[Federal Register Volume 83, Number 205 (Tuesday, October 23, 2018)]
[Notices]
[Page 53468]
[FR Doc No: 2018-23113]

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DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Docket No. CP18-508-000]

Columbia Gas Transmission, LLC; Notice of Schedule for
Environmental Review of the Line Ka1 North Launcher/Receiver Project

    On June 20, 2018, Columbia Gas Transmission, LLC (Columbia) filed
an application in Docket No. CP18-508-000 requesting a Certificate of
Public Convenience and Necessity pursuant to Section 7(c) of the
Natural Gas Act to construct and operate certain natural gas pipeline
facilities. The proposed project is known as the Line KA1 North
Launcher/Receiver Project (Project), and would modify seven discrete
points and install two bi-directional launcher/receivers on Columbia's
existing Line KA1 North pipeline.
    On July 5, 2018, the Federal Energy Regulatory Commission
(Commission or FERC) issued its Notice of Application for the Project.
Among other things, that notice alerted agencies issuing federal
authorizations of the requirement to complete all necessary reviews and
to reach a final decision on a request for a federal authorization
within 90 days of the date of issuance of the Commission staff's
Environmental Assessment (EA) for the Project. This instant notice
identifies the FERC staff's planned schedule for the completion of the
EA for the Project.

Schedule for Environmental Review

Issuance of EA December 5, 2018
90-day Federal Authorization Decision Deadline March 5, 2019

    If a schedule change becomes necessary, additional notice will be
provided so that the relevant agencies are kept informed of the
Project's progress.

Project Description

    In order to enable the use of internal inspection tools along the
KA1 North pipeline for integrity assessment purposes, Columbia would
install one 16-inch by 12-inch launcher/receiver at each end of the
pipeline; and remove, replace, and install various stopples, elbows,
valves, pipe segments, and other components at a total of seven
discrete points along the pipeline in Fayette and Madison Counties,
Kentucky.

Background

    On August 3, 2018, the Commission issued a Notice of Intent to
Prepare an Environmental Assessment for the Proposed Line KA1 North
Launcher/Receiver Project and Request for Comments on Environmental
Issues (NOI). The NOI was sent to affected landowners; federal, state,
and local government agencies; elected officials; environmental and
public interest groups; Native American tribes; other interested
parties; and local libraries and newspapers. In response to the NOI,
the Commission received comments from two Native American tribes. The
primary issues raised by the commentors pertain to cultural resources.
All substantive comments will be addressed in the EA.

Additional Information

    In order to receive notification of the issuance of the EA and to
keep track of all formal issuances and submittals in specific dockets,
the Commission offers a free service called eSubscription. This can
reduce the amount of time you spend researching proceedings by
automatically providing you with notification of these filings,
document summaries, and direct links to the documents. Go to
www.ferc.gov/docs-filing/esubscription.asp.
    Additional information about the Project is available from the
Commission's Office of External Affairs at (866) 208-FERC or on the
FERC website (www.ferc.gov). Using the ``eLibrary'' link, select
``General Search'' from the eLibrary menu, enter the selected date
range and ``Docket Number'' excluding the last three digits (i.e.,
CP18-508), and follow the instructions. For assistance with access to
eLibrary, the helpline can be reached at<PHONE_NUMBER>, TTY (202) 502-
8659, or at [email protected]. The eLibrary link on the FERC
website also provides access to the texts of formal documents issued by
the Commission, such as orders, notices, and rule makings.

    Dated: October 16, 2018.
Kimberly D. Bose,
Secretary.
[FR Doc. 2018-23113 Filed 10-22-18; 8:45 am]
 BILLING CODE 6717-01-P


Brian sent your message to my supervisor Pauline Wagner who has forwarded me for reply.

Seed treatment is considered a food use so all colorants have to be approved by EPA.

First of all please provide me with the list of all colorant for which you want exemptions from the requirement of a tolerance or you say approval. Provide me with chemistry and CAS Reg. Nos. and I will look Agency's data base to check if any of them are on our approved list.

Those colorants not on Agency's approved list will require all chemistry, toxicological, environmental, ecological and exposure data and a Notice of Filing for all colorants. This is a lengthy process and I will explain to you in brief so provide me your telephone so we can talk . FILE NAME: AD_ company. wpt ( 1/ 1/ 2006) ( xml) Template Number AD20 ATTENTION:

All commodity terms must comply with the Food and Feed Commodity Vocabulary database ( http:// www. epa. gov/ pesticides/ foodfeed/).

All text in blue font ( instructions for preparing the document), should be removed prior to sending the document to the Federal Register Staff. Instructional text and prompts in green font should also be removed.

COMPANY FEDERAL REGISTER DOCUMENT SUBMISSION TEMPLATE ( 1/ 1/ 2006)

EPA Registration Division contact: [ Pauline Wagner: ( 703) 308 6164]

TEMPLATE:

Syngenta Crop Protection, Inc.

PP EPA has received a pesticide petition ( PP) from Syngenta Crop Protection, Inc., P. O. Box 18300, Greensboro, NC 27410 proposing, pursuant to section 408( d) of the Federal Food, Drug, and Cosmetic Act ( FFDCA), 21 U. S. C. 346a( d), to amend 40 CFR part 180 to establish an exemption from the requirement of a tolerance for [ phosphoric acid, tris( 2 ethyl hexyl) ester as an adjuvant when used in pesticide formulations applied to growing crops which contain pinoxaden, clodinafop propargyl and tralkoxydim] in or on the raw agricultural commodities [ wheat and barley]. EPA has determined that the petition contains data or information regarding the elements set forth in section 408( d)( 2) of the FFDCA; however, EPA has not fully evaluated the sufficiency of the submitted data at this time or whether the data supports granting of the petition. Additional data may be needed before EPA rules on the petition.

A. Residue Chemistry 1. Plant metabolism. [ NA Remove]

2. Analytical method. [ NA Remove]

3. Magnitude of residues. [ NA Remove]

B. Toxicological Profile 1. Acute toxicity. Tris( 2 ethylhexyl) phosphate ( TEHP) is of very low acute toxicity by oral and dermal routes The oral LD50 in rats is greater than 36,800 mg/ kg and the dermal LD50 is greater than 20,000 mg/ kg. The inhalation LC50 is greater than 0.45 mg/ l, indicating a relatively low potential for acute inhalation hazard. TEHP is classified as a moderate skin irritant, is not a dermal sensitizer and is non irritating to the eyes of rabbits.

2. Genotoxicty. TEHP has been tested in a number of well conducted in vivo and in vitro mutagenicity assays. In vitro assays included Ames assay, mammalian cell mutation/ cytogenetics, cytogenicity and sister chromatid exchange. Concentrations ranged from 63.5 microliters/ liter ( limit of solubility) to 251 micrograms/ milliliter. All assay results were negative with or without S9 activation. In vivo assays included bone marrow micronucleus, cytogenicity, and UDS assay. Doses administered ranged from 500 mg/ kg to 2000 mg/ kg ( both gavage and IP) and all results were negative. Therefore, TEHP shows no potential for genotoxicity in a wide array of in vitro and in vivo assays. 3 3. Reproductive and developmental toxicity. No reproductive toxicity studies or developmental toxicity studies are available for TEHP. However, a significant number of reproductive and developmental toxicity studies are available on closely related structures and a likely metabolite of TEHP, 2 ethylhexanol. In a reproduction study in rats triethyl phosphate ( CAS No. 78 40 0) had a NOAEL was 335 mg/ kg/ d; decreased litter size was noted at 670 mg/ kg. Small numbers of animals were tested; maternal toxicity was not clearly defined. There were no effects on testis histopathology. In a developmental study in rats the NOAEL was greater than 625 mg/ kg/ d ( no effects); the maternal NOAEL was 125 mg/ kg bw/ day. Reduced body weight gain, food intake and feces excretion at noted at 625 mg/ kg/ d.

In a reproduction study in rats dibutyl hydrogen phosphate ( CAS No. 107 66 4) had a NOAEL greater than 1000 mg/ kg/ d. No reproduction effects were noted. Parental NOAEL was 30 mg/ kg/ d; reduced food consumption, red urine, histopathology changes in the stomach and the bladder were seen at 100 mg/ kg/ d and higher. Deaths occurred at 1000 mg/ kg/ d. The pup NOAEL was 300 mg/ kg/ d; there was reduced viability at 1000 mg/ kg/ d. In a rat developmental study in rats the NOAEL was 300 mg/ kg. The pup NOAEL in the rat reproduction study, based on reduced viability was established at 1000 mg/ kg/ d. No guideline developmental toxicity studies exist with this compound.

Tributyl phosphate ( CAS No. 126 73 8) had a NOAEL greater than 225 mg/ kg/ d in a rat reproduction study. There were no reproductive effects noted. The maternal NOAEL was greater than 15 mg/ kg/ d ( decreased BW gain 15, 52 and 225 mgk/ g/ d). The pup NOAEL was also greater than 15 mg/ kg/ d ( reduced pup weights). Tributyl phosphate was tested in developmental studies in rats and rabbits. The rat NOAEL was 250 mg/ kg/ d ( increase in short ribs at 500 mg/ kg/ d). The maternal NOAEL was 62.5 mg/ kg/ d ( Reduced body weight gain, food consumption, salivation). In the Rabbit the NOAEL was greater than 400 mg/ kg/ d, and the maternal NOAEL was 150 mg/ kg/ d ( Reduced body weight gain, deaths at 400 mg/ kg/ d).

Tris ( 2 butoxyethyl) phosphate ( CAS No. 78 51 3) was tested in a rat developmental study and had a NOAEL greater than 1500 mg/ kg/ d. No effects were seen in this study.

In addition to the previous comparisons, the presumed 2 ethylhexanol metabolite of TEHP has been well studied. 2 Ethylhexanol is currently exempt from tolerances for pre harvest uses in 40CFR Part 180. Study data with 2 ethylhexanol indicate low potential for developmental toxicity, seen only at high doses in presence of maternal toxicity, as described below. 4 In a developmental toxicity study in rats, 2 ethylhexanol was administered from days 6 15 of gestation by oral gavage at dose levels of 0, 130, 650 and 1300 mg/ kg/ day. The following effects were reported: at 130 mg/ kg there were no effects ( This dose was considered a maternal and developmental NOAEL). At the 650 mg/ kg dose, there was maternal toxicity + ? fetal wt and increased skeletal variations/ delays in ossification, while at 1300 mg/ kg: there was severe maternal toxicity ( BW, FC, deaths) + fetotoxicity + dilated renal pelvis, hydroureter, skeletal malformations.

Thus, significant developmental effects were only seen at a dose level that was severely maternally toxic, and slight effects that reflect delayed development were seen in the presence of less significant maternal toxicity at the LOAEL of 650 mg/ kg/ day. 2 Ethylhexanol did not show a significant potential for developmental toxicity.

Results of a dermal developmental toxicity study in rats with 2 ethylhexanol were consistent with this observation. No teratogenic effects were observed up to the highest dose tested, despite maternal toxicity ( decreased bodyweight gain) at 3 ml/ kg/ day (~ 3000 mg/ kg/ day). In an inhalation developmental toxicity study, groups of Sprague Dawley rats were exposed for 7 hours per day on gestation days 1 19 to 2 ethylhexanol at the highest concentration that could be generated as a vapor. 2 Ethylhexanol reduced maternal feed intake, but did not produce any malformations.

The potential for developmental toxicity of 2 ethylhexanol has also been studied in mice, because a well studied peroxisome proliferator, di( 2 ethylhexyl) phthalate ( DEHP), has been shown to produce developmental effects in this species. Very early work on 2 ethylhexanol had indicated that it was a peroxisome proliferator, along with DEHP. However, more modern techniques and a greater understanding of the sequence of events that lead to " peroxisome proliferation", namely activation of the peroxisome proliferator activating receptor alpha ( PPAR ), call into question whether 2 ethylhexanol was truly a peroxisome proliferator by today's standards in these older studies. In fact, tests on parameters more closely related to PPAR activation clearly showed that 2 ethylhexanol did not produce any effects associated with peroxisome proliferation, whereas DEHP and a phthalate containing metabolite did. Consistent with this, no liver histopathology consistent with peroxisome proliferation was reported in the subchronic or chronic rat and mouse studies conducted on TEHP.

In order to evaluate the relative roles of 2 ethylhexanol and mono( 2 ethylhexyl) phthalate ( MEHP) ( the two major metabolites of DEHP in mice) in developmental toxicity of DEHP, the NTP conducted dietary developmental toxicity studies with DEHP, MEHP and 2 ethylhexanol at equimolar dose levels ( NTP, 1991). No developmental or maternal effects were produced by 2 ethylhexanol in mice at up to 191 mg/ kg/ day, which was equimolar with dose levels of DEHP and MEHP that caused maternal and developmental effects. NTP concluded from this study that the developmental effects of DEHP arise from MEHP, and not 2 ethylhexanol.

In summary, the potential of TEHP to cause reproductive or developmental effects is clearly 5 quite low and is sufficiently understood based on studies with its major metabolite ( 2 ethylhexanol) and closely related alkyl phosphates. All of these related compounds show minimal to no potential to produce reproductive or developmental effects in the absence of maternal toxicity, and were tested up to very high dose levels. The relatively high acute oral toxicity ( LD50) value and subchronic NOAEL values for TEHP also suggest that it possesses less potential for general toxicity than the lower molecular weight alkyl phosphate compounds, which would probably extend to reproductive and developmental NOAEL values as well. In addition the subchronic and chronic testing of TEHP has shown no effects on target organs that would signal concern about developmental or reproductive toxicity, such as the testis, ovaries, or uterus. Therefore, additional testing of TEHP in reproductive and developmental toxicity studies should not be required for the purposes of this determination of TEHP as a low toxicity ( Tier 1) inert.

There is a consistent lack of reproductive and developmental toxicity with this class of compounds, except for certain compounds where some developmental toxicity was observed at maternally toxic doses, and this provides a strong weight of evidence that reproductive/ developmental toxicity is not a concern with TEHP.

4. Subchronic toxicity. In a 14 day range finding study, groups of 5 male and 5 female rats and mice were administered 0, 375, 750, 3000, or 6000 mg/ kg bw/ day of TEHP by gavage in corn oil. No deaths were observed in either rats or mice. Body weights were lower than control in male rats at greater than or equal to 1500 mg/ kg bw/ day, and in female rats at equal to or greater than 3000 mg/ kg bw/ day. There were no effects on body weight in mice up to the highest dose tested ( 6000 mg/ kg bw/ day. In a 90 day rat study, Fischer 344 rats were dosed with 0, 250, 500, 1000, 2000 or 4000 mg/ kg bw/ day of TEHP by gavage, 5 days a week for 13 weeks.. Body weight gain was reduced by 5% at the top dose, but this minimal effect was not considered biologically significant. There were no deaths, no signs of toxicity and no adverse effects upon histopathological examination. The NOAEL was 2860 mg/ kg/ day, the highest dose tested ( 4000 mg/ kg/ day administered 5 of 7 days in a week). Groups of B6C3F1 mice were dosed with 0, 500, 1000, 2000, 4000 or 8000 mg/ kg bw/ day by gavage, 5 days a week for 13 weeks. Body weight gain was reduced by 7% and 5% at the top dose in males and females respectively, but this effect was not considered biologically significant. There were no deaths, no signs of toxicity and no adverse effects upon histopathological examination. The NOAEL was 5710 mg/ kg/ day, the highest dose tested ( 8000 mg/ kg/ day, administered 5 days a week.)

A dose of 30 45 mg/ kg TEHP was applied to clipped intact skin of rabbits once a day for either 10 or 20 days. There were no signs of systemic toxicity. In a 3 month inhalation study, groups of dogs ( 2 per sex) were exposed whole body for 6 hours/ day, 5 days per week to 60 exposures of 0, 10.8, 24.4 or 85 mg/ m3 TEHP. The median particle size of the aerosol was 4.4 m with a GSD of 3.0. No animals died and there was no effect on body weight, a limited set of hematological parameters or plasma and erythrocyte cholinesterase activities. The lungs showed mild, chronic parenchymal inflammatory changes. The performance of the dogs 6 trained in conditional avoidance deteriorated as exposure concentrations increased.

In a companion 3 month inhalation study, groups ( 2 per sex) of rhesus monkeys were exposed whole body for 6 hours/ day, 5 days per week to 60 exposures of 0, 10.8, 24.4 or 85 mg/ m3 TEHP. The median particle size of the aerosol was 4.4 m with a GSD of 3.0. There were no effects of compound on bodyweight, hematological parameters, cholinesterase ( plasma and erythrocyte), organ pathology or the performance of animals in visual discrimination tests.

Groups of 20 male and 20 female guinea pigs were exposed by inhalation to 0, 1.6 or 9.6 mg/ m3 TEHP for 3 months ( 6 hours per day, 5 days per week). Animals were administered tetracycline prophylactically in drinking water. The high dose animals showed significantly higher body weights than controls, and both test groups showed lower kidney to body weight ratios. There was no effect of compound on erythrocyte or plasma cholinesterase or on organ histopathology. There were no pathological changes to nerve myelin sheaths.

5. Chronic toxicity. In a US National Toxicology Program ( NTP) study, TEHP was administered in corn oil ( 10 ml/ kg body weight) by gavage 5 days/ week for 103 weeks to groups of 50 male and 50 female F 344/ N rats and B6C3F1 mice. The doses administered were:

Fischer 344 rats B6C3F1 mice Dose Male Female Male Female Control Vehicle Vehicle Vehicle Vehicle Low Dose 2000 mg/ kg 1000 mg/ kg 500 mg/ kg 500 mg/ kg High Dose 4000 mg/ kg 2000 mg/ kg 1000 mg/ kg 1000 mg/ kg The animals were observed twice daily and body weight was measured weekly for the first 13 weeks and once every 4 weeks thereafter. Clinical examinations were performed once every 4 weeks. Necropsies and histopathological examinations were performed on all animals, but organ weight changes were not reported.

No compound related clinical toxicity was observed in either sex of either species. Decrease in body weight, compared with controls, was limited to male rats at the low dose ( 11.5%) and the high dose ( 15.8%). The decreased body weight did not affect survival.

In male rats the incidence of pheochromocytomas ( benign tumors of the adrenal medulla) of the adrenal gland increased with dose and two ( 4%) were malignant in the high dose group. The incidence of adrenal pheochromocytomas in male rats was: control 2/ 50 ( 4%), low dose 9/ 50 ( 18%) and high dose 12/ 50 ( 24%). In two previous gavage studies in the same laboratory, 7 the incidence of pheochromocytomas in control male rats was 24 and 26%.

In female mice the incidence of hepatocellular carcinomas was: control 0/ 48 ( 0%), low dose 4/ 50 ( 8%) and high dose 7/ 50 ( 14%). The incidence of hepatocellular carcinomas showed a dose related increase and the incidence at the high dose level was statistically significant.

The results of these 2 year gavage studies in rats and mice were interpreted by NTP as showing some evidence of carcinogenicity in female mice based on the increase in hepatocellular carcinomas and equivocal evidence of carcinogenicity in male rats based on the increased incidence of pheochromocytomas. In this same study, TEHP caused a dose related increase in the incidence of follicular cell hyperplasia of the thyroid in male and female B6C3F1 mice. The incidence of hyperplasia was: in males, control 0/ 49 ( 0%), low dose 12/ 48 ( 25%) and high dose 24/ 47 ( 51%); in females, control 1/ 44 ( 2%), low dose 13/ 47 ( 28%) and high dose 12/ 46 ( 26%). There was no dose related increase in thyroid tumours. The LOAEL for thyroid hyperplasia was 357 mg/ kg body weight per day; a NOAEL was not established.

Two toxicology reviews have commented on the significance of the NTP data: The European Centre for Ecotoxicology and Toxicology of Chemicals ( ECETOC) commented that:

" The probability is high that the adrenal pheochromocytoma effect was spurious. The only other statistically significant neoplastic finding was hepatocellular carcinoma in female mice and, on its own, this is insufficient evidence of carcinogenicity. Considering the high dose used, the low incidence rate of the tumours, the lack of genotoxic activity and the inconsistency of tumour development between sexes and species, a carcinogenic action in man would be highly improbable at exposure levels which do not produce other toxic effects."

The World Health Organization ( WHO) concluded that:

" Although there were increases in adrenal pheochromocytomas in both dose groups of male rats and in hepatocellular carcinomas in female mice in the high dose group, these results are not considered to indicate that TEHP presents a significant carcinogenic risk to humans. Pheochromocytomas show a variable background incidence in rats. The incidences of these tumours in two previous National Toxicology Programme ( NTP) bioassays were equal to the incidence observed in the TEHP bioassay. The only other significant neoplastic finding was hepatocellular carcinomas in the high dose group of female mice. Considering the low incidence of this tumour, its occurrence in only one sex of one species, the lack of evidence of genetic 8 toxicity, and the low exposure of humans to TEHP, it is unlikely that TEHP poses a significant carcinogenic risk to humans."

In summary, the chronic toxicity/ oncogenicity studies with TEHP in rats and mice demonstrate very limited toxicity at relatively high dose levels ( up to 4000mg/ kg/ day in the rat and 1000mg/ kg/ day in the mouse), reflecting the low repeat dose toxicity of this chemical in rodents. In male and female mice, the lowest observed adverse effect level ( LOAEL) for thyroid follicular cell hyperplasia was 357 mg/ kg bodyweight per day. A NOAEL in mice was not established. TEHP is not considered to show any convincing evidence for carcinogenic potential. This position is in agreement with the conclusion of two expert reviews of the database.

6. Animal metabolism. In an inhalation study rats received a single 20 minute head only exposure to aerosols of [ 32P] TEHP ( concentrations 0.72 and 0.91 mg/ L). Animals were killed after 5 min, 30 min, 1, 4, 17, 18, 24, 48 and 72 hours ( 1 animal per time point). TEHP and its metabolites were found in the lungs ( 13% after 5 mins.), stomach ( 64% after 1 hour), brain and liver ( 9 and 16% after 30 mins.). Fecal excretion was high, urinary excretion was low. Partial biotransformation was confirmed but the metabolites were not identified. Regarding metabolism of trialkyl phosphate esters, the following statements have been made in prior reviews ( American Chemistry Council [ ACC] and Beratergremium fur Umweltrelevante Altstoffe [ BUA]) " In mammalian metabolism, the phosphoric acid tri esters are, as a rule, degraded to the corresponding di ester. Only a small amount is further metabolized to the monophosphates." Therefore, TEHP is assumed to be hydrolysed to 2 ethylhexanol ( CAS 104 76 7) and bis ( 2 ethylhexyl) hydrogen phosphate ( CAS 298 07 7). No confirmatory data exist, but this pattern would be consistent with other compounds containing 2 ethylhexyl ester groups.

7. Metabolite toxicology. [ NA Remove]

8. Endocrine disruption. There is no information in the literature to suggest that TEHP possesses any potential for endocrine disruption. Several well known international organizations have studied the toxicity of TEHP in the literature, analyzing data from a number of studies that utilized a many different test systems under short, intermediate and long term exposure, with no suggestion of the potential for endocrine disruption from exposure to TEHP. 9 C. Aggregate Exposure 1. Dietary exposure. Potential dietary exposure will be limited, given the proposed exempted use will only be on wheat and barley crops in conjunction with herbicide applications at the early stage of crop growth for wheat and barley, well before seed head development.

i. Food. Given the favorable safety profile for TEHP, coupled with the timing of application to growing crops for herbicide formulations that contain TEHP that minimizes potential for residues, it can be concluded there will be minimal to no exposure to TEHP in food. In addition, 2 ethylhexanol, a likely metabolite of TEHP, is currently exempt from the requirement of a tolerance for use as an inert in pesticide formulations applied to growing crops and for post harvest use on raw agricultural food commodities under 40CFR Part 180.910 and 180.912.

ii. Drinking water. The solubility of TEHP is extremely low ( 2mg/ liter), which makes the compound virtually insoluble, and the octanol/ water partition coefficient of 4.2 indicates that TEHP will bind strongly to soil and suggests the compound is largely immobile. There has been some water monitoring in rivers in Europe in which very small amounts of TEHP have been detected. These detections were believed to be due to point source discharges from production operations, and not as a result of leaching or runoff. Because of these factors, it is highly unlikely that TEHP will migrate to ground or surface water used as drinking water.

2. Non dietary exposure. TEHP has been used as a flame retardant for many years. There have been no other uses identified. The low vapor pressure would suggest that it is unlikely to reach the atmosphere. The photolytic half life has been modeled to be about 1.3 hours, which is relatively rapid. Further, the solubility is very low and as noted above the available data suggests the compound is largely immobile. Therefore, it is concluded that non dietary exposure to TEHP as a result of applications to growing crops is expected to be minimal.

D. Cumulative Effects TEHP does not display toxicity concerns as a result of an evaluation of a multitude of different tests on mammalian systems. Based on these data there does not appear to be any evidence for a " common mechanism" of toxicity with other substances. 10 E. Safety Determination 1. U. S. population. The toxicology data base is sufficient to make a safety determination for use of TEHP as an inert in pesticide formulations. TEHP has a very low acute toxicity, is non genotoxic, and has low potential for developmental or reproductive effects based on lack of effects in structurally similar compounds as well as it's major metabolite, 2 ethylhexanol. Further TEHP has low subchronic/ chronic toxicity based on a number of well conducted studies, and is unlikely to be carcinogenic to humans. Therefore, there is a reasonable certainty that no harm will result to the general population, including children and infants, and TEHP can be used safely in pesticide formulations used on wheat and barley.

2. Infants and children. There are no indications in the available published literature that infants and children are more susceptible to toxicity from exposure to TEHP than are adults. Several international organizations have evaluated TEHP's toxicity and no concerns have been raised. Therefore there is a reasonable certainty that no harm to infants and children will result from TEHP.

F. International Tolerances No tolerances or exemptions for tolerance for TEHP have been previously requested by Syngenta Crop Protection, Inc. A maximum residue level ( MRL) for TEHP has not been established by the Codex Alimentarus Commission.

BILLLING CODE 6560 50 S


[Federal Register: May 9, 2008 (Volume 73, Number 91)]
[Notices]
[Page 26466]
[DOCID:fr09my08-127]

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DEPARTMENT OF TRANSPORTATION

Federal Aviation Administration

Notice of Opportunity for Public Comment on Surplus Property
Release at Myrtle Beach International Airport

AGENCY: Federal Aviation Administration (FAA), DOT.

ACTION: Notice.

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SUMMARY: Under the provisions of Title 49, U.S.C. Section 47 153(c),
notice is being given that the FAA is considering a request from Horry
County to waive the requirement that a 0.389 acre parcel of surplus
property. located at the Myrtle Beach International Airport, be used
for aeronautical purposes.

DATES: Comments must be received on or before June 9, 2008.

ADDRESSES: Comments on this notice may be mailed or delivered in
triplicate to the FAA at the following address: Atlanta Airports
District Office, Attn: Parks Preston, Program Manager, 1701 Columbia
Ave., Suite 2-260, Atlanta, GA 30337-2747.
    In addition, one copy of any comments submitted to the FAA must be
mailed or delivered to Robert J. Kemp, Director of Airports, at the
following address: Myrtle Beach International Airport, 1100 Jetport
Road, Myrtle Beach, SC 29577.

FOR FURTHER INFORMATION CONTACT: Parks Preston, Program Manager,
Atlanta Airports District Office, 1701 Columbia Ave., Suite 2-260,
Atlanta, GA 30337-2747,<PHONE_NUMBER>. The application may be reviewed
in person at this same location.

SUPPLEMENTARY INFORMATION: The FAA is reviewing a request by Horry
County to release 0.389 acres of surplus property at the Myrtle Beach
International Airport. The property will be purchased to allow for the
realignment of Shine Avenue. The net proceeds from the sale of this
property will be used for airport purposes. The proposed use of this
property is compatible with airport operations.
    Any person may inspect the request in person at the FAA office
listed above under FOR FURTHER INFORMATION CONTACT.
    In addition, any person may, upon request, inspect the request,
notice, and other documents germane to the request in person at the
Myrtle Beach International Airport.

    Issued in Atlanta, Georgia on March 25, 2008.
Larry F. Clark,
Acting Manager, Atlanta Airports District Office, Southern Region.
 [FR Doc. E8-10186 Filed 5-8-08; 8:45 am]

BILLING CODE 4910-13-M