[Federal Register Volume 76, Number 182 (Tuesday, September 20, 2011)]
[Notices]
[Page 58263]
[FR Doc No: 2011-24091]

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

DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Docket No. OR11-21-000]

Kenai Pipe Line Company; Tesoro Alaska Company; Tesoro Logistics
Operations, LLC; Notice of Request for Jurisdictional Determination or
Temporary Waiver of Tariff Filing and Reporting Requirements

    Take notice that on September 1, 2011, Kenai Pipe Line Company
(KPL), Tesoro Alaska Company (Tesoro Alaska), and Tesoro Logistics, LLC
(TLO) (collectively, Tesoro) filed a Request for Jurisdictional
Determination, or, in the Alternative, Temporary Waiver of Tariff
Filing and Reporting Requirements.
    Tesoro requests that the Commission determine that two crude oil
pipelines, as well as several crude oil and refined petroleum products
pipeline spurs that are part of Tesoro Alaska's internal refinery
operations, are not subject to the Commission's jurisdiction under the
Interstate Commerce Act (ICA).
    Tesoro also requests that the Commission determine that a dock and
tank storage that Tesoro also uses as part of its internal refinery
operation are not subject to the Commission's jurisdiction.
    Any person desiring to intervene or to protest in the above
proceeding must file in accordance with Rules 211 and 214 of the
Commission's Rules of Practice and Procedure (18 CFR 385.211 and
385.214) on or before 5 p.m. Eastern time on the specified comment
date. It is not necessary to separately intervene again in a subdocket
related to a compliance filing if you have previously intervened in the
same docket. Protests will be considered by the Commission in
determining the appropriate action to be taken, but will not serve to
make protestants parties to the proceeding. Anyone filing a motion to
intervene or protest must serve a copy of that document on the
Applicant. In reference to filings initiating a new proceeding,
interventions or protests submitted on or before the comment deadline
need not be served on persons other than the Applicant.
    The Commission encourages electronic submission of protests and
interventions in lieu of paper, using the FERC Online links at http://www.ferc.gov. To facilitate electronic service, persons with Internet
access who will eFile a document and/or be listed as a contact for an
intervenor must create and validate an eRegistration account using the
eRegistration link. Select the eFiling link to log on and submit the
intervention or protests.
    Persons unable to file electronically should submit an original and
14 copies of the intervention or protest to the Federal Energy
Regulatory Commission, 888 First St., NE., Washington, DC 20426.
    The filings in the above proceedings are accessible in the
Commission's eLibrary system by clicking on the appropriate link in the
above list. They are also available for review in the Commission's
Public Reference Room in Washington, DC. There is an eSubscription link
on the Web site that enables subscribers to receive e-mail notification
when a document is added to a subscribed docket(s). For assistance with
any FERC Online service, please e-mail<EMAIL_ADDRESS>or
call<PHONE_NUMBER> (toll free). For TTY, call<PHONE_NUMBER>.
    Comment Date: 5 p.m. Eastern time on Friday, September 30, 2011.

    Dated: September 14, 2011.
Kimberly D. Bose,
Secretary.
[FR Doc. 2011-24091 Filed 9-19-11; 8:45 am]
BILLING CODE 6717-01-P


TXR NO. 0051956 DATE: June 13, 2003 MEMORANDUM SUBJECT: 2,4 DB and 2,4 DB DMA  Report of the Hazard Identification Assessment Review Committee.

FROM: Kit Farwell, D. V. M. Reregistration Branch 1 Health Effects Division ( 7509C)

THROUGH: Jess Rowland, Co Chair and Elizabeth Doyle, Co Chair Hazard Identification Assessment Review Committee Health Effects Division ( 7509C)

TO: Jeff Dawson, Risk Assessor Reregistration Branch 1 Health Effects Division ( 7509C)

PC Code: 030801 ( 2,4 DB) 030819 ( 2,4 DB DMA)

On May 6, 2003, the Health Effects Division ( HED) Hazard Identification Assessment Review Committee ( HIARC) reviewed the recommendations of the toxicology reviewer for 2,4 DB and 2,4 DB DMA with regard to the acute and chronic Reference Doses ( RfDs) and the toxicological endpoint selection for use as appropriate in occupational/ residential exposure risk assessments. The potential for increased susceptibility of infants and children from exposure to 2,4 DB and 2,4 DB DMA was also evaluated as required by the Food Quality Protection Act ( FQPA) of 1996 using the 2002 OPP 10X Guidance Document. The conclusions drawn at this meeting are presented in this report. 2 Committee Members in Attendance Members present were: Ayaad Assaad, William Burnam, Jonathan Chen, Elizabeth Doyle, Pamela Hurley, John Liccione, Elizabeth Mendez, PV Shah, Jess Rowland, Brenda Tarplee Member( s) in absentia: Donna Davis, Paula Deschamp, William Dykstra, Susan Makris Data evaluation prepared by: Kit Farwell, D. V. M.

Also in attendance were: Whang Phang, Michael Metzger, Jeff Dawson, and Cecelia Watson ( SRRD)

Data Evaluation / Report Presentation Kit Farwell, D. V. M. Toxicologist 3 INTRODUCTION On May 6, 2003, the Health Effects Division ( HED) Hazard Identification Assessment Review Committee ( HIARC) reviewed the recommendations of the toxicology reviewer for 2,4 DB and 2,4 DBDMA with regard to the acute and chronic Reference Doses ( RfDs) and the toxicological endpoint selection for use as appropriate in occupational/ residential exposure risk assessments. The potential for increased susceptibility of infants and children from exposure to 2,4 DB and 2,4 DB DMA was also evaluated as required by the Food Quality Protection Act ( FQPA) of 1996 using the 2002 OPP 10X Guidance Document. The conclusions drawn at this meeting are presented in this report.

Both 2,4 DB and 2,4 DB DMA are chlorophenoxy herbicides which function by mimicking the action of auxins, plant growth hormones. They are broadleaf herbicides used in agriculture with no current residential uses. 2,4 DB ( PC code 030801) is the acid form and has the chemical name of 2,4 dichlorophenoxy butyric acid. 2,4 DB DMA ( PC code 030801) is its salt and has the chemical name of 2,4 dichlorophenoxy butyric acid, dimethyl amine salt.

The database for 2,4 DB is complete. The database for 2,4 DB DMA is more limited: the guideline studies available for this chemical are subchronic feeding study in rats, developmental toxicity in rats, dermal toxicity in rabbits, and mutagenicity studies. Toxicity and LOAELs for 2,4 DB and 2,4 DB DMA were generally similar in the 2 subchronic rat studies and in the 2 developmental rat studies.

A metabolism study in rats showed that 2,4 DB DMA dissociates to 2,4 DB, after which they share the same metabolic pathway. The toxicity studies for 2,4 DB were therefore also used to evaluate toxicity and to select endpoints for 2,4 DB DMA.

I. FQPA HAZARD CONSIDERATIONS 1. Adequacy of the Toxicity Data Base There are acceptable developmental toxicity studies in rats with 2,4 DB and 2,4 DB DMA and an acceptable developmental study in rabbits and a 2 generation reproduction study in rats with 2,4 DB. The HIARC concluded that the toxicology database for 2,4 DB and 2,4 DB DMA is complete for evaluation of residual concerns under FQPA.

2. Evidence of Neurotoxicity No neurotoxicity studies are available for 2,4 DB or 2,4 DB DMA. Clinical signs suggestive of neurotoxicity occurred only at lethal doses. The HIARC concluded that these effects were agonal in nature and there is not a concern for neurotoxicity resulting from exposure to 2,4 DB and 2,4 DB DMA. 4 3. Developmental Toxicity Study Conclusions Rat Developmental Toxicity Study with 2,4 DB:

In the range finding developmental toxicity study ( MRID 41382701) , 5 Crl: CD BR impregnated rats were dosed by gavage with 0, 125, 250, 500 or 1000 mg/ kg/ day 2, 4 DB ( 98.1% a. i., HLA Sample 90300425) on Days 6 through 15 of gestation. All rats in the 500 and 1000 mg/ kg/ day groups died or were euthanized by day 15 of gestation; only 20% of the 250 mg/ kg/ day group survived to day 20 of gestation. There were no deaths or clinical signs of toxicity in the control and 125 mg/ kg/ day groups. A variety of clinical signs, including languidness, prostration and reduced activity, were observed at 250 mg/ kg/ day and above. Body weight was statistically significantly reduced in all treated groups. There were no significant differences in pre and postimplantation losses, percent of live or resorbed fetuses at 125 mg/ kg/ day. However, 3 of 4 litters in this group had early resorptions and an increased post implantation loss ( 10.8% vs. 1.3% for controls).

In the main developmental toxicity study ( MRID 41382702), 2, 4 DB ( 98.1% a. i., HLA Sample 90300425) was administered to 25 Crl: CD rats/ dose in by gavage at dose levels of 0, 31.25, 62.5 or 125 mg/ kg bw/ day from days 6 through15 of gestation. The death of one dam in the 125 mg/ kg/ day group was attributed to treatment. Clinical signs of toxicity observed at 125 mg/ kg/ day included emaciation, hunched appearance, languidness, poor muscle tone, cold to touch, piloerection and urogenital staining. Mean body weight was statistically significantly reduced in the 125 mg/ kg/ day group ( 18% of control) and non significantly in the 62.5 mg/ kg/ day group ( 87%) for days 6 16; body weight gain was significantly decreased in the 125 mg/ kg/ day ( 73%) and 62.5 ( 73%) groups for days 0 20.

The pregnancy rates were 100% for the control and 96% for all treated groups. In the 125 mg/ kg/ day group, 4 ( 17%) of the 23 dams that were pregnant on gestation day 20 had complete litter resorptions. This group had higher post implantation losses and decreased live fetuses due to the increase in early resorptions.

The maternal NOAEL is 31.25 mg/ kg/ day and the maternal LOAEL is 62.5 mg/ kg/ day based on decreased body weight ( days 6 16) and body weight gain ( days 0 20).

Mean fetal weight was significantly reduced ( 83% of control value) in the 125 mg/ kg/ day group. Also in this group, there was a non significant increase in undeveloped renal papillae and a decrease in distended ureters; these effects were not considered treatment related. In the 125 mg/ kg/ day group, three fetuses in two litters had microphthalmia. Two fetuses in two litters and one fetus in one litter in the 125 and 32.5 mg/ kg/ groups, respectively, had retro esophageal aortic arches. Both fetal and litter incidences of unossified hyoid body of the skull bone, reduced cervical arches and thoracic centra, unossified sternebrae # 2, and malformed ribs were increased on a litter basis in the 125 mg/ kg/ day group. Skeletal variations were not increased on a litter basis in the 62.5 mg/ kg/ day group.

The developmental NOAEL is 62.5 mg/ kg/ day. The developmental LOAEL is 125 mg/ kg/ day, based on decreased fetal body weight, microphthalmia, retro esophageal aortic 5 arches, skeletal malformations/ variations, and increased postimplantation loss ( early resorptions).

This developmental toxicity study in the rat is classified acceptable ( guideline); and satisfies the guideline requirement for a developmental toxicity study ( OPPTS 870.3700; OECD 414) in the rat.

Rat Developmental Toxicity Study with 2,4 DB DMA:

In the range finding developmental toxicity study ( MRID 42536101), six Crl: CD BR VAF/ Plus impregnated rats were dosed by gavage with 0, 25, 50, 100, 175 or 275 mg/ kg/ day Butyrac 200 ( 25.8% a. i., lot # 50215006) on Days 6 through 15 of gestation. Maternal toxicity was observed at dose levels of 100 mg/ kg/ day and above as evidenced by increased mortality ( 275 mg/ kg/ day; 4/ 6 dams), increased clinical signs ( 175 and 275 mg/ kg/ day); decreased body weight/ body weight gain ( 100, 175 and 275 mg/ kg/ day). Developmental toxicity was observed at 175 and 275 mg/ kg/ day as evidenced by decreased fetal weight in both dose groups and increased mortality and resorptions at 175 mg/ kg/ day. Only two dams survived in the 275 mg/ kg/ day group; therefore, the fetal effects were not manifested in this group.

In the main study ( MRID 42595201), 25 Crl: CD BR VAF/ Plus impregnated rats were dosed by gavage with 0, 31.25, 62.5 or 125 mg/ kg/ day Butyrac 200, adjusted for test article activity, ( 25.8% a. i., lot # 50215906) on Days 6 through 15 of gestation. One female in the 125 mg/ kg/ day group was sacrificed in moribund condition on gestation day ( GD) 13 and two other females died on GDs 16 and 20. No abortions were reported. Clinical signs observed at 125 mg/ kg/ day included decreased activity, hunched posture, ataxia, cool to touch, rales, few feces, soft stool, no feces, mucoid stools, red vaginal discharge, emaciation, rough coat, fecal stain, urine stain and pale extremities. At 62.5 mg/ kg/ day, clinical signs were limited to few feces and emaciation. Mean body weight gain was statistically significantly decreased in the 125 mg/ kg/ day group during GDs 6 16 ( 38% of control) value and during GDs 0 20 ( 74%). Mean body weight was also nonsignificantly decreased during GDs 6 16 in the 62.5 mg/ kg/ day group ( 81%). Corrected body weight gain was non significantly decreased in the 31.25 ( 90%), 62.5 ( 87%) and 125 mg/ kg/ day ( 69%) groups. Mean food consumption was significantly decreased during GDs 6 16 ( 72% of control) and during GDs 0 20 ( 88%) in the 125 mg/ kg/ day group and non significantly during GDs 6 16 ( 91%) in the 62.5 mg/ kg/ day group. There was a rebound after treatment ( GDs 16 20) in which both the 62.5 and 125 mg/ kg/ day groups had significantly increased food consumption.

Two dams in the 125 mg/ kg/ day group had 100% resorption of their litters. A non significant increase in early resorptions in this dose group, principally due to the 2 dams with total resorptions, resulted in a statistically significant decrease in the number of live fetuses/ dam. Fetal weight/ litter was also significantly decreased in this group.

There was an increase in the number of skeletal malformations in the 125 mg/ kg/ day group, including vertebral anomalies with/ without rib anomalies ( 3 fetuses/ 2 litters) and rib anomalies ( 4 fetuses/ 2 litters) as compared to none in the control group. Microphthalmia was noted in 1 fetus in the 31.25 mg/ kg/ day group and in 3 fetuses in 1 litter in the 125 mg/ kg/ day group; this malformation was also noted in the rat developmental study with 2,4 DB ( MRID 41382702). 6 The maternal NOAEL is 31.25 mg/ kg/ day. The maternal LOAEL is 62.5 mg/ kg/ day, based on clinical signs of toxicity ( including emaciation) and decreased body weight gain and food consumption. At 125 mg/ kg/ day, there were 3 deaths and clinical signs including ataxia, decreased activity and hunched posture.

The developmental NOAEL is 62.5 mg/ kg/ day. The developmental LOAEL is 125 mg/ kg/ day based on increased post implantation loss ( early resorptions) and decreased number of live fetuses per dam, decreased fetal weight, skeletal malformations and microphthalmia.

This developmental toxicity study in the rat is classified acceptable ( guideline) and satisfies the guideline requirement for a developmental toxicity study ( OPPTS 870.3700a; OECD 414) in rats.

Rabbit Developmental Toxicity Study with 2,4 DB:

In a range finding developmental toxicity study ( MRID 41529903), 8 female Hra: ( NZW) SPF rabbits were dosed by gavage with 0, 50, 100, 200 or 400 mg/ kg/ day 2, 4 DB ( 98.1% a. i., HLA Sample 90300425) on Days 7 through 19 of gestation. All rabbits in the 200 or 400 mg/ kg/ day groups died or were sacrificed moribund by Day 13 of gestation. The percent of animals surviving to the end of the study was 100%, 88% and 25% for the control, 50 mg/ kg/ day and 100 mg/ kg/ day groups. Clinical signs of toxicity, including ataxia, prostration, pale eyes and emaciation, were observed at all dose levels. Body weight and body weight gain were significantly decreased at all dose levels. Gross necropsy lesions ( stomach erosions) were observed at

100 mg/ kg/ day. There were no effects on developmental toxicity parameters.

In the main developmental toxicity study ( MRID 41529902), 2, 4 DB ( 98.1% a. i., HLA Sample 90300425) was administered to 16 impregnated Hra:( NZW) SPF rabbits/ group by gavage at dose levels of 0, 15, 30 or 60 mg/ kg bw/ day from days 7 through 19 of gestation. There were two control does and one 30 mg/ kg/ day doe that aborted and were sacrificed. At 30 mg/ kg/ day, one doe died, apparently from dosing trauma. At 60 mg/ kg/ day, two does aborted and were sacrificed and two does were sacrificed in extremis due to treatment related effects. Clinical signs of toxicity, including loss of coordination, reduced activity, ataxia, prostration and/ or yellow discharge from the eyes were observed at 60 mg/ kg/ day. At this dose, body weight gain was also decreased ( 54% of control for days 7 20). There were no treatment related effects on pregnancy rates, which were 69%, 81%, 75% and 56% at the 0, 15, 30 and 60 mg/ kg/ day groups, respectively. No maternal toxicity was observed at 15 or 30 mg/ kg/ day. The maternal LOAEL was 60 mg/ kg bw/ day, based on death ( sacrifice in extremis) clinical signs of toxicity and decreased body weight gains. The maternal NOAEL was 30 mg/ kg bw/ day.

There were no treatment related effects on fetal body weight, viability or external, visceral or skeletal variations and malformations. The developmental LOAEL was not determined. The developmental NOAEL was 60 mg/ kg/ day ( HDT).

The developmental toxicity study in the rabbit is classified acceptable ( guideline) and satisfies the guideline requirement for a developmental toxicity study ( OPPTS 870.3700; OECD 414) in rabbits. 7 4. Reproductive Toxicity Study Conclusions In a two generation reproduction study ( MRID 40257503) 2,4 DB ( 97.7% a. i., batch # 853686)] was administered to 28 Crl: COBS CD( SD) BR rats/ sex/ dose in the diet at dose levels of 0,60, 300 or 1500 ppm ( equivalent to approximately 0, 5, 25 or 112 mg/ kg bw/ day for males and 0, 6, 30 and 133 mg/ kg/ day for females). After weaning of the F 1 A generation at 21 days, males and females were remated using alternative pairings to produce the F 1 B generation. Weanlings from the F 1 B generation were selected as parental animals for the F 2 generation. Due to the loss of almost all litters in the two matings of the F 0 generation at 1500 ppm, it was impossible to rear a second generation at this concentration.

The only treatment related clinical sign was diffuse or patchy alopecia on the back of F 0 generation females at 1500 ppm. Ten adults died during the study but there was no evidence of a treatment related effect. Females in the F 0 generation treated at 1500 ppm had a higher water intake ( 8 20% increase) than the control group. Overall ( 10 weeks) premating food consumption in the F 0 generation was decreased in males ( 8%) and females ( 7%) at 1500 ppm at the first mating. No effect on food consumption was reported for other parental animals. Food conversion ( food consumption/ body weight gain) was increased only in the F 0 generation females at 1500 ppm. During gestation and lactation of the F 0 generation, body weight was decreased approximately 10% in females at 1500 ppm.

There was no evidence of a treatment related effect on reproduction parameters, except for a slightly longer mean gestational period with the 1500 ppm group ( 22.9 days vs 22.3 days for controls during the first mating; 22.7 days vs 22.2 days for controls for the second mating). The toxicological significance of the finding is questionable due to the minimal non significant effect. On necropsy of the parental animals from the F 0 generation, there were several statistically significant organ weight changes. The weight ( adjusted for body weight as a covariate) of the liver was decreased and the kidneys increased in males at 1500 ppm. In females at 1500 ppm, there was a decrease in the weight of the heart and spleen ( using body weight as a covariate) along with decreases in adrenal and ovarian weights. On macroscopic examination of F 0 generation adults at termination, there was a higher incidence of pallor of the kidneys in females and irregular renal cortical scarring in males at 1500 ppm.

The mean litter size and mean litter weight were lower at birth for offspring in the 1500 ppm group at both matings of the F 0 generation. From birth to Day 21, all litters in this group were lost, except for one from the first mating and three from the second mating. The percentage of males in all treated groups of the first mating of the F 0 generation and in the 300 ppm group of the first mating of the F 1 generation was statistically significantly decreased in comparison to the controls. The toxicological significance of this change is questionable since it was not a consistent finding at all matings. On necropsy of offspring from the F 0 generation females, there was an increased incidence of animals with a small thymus, distended bladder with bloody/ dark urine and ocular opacity in the 1500 ppm group. There was a dose related increase in the renal pelvic dilatation in the 60 and 300 ppm groups in both generations. The toxicological significance of this finding is questionable as there was no increase at 1500 ppm in the F 0 generation.

The parental NOAEL is 300 ppm ( 25 mg/ kg bw/ day in males and 30 mg/ kg bw/ day in 8 females). The parental LOAEL is 1500 ppm ( approximately 112 mg/ kg bw/ day in males and 133 mg/ kg bw/ day in females), based on increased water consumption ( females), decreased food consumption and body weight, increased food conversion ratio ( females), organ weight changes and macroscopic renal findings.

The offspring NOAEL is 300 ppm ( 25 mg/ kg bw/ day in males and 30 mg/ kg bw/ day in females). The offspring LOAEL is 1500 ppm ( approximately 112 mg/ kg bw/ day in males and 133 mg/ kg bw/ day in females), based on increased mortality, decreased mean litter weight and increased incidence of necropsy findings ( small thymus, distended bladder with bloody/ dark urine and ocular opacity).

As there was no treatment related effect on reproduction parameters, the reproductive LOAEL is not established. The reproductive NOAEL is 1500 ppm ( HDT) ( approximately 112 mg/ kg bw/ day in males and 133 mg/ kg bw/ day in females).

This study is classified acceptable ( guideline) and satisfies the guideline requirement for a twogeneration reproductive study ( OPPTS 870.3800); OECD 416 in rats.

5. Additional Information from Literature Sources No information related to developmental or reproductive susceptibility from 2,4 DB or 2,4 DBDMA was found in a Toxline search.

6. Pre and/ or Postnatal Toxicity The HIARC concluded that there is concern for postnatal toxicity resulting from exposure to 2,4 DB or 2,4 DB DMA.

A. Determination of Susceptibility There was no prenatal susceptibility in the developmental rat study with 2,4 DB; developmental effects occurred at doses two fold higher than the doses that caused maternal toxicity. There was no prenatal susceptibility in the developmental rat study with 2,4 DB DMA, either; developmental effects occurred at doses two fold higher than the doses that caused maternal toxicity. There was no prenatal susceptibility in the rabbit developmental toxicity study with 2,4 DB because no developmental toxicity occurred.

There was qualitative, but not quantitative susceptibility in the 2 generation reproduction study with 2,4 DB because offspring mortality occurred at a dose where parental toxicity was less severe. The parental NOAEL was 30 mg/ kg/ day and the parental LOAEL was 133 mg/ kg/ day based on decreased food consumption and body weight, increased food conversion ratio, increased water consumption, organ weight changes, and macroscopic renal findings ( kidney pallor and cortical scarring). The offspring NOAEL was 30 mg/ kg/ day and the offspring LOAEL was 133 mg/ kg/ day based on mortality, decreased mean litter weight, and increased incidence of necropsy findings ( small thymus, distended bladder with bloody/ dark urine and ocular opacity). There was no effect upon reproductive parameters. 9 B. Degree of Concern Analysis and Residual Uncertainties Since there was evidence of increased susceptibility of offspring following exposure to 2,4 DB in the reproduction study, HIARC performed a Degree of Concern Analysis to: 1) determine the level of concern for the effects observed when considered in the context of all available toxicity data; and 2) identify any residual uncertainties after establishing toxicity endpoints and traditional uncertainty factors to be used in the risk assessment for this chemical. If residual uncertainties are identified, HIARC examines whether these residual uncertainties can be addressed by a special FQPA safety factor and, if so, the size of the factor needed. The results of the HIARC Degree of Concern analysis for 2,4 DB follow.

The HIARC concluded that there is low concern for the qualitative susceptibility because: the offspring toxicity was well characterized and was accompanied by maternal toxicity; there was a clear NOAEL/ LOAEL for offspring toxicity; and because the dose/ endpoint selected for longterm risk assessments is considerably lower and would address the concerns for offspring toxicity seen in this study. Therefore, the Committee concluded that there are no residual uncertainties for pre and/ or postnatal toxicity.

C. Special FQPA Safety Factor( s):

Based upon the above data, no special FQPA Safety Factor is needed ( i. e. 1X) since there are no residual uncertainties for pre and/ or postnatal toxicity.

The Special FQPA Safety Factor recommended by the HIARC assumes that the exposure databases ( dietary food, drinking water, and residential) are complete and that the risk assessment for each potential exposure scenario includes all metabolites and/ or degradates of concern and does not underestimate the potential risk for infants and children.

7. Recommendation for a Developmental Neurotoxicity Study The HIARC concluded that there is not a concern for developmental neurotoxicity resulting from exposure to 2,4 DB or 2,4 DB DMA. Clinical signs suggestive of neurotoxicity in the developmental toxicity studies only occurred at lethal doses and were agonal in nature. There was no indication of toxicity to the central nervous system in developmental and/ or reproductive studies with 2,4 DB and 2,4 DB DMA.

Based on the weight of evidence presented, the HIARC concluded that a developmental neurotoxicity study is not required for 2,4 DB or 2,4 DB DMA.

II. HAZARD IDENTIFICATION 10 1. Acute Reference Dose ( aRfD)  Females 13+ years of age Study Selected: Developmental toxicity in rats ( 2,4 DB) Developmental toxicity in rats ( 2,4 DB DMA)

OPPTS 870.3700a [ § 83 3a]; OECD 414 MRID Nos.: 41382701 and 41382702 ( 2,4 DB) 42536101 and 42595201 ( 2,4 DB DMA)

Executive Summaries: See developmental toxicity section.

Dose and Endpoint for Establishing aRfD: Developmental NOAEL = 62.5 mg/ kg/ day and LOAEL = 125 mg/ kg/ day in both studies. The developmental LOAEL is based on skeletal variations/ malformations, microphthalmia, and post implantation loss.

Uncertainty Factor ( UF): 100 ( 10 for interspecies extrapolation and 10 for intraspecies variability)

Comments about Study/ Endpoint/ Uncertainty Factor: The endpoint ( developmental toxicity) is presumed to occur after a single dose.

Acute RfD ( Females 13+) = 62.5 mg/ kg ( NOAEL) = 0.6 mg/ kg/ day 100 ( UF)

2. Acute Reference Dose ( aRfD)  General Population, Including Infants and Children Study Selected: None MRID No.: N/ A Executive Summary: N/ A Dose and Endpoint for Establishing aRfD: N/ A Comments about Endpoint: Data do not show a toxicity endpoint attributable to a single exposure appropriate for the general population.

3. Chronic Reference Dose ( cRfD)

Study Selected: Combined Chronic Toxicity/ Carcinogenicity Rat Feeding Study OPPTS 870.4300 ( OPP § 83 5)

MRID No.: 40257501 11 Executive Summary: In a combined chronic/ carcinogenicity study ( MRID 40257501) 2,4 DB ( 97.74% a. i., batch/ lot # not provided) was administered to 50 Crl: CD ® ( SD) BR rats/ sex/ dose in the diet at dose levels of 0, 60, 600 or 1800 ppm ( equivalent to 0, 3, 30 or 90 mg/ kg bw/ day based on 1 ppm equals 0.05 mg/ kg) for 24 months to test the carcinogenic potential of the chemical. An additional 20 rats/ sex/ group were administered 2,4 DB in the diet at the same concentrations for 24 months to test the chronic toxicity of the chemical. Ten ( 10) rats/ sex/ group were treated for 12 months at the same concentrations and then sacrificed. Ten ( 10) were treated at 0 or 1800 ppm for 12 months and then untreated for another 4 weeks before sacrifice to test the reversibility of toxicity.

There was no treatment related effect on the survival or clinical signs of toxicity. Mean body weight was statistically significantly decreased in 1800 males ( 87 97% of control value) and females ( 77 93% of control) and in 600 ppm females ( 91 97% of control). Mean body weight gain was significantly decreased in 1800 ppm males ( 82 90% control) and females ( 69 76% of control) and in 600 ppm females ( 88 91% of control). Mean weekly food consumption was significantly decreased in the 1800 ppm males during the first 50 weeks of the study. Females in the 1800 and 600 ppm groups had significantly decreased food consumption during the first 13 weeks and first 10 weeks, respectively.

Hematology parameters ( RBC, hemoglobin, hematocrit) were significantly decreased and MCHC increased in the 1800 ppm females at various periods ( 6 and 12 months most frequently). Platelet counts were significantly decreased in the 1800 ppm males ( 3 and 6 months) and females ( 6 months). Multiple clinical chemistry parameters were significantly changed in the 1800 ppm males and females at several testing periods; a few parameters were altered in the 600 ppm males and females. The following clinical chemistry parameters were altered in the 1800 ppm males and females: decreased total protein, globulin, total bilirubin, cholesterol, LDH, CK, K, glucose ( females), Ca ( females) and P ( females); increased A/ G ratio, AST ( males), ALT ( males) and AP. The following parameters were altered in the 600 ppm males and females: increased A/ G ratio, decreased total protein ( females), decreased cholesterol, decreased CK ( males). The toxicological significance of the clinical pathology changes in the 600 ppm groups is questionable as there were no gross or microscopic alterations.

Absolute weight of the spleen was significantly decreased in the 1800 ppm males ( 12 and 24 month sacrifices) and females ( 12 and 13 month sacrifices). The weights of the heart and liver were significantly decreased in 1800 ppm males and females. Absolute and relative ( to body weight) weights of one or both kidneys were decreased at the 12 and 24 month ( females) sacrifices. At gross necropsy, there was an increased incidence of depressed focus in the kidneys in males at 1800 ppm. On microscopic examination, there was a significant increased incidence of kidney infarcts in both sexes at 1800 ppm and an increase in mononuclear cell infiltration and spongy degeneration of the liver in the 1800 ppm males.

The LOAEL in males is 1800 ppm ( 90 mg/ kg/ day) based on decreased body weight, body weight gain and food consumption, clinical pathology changes and necropsy alterations ( decreased kidney weights, increased incidence of kidney foci and infarcts and liver mononuclear infiltration and spongy degeneration). The LOAEL in females is 600 ppm ( 30 12 mg/ kg/ day), based on decreased body weight gain and food consumption. The NOAEL in males is 600 pp ( 30 mg/ kg/ day). The NOAEL in females is 60 ppm ( 3 mg/ kg/ day). This chronic/ carcinogenicity study in the rat is classified acceptable ( guideline) and satisfies the guideline requirement for a chronic/ carcinogenicity study OPPTS 870.4300); OECD 453] in rat.

Dose and Endpoint for Establishing cRfD: NOAEL = 3 mg/ kg/ day based upon decreased body weight gain and food consumption in females at the LOAEL of 30 mg/ kg/ day.

Uncertainty Factor( s): 100 ( 10 for interspecies extrapolation and 10 for intraspecies variations)

Comments about Study/ Endpoint/ Uncertainty Factor: Consideration was given to using an endpoint from the chronic dog study. The dog is more sensitive to toxicity from 2,4 DB than is the rat, as is the case for 2,4 D and MCPA. Pharmacokinetic data on dogs are not available for 2,4 DB. However, compounds closely related structurally to 2,4 DB, including 2,4 D, triclopyr, MCPA, and other organic acids have a decreased clearance in dogs relative to that predicted from the allometric relationship, whereas humans, rats, mice, and other species all fit the relationship. Although absorption and distribution of chlorophenoxy herbicides and other organic acids is similar across all species evaluated, the half life of elimination for dogs is significantly longer than for all other species considered. For 2,4 D, dogs exhibited half lives of 31 to 106 hours for doses of 1 to 5 mg/ kg and in other species ( mice, rats, pigs, cats and humans) half lives ranged from 0.75 to 11.6 hours for similar doses. The decreased capacity of the dog to eliminate organic acids results in higher blood levels and a longer elimination half life for these compounds in the dog, relative to those found in the rat and other species, and consequently, effects are seen at lower dose levels in the dog than in the rat. ( See HIARC reports for 2,4 D [ TXR 0051866] and MCPA [ TXR 0051862] for more details.) The difference in the elimination pattern among dogs and other mammalian species persuaded HIARC that the rat was a better predictor than the dog of the potential toxicity of 2,4 DB and 2,4 DB DMA to humans.

Chronic RfD = 3 mg/ kg/ day ( NOAEL) = 0.03mg/ kg/ day 100 ( UF)

4. Incidental Oral Exposure: Short Term ( 1 30 days)

Study Selected: Developmental toxicity in rats ( 2,4 DB) Developmental toxicity in rats ( 2,4 DB DMA)

OPPTS 870.3700a [ § 83 3a]; OECD 414 MRID No.: 41382701 and 41382702 ( 2,4 DB) 42536101 and 42595201 ( 2,4 DB DMA)

Executive Summary: See developmental toxicity section. 13 Dose and Endpoint for Risk Assessment: Maternal NOAEL = 31.25 mg/ kg based on decreased body weight, body weight gain, and food consumption and clinical signs of toxicity ( emaciation, few feces) at the LOAEL of 62.5 mg/ kg/ day.

Comments about Study/ Endpoint: This study is appropriate for the population of concern ( infants and children) and for the route and duration of exposure. There was confidence in the endpoint because NOAEL values and the types of toxicity seen were comparable in the rat studies with both 2,4 DB and 2,4 DB DMA.

5. Incidental Oral Exposure: Intermediate Term ( 1  6 Months)

Study Selected: 90 Day Feeding Study in Rats with 2,4 DB OPPTS 870.3100 [ § 82 1a]

MRID No.: 00104739 Executive Summary: In a 90 day oral toxicity study ( MRID 00104739) 2,4 DB [ 98.5% a. i ( from MRID 00092165), batch/ lot # 811012] was administered to 10 Charles River albino rats/ sex/ dose in the diet at dose levels of 0, 316, 1000 or 3160 ppm ( 0, 15.8, 50 or 158 mg/ kg/ day based on 1 ppm equals 0.05 mg/ kg/ day) for three months. An additional group of 10 rats/ sex was administered 100 ppm ( 5 mg/ kg/ day) for three months starting seven weeks after initiation of treatment in the other groups. Clinical pathology measurements were performed on 5 animals/ sex/ group. Microscopic examinations at necropsy were conducted on 5 rats/ sex from the control and 3160 ppm groups. The thyroids, liver, kidneys and any unusual lesions were examined in 5 rats/ sex of the 1000 ppm group. The liver, kidneys and any unusual lesions were examined in 5 rats/ sex of the 100 and 316 ppm groups.

All animals survived to study termination. The only clinical signs of toxicity were bloated appearance and soft feces in five of ten males in the 3160 ppm group. Mean body weights were decreased in the 3160 ppm males ( 80 91% of control) and females ( 75 92%) and slightly in the 1000 ppm females ( 90 93%). Mean body weight gain over the course of the study was decreased in the 3160 ppm males ( 77%) and females ( 61%) and slightly in the 1000 ppm females ( 89%). There were slight alterations in clinical chemistry values ( decreased glucose, increased SGPT, alkaline phosphatase) in the 3160 ppm group males and females.

At necropsy, the absolute weight of the heart, spleen and adrenals was significantly decreased in the 3160 ppm males; the absolute weight of the thyroids, heart and adrenals was significantly increased in the 3160 ppm females. The relative weight ( to body weight) of the liver and kidneys was increased in the 3160 ppm males and females and in the 1000 ppm males. On microscopic examination, there was increased activity in the thyroid glands of the 3160 ppm males and females as evidenced by an increased number of small follicles. In both sexes of the 1000 and 3160 ppm groups, there was an increased incidence and severity of the following lesions: hepatocyte hypertrophy and increased pigment in the liver, regenerative epithelium in the kidneys and mucosal edema of the stomach. 14 The NOAEL is 316 ppm ( 15.8 mg/ kg/ day). The LOAEL is 1000 ppm ( 50 mg/ kg/ day), based on slightly decreased body weight gain ( females), increased relative weight of the liver and kidneys ( males) and increased incidence of microscopic alterations in the liver, kidneys and stomach.

Although microscopic examinations of target tissues were not performed on all dose groups, a NOAEL for microscopic effects can be determined in conjunction with the chronic toxicity study in rats with 2,4 DB ( MRID 40257501). This 90 day oral toxicity study in the rat is classified acceptable ( guideline) and satisfies the guideline requirement for a 90 day oral toxicity study ( OPPTS 870.3100; OECD 408) in the rat.

Dose and Endpoint for Risk Assessment: NOAEL = 15.8 mg/ kg/ day based upon slightly decreased body weight gain ( females), increased relative weight of the liver and kidneys ( males) and increased incidence of microscopic changes ( hepatocyte hypertrophy, regenerative kidney epithelium, gastric mucosal edema) at the LOAEL of 50 mg/ kg/ day.

Comments about Study/ Endpoint: This endpoint is appropriate for the population of concern ( infants and children) and for the route and duration of exposure. Consideration was given to using the subchronic rat study with 2,4 DB DMA, which has a lower NOAEL ( 4mg/ kg/ day in males and 5 mg/ kg/ day). However, the lower NOAEL in the 2,4 DB DMA study is believed to be due to dose spacing because the LOAEL for both studies was the mid dose ( 50 mg/ kg/ day) and the low dose ( NOAEL) for 2,4 DB was 16 mg/ kg/ day and for 2,4 DB DMA was only 5 mg/ kg/ day.

6. Dermal Absorption Dermal Absorption Factor: 23%

This value is from a dermal absorption study with 2,4 DB DMA ( MRID 44729501) and is the value from a 120 ug/ cm2 exposure determined at 96 hours after a wash at 10 hours.

Although this value is from a dermal absorption study with 2,4 DB DMA, it should also be used for 2,4 DB because there is no dermal absorption study with 2,4 DB. This dermal absorption value is quite protective because the NOAELs for systemic toxicity from 21 day dermal toxicity studies in rabbits were 2000 mg/ kg/ day for 2,4 DB and 1500 mg/ kg/ day for 2,4 DB DMA, the highest doses tested.

7. Dermal Exposure: Short Term ( 1 30 days) Exposure Study Selected: None MRID No.: N/ A Executive Summary: N/ A Dose and Endpoint for Establishing aRfD: N/ A 15 Comments about Endpoint: Quantification of short term dermal exposure is not required. No systemic toxicity developed in 21 day dermal toxicity studies with 2,4 DB and 2,4 DB DMA. There were no effects on body weight, food consumption, clinical signs, hematology, clinical chemistry, organ weights, and gross or microscopic pathology of organs, including liver and kidney. Dermal irritation ( moderate) occurred with 2,4 DB DMA treatment. The systemic NOAEL and highest dose tested was 2000 mg/ kg/ day with 2,4 DB and 1500 mg/ kg/ day with 2,4 DB DMA.

There are no developmental toxicity concerns. This is because developmental toxicity in rats only occurred at doses two fold greater than those causing maternal toxicity, and no systemic toxicity occurred in the dermal studies with 2,4 DB and 2,4 DB DMA. Furthermore, developmental toxicity in rats ( skeletal variations/ malformations, microphthalmia, and post implantation loss), occurred only at a dose that was lethal to the dams. In rabbits, no developmental toxicity occurred, even at a dose causing maternal mortality and clinical signs.

8. Dermal Exposure: Intermediate Term ( 1  6 Months)

Study Selected: 90 Day Feeding Study in Rats with 2,4 DB OPPTS 870.3100 [ § 82 1a]

MRID No.: 00104739 Executive Summary: See intermediate term incidental oral section of this report.

Dose and Endpoint for Risk Assessment: NOAEL = 15.8 mg/ kg/ day based upon slightly decreased body weight gain ( females), increased relative weight of the liver and kidneys ( males) and increased incidence of microscopic changes ( hepatocyte hypertrophy, regenerative kidney epithelium, gastric mucosal edema) at the LOAEL of 50 mg/ kg/ day.

Comments about Study/ Endpoint: The duration of exposure is appropriate for this endpoint. The 21 day dermal toxicity study in rabbits was not used for this endpoint because the duration of exposure ( 21 days) was considered too short for liver and kidney toxicity to develop. Consideration was also given to using the subchronic rat study with 2,4 DB DMA, which has a lower NOAEL ( 4 mg/ kg/ day in males and 5 mg/ kg/ day). However, the lower NOAEL in the 2,4 DB DMA study is believed to be an artifact of dose spacing, as described in Section II. 5 ( Incidental oral, intermediate term exposure). Since an oral dose was selected, the 23% dermal absorption factor should be used for route to route extrapolation.

9. Dermal Exposure Long Term (> 6 Months)

Study Selected: Combined Chronic Toxicity/ Carcinogenicity Rat Feeding Study OPPTS 870.4300 ( OPP § 83 5 MRID No.: 40257501 16 Executive Summary: See chronic dietary section.

Dose and Endpoint for Risk Assessment: NOAEL = 3 mg/ kg/ day based upon decreased body weight gain and food consumption in females at the LOAEL of 30 mg/ kg/ day.

Comments about Study/ Endpoint: This dose/ endpoint/ study was also used for establishing the chronic RfD. See Comments section for the Chronic RfD in this report for more details. Since an oral dose was selected, the 23% dermal absorption factor should be used for route to route extrapolation.

10. Inhalation Exposure: Short  Term ( 1 30 days)

Study Selected: Developmental toxicity in rats ( 2,4 DB) Developmental toxicity in rats ( 2,4 DB DMA)

OPPTS 870.3700a [ § 83 3a]; OECD 414 MRID No.: 41382701 and 41382702 ( 2,4 DB) 42536101 and 42595201 ( 2,4 DB DMA)

Executive Summary: See developmental toxicity section.

Dose and Endpoint for Risk Assessment: Maternal NOAEL = 31.25 mg/ kg based on decreased body weight, body weight gain, and food consumption and clinical signs of toxicity ( emaciation, few feces) at the LOAEL of 62.5 mg/ kg/ day.

Comments about Study/ Endpoint: In the absence of a repeated exposure inhalation study, an oral dose was selected. There was confidence in the endpoint because NOAEL values and the types of toxicity seen were comparable in the rat studies with both 2,4 DB and 2,4 DB DMA. Absorption via the inhalation route is presumed to be equivalent to oral absorption.

11. Inhalation Exposure: Intermediate Term ( 1 6Months)

Study Selected: 90 Day Feeding Study in Rats with 2,4 DB OPPTS 870.3100 [ § 82 1a]

MRID No.: 00104739 Executive Summary: See intermediate term incidental oral section of this report.

Dose and Endpoint for Risk Assessment: NOAEL = 15.8 mg/ kg/ day based upon slightly decreased body weight gain ( females), increased relative weight of the liver and kidneys ( males) and increased incidence of microscopic changes ( hepatocyte hypertrophy, regenerative kidney epithelium, gastric mucosal edema) at the LOAEL of 50 mg/ kg/ day. 17 Comments about Study/ Endpoint: In the absence of a repeated exposure inhalation study, an oral dose was selected. Absorption via the inhalation route is presumed to be equivalent to oral absorption.

12. Inhalation Exposure: Long Term (> 6 Months)

Study Selected: Combined Chronic Toxicity/ Carcinogenicity Rat Feeding Study OPPTS 870.4300 ( OPP § 83 5 MRID No.: 40257501 Executive Summary: See chronic dietary section.

Dose and Endpoint for Risk Assessment: NOAEL = 3 mg/ kg/ day based upon decreased body weight gain and food consumption in females at the LOAEL of 30 mg/ kg/ day.

Comments about Study/ Endpoint: This dose/ endpoint/ study was also selected for establishing the chronic RfD and long term dermal risk assessments. See Comments section for the Chronic RfD in this report for more details. Absorption via the inhalation route is presumed to be equivalent to oral absorption.

13. Margins of Exposure Summary of target Margins of Exposure ( MOEs) for risk assessment.

Route Duration Short Term ( 1 30 Days) Intermediate Term ( 1  6 Months) Long Term (> 6 Months)

Occupational ( Worker) Exposure Dermal N/ A 100 100 Inhalation 100 100 100 Residential ( Non Dietary) Exposure Oral 100 100 N/ A Dermal N/ A 100 100 Inhalation 100 100 100 For Occupational exposure: This is based on the conventional uncertainty factor of 100 ( 10 for intraspecies extrapolation and 10 for interspecies variation) For Residential exposure: This is based on the conventional uncertainty factor of 100 ( 10 for intraspecies extrapolation and 10 for interspecies variation). 18 14. Recommendation for Aggregate Exposure Risk Assessments As per FQPA, 1996, when there are potential residential exposures to the pesticide, aggregate risk assessment must consider exposures from three major sources: oral, dermal and inhalation exposures. For intermediate term and long term aggregate exposure risk assessments, the oral, dermal, and inhalation routes can be combined because a common toxicity endpoint ( using oral equivalents) was identified for all 3 routes of exposure. For short term aggregate exposure risk assessments, the oral and inhalation routes can be combined because a common toxicity endpoint ( using oral equivalents) was identified; quantification of short term dermal exposure is not required ( see short term dermal exposure section of this document).

III. CLASSIFICATION OF CARCINOGENIC POTENTIAL 1. Combined Chronic Toxicity/ Carcinogenicity Study in Rats MRID No. 40257501 Executive Summary: See chronic dietary section of this document.

Discussion of Tumor Data: There was no treatment related increase in tumor incidence when compared to controls.

Adequacy of the Dose Levels Tested: Dosing was considered adequate based on the effects on body weight, body weight gain, food consumption, clinical pathology and necropsy findings.

2. Carcinogenicity Study in Mice MRID No.: 42387301 Executive Summary: In a carcinogenicity study ( MRIDs 40257502, 41936201 and 42387301) 2,4 DB ( 97.4% a. i., no batch/ lot # provided) was administered to 50 Crl: CD1 ( CR) BR mice/ sex/ dose in the diet at dose levels of 0, 25, 250 or 750 ppm ( equivalent to 0, 3.75, 37.5 and 112.5 mg/ kg bw/ day based on 7 ppm in the diet equals 1 mg/ kg/ day) for 78 weeks, except males at 750 ppm were terminated at 66 weeks. An additional 20 animals/ sex/ group were terminated after receiving the same doses for 52 weeks.

Males dosed at 750 ppm had a dramatic increase in mortality beginning about weeks 58 61; therefore, all males in this group were terminated at week 66. There were no treatment related effects on body weight, body weight gain, food consumption, ophthalmological examinations or clinical pathology parameters. At the 12 month and terminal sacrifices, the absolute and relative ( to body weight) weights of the left and right kidneys were increased in the 750 ppm males ( 6 19%) and females ( 8 20%), although not always statistically significantly and not always in a dose related manner. Liver absolute and relative weights at the 12 month sacrifice were also increased in the 750 ppm males ( 7 10%) and females ( 22 24%), although not significantly, and in 19 750 ppm males ( 14%) at the terminal sacrifice. The absolute weight of the heart was significantly increased in the 750 ppm males at the terminal sacrifice. On gross pathological examination at the terminal necropsy, there was a statistically significant increased incidence of irregularly shaped kidneys, diffusely dark livers and light foci in the heart of males at 750 ppm. On microscopic examination, males at 750 ppm had an increased incidence of amyloidosis in a number of organs and a significant increase in hepatocellular enlargement at the terminal sacrifice. The LOAEL is 750 ppm ( 112.5 mg/ kg/ day), based on increased mortality in males and increased absolute and relative organ weights ( liver and kidney in both sexes, heart in males), gross pathological changes in liver and kidney ( males) and increased amyloidosis and hepatocellular enlargement ( males). The NOAEL is 250 ppm ( 37.5 mg/ kg/ day). This carcinogenicity study in the mice is acceptable ( guideline) and satisfies guideline requirements for a carcinogenicity study [ OPPTS 870.4200; OECD 451] in mice.

Discussion of Tumor Data: There was no treatment related increase in tumor incidence.

Adequacy of the Dose Levels Tested: The high dose male group ( 750 ppm) was sacrificed at week 66 due to high mortality. This left 2 dose groups for males ( 25 and 250 ppm). However, dosing was considered adequate in males and females based on the findings of the 4 week rangefinding study ( MRID 42387301). In this study, 10 Crl: CD1 ( CR) BR mice/ sex/ dose were dosed with 0, 30, 100, 300, 1000 or 3000 ppm 2,4 DB in the diet for 4 weeks. At 300 ppm, body weight gain was decreased by 15% and 18% in males and females, respectively. At 1000 ppm, mean body weight gains were decreased 17% and 15% in males and females, respectively ( in the absence of any palatability problems) and liver weights were increased in both sexes. At 3000 ppm, there was decreased survival in both sexes, decreased body weight gain and food consumption and increased absolute and relative liver weights.

3. Classification of Carcinogenic Potential In accordance with the 1999 Draft Guidelines for Cancer Risk Assessment ( July, 1999), the HIARC classified 2,4 DB as " not likely to be carcinogenic to humans". This classification was based on the lack of evidence of carcinogenicity in mice and rats.

IV. MUTAGENICITY The HIARC concluded that there is not a concern for mutagenicity resulting from exposure to 2,4 DB or 2,4 DB DMA. 20 Mutagenicity Testing with 2,4 DB and 2,4 DB DMA Gene Mutation 2,4 DB Negative for reverse gene mutations in Salmonella typhimurium strains TA1535, TA1537, TA1538, TA98 and TA100 up to a concentration exceeding the limit dose. ( MRID 40257504)

2,4 DB DMA ( 26%) Negative for reverse gene mutations in Salmonella typhimurium strains TA1535, TA1537, TA1538, TA98 and TA100 up to a concentration that exceeded the limit dose. ( MRID 41256101).

2,4 DB Negative for forward gene mutations at the HGPRT locus in Chinese hamster ovary ( CHO) cells  S9 at 1000

g/ mL; cytotoxicity was not seen at this level. Equivocal increases in mutation frequency + S9 ( 2 of 3 trials), but not dose related; mostly in only 1 replicate of the 2 cultures at each concentration. All increased MF were within historical spontaneous range for this cell line and below the MF considered necessary by the International Standardization of Genotoxicity Workgroup to be declared a positive response in this test system ( MRID 40257505).

2,4 DB DMA ( 26%) Negative up to a cytotoxic concentration ( MRID 41810701).

Structural Chromosomal Aberrations 2,4 DB There were no significant increases in chromosome aberrations + S9, up to solubility limits. Chromosomal aberrations were noted  S9, but only at cytotoxic doses ( MRID 40257506).

2,4 DB DMA ( 26%) Not clastogenic in CHO cells up to the limit dose ( MRID 41224403).

Other Mutagenic Mechanisms 2,4 DB No evidence of unscheduled DNA synthesis ( UDS) in primary rat hepatocytes up to a lethal dose ( MRID 40257507).

2,4 DB DMA ( 26%) Positive at the 2 highest concentrations ( 101 and 252

g/ mL) for induction of UDS in primary rat hepatocytes. Increases in both the mean net nuclear grains/ nucleus and percentage of the cells with  6 net nuclear grains were scored at these levels ( MRID 41358901).

V. HAZARD CHARACTERIZATION 2,4 DB and 2,4 DB DMA are chlorophenoxy herbicides. This class of herbicides function by mimicking the action of auxins, plant growth hormones. 2,4 DB ( 2,4 dichlorophenoxy butyric acid) is an acid and 2,4 DB DMA ( 2,4 dichlorophenoxy butyric acid, dimethyl amine salt) is its dimethyl amine salt.

A metabolism study in rats showed that 2,4 DB DMA dissociates to 2,4 DB, after which they share the same metabolic pathway. Urine is the major route of excretion; 2,4 D and conjugated dichlorophenol are the major metabolites for both chemicals.

The database for 2,4 DB and 2,4 DB DMA is adequate for establishing toxicity endpoints for risk assessment. Most studies were conducted with 2,4 DB. Studies with 2,4 DB DMA include subchronic feeding study in rats, developmental toxicity in rats, dermal toxicity in rabbits, and mutagenicity studies. Toxicity and LOAELs for 2,4 DB and 2,4 DB DMA were generally similar in the 2 subchronic rat 21 studies and in the 2 developmental rat studies. The DMA salt form appears more irritating than the acid form, based on skin irritation in the dermal toxicity study and inflamed lacrimal glands in the subchronic rat study. Toxicity in the following section generally refers to studies with 2,4 DB, unless otherwise specified.

Some form of liver toxicity was noted in all the subchronic and chronic toxicity studies with 2,4 DB and in the subchronic rat study with 2,4 DB DMA. Liver weights were increased in subchronic rat studies with 2,4 DB and 2,4 DB DMA, the subchronic dog study, and the mouse carcinogenicity study. Liver enzymes ( ALT, AST, and/ or alkaline phosphatase) were elevated in the subchronic and chronic dog studies with 2,4 DB and in the subchronic rat study with 2,4 DB DMA. Hepatocyte hypertrophy was noted in the subchronic rat study with 2,4 DB. In the subchronic dog study with 2,4 DB, BSP retention was increased, and icterus and pale livers were noted.

Kidney toxicity was noted in several studies. Kidney weights were increased in the subchronic dog study and in the subchronic rat study with 2,4 DB. In the chronic rat study with 2,4 DB, kidney weights were decreased and kidney infarcts were noted. BUN was increased in the subchronic and chronic dog studies with 2,4 DB.

Other toxicity included decreased hematological parameters in the chronic rat study and the subchronic and chronic dog studies with 2,4 DB and in the subchronic rat study with 2,4 DB DMA. Heart weights were increased in the subchronic and chronic rat studies and the mouse carcinogenicity study with 2,4 DB. Light foci in the heart were also noted in the mouse carcinogenicity study. Inflamed lacrimal glands were noted in the subchronic rat study with 2,4 DB DMA.

No systemic toxicity was noted in 21 day dermal studies in rabbits with either 2,4 DB or 2,4 DB DMA, although dermal irritation occurred in the dermal study with 2,4 DB DMA.

Although neurotoxicity has been noted with other phenoxy herbicides, neurotoxicity with 2,4 DB and 2,4 DB DMA only occurred at lethal doses.

No developmental toxicity occurred in the developmental study in rabbits. Developmental toxicity in rat studies occurred at the same dose as maternal mortality and there were no concerns for increased susceptibility of offspring from the developmental toxicity studies.

Offspring toxicity in the 2 generation reproduction study with 2,4 DB included mortality, decreased mean litter weight, and increased incidence of necropsy findings ( small thymus, distended bladder with bloody/ dark urine and ocular opacity); parental effects at the same dose included decreased food consumption and body weight, increased food conversion ratio, increased water consumption, organ weight changes, and macroscopic renal findings ( kidney pallor and cortical scarring). There was no effect upon reproductive parameters.

The dog is more sensitive to toxicity from 2,4 DB than is the rat, as is the case for 2,4 D and MCPA. Pharmacokinetic data on dogs are not available for 2,4 DB. However, compounds closely related structurally to 2,4 DB, including 2,4 D, triclopyr, MCPA, and other organic acids have a decreased clearance in dogs relative to that predicted from the allometric relationship, whereas humans, rats, mice, 22 and other species all fit the relationship. Although absorption and distribution of chlorophenoxy herbicides and other organic acids is similar across all species evaluated, the half life of elimination for dogs is significantly longer than for all other species considered. For 2,4 D, dogs exhibited half lives of 31 to 106 hours for doses of 1 to 5 mg/ kg and in other species ( mice, rats, pigs, cats and humans) halflives ranged from 0.75 to 11.6 hours for similar doses. The decreased capacity of the dog to eliminate organic acids results in higher blood levels and a longer elimination half life for these compounds in the dog, relative to those found in the rat and other species, and consequently, effects are seen at lower dose levels in the dog than in the rat. ( See HIARC reports for 2,4 D and MCPA for more details.) The difference in the elimination pattern among dogs and other mammalian species persuaded HIARC that the rat was a better predictor than the dog of the potential toxicity of 2,4 DB and 2,4 DB DMA to humans.

VI. DATA GAPS / REQUIREMENTS A 28 day inhalation study is required because the use pattern indicates potential repeated exposure via this route. This study should be conducted with 2,4 DB DMA because of possible irritancy observed in the subchronic dermal and feeding studies. 23 VII. ACUTE TOXICITY Acute Toxicity of 2,4 DB Guideline No. Study Type MRID # s Results Toxicity Category 81 1 Acute Oral 00128854 0092159 LD50 = 1935 mg/ kg LD50 = 1715 mg/ kg III 81 2 Acute Dermal 0128854 LD50 = > 2000 mg/ kg III 81 3 Acute Inhalation 41774001 LC50 > 2.3 mg/ L IV 81 4 Primary Eye Irritation 0128854 00092160 Eye irritation with complete clearing by day 7 III 81 5 Primary Skin Irritation 0128854 No irritation IV 81 6 Dermal Sensitization  Under review   Acute Toxicity of 2 4 DB DMA ( 26%)

Guideline No. Study Type MRID # Results Toxicity Category 81 1 Acute Oral 41224401 LD50 = 3583 mg/ kg III 81 2 Acute Dermal ( rabbit) 41224402 LD50 > 2000 mg/ kg III 81 3 Acute Inhalation 41370101 LC50 > 7.98 mg/ L IV 81 4 Primary Eye Irritation 4195801 Persistent corneal opacity, iritis, erythema I 81 5 Primary Skin Irritation 250871 Irritation score = 0.99 IV 81 6 Dermal Sensitization  Under review   24 VIII. SUMMARY OF TOXICOLOGY ENDPOINT SELECTION Summary of Toxicological Dose and Endpoints for 2,4 DB and 2,4 DB DMA Exposure Scenario Dose for Risk Assessment and Uncertainty Factor Special FQPA Safety Factor and Level of Concern Study and Toxicological Effects Acute Dietary ( Females 13 50 years of age) NOAEL = 62.5 mg/ kg/ day UF = 100 Acute RfD = 0.6 mg/ kg/ day FQPA SF = 1X aPAD = acute RfD FQPA SF = 0.6 mg/ kg/ day Rat developmental toxicity. LOAEL = 125 mg/ kg/ day based on skeletal variations/ malformations, microphthalmia, post implantation loss Acute Dietary ( General population including infants and children) None N/ A No appropriate endpoint attributable to a single dose from oral toxicity studies.

Chronic Dietary ( All populations) NOAEL= 3 mg/ kg/ day UF = 100 Chronic RfD = 0.03 mg/ kg/ day FQPA SF = 1X cPAD = chronic RfD FQPA SF = 0.03 mg/ kg/ day Chronic/ carcinogenicity study in rats. LOAEL = 30 mg/ kg/ day based on decreased body weight gain and food consumption in females.

Short Term Incidental Oral ( 1 30 days) NOAEL = 31.25 mg/ kg/ day Residential LOC for MOE = 100 Occupational = NA Rat developmental toxicity. LOAEL = 62.5 mg/ kg/ day based on decreased maternal body weight, body weight gain, and food consumption, and clinical signs ( emaciation, few feces)

Intermediate Term Incidental Oral ( 1 6 months) NOAEL = 15.8 mg/ kg/ day Residential LOC for MOE = 100 Occupational = NA Subchronic rat toxicity ( 2,4 DB study). LOAEL = 50 mg/ kg/ day based on decreased body weight gain ( females), increased relative liver/ kidney weight, and microscopic changes Short Term Dermal ( 1 to 30 days) None N/ A Quantitation not required. No systemic toxicity via the dermal route and there are no developmental concerns.

Intermediate Term Dermal ( 1 to 6 months) Oral NOAEL = 15.8 mg/ kg/ day Residential LOC for MOE = 100 Occupational = 100 Subchronic rat toxicity ( 2,4 DB study) LOAEL = 50 mg/ kg/ day based on decreased body weight gain, increased relative liver/ kidney weight, and microscopic changes Exposure Scenario Dose for Risk Assessment and Uncertainty Factor Special FQPA Safety Factor and Level of Concern Study and Toxicological Effects 25 Long Term Dermal (> 6 months) Oral NOAEL = 3 mg/ kg/ day ( dermal absorption = 23%) Residential LOC for MOE = 100 Occupational LOC for MOE = 100 Chronic/ carcinogenicity study in rats. LOAEL = 30 mg/ kg/ day based on decreased body weight gain and food consumption in females.

Short Term Inhalation ( 1 to 30 days) Oral NOAEL = 31 mg/ kg/ day ( inhalation absorption = 100%) Residential LOC for MOE = 100 Occupational LOC for MOE = 100 Rat developmental toxicity. LOAEL = 62.5 mg/ kg/ day based on decreased maternal body weight, body weight gain, and food consumption, and clinical signs ( emaciation, few feces)

Intermediate Term Inhalation ( 1 to 6 months) Oral NOAEL = 15.8 mg/ kg/ day ( inhalation absorption = 100%) Residential LOC for MOE = 100 Occupational LOC for MOE = 100 Subchronic rat toxicity ( 2,4 DB study). LOAEL = 50 mg/ kg/ day based on decreased body weight gain, increased relative liver/ kidney weight, and microscopic changes Long Term Inhalation (> 6 months) Oral NOAEL = 3 mg/ kg/ day ( inhalation absorption = 100%) Residential LOC for MOE = 100 Occupational LOC for MOE = 100 Chronic/ carcinogenicity study in rats. LOAEL = 30 mg/ kg/ day based on decreased body weight gain and food consumption in females.

Cancer None N/ A Classified " not likely to be a human carcinogen".

UF = uncertainty factor, FQPA SF = Special FQPA safety factor, NOAEL = no observed adverse effect level, LOAEL = lowest observed adverse effect level, PAD = population adjusted dose, ( a = acute, c = chronic) RfD = reference dose, MOE = margin of exposure, LOC = level of concern, NA = Not Applicable NOTE: The Special FQPA Safety Factor recommended by the HIARC assumes that the exposure databases ( dietary food, drinking water, and residential) are complete and that the risk assessment for each potential exposure scenario includes all metabolites and/ or degradates of concern and does not underestimate the potential risk for infants and children.


[Federal Register: February 9, 2009 (Volume 74, Number 25)]
[Notices]
[Page 6447-6449]
[DOCID:fr09fe09-73]

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

SECURITIES AND EXCHANGE COMMISSION

[Release No. 34-59344; File No. SR-NYSEALTR-2009-03]

Self-Regulatory Organizations; Notice of Filing and Immediate
Effectiveness of Proposed Rule Change by NYSE Alternext U.S. LLC Making
Changes to Certain NYSE Alternext Equities Rules to Conform With
Amendments to Corresponding Rules Recently Filed for Immediate
Effectiveness by the New York Stock Exchange LLC and To Make Other
Technical Changes

February 2, 2009.
    Pursuant to Section 19(b)(1) \1\ of the Securities Exchange Act of
1934 (the ``Act'') \2\ and Rule 19b-4 thereunder,\3\ notice is hereby
given that, on January 23, 2009, NYSE Alternext U.S. LLC (the
``Exchange'' or ``NYSE Alternext'') 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 self-regulatory organization. NYSE Alternext filed the proposed
rule change pursuant to Section 19(b)(3)(A) of the Act \4\ and Rule
19b-4(f)(6) thereunder,\5\ which renders it effective upon filing with
the Commission. 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\ 15 U.S.C. 78a.
    \3\ 17 CFR 240.19b-4.
    \4\ 15 U.S.C. 78s(b)(3)(A).
    \5\ 17 CFR 240.19b-4(f)(6).
---------------------------------------------------------------------------

I. Self-Regulatory Organization's Statement of the Terms of Substance
of the Proposed Rule Change

    The Exchange proposes to (i) make changes to certain NYSE Alternext
Equities Rules to conform with

amendments to corresponding rules recently filed for immediate
effectiveness by the New York Stock Exchange LLC (``NYSE''); \6\ and
(ii) make technical changes to Rule 431--NYSE Alternext Equities.
---------------------------------------------------------------------------

    \6\ See Securities Exchange Act Release No. 59077 (December 10,
2008), 73 FR 76691 (December 17, 2008) (SR-NYSE-2008-127) (clean-up
amendments related to the New Market Model).
---------------------------------------------------------------------------

    The text of the proposed rule change is available at http: //
www.nyse.com, the Exchange, and 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 those statements may be examined at
the places specified in Item IV below. The Exchange has prepared
summaries, set forth in sections A, B, and C below, of the most
significant parts 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 the proposed rule changes is to (i) make changes to
certain NYSE Alternext Equities Rules to conform with amendments to
corresponding NYSE Rules recently filed for immediate effectiveness by
the NYSE; and (ii) make technical changes to Rule 431--NYSE Alternext
Equities.
Background
    As described more fully in a related rule filing,\7\ NYSE Euronext
acquired The Amex Membership Corporation (``AMC'') pursuant to an
Agreement and Plan of Merger, dated January 17, 2008 (the ``Merger'').
In connection with the Merger, the Exchange's predecessor, the American
Stock Exchange LLC (``Amex''), a subsidiary of AMC, became a subsidiary
of NYSE Euronext called NYSE Alternext U.S. LLC, and continues to
operate as a national securities exchange registered under Section 6 of
the Act.\8\ The effective date of the Merger was October 1, 2008.
---------------------------------------------------------------------------

    \7\ See Securities Exchange Act Release No. 58673 (September 29,
2008), 73 FR 57707 (October 3, 2008) (SR-NYSE-2008-60 and SR-Amex
2008-62) (approving the Merger).
    \8\ 15 U.S.C. 78f.
---------------------------------------------------------------------------

    In connection with the Merger, on December 1, 2008, the Exchange
relocated all equities trading conducted on the Exchange legacy trading
systems and facilities located at 86 Trinity Place, New York, New York,
to trading systems and facilities located at 11 Wall Street, New York,
New York (the ``Equities Relocation''). The Exchange's equity trading
systems and facilities at 11 Wall Street (the ``NYSE Alternext Trading
Systems'') are operated by the NYSE on behalf of the Exchange.\9\
---------------------------------------------------------------------------

    \9\ See Securities Exchange Act Release No. 58705 (October 1,
2008), 73 FR 58995 (October 8, 2008) (SR-Amex 2008-63) (approving
the Equities Relocation).
---------------------------------------------------------------------------

    As part of the Equities Relocation, NYSE Alternext adopted NYSE
Rules 1-1004, subject to such changes as necessary to apply the Rules
to the Exchange, as the NYSE Alternext Equities Rules to govern trading
on the NYSE Alternext Trading Systems.\10\ The NYSE Alternext Equities
Rules, which became operative on December 1, 2008, are substantially
identical to the current NYSE Rules 1-1004 and the Exchange continues
to update the NYSE Alternext Equities Rules as necessary to conform
with rule changes to corresponding NYSE Rules filed by the NYSE.
---------------------------------------------------------------------------

    \10\ See Securities Exchange Act Release No. 58705 (October 1,
2008), 73 FR 58995 (October 8, 2008) (SR-Amex 2008-63) (approving
the Equities Relocation); Securities Exchange Act Release No. 58833
(October 22, 2008), 73 FR 64642 (October 30, 2008) (SR-NYSE-2008-
106) and Securities Exchange Act Release No. 58839 (October 23,
2008), 73 FR 64645 (October 30, 2008) (SR-NYSEALTR-2008-03)
(together, approving the Bonds Relocation); Securities Exchange Act
Release No. 59022 (November 26, 2008), 73 FR 73683 (December 3,
2008) (SR-NYSEALTR-2008-10) (adopting amendments to NYSE Alternext
Equities Rules to track changes to corresponding NYSE Rules);
Securities Exchange Act Release No. 59027 (November 28, 2008), 73 FR
73681 (December 3, 2008) (SR-NYSEALTR-2008-11) (adopting amendments
to Rule 62-NYSE Alternext Equities to track changes to corresponding
NYSE Rule 62).
---------------------------------------------------------------------------

Proposed Conforming Amendments to Certain NYSE Alternext Equities
Rules:
    As noted above, the Exchange proposes to make changes to certain
NYSE Alternext Equities Rules to conform with amendments to
corresponding NYSE Rules recently filed for immediate effectiveness by
the NYSE. Unless specifically noted, and subject to such technical
changes as are necessary to apply the Rules to the Exchange, NYSE
Alternext is proposing to adopt the NYSE's rule changes in the form
that they were filed with the Commission. The NYSE's rule changes and
the Exchange's proposed conforming rule changes are described below.
NYSE Rule Filing SR-NYSE-2008-127 \11\
---------------------------------------------------------------------------

    \11\ See Securities Exchange Act Release No. 59077 (December 10,
2008), 73 FR 76691 (December 17, 2008).
---------------------------------------------------------------------------

    In this filing, the NYSE proposed to (i) amend the operative
duration of Rule 104T (Dealings by DMMs), (ii) delete text from Rules
104T and 123 (Record of Orders) relating to orders received by NYSE
systems and DMM yielding, (iii) change internal cross-references in
Rules 98 (Operation of a DMM Unit) and 123E (DMM Combination Review
Policy), (iv) add the terms ``market maker'' and ``market making'' to
certain provisions of Rule 431 (Margin Requirements), and (v) make
technical ``clean-up'' changes to other NYSE Rules by substituting
``DMM'' for ``specialist''.
    Most of the changes noted above were adopted by the Exchange for
the NYSE Alternext Equities Rules in a prior filing tracking changes to
NYSE Rules.\12\ However, the Exchange proposes the following conforming
changes that still need to be made to the NYSE Alternext Equities
Rules: (i) In Rule 70.25(a)(viii) clarifying ``DMM unit'' rather than
``DMM''; (ii) in Rule 98(c)(2)(D), removing the cross-reference to
paragraph (b) of Rule 103.20; (iii) in Rule 431(f)(2)(M)(iv)(10)(F)
adding in the terms ``market maker'' and ``market making''; and (iv) in
the chart contained in Rule 900(b), clarifying that, for Rule 98A, the
second sentence of the first paragraph of that Rule does not apply to
after-hours trading on the Exchange.
---------------------------------------------------------------------------

    \12\ See Securities Exchange Act Release No. 59022 (November 26,
2008), 73 FR 73683 (December 3, 2008) (SR-NYSEALTR-2008-10).
---------------------------------------------------------------------------

Proposed Technical Amendments to Rule 431-NYSE Alternext Equities
    The Exchange also proposes to make additional technical changes to
Rule 431-NYSE Alternext Equities to correct references to
``specialist'' that were incorrectly changed to ``DMM'' in a prior rule
filing.\13\ The term ``specialist'' as used in that Rule is used in
conformity with federal rules and, unlike the term ``DMM'', is not
Exchange-specific.
---------------------------------------------------------------------------

    \13\ See Securities Exchange Act Release No. 59022 (November 26,
2008), 73 FR 73683 (December 3, 2008) (SR-NYSEALTR-2008-10).
---------------------------------------------------------------------------

2. Statutory Basis
    The Exchange believes that its proposal is consistent with Section
6(b) of the Act,\14\ in general, and furthers the objectives of Section
6(b)(5) of the Act,\15\ in particular, in that it is designed to
promote just and equitable principles of

trade, to foster cooperation and coordination with persons engaged in
regulating, clearing, settling, processing information with respect to,
and facilitating transactions in, securities, to remove impediments to
and perfect the mechanism of a free and open market and a national
market system, and, in general, to protect investors and the public
interest. The proposal also supports the principles of Section
11A(a)(1) \16\ of the Act in that it seeks to ensure the economically
efficient execution of securities transactions, to make it practicable
for brokers to execute investors' orders in the best market, and to
provide an opportunity for investors' orders to be executed without the
participation of a dealer.
---------------------------------------------------------------------------

    \14\ 15 U.S.C. 78f(b).
    \15\ 15 U.S.C. 78f(b)(5).
    \16\ 15 U.S.C. 78k-1(a)(1).
---------------------------------------------------------------------------

    The Exchange believes that the proposed rule changes are necessary
and appropriate to update the NYSE Alternext Equities Rules in
conformity with changes made to the corresponding NYSE Rules on which
they are based and to make other technical amendments to correct the
Rules. To the extent the Exchange has proposed changes that differ from
the NYSE version of the Rules, such changes are technical in nature and
do not change the substance of the proposed Rules.

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 the purposes of the Act.

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

    No written comments were solicited or received with respect to the
proposed rule change.

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

    Because the foregoing proposed rule change: (1) Does not
significantly affect the protection of investors or the public
interest; (2) does not impose any significant burden on competition;
and (3) by its terms, does not become operative for 30 days after the
date of filing, or such shorter time as the Commission may designate if
consistent with the protection of investors and the public interest,
the proposed rule change has become effective pursuant to Section
19(b)(3)(A) of the Act \17\ and Rule 19b-4(f)(6) thereunder.\18\
---------------------------------------------------------------------------

    \17\ 15 U.S.C. 78s(b)(3)(A).
    \18\ 17 CFR 240.19b-4(f)(6).
---------------------------------------------------------------------------

    A proposed rule change filed under Rule 19b-4(f)(6) normally does
not become operative for 30 days after the date of filing.\19\ However,
Rule 19b-4(f)(6)(iii) permits the Commission to designate a shorter
time if such action is consistent with the protection of investors and
the public interest. The Exchange requested that the Commission waive
the 30-day operative delay, as specified in Rule 19b-4(f)(6)(iii),\20\
which would make the rule change effective and operative upon filing.
---------------------------------------------------------------------------

    \19\ 17 CFR 240.19b-4(f)(6)(iii). In addition, Rule 19b-
4(f)(6)(iii) requires the self-regulatory organization to give the
Commission notice of its intent to file the proposed rule change,
along with a brief description and text of the proposed rule change,
at least five business days prior to the date of filing of the
proposed rule change, or such shorter time as designated by the
Commission. NYSE has satisfied this requirement.
    \20\ 17 CFR 240.19b-4(f)(6)(iii).
---------------------------------------------------------------------------

    The Commission believes that waiving the 30-day operative delay is
consistent with the protection of investors and the public interest
because it will conform the rule text to language that was previously
approved by the Commission in prior proposed rule changes, and make
technical clarifications to those rules.\21\ Waiving the operative
delay will ensure that the rule text of the Exchange is accurate and
will avoid potential confusion by eliminating technical errors.
Accordingly, the Commission designates the proposed rule change as
operative upon filing with the Commission.\22\
---------------------------------------------------------------------------

    \21\ See supra notes 11 and 12.
    \22\ For purposes only of waiving the operative delay for this
proposal, the Commission has considered the proposed rule's impact
on efficiency, competition, and capital formation. See 15 U.S.C.
78c(f).
---------------------------------------------------------------------------

    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.\23\
---------------------------------------------------------------------------

    \23\ 15 U.S.C. 78s(b)(3)(C).
---------------------------------------------------------------------------

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-NYSEALTR-2009-03 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-NYSEALTR-2009-03. 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 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-NYSEALTR-2009-03 and should
be submitted on or before March 2, 2009.

    For the Commission, by the Division of Trading and Markets,
pursuant to delegated authority.\24\
---------------------------------------------------------------------------

    \24\ 17 CFR 200.30-3(a)(12).
---------------------------------------------------------------------------

Florence E. Harmon,
Deputy Secretary.
[FR Doc. E9-2580 Filed 2-6-09; 8:45 am]

BILLING CODE 8011-01-P