49932 Federal Register / Vol. 78, No. 159 / Friday, August 16, 2013 / Rules and Regulations 

PART 180—[AMENDED] 

■ 1. The authority citation for part 180 

continues to read as follows: 

Authority: 21 U.S.C. 321(q), 346a and 371. 

■ 2. Amend § 180.490 as follows: 

■ a. Revise the section heading; 

■ b. Revise the introductory text in 

paragraph (a)(1) and add alphabetically 

the following commodity to the table; 

■ c. Revise the introductory text in 

paragraph (a)(2); and 

■ d. Revise the heading in paragraph (c). 

The amendments read as follows: 

§ 180.490 Imazapic; tolerances for 

residues. 

(a) General. (1) Tolerances are 

established for residues of the herbicide 

imazapic, including its metabolites and 

degradates, in or on the commodities 

listed in the following table. 

Compliance with the tolerance levels 

specified is to be determined by 

measuring the sum of imazapic (2-[4,5- 

dihydro-4-methyl-4-(1-methylethyl)-5- 

oxo-1H-imidazol-2-yl]-5-methyl-3- 

pyridinecarboxylic acid) and its 

metabolites (±)-2-[4,5-dihydro-4-methyl4-(1-methylethyl)-5-oxo-1H-imidazol-2- 

yl]-5-hydroxymethyl-3- 

pyridinecarboxylic acid and (±)-2-[4,5- 

dihydro-4-methyl-4-(1-methylethyl)-5- 

oxo-1H-imidazol-2-yl]-5-(b-Dglucopyranosyloxy)methyl-3- 

pyridinecarboxylic acid, calculated as 

the stoichiometric equivalent of 

imazapic. 

Commodity Parts per 

million 

* * * * * 

Sugarcane, cane .................. 0.03 

(2) Tolerances are established for 

residues of the herbicide imazapic, 

including its metabolites and 

degradates, in or on the commodities 

listed in the following table. 

Compliance with the tolerance levels 

specified is to be determined by 

measuring the sum of imazapic (2-[4,5- 

dihydro-4-methyl-4-(1-methylethyl)-5- 

oxo-1H-imidazol-2-yl]-5-methyl-3- 

pyridinecarboxylic acid) and its 

metabolite (±)-2-[4,5-dihydro-4-methyl4-(1-methylethyl)-5-oxo-1H-imidazol-2- 

yl]-5-hydroxymethyl-3- 

pyridinecarboxylic acid, calculated as 

the stoichiometric equivalent of 

imazapic. 

* * * * * 

(c) Tolerances with regional 

registrations. [Reserved] 

* * * * * 

[FR Doc. 2013–19867 Filed 8–15–13; 8:45 am] 

BILLING CODE 6560–50–P 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 180 

[EPA–HQ–OPP–2012–0405; FRL–9395–6] 

Emamectin; Pesticide Tolerance 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Final rule. 

SUMMARY: This regulation establishes a 

tolerance for residues of emamectin 

benzoate in or on wine grapes. Syngenta 

Crop Protection, LLC, requested this 

tolerance under the Federal Food, Drug, 

and Cosmetic Act (FFDCA). This 

document also makes a technical 

correction to the tolerance expression in 

the section. 

DATES: This regulation is effective 

August 16, 2013. Objections and 

requests for hearings must be received 

on or before October 15, 2013, and must 

be filed in accordance with the 

instructions provided in 40 CFR part 

178 (see also Unit I.C. of the 

SUPPLEMENTARY INFORMATION). 

ADDRESSES: The docket for this action, 

identified by docket identification (ID) 

number EPA–HQ–OPP–2012–0405, is 

available at http://www.regulations.gov 

or at the Office of Pesticide Programs 

Regulatory Public Docket (OPP Docket) 

in the Environmental Protection Agency 

Docket Center (EPA/DC), EPA West 

Bldg., Rm. 3334, 1301 Constitution Ave. 

NW., Washington, DC 20460–0001. The 

Public Reading Room is open from 8:30 

a.m. to 4:30 p.m., Monday through 

Friday, excluding legal holidays. The 

telephone number for the Public 

Reading Room is (202) 566–1744, and 

the telephone number for the OPP 

Docket is (703) 305–5805. Please review 

the visitor instructions and additional 

information about the docket available 

at http://www.epa.gov/dockets. 

FOR FURTHER INFORMATION CONTACT: Lois 

Rossi, Registration Division, (7505P), 

Office of Pesticide Programs, 

Environmental Protection Agency, 1200 

Pennsylvania Ave. NW., Washington, 

DC 20460–0001; telephone number: 

(703) 305–7090; email address: 

RDFRNotices@epa.gov. 

SUPPLEMENTARY INFORMATION: 

I. General Information 

A. Does this action apply to me? 

You may be potentially affected by 

this action if you are an agricultural 

producer, food manufacturer, or 

pesticide manufacturer. The following 

list of North American Industrial 

Classification System (NAICS) codes is 

not intended to be exhaustive, but rather 

provides a guide to help readers 

determine whether this document 

applies to them. Potentially affected 

entities may include: 

• Crop production (NAICS code 111). 

• Animal production (NAICS code 

112). 

• Food manufacturing (NAICS code 

311). 

• Pesticide manufacturing (NAICS 

code 32532). 

B. How can I get electronic access to 

other related information? 

You may access a frequently updated 

electronic version of EPA’s tolerance 

regulations at 40 CFR part 180 through 

the Government Printing Office’s e-CFR 

site at http://www.ecfr.gov/cgi-bin/textidx?&c=ecfr&tpl=/ecfrbrowse/Title40/ 

40tab_02.tpl. 

C. How can I file an objection or hearing 

request? 

Under FFDCA section 408(g), 21 

U.S.C. 346a, any person may file an 

objection to any aspect of this regulation 

and may also request a hearing on those 

objections. You must file your objection 

or request a hearing on this regulation 

in accordance with the instructions 

provided in 40 CFR part 178. To ensure 

proper receipt by EPA, you must 

identify docket ID number EPA–HQ– 

OPP–2012–0405 in the subject line on 

the first page of your submission. All 

objections and requests for a hearing 

must be in writing, and must be 

received by the Hearing Clerk on or 

before October 15, 2013. Addresses for 

mail and hand delivery of objections 

and hearing requests are provided in 40 

CFR 178.25(b). 

In addition to filing an objection or 

hearing request with the Hearing Clerk 

as described in 40 CFR part 178, please 

submit a copy of the filing (excluding 

any Confidential Business Information 

(CBI)) for inclusion in the public docket. 

Information not marked confidential 

pursuant to 40 CFR part 2 may be 

disclosed publicly by EPA without prior 

notice. Submit the non-CBI copy of your 

objection or hearing request, identified 

by docket ID number EPA–HQ–OPP– 

2012–0405, by one of the following 

methods: 

• Federal eRulemaking Portal: http:// 

www.regulations.gov. Follow the online 

instructions for submitting comments. 

Do not submit electronically any 

information you consider to be CBI or 

other information whose disclosure is 

restricted by statute. 

• Mail: OPP Docket, Environmental 

Protection Agency Docket Center (EPA/ 

DC), (28221T), 1200 Pennsylvania Ave. 

NW., Washington, DC 20460–0001. 


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Federal Register / Vol. 78, No. 159 / Friday, August 16, 2013 / Rules and Regulations 49933 

• Hand Delivery: To make special 

arrangements for hand delivery or 

delivery of boxed information, please 

follow the instructions at http:// 

www.epa.gov/dockets/contacts.html. 

Additional instructions on 

commenting or visiting the docket, 

along with more information about 

dockets generally, is available at http:// 

www.epa.gov/dockets. 

II. Summary of Petitioned-For 

Tolerance 

In the Federal Register of August 22, 

2012 (77 FR 50661) (FRL–9358–9) EPA 

issued a document pursuant to FFDCA 

section 408(d)(3), 21 U.S.C. 346a(d)(3), 

announcing the filing of a pesticide 

petition (PP 2E8018) by Syngenta Crop 

Protection, LLC, P.O. Box 18300, 

Greensboro, NC 27419. The petition 

requested that 40 CFR 180.505 be 

amended by establishing tolerances for 

residues of the insecticide emamectin 

benzoate (a benzoate salt mixture of a 

minimum of 90% 4′-epi-methylamino4′- deoxyavermectin B1a and a 

maximum of 10% 4′-epi-methylamino4′-deoxyavermectin B1b) resulting from 

the application of emamectin benzoate 

in or on imported wine at 0.005 parts 

per million (ppm). That document 

referenced a summary of the petition 

prepared by Syngenta Crop Protection, 

LLC, the registrant, which is available in 

the docket, http://www.regulations.gov. 

There were no comments received in 

response to the notice of filing. 

Based upon review of the data 

supporting the petition, EPA has 

modified the requested tolerance to 

emamectin, including its metabolites 

and degradates, in or on grape, wine at 

0.03 ppm. The reason for this change is 

explained in Unit IV.C. 

This final rule also corrects a 

typographical error (one ‘‘ZB’’ missing) 

in the currently published tolerance 

expression for § 180.505(a)(2). 

III. Aggregate Risk Assessment and 

Determination of Safety 

Section 408(b)(2)(A)(i) of FFDCA 

allows EPA to establish a tolerance (the 

legal limit for a pesticide chemical 

residue in or on a food) only if EPA 

determines that the tolerance is ‘‘safe.’’ 

Section 408(b)(2)(A)(ii) of FFDCA 

defines ‘‘safe’’ to mean that ‘‘there is a 

reasonable certainty that no harm will 

result from aggregate exposure to the 

pesticide chemical residue, including 

all anticipated dietary exposures and all 

other exposures for which there is 

reliable information.’’ This includes 

exposure through drinking water and in 

residential settings, but does not include 

occupational exposure. Section 

408(b)(2)(C) of FFDCA requires EPA to 

give special consideration to exposure 

of infants and children to the pesticide 

chemical residue in establishing a 

tolerance and to ‘‘ensure that there is a 

reasonable certainty that no harm will 

result to infants and children from 

aggregate exposure to the pesticide 

chemical residue . . . .’’ 

Consistent with FFDCA section 

408(b)(2)(D), and the factors specified in 

FFDCA section 408(b)(2)(D), EPA has 

reviewed the available scientific data 

and other relevant information in 

support of this action. EPA has 

sufficient data to assess the hazards of 

and to make a determination on 

aggregate exposure for emamectin 

benzoate including exposure resulting 

from the tolerances established by this 

action. EPA’s assessment of exposures 

and risks associated with emamectin 

benzoate follows. 

A. Toxicological Profile 

EPA has evaluated the available 

toxicity data and considered its validity, 

completeness, and reliability as well as 

the relationship of the results of the 

studies to human risk. EPA has also 

considered available information 

concerning the variability of the 

sensitivities of major identifiable 

subgroups of consumers, including 

infants and children. Emamectin acts by 

binding to gamma-aminobutyric acid 

(GABA) gated chloride channels at two 

different sites, a high affinity binding 

site that activates the channel and a 

low-affinity site that blocks the channel. 

GABA plays a critical role in nervous 

system development through both nonsynaptic and synaptic mechanisms. 

Consequently, emamectin may have the 

potential to influence GABA-mediated 

events important to brain development. 

Within the mammalian brain, a member 

of this class of compound (abamectin) 

has been shown to have widespread 

binding but particularly abundant in the 

cerebellum. Through action on the 

enteric nervous system and induction of 

longitudinal rhythmic contractions in 

the isolated ileum, emamectin like 

abamectin may therefore influence 

GABA-mediated regulation of 

metabolism, food intake and body 

weight at multiple sites. Although 

GABA receptor mediated neurotoxicity 

is a solid hypothesis, data in 

mammalian preparations linking 

alterations in GABA receptor function to 

disruptions in neuronal excitability in 

vitro and in vivo, and ultimately adverse 

outcome are currently lacking. 

Integral to its mechanism of action in 

mammals, this class of compounds is 

also a substrate for (i.e., binds to) Pglycoprotein (P-gp). P-glycoprotein is a 

member of the adenosine triphosphate 

(ATP) binding cassette transporter 

proteins, which reside in the plasma 

membrane and function as a 

transmembrane efflux pump, moving 

xenobiotics from intracellular to the 

extracellular domain against a steep 

concentration gradient with ATPhydrolysis providing the energy for 

active transport. P-gp is found in the 

canallicular surface of hepatocytes, the 

apical surface of proximal tubular cells 

in the kidneys, brush border surface of 

enterocytes, luminal surface of blood 

capillaries of the brain (blood brain 

barrier), placenta, ovaries, and the 

testes. As an efflux transporter, P-gp acts 

as a protective barrier to keep 

xenobiotics out of the body by excreting 

them into bile, urine, and intestinal 

lumen and prevents accumulation of 

these compounds in the brain and 

gonads, as well as the fetus. Therefore, 

some test animals, in which genetic 

polymorphisms compromise P-gp 

expression, are particularly susceptible 

to abamectin or emamectin-induced 

neurotoxicity. An example is the CF–1 

mouse. Some CF–1 mice are deficient in 

P-gp and are found to be highly 

sensitive to the neurotoxicity of 

abamectin. A small population of 

humans is also found to be deficient of 

ATP binding cassette (ABC) transporter 

proteins due to polymorphism in the 

gene encoding ABC transporter proteins 

(Dubin-Johnson Syndrome). In addition, 

collie dogs have been known to be 

deficient in P-gp. 

Consistent with the mode of action, 

the main target organ for emamectin is 

the nervous system; clinical signs 

(tremors, ptosis, ataxia, and hunched 

posture) and neuropathology (neuronal 

degeneration in the brain and in 

peripheral nerves, muscle fiber 

degeneration) were found in most of the 

emamectin studies in rats, dogs, and 

mice. The dose/response curve was very 

steep in several studies (most notably 

with CF–1 mice and dogs), with severe 

effects (morbid sacrifice and 

neuropathology) sometimes seen at the 

lowest-observed-adverse-effect-levels 

(LOAELs) (0.1 milligram/kiolgram/day 

(mg/kg/day) with no-observed-adverseeffect-level (NOAEL) of 0.075 mg/kg/ 

day). Although no increased sensitivity 

was seen in developmental toxicity 

studies in rats and rabbits, increased 

qualitative and/or quantitative 

sensitivity of rat pups was seen in the 

reproductive toxicity and in the 

developmental neurotoxicity studies. 

The carcinogenicity and mutagenicity 

studies provide no indication that 

emamectin is carcinogenic or 

mutagenic. Emamectin is classified as 

‘‘not likely to be carcinogenic to 

humans.’’ 


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The available emamectin data show 

that there is a difference in species 

sensitivity, and the data suggest the 

following order: Rat NOAELs/LOAELs 

greater than dog NOAELs/LOAELs 

greater than mouse NOAELs/LOAELs. 

The toxicity endpoints and points of 

departure for risk were selected from the 

results of the 15-day CF–1 mouse oral 

toxicity study. 

Specific information on the studies 

received and the nature of the adverse 

effects caused by emamectin benzoate as 

well as the NOAEL and the LOAEL from 

the toxicity studies can be found at 

http://www.regulations.gov on pp. 29– 

35 of the document entitled 

‘‘Emamectin Benzoate. Human Health 

Risk Assessment for a Proposed 

Tolerance on Imported Wine Grapes’’ in 

docket ID number EPA–HQ–OPP–2012– 

0405. 

B. Toxicological Points of Departure/ 

Levels of Concern 

Once a pesticide’s toxicological 

profile is determined, EPA identifies 

toxicological points of departure (POD) 

and levels of concern to use in 

evaluating the risk posed by human 

exposure to the pesticide. For hazards 

that have a threshold below which there 

is no appreciable risk, the toxicological 

POD is used as the basis for derivation 

of reference values for risk assessment. 

PODs are developed based on a careful 

analysis of the doses in each 

toxicological study to determine the 

dose at which no adverse effects are 

observed (the NOAEL) and the lowest 

dose at which adverse effects of concern 

are identified (the LOAEL). Uncertainty/ 

safety factors are used in conjunction 

with the POD to calculate a safe 

exposure level—generally referred to as 

a population-adjusted dose (PAD) or a 

reference dose (RfD)—and a safe margin 

of exposure (MOE). For non-threshold 

risks, the Agency assumes that any 

amount of exposure will lead to some 

degree of risk. Thus, the Agency 

estimates risk in terms of the probability 

of an occurrence of the adverse effect 

expected in a lifetime. For more 

information on the general principles 

EPA uses in risk characterization and a 

complete description of the risk 

assessment process, see http://www.epa.

gov/pesticides/factsheets/

riskassess.htm. 

A summary of the toxicological 

endpoints for emamectin benzoate used 

for human risk assessment is shown in 

Table 1 of this unit. 

TABLE 1—SUMMARY OF TOXICOLOGICAL DOSES AND ENDPOINTS FOR EMAMECTIN BENZOATE FOR USE IN HUMAN HEALTH

RISK ASSESSMENT

Exposure/ 

scenario 

Point of departure and 

uncertainty/safety factors 

RfD, PAD, LOC for 

risk assessment Study and toxicological effects 

Acute dietary (All 

populations).

NOAEL = 0.075 mg/kg/day .........

UFA = 10x ...................................

UFH = 10x ...................................

FQPA SF = 3x .............................

Acute RfD = 0.00025 mg/kg/day 

aPAD = 0.00025 mg/kg/day.

15-day mouse study LOAEL = 0.1 mg/kg/day 

based on tremors on day 3 of dosing. At the 

next higher dose (0.3 mg/kg/day), tremors were 

seen at day 2 of treatment. 

Chronic dietary (All 

populations).

NOAEL= 0.075 mg/kg/day ..........

UFA = 10x ...................................

UFH = 10x ...................................

FQPA SF = 10x ...........................

Chronic RfD = 0.000075 mg/kg/ 

day cPAD = 0.000075 mg/kg/ 

day.

15-day mouse study LOAEL = 0.1 mg/kg/day 

based on moribund sacrifices, clinical signs of 

neurotoxicity, decreases in body weight and 

food consumption, and histopathological lesions 

in the sciatic nerve. 

FQPA SF = Food Quality Protection Act Safety Factor. LOC = level of concern. LOAEL = lowest-observed-adverse-effect-level. mg/kg/day = 

milligram/kilogram/day. NOAEL = no-observed-adverse-effect-level. PAD = population adjusted dose (a = acute, c = chronic). RfD = reference 

dose. UF = uncertainty factor. UFA = extrapolation from animal to human (interspecies). UFH = potential variation in sensitivity among members 

of the human population (intraspecies). 

C. Exposure Assessment 

1. Dietary exposure from food and 

feed uses. In evaluating dietary 

exposure to emamectin benzoate, EPA 

considered exposure under the 

petitioned-for tolerances as well as all 

existing emamectin benzoate tolerances 

in 40 CFR 180.505. EPA assessed dietary 

exposures from emamectin benzoate in 

food as follows: 

i. Acute exposure. Quantitative acute 

dietary exposure and risk assessments 

are performed for a food-use pesticide, 

if a toxicological study has indicated the 

possibility of an effect of concern 

occurring as a result of a 1-day or single 

exposure. 

Such effects were identified for 

emamectin benzoate. In estimating acute 

dietary exposure, EPA used food 

consumption information from the U.S. 

Department of Agriculture (USDA) 

2003–2008 National Health and 

Nutrition Examination Survey, What We 

Eat in America (NHANES/WWEIA). As 

to residue levels in food, a probabilistic 

acute dietary exposure assessment was 

conducted. The anticipated residue 

estimates, used for most crops, were 

based on field trial data. Tolerance-level 

residues were used for cottonseed oil, 

tree nuts (including pistachios), and 

wine. Pesticide Data Program (PDP) 

monitoring data for years 2009 and 2010 

were used for apples since apple juice 

had a significant impact on exposure. 

The Dietary Exposure Evaluation Model 

(DEEM) default processing factors were 

used except for commodities with 

chemical-specific processing studies. 

Percent crop treated (PCT) data were 

used. 

ii. Chronic exposure. In conducting 

the chronic dietary exposure assessment 

EPA used the food consumption data 

from the USDA 2003–2008 NHANES/ 

WWEIA. As to residue levels in food, a 

somewhat refined chronic dietary 

exposure assessment was conducted. 

The anticipated residue estimates, used 

for most crops, were single-point 

estimates (averages) based on field trial 

data. Tolerance-level residues were used 

for cottonseed oil, tree nuts (including 

pistachios), and wine. DEEM default 

processing factors were used except for 

commodities with chemical-specific 

processing studies. PCT data were used. 

iii. Cancer. Based on the data 

summarized in Unit III.A., EPA has 

concluded that emamectin benzoate 

does not pose a cancer risk to humans. 

Therefore, a dietary exposure 

assessment for the purpose of assessing 

cancer risk is unnecessary. 

iv. Anticipated residue and PCT 

information. Section 408(b)(2)(E) of 

FFDCA authorizes EPA to use available 

data and information on the anticipated 

residue levels of pesticide residues in 

food and the actual levels of pesticide 

residues that have been measured in 

food. If EPA relies on such information, 

EPA must require pursuant to FFDCA 

section 408(f)(1) that data be provided 5 

years after the tolerance is established, 

modified, or left in effect, demonstrating 

that the levels in food are not above the 


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Federal Register / Vol. 78, No. 159 / Friday, August 16, 2013 / Rules and Regulations 49935 

levels anticipated. For the present 

action, EPA will issue such data call-ins 

as are required by FFDCA section 

408(b)(2)(E) and authorized under 

FFDCA section 408(f)(1). Data will be 

required to be submitted no later than 

5 years from the date of issuance of 

these tolerances. 

Section 408(b)(2)(F) of FFDCA states 

that the Agency may use data on the 

actual percent of food treated for 

assessing chronic dietary risk only if: 

• Condition a: The data used are 

reliable and provide a valid basis to 

show what percentage of the food 

derived from such crop is likely to 

contain the pesticide residue. 

• Condition b: The exposure estimate 

does not underestimate exposure for any 

significant subpopulation group. 

• Condition c: Data are available on 

pesticide use and food consumption in 

a particular area, the exposure estimate 

does not understate exposure for the 

population in such area. 

In addition, the Agency must provide 

for periodic evaluation of any estimates 

used. To provide for the periodic 

evaluation of the estimate of PCT as 

required by FFDCA section 408(b)(2)(F), 

EPA may require registrants to submit 

data on PCT. 

For the acute dietary assessment, the 

Agency estimated the maximum PCT for 

existing uses as follows: Almonds, 

2.5%; apples, 20%; broccoli, 20%; 

cabbage, 25%; cauliflower, 20%; celery, 

40%; cotton, 2.5%; lettuce, 20%; pears, 

20%; peppers, 15%; spinach, 10%; and 

tomatoes, 20%. 

For the chronic dietary assessment, 

the Agency estimated the PCT for 

existing uses as follows: Almonds, 1%; 

apples, 10%; broccoli, 5%; cabbage, 

10%; cauliflower, 10%; celery, 25%; 

cotton, 1%; lettuce, 10%; pears, 5%; 

peppers, 5%; spinach, 5%; and 

tomatoes, 10%. 

In most cases, EPA uses available data 

from United States Department of 

Agriculture/National Agricultural 

Statistics Service (USDA/NASS), 

proprietary market surveys, and the 

National Pesticide Use Database for the 

chemical/crop combination for the most 

recent 6–7 years. EPA uses an average 

PCT for chronic dietary risk analysis. 

The average PCT figure for each existing 

use is derived by combining available 

public and private market survey data 

for that use, averaging across all 

observations, and rounding to the 

nearest 5%, except for those situations 

in which the average PCT is less than 

one. In those cases, 1% is used as the 

average PCT and 2.5% is used as the 

maximum PCT. EPA uses a maximum 

PCT for acute dietary risk analysis. The 

maximum PCT figure is the highest 

observed maximum value reported 

within the recent 6 years of available 

public and private market survey data 

for the existing use and rounded up to 

the nearest multiple of 5%. 

Also for the acute dietary assessment, 

the Agency used the following PCT 

estimates for the following recently 

approved uses: Cantaloupe, 51%; 

cucumber, 26%; squash, 46%; and 

watermelon, 21%. For the chronic 

dietary assessment, the Agency used the 

following PCT estimates for the 

following recently approved uses: 

Cantaloupe, 40%; cucumber, 14%; 

squash, 29%; and watermelon, 19%. 

These PCT estimates for recently 

approved uses represent the upper 

bound of the use expected during the 

pesticide’s initial 5 years of registration; 

that is, PCT for new uses of emamectin 

benzoate is a threshold of use that EPA 

is reasonably certain will not be 

exceeded for each registered use site. 

The PCT recommended for use in the 

chronic dietary assessment for new uses 

is calculated as the average PCT of the 

market leader or leaders, (i.e., the 

pesticide(s) with the greatest PCT) on 

that site over the 3 most recent years of 

available data. The PCT recommended 

for use in the acute dietary assessment 

for new uses is the maximum observed 

PCT over the same period. Comparisons 

are only made among pesticides of the 

same pesticide types (e.g., the market 

leader for insecticides on the use site is 

selected for comparison with a new 

insecticide). The market leader included 

in the estimation may not be the same 

for each year since different pesticides 

may dominate at different times. 

Typically, EPA uses USDA/NASS as 

the source data because it is publicly 

available and directly reports values for 

PCT. When a specific use site is not 

reported by USDA/NASS, EPA uses 

proprietary data and calculates the PCT 

given reported data on acres treated and 

acres grown. If no data are available, 

EPA may extrapolate PCT for new uses 

from other crops, if the production area 

and pest spectrum are substantially 

similar. 

A retrospective analysis to validate 

this approach shows few cases where 

the PCT for the market leaders were 

exceeded. Further review of these cases 

identified factors contributing to the 

exceptionally high use of a new 

pesticide. To evaluate whether the PCT 

for new uses for emamectin benzoate 

could be exceeded, EPA considered 

whether there may be unusually high 

pest pressure, as indicated in emergency 

exemption requests for emamectin 

benzoate; the pest spectrum of the new 

pesticide in comparison with the market 

leaders and whether the market leaders 

are well established for that use; and 

whether pest resistance issues with past 

market leaders provide emamectin 

benzoate with significant market 

potential. Given currently available 

information, EPA concludes that it is 

unlikely that actual PCT for emamectin 

benzoate will exceed the estimated PCT 

for new uses during the next 5 years. 

The Agency believes that the three 

conditions discussed in Unit III.C.1.iv. 

have been met. With respect to 

Condition a, PCT estimates are derived 

from Federal and private market survey 

data, which are reliable and have a valid 

basis. The Agency is reasonably certain 

that the percentage of the food treated 

is not likely to be an underestimation. 

As to Conditions b and c, regional 

consumption information and 

consumption information for significant 

subpopulations is taken into account 

through EPA’s computer-based model 

for evaluating the exposure of 

significant subpopulations including 

several regional groups. Use of this 

consumption information in EPA’s risk 

assessment process ensures that EPA’s 

exposure estimate does not understate 

exposure for any significant 

subpopulation group and allows the 

Agency to be reasonably certain that no 

regional population is exposed to 

residue levels higher than those 

estimated by the Agency. Other than the 

data available through national food 

consumption surveys, EPA does not 

have available reliable information on 

the regional consumption of food to 

which emamectin benzoate may be 

applied in a particular area. 

2. Dietary exposure from drinking 

water. The Agency used screening level 

water exposure models in the dietary 

exposure analysis and risk assessment 

for emamectin benzoate in drinking 

water. These simulation models take 

into account data on the physical, 

chemical, and fate/transport 

characteristics of emamectin benzoate. 

Further information regarding EPA 

drinking water models used in pesticide 

exposure assessment can be found at 

http://www.epa.gov/oppefed1/models/ 

water/index.htm. 

Based on the Pesticide Root Zone 

Model/Exposure Analysis Modeling 

System (PRZM/EXAMS) and Screening 

Concentration in Ground Water (SCI– 

GROW) models, the estimated drinking 

water concentrations (EDWCs) of 

emamectin benzoate for acute exposures 

are estimated to be between 0 and 0.465 

parts per billion (ppb) for surface water 

and 0.00054 ppb for ground water, and 

for chronic exposures are estimated to 

be 0.150 ppb for surface water and 

0.00054 ppb for ground water. 


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Modeled estimates of drinking water 

concentrations were directly entered 

into the dietary exposure model. For 

acute dietary risk assessment, a drinking 

water residue distribution based on the 

PRZM/EXAMS modeling was used. For 

chronic dietary risk assessment, the 

water concentration value of 0.150 ppb 

was used to assess the contribution to 

drinking water. 

3. From non-dietary exposure. The 

term ‘‘residential exposure’’ is used in 

this document to refer to nonoccupational, non-dietary exposure 

(e.g., for lawn and garden pest control, 

indoor pest control, termiticides, and 

flea and tick control on pets). 

Emamectin benzoate is not registered for 

any specific use patterns that would 

result in residential exposure. 

4. Cumulative effects from substances 

with a common mechanism of toxicity. 

Section 408(b)(2)(D)(v) of FFDCA 

requires that, when considering whether 

to establish, modify, or revoke a 

tolerance, the Agency consider 

‘‘available information’’ concerning the 

cumulative effects of a particular 

pesticide’s residues and ‘‘other 

substances that have a common 

mechanism of toxicity.’’ 

OPP’s Guidance for Identifying 

Pesticide Chemicals and Other 

Substances that have a Common 

Mechanism of Toxicity (EPA, 1999) 

describes the weight of the evidence 

approach for determining whether or 

not a group of pesticides share a 

common mechanism of toxicity. This 

guidance defines mechanism of toxicity 

as the major steps leading to a toxic 

effect following interaction of a 

pesticide with biological targets. All 

steps leading to an effect do not need to 

be specifically understood. Rather, it is 

the identification of the crucial events 

following chemical interaction that are 

required in order to describe a 

mechanism of toxicity. For example, a 

mechanism of toxicity may be described 

by knowing the following: A chemical 

binds to a given biological target in 

vitro, and causes the receptor-related 

molecular response; in vivo it also leads 

to the molecular response and causes a 

number of intervening biological and 

morphological steps that result in an 

adverse effect. In this context a common 

mechanism of toxicity pertains to two or 

more pesticide chemicals or other 

substances that cause a common toxic 

effect to human health by the same, or 

essentially the same, sequence of major 

biochemical events. Hence, the 

underlying basis of the toxicity is the 

same, or essentially the same, for each 

chemical. In the case of the macrocyclic 

lactone pesticides (e.g., abamectin, 

emamectin, and avermectin), there is a 

wealth of data on the insecticidal 

mechanism of action for avermectin: Its 

insecticidal actions are mediated by 

interaction with the glutamate-gated 

chloride channels and GABAA gated 

chloride channels. This is presumed to 

be the insecticidal mechanism of action 

of emamectin and abamectin as well. 

Insecticidal mechanism of action does 

not indicate a common mechanism of 

toxicity for human health. Further, 

mammals lack glutamate-gated chloride 

channels; the toxic actions of 

avermectin appear to be mediated via 

interaction with GABAA and possibly 

glycine gated chloride channels. There 

is evidence that avermectin B1a binds to 

GABAA receptors and activates Cl 

flux into neurons (Abalis et al., 1986; 

Huang and Casida, 1997). However, 

there is a paucity of data regarding the 

resultant alterations in cellular 

excitability of mammalian neurons and 

neural networks (i.e., changes in cellular 

excitability and altered network 

function as documented with 

pyrethroids), as well as in vivo 

measurements of altered excitability 

associated with adverse outcomes. 

Thus, while the downstream steps 

leading to toxicity via disruption of 

GABAA receptor function for avermectin 

can be postulated, experimental data 

supporting these actions are lacking. In 

addition, specific data demonstrating 

GABAA receptor interaction in 

mammalian preparations are lacking for 

abamectin and emamectin. Moreover, 

the specificity of such interaction on the 

adverse outcome would need to be 

shown experimentally. GABAA

receptors have multiple binding sites 

which have been proposed to relate to 

adverse outcomes. For example, Dawson 

et al (2000) showed for a group of 

avermectin-like compounds that rank 

order for anticonvulsant activity did not 

parallel the rank order for affinity at the 

[3H]-ivermectin site. The authors 

hypothesized that these findings may be 

related to differential affinity or efficacy 

at subtypes of the GABAA receptor. 

Other reports have indicated species 

differences in abamectin effects on 

GABAA receptor function in the mouse 

as compared to the rat (Soderlund et al., 

1987). 

In conclusion, although GABAA

receptor mediated neurotoxicity may be 

a common mechanism endpoint for the 

macrocyclic lactone pesticides, data 

demonstrating the interactions of 

emamectin and abamectin with 

mammalian GABAA receptors are not 

available, and data in mammalian 

preparations linking alterations in 

GABAA receptor function to disruptions 

in neuronal excitability in vitro and in 

vivo, and ultimately adverse outcome, 

are also currently lacking for this class 

of compounds. In the absence of such 

data, the key biological steps leading to 

the adverse outcome (i.e., the 

mammalian mechanism of action) 

cannot be established and by extension 

a common mechanism of toxicity (CMT) 

cannot be established. 

For information regarding EPA’s 

efforts to determine which chemicals 

have a common mechanism of toxicity 

and to evaluate the cumulative effects of 

such chemicals, see EPA’s Web site at 

http://www.epa.gov/pesticides/ 

cumulative. 

D. Safety Factor for Infants and 

Children 

1. In general. Section 408(b)(2)(C) of 

FFDCA provides that EPA shall apply 

an additional tenfold (10X) margin of 

safety for infants and children in the 

case of threshold effects to account for 

prenatal and postnatal toxicity and the 

completeness of the database on toxicity 

and exposure unless EPA determines 

based on reliable data that a different 

margin of safety will be safe for infants 

and children. This additional margin of 

safety is commonly referred to as the 

Food Quality Protection Act Safety 

Factor (FQPA SF). In applying this 

provision, EPA either retains the default 

value of 10X, or uses a different 

additional safety factor when reliable 

data available to EPA support the choice 

of a different factor. 

2. Prenatal and postnatal sensitivity. 

Although no increased sensitivity was 

seen in developmental toxicity studies 

in rats and rabbits, increased qualitative 

and/or quantitative sensitivity of rat 

pups was seen in the reproductive 

toxicity study and in the developmental 

neurotoxicity study. In the reproduction 

study, whole body tremors, hind limb 

extension, and hind limb splay were 

seen in the F1 and F2 pups while these 

clinical signs were not seen in F0

parental animals at similar dose levels. 

In addition, a greater incidence of 

decreased fertility was seen in the F1

parental females than in the F0 females. 

In the developmental neurotoxicity 

study, no maternal effect was seen at the 

highest dose tested whereas dose-related 

decrease in open-field motor activity 

was seen in the mid-dose in pups on 

postnatal day 17. Body tremors, hindlimb extension, and auditory startle 

were also found in the high-dose pups. 

3. Conclusion. Based on currently 

available data, EPA is retaining the 10X 

FQPA SF for chronic assessments and is 

using a 3X FQPA SF for acute 

assessments. This decision is based on 

the following findings: 


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i. Completeness of the toxicity 

database. The toxicology database used 

to assess pre- and postnatal exposure to 

emamectin contains all required studies 

with exception of an immunotoxicity 

study and a subchronic inhalation 

toxicity study, which are data gaps. 

The Agency evaluated subchronic, 

chronic, carcinogenicity, 

developmental, and reproduction 

studies as well as acute and subchronic 

neurotoxicity studies for any effects that 

might indicate that emamectin induced 

changes in the organs generally 

associated with immunological toxicity. 

In the studies evaluated, only the 14- 

week oral toxicity study in dogs showed 

an increase in the incidence of thymus 

atrophy at 1 mg/kg/day. In the 1-year 

feeding study in dog, thymus atrophy 

was not reported at similar dose levels 

tested. Currently, the point of departure 

for risk assessment is 0.075 mg/kg/day, 

which is more than 10 times less than 

the dose where thymus atrophy had 

been reported. Therefore, since the 

acute and chronic RfD’s are 0.00025 mg/ 

kg/day and 0.000075 mg/kg/day, 

respectively, the Agency does not 

believe an immunotoxicity study will 

result in a lower POD than that which 

is currently in use for overall risk 

assessment. As such, a database 

uncertainty factor is not necessary to 

account for the lack of an 

immunotoxicity study. 

In regards to the inhalation toxicity 

study, there are currently no residential 

uses registered for emamectin benzoate, 

and therefore, lack of this study does 

not impact the Agency’s assessment of 

pre- and postnatal exposure. 

Another completeness issue with 

regard to the toxicity database is that 

EPA is using a short-term study for longterm risk assessment. The data 

submitted show that CF–1 mice, which 

lack P-gp, are the most sensitive 

species/strand of animal tested. EPA 

only has data on CF–1 mice in shortterm studies. Longer-term studies used 

CD–1 mice. Hence a short-term study in 

CF–1 mice was used to choose the 

chronic POD. The extrapolation from a 

short-term study in CF–1 mice to a longterm POD introduces additional 

uncertainty into the risk assessment 

process. 

ii. Potential pre- and postnatal 

toxicity. Although no increased 

sensitivity was seen in developmental 

toxicity studies in rats and rabbits, 

increased qualitative and/or quantitative 

sensitivity of rat pups was seen in the 

reproductive toxicity study and in the 

developmental neurotoxicity study. A 

degree-of-concern analysis was 

conducted to determine whether or not 

an additional safety factor is needed to 

account for the increased susceptibility 

in pups; it was concluded that the 

degree-of-concern was low for both 2- 

generation reproduction and 

developmental neurotoxicity studies. 

The reasons are as follows: 

a. For the 2-generation reproduction 

study: 

• There was a clear NOAEL for the 

offspring toxicity. 

• The decreased fertility seen in F1

adults might have been due to 

histopathological lesions in the brain 

and central nervous system (seen in 

both F0 and F1 generations), rather than 

due to a direct effect on the 

reproductive system. 

b. For the developmental 

neurotoxicity study: 

• Although multiple offspring effects 

(including decreased pup body weight, 

head and body tremors, hindlimb 

extension and splay, changes in motor 

activity and auditory startle) were seen 

at the highest dose, and no maternal 

effects were seen at any dose, there was 

a clear NOAEL for offspring toxicity at 

the low dose. 

• The offspring LOAEL (at the mid 

dose) is based on a single effect seen on 

only 1 day (decreased motor activity on 

PND 17) and no other offspring toxicity 

was seen at the LOAEL. 

Two other considerations raise 

residual concerns about whether the 

traditional safety factors are protective 

of potential pre- and postnatal toxicity. 

First, the steepness of the dose-response 

curve means that there is a small margin 

of error provided by reliance on the 

study NOAEL. Second, the severity of 

effects at the LOAEL (death and 

neuropathology), exacerbate the concern 

raised by the steep dose response curve. 

iii. The completeness of the exposure 

database. The assessment for food 

incorporates somewhat refined 

anticipated residue estimates for most 

commodities that were derived from 

field trial data and PCT. The availability 

and use of monitoring data and food 

preparation-reduction factors for 

washing, cooking, etc., may have 

resulted in a more refined estimate of 

dietary exposure. Therefore, exposures 

to residues in food are not expected to 

be exceeded. 

The dietary drinking water 

assessment utilizes water concentration 

values generated by model and 

associated modeling parameters which 

are designed to provide conservative, 

health protective, high-end estimates of 

water concentrations which will not 

likely be exceeded. 

Taking all of these findings into 

account, EPA has concluded that there 

are not reliable data supporting 

lowering of the default 10X FQPA SF for 

chronic exposures. Specifically, EPA 

does not have reliable data showing that 

infants and children will be adequately 

protected using the traditional interand intra-species safety factors due to 

the steepness of the dose-response 

curve, the severity of effects at the 

LOAEL (death and neuropathology), and 

the use of a short-term study for longterm risk assessment. The Agency did 

not use a chronic study for the point of 

departure because the chronic studies 

were conducted in rats, dogs, and CD– 

1 mice. 

Taking all of these findings into 

account, for acute exposures, EPA has 

concluded that there are reliable data 

supporting lowering the default 10X 

FQPA SF to 3X. Although the steepness 

of the dose-response curve and the 

severity of the effects at the LOAEL 

introduce uncertainty with regard to 

whether the inter- and intra-species 

safety factors are protective of infants 

and children from acute effects, EPA has 

concluded that use of the 15-day 

neurotoxicity CF–1 mouse study 

provides reliable data to reduce the 

FQPA SF for acute assessments from 

10X to 3X. The Agency determined that 

a 3X FQPA SF is adequate for assessing 

acute dietary risk based on the following 

weight of evidence considerations: 

• An endpoint of concern attributable 

to a single exposure was not identified 

for in utero effects since there was no 

concern for developmental toxicity and 

there was no indication of increased 

susceptibility (qualitative or 

quantitative) of rat or rabbit fetuses to in 

utero exposure to emamectin. 

• Although there was evidence of 

increased susceptibility in the 

developmental neurotoxicity (DNT) 

study, an endpoint of concern was not 

identified for acute dietary risk 

assessment for prenatal exposures 

because the adverse effect at the LOAEL 

(i.e., decrease in open-field motor 

activity) was seen only on postnatal day 

17 and not seen after a single exposure. 

• The POD selected for acute dietary 

risk assessment is a NOAEL (with a 

clear LOAEL) seen after repeated dosing 

but is used for assessing acute risk (i.e., 

a very conservative approach). 

Therefore, the Agency is confident 

that the retention of a 3X FQPA SF (to 

account for the steepness of the dose 

response curve) will not underestimate 

risk and provides reasonable certainty of 

no harm from exposure to emamectin 

benzoate. 

E. Aggregate Risks and Determination of 

Safety 

EPA determines whether acute and 

chronic dietary pesticide exposures are 

safe by comparing aggregate exposure 


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estimates to the acute PAD (aPAD) and 

chronic PAD (cPAD). For linear cancer 

risks, EPA calculates the lifetime 

probability of acquiring cancer given the 

estimated aggregate exposure. Short-, 

intermediate-, and chronic-term risks 

are evaluated by comparing the 

estimated aggregate food, water, and 

residential exposure to the appropriate 

PODs to ensure that an adequate MOE 

exists. 

1. Acute risk. Using the exposure 

assumptions discussed in this unit for 

acute exposure, the acute dietary 

exposure from food and drinking water 

to emamectin benzoate will occupy 91% 

of the aPAD for females 13–49 years old, 

the population group receiving the 

greatest exposure. 

2. Chronic risk. Using the exposure 

assumptions described in this unit for 

chronic exposure, EPA has concluded 

that chronic exposure to emamectin 

benzoate from food and water will 

utilize 16% of the cPAD for all infants 

less than 1 year old, the population 

group receiving the greatest exposure. 

There are no residential uses for 

emamectin benzoate. 

3. Short-term risk. Short- and 

intermediate-term aggregate exposure 

takes into account short- and 

intermediate-term residential exposure 

plus chronic exposure to food and water 

(considered to be a background 

exposure level). 

Both short- and intermediate-term 

adverse effects were identified; 

however, emamectin benzoate is not 

registered for any use patterns that 

would result in either short- or 

intermediate-term residential exposure. 

Short- and intermediate-term risk is 

assessed based on short- and 

intermediate-term residential exposure 

plus chronic dietary exposure. Because 

there is no short- or intermediate-term 

residential exposure and chronic dietary 

exposure has already been assessed 

under the appropriately protective 

cPAD (which is at least as protective as 

the POD used to assess short- or 

intermediate-term risk), no further 

assessment of short- or intermediateterm risk is necessary, and EPA relies on 

the chronic dietary risk assessment for 

evaluating short- and intermediate-term 

risk for emamectin benzoate. 

4. Aggregate cancer risk for U.S. 

population. Based on the lack of 

evidence of carcinogenicity in two 

adequate rodent carcinogenicity studies, 

emamectin benzoate is not expected to 

pose a cancer risk to humans. 

5. Determination of safety. Based on 

these risk assessments, EPA concludes 

that there is a reasonable certainty that 

no harm will result to the general 

population or to infants and children 

from aggregate exposure to emamectin 

benzoate residues. 

IV. Other Considerations 

A. Analytical Enforcement Methodology 

Adequate enforcement methodology 

(high performance liquid 

chromatography with fluorescence 

detection (HPLC/FLD)) is available to 

enforce the tolerance expression. 

The method may be requested from: 

Chief, Analytical Chemistry Branch, 

Environmental Science Center, 701 

Mapes Rd., Ft. Meade, MD 20755–5350; 

telephone number: (410) 305–2905; 

email address: 

residuemethods@epa.gov. 

B. International Residue Limits 

In making its tolerance decisions, EPA 

seeks to harmonize U.S. tolerances with 

international standards whenever 

possible, consistent with U.S. food 

safety standards and agricultural 

practices. EPA considers the 

international maximum residue limits 

(MRLs) established by the Codex 

Alimentarius Commission (Codex), as 

required by FFDCA section 408(b)(4). 

The Codex Alimentarius is a joint 

United Nations Food and Agriculture 

Organization/World Health 

Organization food standards program, 

and it is recognized as an international 

food safety standards-setting 

organization in trade agreements to 

which the United States is a party. EPA 

may establish a tolerance that is 

different from a Codex MRL; however, 

FFDCA section 408(b)(4) requires that 

EPA explain the reasons for departing 

from the Codex level. 

Harmonization issues regarding the 

tolerance expression are associated with 

this petition. There is a Codex MRL for 

grapes of 0.03 ppm. The Codex residue 

definition for the MRL and for the risk 

assessment is emamectin B1a benzoate. 

The recommended U.S. tolerance is 0.03 

ppm to harmonize with Codex but the 

U.S. residue definition includes 

additional analytes. 

C. Revisions to Petitioned-For 

Tolerances 

The difference in the proposed 

tolerance level of 0.005 ppm and the 

recommended tolerance level of 0.03 

ppm is because EPA does not set 

tolerances on wine but rather on the raw 

commodity wine grapes. The 

recommended tolerance level reflects 

the harmonized residue values in the 

raw commodity as described in Unit 

IV.B. 

EPA has revised the tolerance 

expression to clarify: 

1. That, as provided in FFDCA section 

408(a)(3), the tolerance covers 

metabolites and degradates of 

emamectin benzoate not specifically 

mentioned. 

2. That compliance with the specified 

tolerance levels is to be determined by 

measuring only the specific compounds 

mentioned in the tolerance expression. 

V. Conclusion 

Therefore, a tolerance is established 

for residues of emamectin, including its 

metabolites and degradates, in or on 

grape, wine at 0.03 ppm. Compliance 

with the tolerance levels specified is to 

be determined by measuring only the 

sum of emamectin (a mixture of a 

minimum of 90% 4′-epi-methylamino4′-deoxyavermectin B1a and maximum 

of 10% 4′-epi-methylamino-4′- 

deoxyavermectin B1b) and its 

metabolites 8,9-isomer of the B1a and B1b

component of the parent (8,9-ZMA), or 

4′-deoxy-4′-epi-amino-avermectin B1a

and 4′-deoxy-4′-epi-amino-avermectin 

B1b; 4′-deoxy-4′-epi-amino avermectin 

B1a (AB1a); 4′-deoxy-4′-epi-(N-formyl-Nmethyl)amino-avermectin (MFB1a); and 

4′-deoxy-4′-epi-(N-formyl)aminoavermectin B1a (FAB1a), calculated as 

the stoichiometric equivalent of 

emamectin. 

VI. Statutory and Executive Order 

Reviews 

This final rule establishes tolerances 

under FFDCA section 408(d) in 

response to a petition submitted to the 

Agency. The Office of Management and 

Budget (OMB) has exempted these types 

of actions from review under Executive 

Order 12866, entitled ‘‘Regulatory 

Planning and Review’’ (58 FR 51735, 

October 4, 1993). Because this final rule 

has been exempted from review under 

Executive Order 12866, this final rule is 

not subject to Executive Order 13211, 

entitled ‘‘Actions Concerning 

Regulations That Significantly Affect 

Energy Supply, Distribution, or Use’’ (66 

FR 28355, May 22, 2001) or Executive 

Order 13045, entitled ‘‘Protection of 

Children from Environmental Health 

Risks and Safety Risks’’ (62 FR 19885, 

April 23, 1997). This final rule does not 

contain any information collections 

subject to OMB approval under the 

Paperwork Reduction Act (PRA) (44 

U.S.C. 3501 et seq.), nor does it require 

any special considerations under 

Executive Order 12898, entitled 

‘‘Federal Actions to Address 

Environmental Justice in Minority 

Populations and Low-Income 

Populations’’ (59 FR 7629, February 16, 

1994). 

Since tolerances and exemptions that 

are established on the basis of a petition 

under FFDCA section 408(d), such as 

the tolerance in this final rule, do not 


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Federal Register / Vol. 78, No. 159 / Friday, August 16, 2013 / Rules and Regulations 49939 

require the issuance of a proposed rule, 

the requirements of the Regulatory 

Flexibility Act (RFA) (5 U.S.C. 601 et 

seq.), do not apply. 

This final rule directly regulates 

growers, food processors, food handlers, 

and food retailers, not States or tribes, 

nor does this action alter the 

relationships or distribution of power 

and responsibilities established by 

Congress in the preemption provisions 

of FFDCA section 408(n)(4). As such, 

the Agency has determined that this 

action will not have a substantial direct 

effect on States or tribal governments, 

on the relationship between the national 

government and the States or tribal 

governments, or on the distribution of 

power and responsibilities among the 

various levels of government or between 

the Federal Government and Indian 

tribes. Thus, the Agency has determined 

that Executive Order 13132, entitled 

‘‘Federalism’’ (64 FR 43255, August 10, 

1999) and Executive Order 13175, 

entitled ‘‘Consultation and Coordination 

with Indian Tribal Governments’’ (65 FR 

67249, November 9, 2000) do not apply 

to this final rule. In addition, this final 

rule does not impose any enforceable 

duty or contain any unfunded mandate 

as described under Title II of the 

Unfunded Mandates Reform Act of 1995 

(UMRA) (2 U.S.C. 1501 et seq.). 

This action does not involve any 

technical standards that would require 

Agency consideration of voluntary 

consensus standards pursuant to section 

12(d) of the National Technology 

Transfer and Advancement Act of 1995 

(NTTAA) (15 U.S.C. 272 note). 

VII. Congressional Review Act 

Pursuant to the Congressional Review 

Act (5 U.S.C. 801 et seq.), EPA will 

submit a report containing this rule and 

other required information to the U.S. 

Senate, the U.S. House of 

Representatives, and the Comptroller 

General of the United States prior to 

publication of the rule in the Federal 

Register. This action is not a ‘‘major 

rule’’ as defined by 5 U.S.C. 804(2). 

List of Subjects in 40 CFR Part 180 

Environmental protection, 

Administrative practice and procedure, 

Agricultural commodities, Pesticides 

and pests, Reporting and recordkeeping 

requirements. 

Dated: August 7, 2013. 

Lois Rossi, 

Director, Registration Division, Office of 

Pesticide Programs. 

Therefore, 40 CFR chapter I is 

amended as follows: 

PART 180—[AMENDED] 

■ 1. The authority citation for part 180 

continues to read as follows: 

Authority: 21 U.S.C. 321(q), 346a and 371. 

■ 2. In § 180.505: 

■ a. Add alphabetically the following 

commodity and footnote 1 to the table 

in paragraph (a)(1). 

■ b. Revise the introductory text of 

paragraph (a)(2). 

The amendments read as follows: 

§ 180.505 Emamectin; tolerances for 

residues. 

(a) * * * 

(1) * * * 

Commodity Parts per 

million 

* * * * * 

Grape, wine 1 ........................ 0.03 

* * * * * 

1There are no U.S. registrations for use of 

emamectin on grape, wine. 

(2) Tolerances are established for 

emamectin, including its metabolites 

and degradates, in or on the 

commodities in the following table. 

Compliance with the tolerance levels 

specified in the following table is to be 

determined by measuring only the sum 

of emamectin (MAB1a + MAB1b isomers) 

and the associated 8,9-Z isomers (8,9- 

ZB1a and 8,9-ZB1b). 

* * * * * 

[FR Doc. 2013–19863 Filed 8–15–13; 8:45 am] 

BILLING CODE 6560–50–P 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 300 

[EPA–HQ–SFUND–1986–0005; FRL–9846–4] 

National Oil and Hazardous 

Substances Pollution Contingency 

Plan; National Priorities List: Partial 

Deletion of the Torch Lake Superfund 

Site 

AGENCY: U.S. Environmental Protection 

Agency. 

ACTION: Direct final rule. 

SUMMARY: The U.S. Environmental 

Protection Agency Region 5 is 

publishing a direct final Notice of 

Deletion of the Quincy Smelter and 

Calumet Lake parcels of Operable Unit 

3 (OU3) of the Torch Lake Superfund 

Site (Site), located in Houghton County, 

Michigan, from the National Priorities 

List (NPL). The NPL, promulgated 

pursuant to Section 105 of the 

Comprehensive Environmental 

Response, Compensation, and Liability 

Act (CERCLA) of 1980, as amended, is 

an appendix of the National Oil and 

Hazardous Substances Pollution 

Contingency Plan (NCP). This direct 

final partial deletion is being published 

by EPA with the concurrence of the 

State of Michigan, through the Michigan 

Department of Environmental Quality 

(MDEQ), because EPA has determined 

that all appropriate response actions at 

these identified parcels under CERCLA, 

other than operation, maintenance, and 

five-year reviews, have been completed. 

However, this partial deletion does not 

preclude future actions under 

Superfund. 

This partial deletion pertains to the 

surface tailings and slag deposits of the 

Quincy Smelter and Calumet Lake 

parcels of OU3. The following parcels or 

areas will remain on the NPL and are 

not being considered for deletion as part 

of this action: Dollar Bay, Point Mills, 

Boston Pond, and North Entry. 

DATES: This direct final partial deletion 

is effective October 15, 2013 unless EPA 

receives adverse comments by 

September 16, 2013. If adverse 

comments are received, EPA will 

publish a timely withdrawal of the 

direct final partial deletion in the 

Federal Register informing the public 

that the deletion will not take effect. 

ADDRESSES: Submit your comments, 

identified by Docket ID No. EPA–HQ– 

SFUND–1986–0005, by one of the 

following methods: 

• http://www.regulations.gov: Follow 

online instructions for submitting 

comments. 

• Email: Nefertiti DiCosmo, Remedial 

Project Manager, at dicosmo.nefertiti@

epa.gov or Dave Novak, Community 

Involvement Coordinator, at 

novak.dave@epa.gov. 

• Fax: Gladys Beard at (312) 697– 

2077. 

• Mail: Nefertiti DiCosmo, Remedial 

Project Manager, U.S. Environmental 

Protection Agency (SR–6J), 77 West 

Jackson Boulevard, Chicago, IL 60604, 

(312) 886–6148 or Dave Novak, 

Community Involvement Coordinator, 

U.S. Environmental Protection Agency 

(SI–7J), 77 West Jackson Boulevard, 

Chicago, IL 60604, (312) 886–7478 or 

toll free at 1 (800) 621–8431. 

• Hand delivery: Dave Novak, 

Community Involvement Coordinator, 

U.S. Environmental Protection Agency 


tkelley on DSK3SPTVN1PROD with RULES