. Genotoxicty. A battery of tests has been conducted to assess the
genotoxic potential of technical fluazinam.  Assays conducted included
two gene mutation tests in bacteria, a chromosomal aberration test in
mammalian cells, a mouse micronucleus test and a DNA repair test in
bacteria.  Technical fluazinam did not elicit a genotoxic response in
any of the studies conducted.>

<	3. Reproductive and developmental toxicity. In a two-generation
reproductive toxicity study, the NOAEL for reproductive effects was 100
ppm (10.6 mg/kg bw/day).  The NOAEL for parental toxicity was 20 ppm
(1.9 mg/kg bw/day).>

    In a rat developmental study, there were no developmental effects
observed at non-maternally toxic doses.  The developmental NOAEL was 50
mg/kg bw/day and the LOAEL was 250 mg/kg bw/day, based upon decreased
mean fetal body weight and other evidence suggestive of delayed fetal
development related to maternal toxicity. The maternal NOAEL was shown
to be 50 mg/kg bw/day.

    In a rabbit developmental study, there were no developmental effects
observed at non-maternally toxic doses.  The developmental NOAEL was 7
mg/kg bw/day and the LOAEL was 12 mg/kg bw/day, based on increased
incidence of total litter loss and possible slightly increased
incidences of fetal findings at this dose.  It was concluded that the
maternal NOAEL was 4 mg/kg bw/day.

<	4. Subchronic toxicity. The NOAEL for the 13-week feeding study in
rats was 50 ppm (3.8 mg/kg bw/day in males, 4.3 mg/kg bw/day in
females).  The LOAEL was 500 ppm (38 mg/kg bw/day in males, 44 mg/kg
bw/day in females), based on periacinar hepatocellular hypertrophy and
sinusoidal chronic inflammation in males, increased liver weights in
males and increased lung weights in females.

    In a 13-week dog study, the NOAEL was 10 mg/kg bw/day.  The LOAEL
was 100 mg/kg bw/day, based on ocular change observed
ophthalmoscopically and liver effects consisting of increased relative
liver to body weight, bile duct hyperplasia with or without
cholangiofibrosis and increased plasma phosphatase levels.

    In a 21-day dermal study, the NOAEL for systemic effects was 10
mg/kg bw/day.  The LOAEL was 100 mg/kg bw/day, based on hepatocelluar
hypertrophy and increases in AST and cholesterol levels.

    In a subchronic neurotoxicity study, no effects considered to be
indicative of neurotoxicity were observed at the highest dose tested,
3000 ppm (233 mg/kg bw/day in males, 280 mg/kg bw/day in females).  The
NOAEL for systemic toxicity (body weight differences) was 1000 ppm (74
mg/kg bw/day).

    In a developmental neurotoxicity study in rats, fluazinam was
administered by gavage to female rats from Day 6 after mating to Day 20
of lactation and additionally to their offspring from Day 7 of age to
Day 20 or 21 of age.  The author concluded that the maternal NOAEL was 2
mg/kg bw/day based on reduced body weights and lower food intake.  No
effects were seen on the microscopic structure of the nervous system of
the dams at any dose level (maximum dose of 50 mg/kg bw/day).  The NOAEL
for behavior and nervous system of the dams was >50 mg/kg bw/day, the
highest dose tested.  No adverse effect of treatment at any dose level
was seen on number of implantations, litter size or offspring survival.
Signs of general toxicity in the offspring were evident based on lower
Day 1 body weights and lower weight gains at 10 and 50 mg/kg bw/day
through weaning.  The NOAEL for general toxicity to offspring was 2
mg/kg bw/day.  There was no evidence of developmental neurotoxicity in
the offspring.  The NOAEL for the functional and morphological
development of the nervous system in the offspring was >50 mg/kg bw/day,
the highest dose tested.  There was no increased sensitivity of the
fetus or young rat pups to fluazinam as compared to the dams.>

<	5. Chronic toxicity. Fluazinam was not carcinogenic in rats.  A NOAEL
of 10 ppm (Males: 0.38 mg/kg bw/day; Females: 0.47 mg/kg bw/day) of
fluazinam was established based on the following effects at 1000 and/or
100 ppm: lower food consumption and efficiency of food utilization,
slight anemia, elevated cholesterol, increased liver weights, an
increased number of macroscopic liver and testes lesions and an
increased incidence of microscopically observed lung, liver, pancreas,
lymph node and testes lesions.

    An additional study was conducted to further define the NOAEL for
long-term effects in the rat.  In the second study, a NOAEL of 50 ppm
(2.2 mg/kg bw/day) was established based on liver and testes effects.

    Two long-term feeding studies were conducted in mice.  In the first,
the NOAEL for all effects was 10 ppm (Males: 1.1 mg/kg bw/day; Females:
1.2 mg/kg bw/day) and the LOAEL was 100 ppm (Males: 10.7 mg/kg bw/day;
Females: 11.7 mg/kg bw/day) based on the treatment-related effects
observed in the liver.

    A second oncogenicity study in mice was conducted at 1000, 3000 and
7000 ppm to ensure that an MTD dose was studied.  Findings included
increased female mortality, reduced body weight gains, increased brain
weights and/or liver weights.  An impurity in the test material used in
this study resulted in vacuolation of the white matter of the brain and
cervical spinal cord in treated animals. A statistically significant
higher incidence of hepatocellular adenomas was observed in the 3000 ppm
dose males.  Hepatocellular adenomas are common tumors in male mice.
There was no dose relationship in the induction of the adenoma and no
increase in hepatocellular carcinomas.  It was concluded that fluazinam
is not carcinogenic in the mouse.

    In a chronic dog study, the NOAEL was determined to be 1 mg/kg
bw/day.  The LOAEL was 10 mg/kg bw/day based on generalized, nonspecific
toxicity.  No ocular effects were observed ophthalmoscopally at any dose
in this study.>

<	6. Animal metabolism. After an oral dose of fluazinam the median peak
time for blood concentration of radiolabel activity for both sexes was 6
hours.  The major route of excretion was the feces with urine
contributing as a minor route. Less than 1% of the administered dose was
found in the terminated animals.  The highest concentration in tissues
was found in the liver.  There were no major differences related to sex
or dose level in the findings.  It was concluded that fluazinam is
metabolized by both reduction and glutathione and glucuronide
conjugation and further metabolism.>

<	7. Metabolite toxicology. The same metabolic processes occur in plants
and animals but metabolism in plants is more extensive than in animals.
All of the major identified metabolites in both plants and animals
retain the phenylpyridinylamine structure.  Many of the metabolites
resulting from fluazinam are similar in plants and animals and,
therefore, have already been evaluated toxicologically.

    Because of the rapid and complete elimination (in animals) and
re-incorporation (in plants) of fluazinam, the toxicity of metabolites
is expected to be similar to but lower than the toxicity of the parent
compound.  The residue of concern is parent fluazinam only in most crops
and parent fluazinam plus its minor metabolite AMGT on/in fruit crops
such as grape and blueberry.>

<	8. Endocrine disruption. The toxicological profile of fluazinam shows
no evidence of physiological effects characteristic of the disruption of
the hormone estrogen in mammalian chronic studies or in mammalian or
avian reproduction studies.   It is therefore considered that there is
an adequate level of safety over the reference dose for possible
endocrine effects and that an additional safety factor for possible
endocrine effects is not warranted.>

<C. Aggregate Exposure>

<	1. Dietary exposure. Potential dietary exposures from food were
estimated using the proposed tolerances for all crops (except apples as
noted below), using the Dietary Exposure Evaluation Model-Food
Consumption Intake Database (DEEM-FCIDTM) and percent crop treated of
100% (with the exception of imported wine grapes as discussed below).
The following raw agricultural commodities were included: apple, carrot,
 brassica (cole) leafy vegetables (Group 5) including turnip greens,
bean (Groups 6A, 6B and 6C), bushberry (Group 13-07B), ginseng, head
lettuce, leaf lettuce, bulb onion (Crop 3-07A), peanut, potato,
pepper/eggplant subgroup 8-10B,  melon subgroup 9A, soybeans, imported
wine grapes and sherry and resulting secondary residues in meat and
milk.  For acute dietary exposure, the acute population adjusted dose
(aPAD) was based on the NOAEL of 50 mg/kg bw/day from an acute rat
neurotoxicity study.   For females 13-49 years of age, the NOAEL of 7
mg/kg bw/day from the rabbit developmental toxicity study was used for
acute dietary exposure.  For chronic dietary exposure, the chronic
population adjusted dose (cPAD) was based on the NOAEL from the mouse
carcinogenicity study (1.1 mg/kg bw/day).  An uncertainty factor of 100
was used in both cases since the results of a DNT study confirmed there
was no increased sensitivity of the fetus or young rat pups to fluazinam
as compared to the dams and the FQPA uncertainty factor could be reduced
to one (1).>

<	i. Food. Acute Risk Tier 1 acute dietary exposure analyses were
conducted for fluazinam to determine the exposure contribution of the
above mentioned commodities to the diet and to ascertain the acute risk
potential.  The estimates were based on: proposed tolerance level
residues for all the crops; apple, peanut and potato processing studies;
market share assumptions of 100% crop treated (except wine grapes where
it was assumed that 100% of the imported wine grapes would be treated
and 39% of wine consumed in the US is imported); screening-level acute
EDWC of 218 ppb for water; and consumption data from USDA’s CSFII
(1994 through 1998) continuing survey of food intake.

    Even using all of the worst-case exposure scenarios listed above,
the Tier 1 95th percentile acute dietary exposure (per capita) from food
and drinking water for the U.S. population was estimated to be 0.024402
mg/kg bw/day or 4.9% of the aPAD. The highest acute exposure estimate
(95th percentile) was observed in the females 13-49 yrs. subpopulation:
0.018334 mg/kg bw/day.  This corresponds to 26.1% of the aPAD.

    Chronic Risk Tier 1 dietary exposure analyses were conducted for
fluazinam to determine the exposure contribution of the above mentioned
commodities to the diet and to ascertain the chronic risk potential. The
estimates were based on: proposed tolerance level residues for all the
crops, accept apples where average field residues were used; apple,
peanut and potato processing studies; market share assumptions of 100%
crop treated (except wine grapes where it was assumed that 100% of the
imported wine grapes would be treated and 39% of wine consumed in the US
is imported); screening-level chronic EDWC of 37 ppb; and consumption
data from USDA’s CSFII (1994 through 1998) continuing survey of food
intake.

    Even using all of the worst-case exposure scenarios listed above,
the Tier 1 chronic dietary exposure estimates resulted in an estimated
exposure for the U.S. population of 0.001924 mg/kg bw/day.  This
exposure corresponds to 17.5% of the cPAD of 0.011mg/kg bw/day.  The
highest exposure estimate was calculated for the all infants (<1 year)
population subgroup.  This exposure was determined to be 0.005609 mg/kg
bw/day (51.0% of the cPAD) most of which was due to the water
contribution.

    It can be concluded that acute or long-term dietary exposure to
fluazinam through residues on treated apple, carrot, brassica (cole)
leafy vegetables (Group 5) including turnip greens, bean (Groups 6A, 6B
and 6C), bushberry (Group 13-07B), ginseng, head lettuce, leaf lettuce,
bulb onion (Crop 3-07A), peanut, potato, pepper/eggplant subgroup 8-10B,
 melon subgroup 9A, soybeans, imported wine grapes and sherry should not
be of cause for concern.>

<	ii. Drinking water. Since fluazinam is intended for application
outdoors to field grown crops, the potential exists for parent and/or
metabolites to reach ground or surface water that may be used for
drinking water.  The potential estimated drinking water concentrations
(EDWCs) associated with the application of fluazinam to soybeans, is
less than the maximum values estimated for turf.  Thus, the more
conservative screening-level acute EDWC (218 ppb) and chronic EDWC (37
ppb) for turf were incorporated into the DEEM-FCID model to estimate
dietary exposure.>

<	2. Non-dietary exposure. A registration for the use of fluazinam on
golf courses is pending.  Applications are to be made by golf course
workers only, thus no residential handler exposure is expected.
However, post-application dermal exposure from contact with the treated
turf on golf courses may occur.  Thus, post-application dermal exposure
was calculated for adults and for youth playing golf, using the general
US population subgroup and youth, 13-19 years subgroup.   The Margins of
Exposure (MOE) for both the adults (21,800) and the youth (14,300) were
well above the acceptable MOE of 100.  >

<D. Cumulative Effects>

<	Fluazinam is a phenylpyridinylamine fungicide.   Since there are no
other members of this class of fungicides, it is considered unlikely
that fluazinam would have a common mechanism of toxicity with any other
pesticide in use at this time.>

<E. Safety Determination>

<	1. U.S. population. Dietary and post-application dermal exposure from
recreational contact with treated turf on golf courses will be the
routes of exposure to the U.S. population.  Ample margins of safety have
been demonstrated for both situations. For the general U.S. population,
the chronic aggregate risk assessment is based on exposure from food and
drinking water only, since no residential uses exist.  As noted above,
the chronic dietary exposure to fluazinam represents 17.5% of the cPAD
for the overall U.S. population, using the conservative Tier I
assumptions. A cancer dietary assessment was not conducted because this
product has been classified as “suggestive evidence of
carcinogenicity, but not sufficient to assess human carcinogenic
potential.”

An acute aggregate risk assessment is required for the general
population and for the subgroup of females 13-49 years old.  For both of
these populations, the acute dietary (food and drinking water) risk
assessment represents acute aggregate risk since the dietary route alone
is relevant for acute exposure and risk assessment. As noted above, the
acute dietary exposure to fluazinam is estimated to be 4.9% of the aPAD
for the overall U.S. population, and 26.1% of the aPAD for the subgroup
of females 13-49 years old. These values were presented above and are
below the Agency’ level of concern.

Short-term and intermediate-term aggregate risks include chronic dietary
and short-term residential sources of exposure. Since Fluazinam is
proposed for use on golf courses there is potential for post-application
exposure to adults and youths from playing golf.  The US general
population was chosen as the representative short-term population for
adults, while the dietary subpopulation youths aged 13 to 19 was chosen
to match with the youth golfer residential exposure.  The dietary (food
and drinking water) exposure was based on the Tier I chronic exposure
assessment as noted above but converted to an MOE.  This was aggregated
with the appropriate post-application residential golfer MOE to yield
the following aggregate short/intermediate-term MOEs: US general
population MOE = 1811; youths, 13-19 = 2779.  These aggregate risks are
well above 100 for all populations, indicating acceptable risks for both
adults and youth.

Based on this information, it can be concluded that there is reasonable
certainty that no harm will result from acute, short/intermediate term
or chronic exposure to fluazinam.>

<	2. Infants and children. Data from developmental toxicity studies in
the rat and rabbit, a 2-generation reproduction study and a
developmental neurotoxicity study were considered.  These studies, that
were described earlier, demonstrated no increased sensitivity of rats or
rabbits to in utero or gavage exposure of pups to fluazinam.  In
addition, the multigeneration reproductive toxicity study did not
identify any increased sensitivity of rats to in utero or postnatal
exposure.  For all four studies, parental NOAELs were lower than or
equivalent to the developmental or offspring NOAELs.  It is concluded
that the standard margin of safety will protect the safety of infants
and children and that an additional FQPA safety factor is not warranted.

    The dietary exposure of fluazinam to infants and children is
estimated to be less than any level of concern. The proposed tolerances
plus drinking water input will utilize 20.5% of the aPAD for the
“Children (1-2 years)” subgroup, and 51.0% of the cPAD for the
“All Infants (<1 year) “subgroup.  (These were the most sensitive
infant/child subgroups.) Thus, it can be concluded that there is
reasonable certainty that no harm will result to infants and children
from acute or chronic exposure to fluazinam.]>

<F. International Tolerances>

<	[There are presently no Codex maximum residue levels (MRLs)
established for residues of fluazinam on any crop.  The Canadian
established MRLs for brassicas (crop group 5A & 5B), bushberries (crop
group 13B), dry beans, lima beans, snap beans, and the Mexican MRLs for
beans and potatoes are similar to the tolerances established for these
crops in the USA.]>

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