18504 Federal Register / Vol. 78, No. 59 / Wednesday, March 27, 2013 / Rules and Regulations 

§ 218.32 Objection time periods. 

(a) Time to file an objection. Written 

objections, including any attachments, 

must be filed with the reviewing officer 

within 30 days following the 

publication date of the legal notice of 

the EA or final EIS in the newspaper of 

record or the publication date of the 

notice in the Federal Register when the 

Chief is the responsible official (see 

§ 218.6(c)). It is the responsibility of 

objectors to ensure that their objection 

is received in a timely manner. 

(b) Time for responding to an 

objection. The reviewing officer must 

issue a written response to the 

objector(s) concerning their objection(s) 

within 30 days following the end of the 

objection filing period. 

Dated: March 20, 2013. 

Harris D. Sherman, 

Under Secretary, Natural Resources and 

Environment (NRE). 

[FR Doc. 2013–06857 Filed 3–26–13; 8:45 am] 

BILLING CODE 3410–11–P 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 180 

[EPA–HQ–OPP–2011–0665; FRL–9381–4] 

Emamectin Benzoate; Pesticide 

Tolerance 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Final rule. 

SUMMARY: This regulation establishes a 

tolerance for residues of emamectin 

benzoate in or on the cucurbit vegetable 

crop group 9. Interregional Research 

Project Number 4 (IR–4) requested this 

tolerance under the Federal Food, Drug, 

and Cosmetic Act (FFDCA). 

DATES: This regulation is effective 

March 27, 2013. Objections and requests 

for hearings must be received on or 

before May 28, 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–2011–0665, 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: 

Andrew Ertman, Registration Division 

(7505P), Office of Pesticide Programs, 

Environmental Protection Agency, 1200 

Pennsylvania Ave. NW., Washington, 

DC 20460–0001; telephone number: 

(703) 308–9367; email address: 

ertman.andrew@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–2011–0665 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 May 28, 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– 

2011–0665, 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 

Confidential Business Information (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. 

• 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.htm. 

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 September 

7, 2011 (76 FR 55329) (FRL–8886–7), 

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 1E7904) by IR–4, 

500 College Rd. East, Suite 201 W, 

Princeton, NJ 08540. The petition 

requested that 40 CFR 180.505 be 

amended by establishing tolerances for 

residues of the insecticide emamectin 

benzoate, 4′-epimethylamino-4′- 

deoxyavermectin B1 benzoate (a 

mixture of a minimum of 90% 4′-epimethylamino-4′-deoxyavermectin B1a 

and a maximum of 10% 4′-epimethlyamino-4′deoxyavermectin B1b 

benzoate), and its metabolites 8,9 isomer 

of the B1a and B1b component of the 

parent insecticide, in or on vegetable, 

cucurbit, group 9 at 0.03 parts per 

million (ppm). That document 

referenced a summary of the petition 

prepared by Syngenta, the registrant, 

which is available in the docket, http://

www.regulations.gov. There were no 

comments received in response to the 

notice of filing. 


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Based upon review of the data 

supporting the petition, EPA has 

modified the level at which the 

tolerance is being established. The 

reason for this change is explained in 

Unit IV.C. 

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-glycoprotein (P-gp) 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 

LOAELs (0.1 milligram/kilogram/day 

(mg/kg/day) with 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.’’ 

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 no-observed-adverse-effectlevel (NOAEL) and the lowest-observedadverse-effect-level (LOAEL) from the 

toxicity studies can be found at http:// 

www.regulations.gov on pages 43–50 of 

the document titled ‘‘Emamectin 

Benzoate. Revised Human Health Risk 

Assessment for Proposed Uses on 

Cucurbits and Outdoor-Grown Plants in 

Commercial Nursery Production’’ in 

docket ID number EPA–HQ–OPP–2011– 

0665. 

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/ 


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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 

(mg/kg/day) 

Study and toxicological effects 

Acute dietary (All Populations) NOAEL = 0.075 mg/ 

kg/day.

UFA = 10x 

UFH = 10x 

FQPA SF = 3x 

aRfD = 0.00025 .......

aPAD = 0.00025 

15-day mouse. 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 

cRfD = 0.000075 .....

cPAD = 0.000075 

15-day mouse. 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. 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 tree nuts 

(including pistachios) and cottonseed 

oil. Pesticide Data Program (PDP) 

monitoring data for years 2009 and 2010 

were used for apples since apple juice 

had a significant impact on exposure. 

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 tree nuts (including pistachios) and 

cottonseed oil. 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 

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 PCT for existing 

uses as follows: 

Almonds, 2.5%; apples, 20%; 

broccoli, 20%; cabbage, 25%; 


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cauliflower, 20%; celery, 40%; cotton, 

2.5%; lettuce, 20%; pears, 20%; 

peppers, 15%; spinach, 10%; 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%; 

tomatoes, 10%. 

In most cases, EPA uses available data 

from USDA/National Agricultural 

Statistics Service (NASS), proprietary 

market surveys, and the National 

Pesticide Use Database for the chemical/ 

crop combination for the most recent 6 

to 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 1. 

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%. 

For the acute dietary assessment, the 

Agency estimated the PCT for new uses 

as follows: 

Cantaloupe, 51%; cucumber, 26%; 

squash, 46%; watermelon, 21%. 

For the chronic dietary assessment, 

the Agency estimated the PCT for new 

uses as follows: 

Cantaloupe, 40%; cucumber, 14%; 

squash, 29%; watermelon, 19%. 

EPA estimates of the PCT for new 

uses of emamectin benzoate 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 three 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. 

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’’ (Ref. 1) 

describes the weight of the evidence 

approach for determining whether or 

not a group of pesticides share a 


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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 (Refs. 2 and 3). 

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. (Ref. 4) 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 (Ref. 5). 

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 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 

FQPA Safety Factor (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 safety factor for chronic 

assessments and is using a 3X FQPA 

safety factor for acute assessments. This 

decision is based on the following 

findings: 

i. Completeness of the toxicity 

database. The toxicology database used 

to assess prenatal 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 dogs, 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 point of departure 

(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 


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not impact the Agency’s assessment of 

prenatal 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 glycoprotein, 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 Point of Departure. The 

extrapolation from a short-term study in 

CF–1 mice to a long-term POD 

introduces additional uncertainty into 

the risk assessment process. 

ii. Potential prenatal 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: 

For the 2-generation reproduction 

study, (1) there was a clear NOAEL for 

the offspring toxicity, and (2) 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. 

For the developmental neurotoxicity 

study, (1) 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, and (2) the 

offspring LOAEL (at the mid dose) is 

based on a single effect seen on only one 

day (decreased motor activity on 

postnatal day 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 prenatal and postnatal 

toxicity. First, the steepness of the doseresponse 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 safety 

factor for chronic exposures. 

Specifically, EPA does not have reliable 

data showing that infants and children 

will be adequately protected using the 

traditional inter- and intra-species safety 

factors due to the steepness of the doseresponse curve, the severity of effects at 

the LOAEL (death and neuropathology), 

and the use of a short-term study for 

long-term risk assessment. The Agency 

did not use a chronic study for the POD 

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 safety factor 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 intraspecies 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 safety factor for acute 

assessments from 10X to 3X. The 

Agency determined that a 3X FQPA 

Safety Factor 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 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 Safety 

Factor (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 

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 60% 

of the aPAD for children 1–2 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. 


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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. 

The Codex has not established a MRL 

for emamectin benzoate on cucurbits. 

C. Revisions to Petitioned-For 

Tolerances 

Based on the review of the residue 

data submitted with the petition, the 

proposed tolerance level of 0.03 ppm is 

being modified to 0.02 ppm. 

Also, 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; and (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 the 

cucurbit vegetable group 9 at 0.02 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′-epimethylamino-4′-deoxyavermectin B1a

and maximum of 10% 4′-epimethylamino-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-aminoavermectin B1a and 4′-deoxy-4′-epiamino-avermectin B1b; 4′-deoxy-4′-epiamino avermectin B1a (AB1a); 4′-deoxy4′-epi-(N-formyl-N-methyl)aminoavermectin (MFB1a); and 4′-deoxy-4′- 

epi-(N-formyl)amino-avermectin B1a

(FAB1a), calculated as the stoichiometric 

equivalent of emamectin. 

VI. References 

The following literature was 

referenced in the preamble of this 

document. 

1. OPP’s ‘‘Guidance for Identifying Pesticide 

Chemicals and Other Substances that 

have a Common Mechanism of Toxicity’’ 

(USEPA, 1999); http://www.epa.gov/ 

fedrgstr/EPA-PEST/1999/February/Day05/6055.pdf. 

2. balis IM, Eldefrawi AT, Eldefrawi ME. 

Actions of avermectin B1a on the gammaaminobutyric acidA receptor and 

chloride channels in rat brain. Journal of 

Biochemical Toxicology. 1986 

Mar;1(1):69–82. 

3. Huang J, Casida JE. (1997) Avermectin B1a

binds to high- and low-affinity sites with 

dual effects on the gama-aminobutyric 

acid-gated chloride channel of cultured 

cerebellar granule neurons. Journal of 

Pharmacology and Experimental 

Therapeutics. 281: 261–266. 

4. Dawson GR, Wafford KA, Smith A, 

Marshall GR, Bayley PJ, Schaeffer JM, 

Meinke PT, McKernan RM. (2000) 

Anticonvulsant and adverse effects of 

avermectin analogs in mice are mediated 

through the gama-aminobutyric acid (A) 

receptor. Journal of Pharmacology and 

Experimental Therapeutics 295: 1051– 

1060. 

5. Soderlund DM, Adams PM, Bloomquist JR. 

Differences in the action of avermectin 

B1a on the GABAA receptor complex of 

mouse and rat. Biochemical Biophysical 

Research Communications. 1987 Jul 

31;146(2):692–8. 

VII. 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 

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 


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Federal Register / Vol. 78, No. 59 / Wednesday, March 27, 2013 / Rules and Regulations 18511 

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: March 19, 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. § 180.505, is amended by: 

■ i. Revise paragraph (a)(1) introductory 

text and paragraph (a)(2) introductory 

text; 

■ ii. Add alphabetically an entry for 

‘‘Vegetable, cucurbit, group 9’’ to the 

table in paragraph (a)(1). 

The added and revised text read as 

follows: 

§ 180.505 Emamectin; tolerances for 

residues. 

(a) General. (1) Tolerances are 

established for emamectin, including its 

metabolites and degradates, in or on the 

commodities in the table below. 

Compliance with the tolerance levels 

specified below is to be determined by 

measuring only the sum of emamectin (a 

mixture of a minimum of 90% 4′-epimethylamino-4′-deoxyavermectin B1a

and maximum of 10% 4′-epimethylamino-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-aminoavermectin B1a and 4’-deoxy-4’-epiamino-avermectin B1b; 4′-deoxy-4′-epiamino avermectin B1a (AB1a); 4′-deoxy4′-epi-(N-formyl-N-methyl)aminoavermectin (MFB1a); and 4′-deoxy-4′- 

epi-(N-formyl)amino-avermectin B1a

(FAB1a), calculated as the stoichiometric 

equivalent of emamectin. 

Commodity Parts per 

million 

* * * * * 

Vegetable, cucurbit, group 9 0.02 

* * * * * 

(2) Tolerances are established for 

emamectin, including its metabolites 

and degradates, in or on the 

commodities in the table below. 

Compliance with the tolerance levels 

specified below is to be determined by 

measuring only the sum of emamectin 

(MAB1a + MAB1b isomers) and the 

associated 8,9-Z isomers (8,9-1a and 8,9- 

ZB1b). 

* * * * * 

[FR Doc. 2013–06758 Filed 3–26–13; 8:45 am] 

BILLING CODE 6560–50–P 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 180 

[EPA–HQ–OPP–2012–0488; FRL–9377–3] 

Thiamethoxam; Pesticide Tolerances 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Final rule. 

SUMMARY: This regulation establishes a 

tolerance for residues of the insecticide 

thiamethoxam in or on tea, and amends 

the existing tolerance for residues of 

thiamethoxam in or on coffee. Syngenta 

Crop Protection, Inc., requested these 

tolerances under the Federal Food, 

Drug, and Cosmetic Act (FFDCA). 

DATES: This regulation is effective 

March 27, 2013. Objections and requests 

for hearings must be received on or 

before May 28, 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–2012–0488, 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: Julie 

Chao, Registration Division (7505P), 

Office of Pesticide Programs, 

Environmental Protection Agency, 1200 

Pennsylvania Ave. NW., Washington, 

DC 20460–0001; telephone number: 

(703) 308–8735; email address: 

chao.julie@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 

Web site at http://www.ecfr.gov/cgi-bin/ 

text-idx?&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 


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