Thiamethoxam; Pesticide Tolerance, 34401-34409 [E7-11794]

Agencies

• ENVIRONMENTAL PROTECTION AGENCY

[Federal Register Volume 72, Number 120 (Friday, June 22, 2007)]
[Rules and Regulations]
[Pages 34401-34409]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E7-11794]


=======================================================================
-----------------------------------------------------------------------

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[EPA-HQ-OPP-2006-0523; FRL-8133-6]


Thiamethoxam; Pesticide Tolerance

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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

SUMMARY: This regulation establishes tolerances for combined residues 
of thiamethoxam and its metabolite (CGA-322704) in or on artichoke, 
globe; caneberry subgroup 13-A, hop, dried cones; grape; grape, raisin; 
brassica,

[[Page 34402]]

head and stem, subgroup 5-A; brassica, leafy greens, subgroup 5-B; 
vegetable, leafy, except brassica group 4. Additionally, tolerance 
levels for barley, grain; barley, hay and barley, straw will be 
amended. Interregional Research Project Number 4 (IR-4) and Syngenta 
Crop Protection Inc. requested these tolerances under the Federal Food, 
Drug, and Cosmetic Act (FFDCA).

DATES: This regulation is effective June 22, 2007. Objections and 
requests for hearings must be received on or before August 21, 2007, 
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:  EPA has established a docket for this action under docket 
identification (ID) number EPA-HQ-OPP-2006-0523. To access the 
electronic docket, go to https://www.regulations.gov, select ``Advanced 
Search,'' then ``Docket Search.'' Insert the docket ID number where 
indicated and select the ``Submit'' button. Follow the instructions on 
the regulations.gov web site to view the docket index or access 
available documents. All documents in the docket are listed in the 
docket index available in regulations.gov. Although listed in the 
index, some information is not publicly available, e.g., Confidential 
Business Information (CBI) or other information whose disclosure is 
restricted by statute. Certain other material, such as copyrighted 
material, is not placed on the Internet and will be publicly available 
only in hard copy form. Publicly available docket materials are 
available in the electronic docket at https://www.regulations.gov, or, 
if only available in hard copy, at the OPP Regulatory Public Docket in 
Rm. S-4400, One Potomac Yard (South Bldg.), 2777 S. Crystal Dr., 
Arlington, VA. The Docket Facility is open from 8:30 a.m. to 4 p.m., 
Monday through Friday, excluding legal holidays. The Docket Facility 
telephone number is (703) 305-5805.

FOR FURTHER INFORMATION CONTACT: Barbara Madden, Registration Division 
(7505P), Office of Pesticide Programs, Environmental Protection Agency, 
1200 Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone 
number: (703) 305-6463; e-mail address: madden.barbara@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. 
Potentially affected entities may include, but are not limited to those 
engaged in the following activities:
     Crop production (NAICS code 111), e.g., agricultural 
workers; greenhouse, nursery, and floriculture workers; farmers.
     Animal production (NAICS code 112), e.g., cattle ranchers 
and farmers, dairy cattle farmers, livestock farmers.
     Food manufacturing (NAICS code 311), e.g., agricultural 
workers; farmers; greenhouse, nursery, and floriculture workers; 
ranchers; pesticide applicators.
     Pesticide manufacturing (NAICS code 32532), e.g., 
agricultural workers; commercial applicators; farmers; greenhouse, 
nursery, and floriculture workers; residential users.
    This listing is not intended to be exhaustive, but rather to 
provide a guide for readers regarding entities likely to be affected by 
this action. Other types of entities not listed in this unit could also 
be affected. The North American Industrial Classification System 
(NAICS) codes have been provided to assist you and others in 
determining whether this action might apply to certain entities. If you 
have any questions regarding the applicability of this action to a 
particular entity, consult the person listed under FOR FURTHER 
INFORMATION CONTACT.

B. How Can I Access Electronic Copies of this Document?

    In addition to accessing an electronic copy of this Federal 
Register document through the electronic docket at https://
www.regulations.gov, you may access this Federal Register document 
electronically through the EPA Internet under the ``Federal Register'' 
listings at https://www.epa.gov/fedrgstr. You may also access a 
frequently updated electronic version of EPA's tolerance regulations at 
40 CFR part 180 through the Government Printing Office's pilot e-CFR 
site at https://www.gpoaccess.gov/ecfr.

C. Can I File an Objection or Hearing Request?

    Under section 408(g) of the FFDCA, 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-2006-0523 in the subject line on the first page of 
your submission. All requests must be in writing, and must be mailed or 
delivered to the Hearing Clerk as required by 40 CFR part 178 on or 
before August 21, 2007.
    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 that does not contain any CBI for inclusion in the public 
docket that is described in ADDRESSES. Information not marked 
confidential pursuant to 40 CFR part 2 may be disclosed publicly by EPA 
without prior notice. Submit this copy, identified by docket ID number 
EPA-HQ-OPP-2006-0523, by one of the following methods:
     Federal eRulemaking Portal: https://www.regulations.gov. 
Follow the on-line instructions for submitting comments.
     Mail: Office of Pesticide Programs (OPP) Regulatory Public 
Docket (7502P), Environmental Protection Agency, 1200 Pennsylvania 
Ave., NW., Washington, DC 20460-0001.
     Delivery: OPP Regulatory Public Docket (7502P), 
Environmental Protection Agency, Rm. S-4400, One Potomac Yard (South 
Bldg.), 2777 S. Crystal Dr., Arlington, VA. Deliveries are only 
accepted during the Docket's normal hours of operation (8:30 a.m. to 4 
p.m., Monday through Friday, excluding legal holidays). Special 
arrangements should be made for deliveries of boxed information. The 
Docket Facility telephone number is (703) 305-5805.

II. Petition for Tolerance

    In the Federal Register of July 12, 2006 (71 FR 39316) (FRL-8074-
3), EPA issued a notice pursuant to section 408(d)(3) of FFDCA, 21 
U.S.C. 346a(d)(3), announcing the filing of pesticide petitions (PP 
6E7060, 0F6142, and 9F5051) Interregional Research Project Number 4 
(IR-4), 681 U.S. Highway 1 South, North Brunswick, NJ 08902-
3390 and Syngenta Crop Protection Inc., P.O. Box 18300, Greensboro, NC 
27419-8300. These petitions requested that 40 CFR 180.565 be amended by 
establishing a tolerance for combined residues of the insecticide, 
thiamethoxam [3-[(2-chloro-5-thiazolyl)methyl]tetrahydro-5-methyl-N-
nitro-4H-1,3,5-oxadiazin-4-imine and its metabolite [N-(2-chloro-
thiazol-5-ylmethyl)-N'-methyl-N'-nitro-guanidine] in or on the 
following commodities:
    PP 6E7060: Caneberry subgroup 13-A at 0.30 parts per million (ppm); 
hops at 0.1 ppm; globe artichoke at 0.4 ppm and amend the existing 
tolerance levels for barley, grain at 0.3 ppm; barley, hay at 0.4 ppm; 
and barley, straw at 0.4 ppm.
    PP 0F6142: Grapes at 0.15 ppm; grape, juice at 0.20 ppm; and 
raisins at 0.30 ppm.

[[Page 34403]]

    PP 9F5051: Vegetable, leafy, except brassica, group 4 at 2.0 ppm; 
brassica, leafy greens, subgroup 5-B at 2.0 ppm; brassica, head and 
stem, subgroup 5-A at 1.0 ppm.
    That notice referenced a summary of the petitions prepared by 
Syngenta Crop Protection Inc., the registrant, which is available to 
the public in the docket, https://www.regulations.gov. Comments were 
received on the notice of filing. EPA's response to these comments is 
discussed in Unit IV.C.
    Based upon review of the data supporting the petitions, EPA has 
determined tolerance levels for artichoke, grape, caneberry subgroup 
13-A, brassica head and stem subgroup 5-A, brassica leafy greens 
subgroup 5-B, vegetable leafy except brassica group 4 should be 
modified and a tolerance for grape juice should not be established. The 
reason for these changes is explained in Unit V.
    EPA is also deleting several established tolerances in Sec.  
180.565(b) that are no longer needed. The tolerance deletions under 
Sec.  180.565(b) are time-limited tolerances established under section 
18 emergency exemptions that are superceded by the establishment of 
general tolerances for thiamethoxam and its metabolite under Sec.  
180.565(a).
    The revisions to Sec.  180.565(b) are as follows:
    1. Delete the time-limited tolerance for artichoke, globe at 0.40 
ppm. A tolerance for artichoke, globe at 0.45 ppm is established by 
this action under Sec.  180.565(a).
    2. Delete the time-limited tolerances for bean, dried at 0.02 ppm 
and bean, succulent at 0.02 ppm as these tolerances have expired and 
are no longer in force.
    3. Delete the time-limited tolerance for hops at 0.10 ppm. A 
tolerance for hop, dried cones at 0.10 ppm is established by this 
action under Sec.  180.565(a).

III. Aggregate Risk Assessment and Determination of Safety

    Section 408(b)(2)(A)(i) of the 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 the 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 the 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. . . 
.'' These provisions were added to the FFDCA by the Food Quality 
Protection Act (FQPA) of 1996.
    Consistent with section 408(b)(2)(D) of FFDCA, and the factors 
specified in section 408(b)(2)(D) of FFDCA, 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 the petitioned-for 
tolerances for combined residues of the insecticide, thiamethoxam [3-
[(2-chloro-5-thiazolyl)methyl]tetrahydro-5-methyl-N-nitro-4H-1,3,5-
oxadiazin-4-imine and its metabolite [N-(2-chloro-thiazol-5-ylmethyl)-
N'-methyl -N'-nitro-guanidine] on artichoke, globe at 0.45 ppm; barley, 
grain at 0.30 ppm; barley, hay at 0.40 ppm; barley, straw at 0.40 ppm; 
Brassica, head and stem, subgroup 5-A at 4.5; brassica, leafy greens, 
subgroup 5-B at 3.0 ppm; caneberry subgroup 13-A at 0.35 ppm; grape at 
0.20 ppm; grape, raisin at 0.30 ppm; hop, dried cones at 0.10 ppm; and 
vegetable, leafy except Brassica, group 4 at 4.0 ppm. EPA's assessment 
of exposures and risks associated with establishing the tolerance 
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. Specific information on the studies received and the nature 
of the adverse effects caused by thiamethoxam as well as the no-
observed-adverse-effect-level (NOAEL) and the lowest-observed-adverse-
effect-level (LOAEL) from the toxicity studies can be found at https://
www.regulations.gov. The referenced document is available in the docket 
established by this action, which is described under ADDRESSES, and is 
identified as EPA-HQ-OPP-2006-0523-0003 in that docket.
    The database for thiamethoxam indicates 4 primary targets for this 
pesticide: The liver, testes, kidney, and hematopoietic system. The 
testicular effects are considered to be toxicologically significant 
effects and most of the endpoints for risk assessment are based on 
these effects. In the liver, enzyme induction and hepatocellular 
hypertrophy in and of themselves are not necessarily considered adverse 
effects. However, other effects were associated with these observations 
that are considered to be toxicologically significant. These include 
necrosis of single hepatocytes, foci of cellular alteration, apoptosis, 
Kupffer cell infiltration, pigmentation and hyperplasia, and benign and 
malignant liver tumors. The majority of the kidney effects may be 
attributed to accumulation of [alpha]2u-globulin, a protein that is 
unique to males rats (it is noted that 1 high-dose female in the 
reproduction study also had similar effects). If the effects in male 
rats are related to accumulation of [alpha]2u-globulin, then these 
particular kidney effects are not relevant to humans. The hematological 
effects are observed in three species. These include increased spleen 
weights, increases in the incidence and severity of hemosiderosis and/
or extramedullary hematopoiesis and a slight reduction in erythrocytes, 
hemoglobin and hematocrit. In the dog, leukopenia and slight microcytic 
anemia have been observed. These effects are not considered to be as 
significant as the testicular, liver, and kidney effects. They often 
appear at very high dose levels and the changes are not dramatic.
    The final rule published in the Federal Register of January 5, 2006 
https://www.epa.gov/fedrgstr/EPA-PEST/2005/January/Day-05/p089.htm) 
reported that the EPA had classified thiamethoxam as ``likely 
carcinogen for humans'' based on increased incidence of hepatocellular 
adenomas and carcinomas in male and female mice. Quantification of risk 
based on most potent unit was based on male mouse liver adenoma and/or 
carcinoma combined tumor rate. The upper bound estimate of unit risk, 
Q1* was calculated as 3.77 x 10-2 in human equivalents.
    EPA re-evaluated this determination based on new data submitted by 
the registrant indicating the mode of action for the mouse liver 
tumors. EPA agreed with the registrant that a plausible mode of action 
has been established for the development of liver tumors in a mouse 
bioassay with thiamethoxam. EPA concluded that the liver tumors in the 
mouse arise through a non-genotoxic mode of action characterized by a 
series of key events that include: Perturbation of cholesterol 
biosynthesis, hepatotoxicity, cell death (both as single cell necrosis 
and apoptosis) and a

[[Page 34404]]

sustained increase in cell replication rates. Neither the key events 
nor an increase in liver tumors are seen in rats fed on diets 
containing up to 3,000 ppm thiamethoxam. The key metabolites, CGA330050 
and CGA265307, responsible for the key events in the mouse are not 
formed in sufficient quantities in the rat and explain the lack of a 
carcinogenic response in this species.
    A sufficient amount of active metabolite must be produced along 
with persistent exposure to the active metabolite to lead to the 
hepatotoxic/regenerative proliferative/neoplastic response in the 
mouse. Limited human in vitro metabolism studies suggest that humans 
are more similar to the rat compared to the mouse in producing the 
active metabolite. The rat does not develop tumors following treatment 
with thiamethoxam. Thus, the mouse appears to be uniquely sensitive to 
this mode of action. Because of the threshold nature of the mode of 
action and the unique sensitivity of the mouse, it is concluded that 
humans are unlikely to be at risk for developing tumors following 
exposures to thiamethoxam.
    After considering EPA's Final Guidelines for Carcinogen Risk 
Assessment, the Agency classified thiamethoxam as ``Not Likely to be 
Carcinogenic to Humans'' based on convincing evidence that a non-
genotoxic mode of action for liver tumors was established in the mouse 
and that the carcinogenic effects are a result of a mode of action 
dependent on sufficient amounts of a hepatotoxic metabolite produced 
persistently. Although humans are qualitatively capable of producing 
the active metabolite, thiamethoxam is unlikely to pose a cancer risk 
to humans unless sufficient amounts of metabolites are persistently 
formed to drive a carcinogenic response. Lastly, the non-cancer 
(chronic) assessment is sufficiently protective of the key events 
(perturbation of liver metabolism, hepatotoxicity/regenerative 
proliferation) in the animal mode of action and, thus, cancer is not an 
issue. Thus, quantification of carcinogenic potential is not required.
    In assessing the human health risks associated with the existing 
and proposed uses of thiamethoxam, EPA has included exposure to 
thiamethoxam as well as its metabolite CGA-322704 when evaluating 
exposure from the dietary (food only) pathway. This approach was 
developed when the Agency received the first food-use request for 
registration of thiamethoxam and determined that the CGA-322704 
metabolite/degradate, as well as the parent compound, are residues of 
concern in food; no exposure to CGA-322704 in drinking water was 
considered likely following application of thiamethoxam. At the time, 
toxicological information regarding CGA-322704 was not available, and 
it was assumed that thiamethoxam and this metabolite are 
toxicologically equivalent for estimation of dietary risk.
    Subsequently, the Agency received a petition requesting 
registration of the insecticide clothianidin. Upon review of that 
petition, the Agency discovered that CGA-322704 and clothianidin are 
identical. With the registration of clothianidin uses, the Agency now 
has a complete toxicological database for both thiamethoxam and CGA-
322704 (referred to in the remainder of this rule as clothianidin). 
While some of the toxic effects observed following sing with the two 
active ingredients are similar, the available information indicate that 
thiamethoxam and clothianidin have different toxicological effects in 
mammals and should be assessed separately. A separate risk assessment 
of clothianidin has been completed in conjunction with the registration 
of clothianidin. The most recent assessment, which provides details 
regarding the toxicology of clothianidin are discussed in the final 
rule published in the Federal Register of December 13, 2006 (https://
www.epa.gov/EPA-PEST/2006/December/Day-13/p20898.htm).

B. Toxicological Endpoints

    For hazards that have a threshold below which there is no 
appreciable risk, the toxicological level of concern (LOC) is derived 
from the highest dose at which no adverse effects are observed (the 
NOAEL) in the toxicology study identified as appropriate for use in 
risk assessment. However, if a NOAEL cannot be determined, the lowest 
dose at which adverse effects of concern are identified (the LOAEL) is 
sometimes used for risk assessment. Uncertainty/safety factors (UF) are 
used in conjunction with the LOC to take into account uncertainties 
inherent in the extrapolation from laboratory animal data to humans and 
in the variations in sensitivity among members of the human population 
as well as other unknowns. Safety is assessed for acute and chronic 
risks by comparing aggregate exposure to the pesticide to the acute 
population adjusted dose (aPAD) and chronic population adjusted dose 
(cPAD). The aPAD and cPAD are calculated by dividing the LOC by all 
applicable uncertainty/safety factors. Short-, intermediate, and long-
term risks are evaluated by comparing aggregate exposure to the LOC to 
ensure that the margin of exposure (MOE) called for by the product of 
all applicable uncertainty/safety factors is not exceeded.
    For non-threshold risks, the Agency assumes that any amount of 
exposure will lead to some degree of risk and estimates risk in terms 
of the probability of occurrence of additional adverse cases. 
Generally, cancer risks are considered non-threshold. For more 
information on the general principles EPA uses in risk characterization 
and a complete description of the risk assessment process, see https://
www.epa.gov/fedrgstr/EPA-PEST/1997/November/Day-26/p30948.htm.
    A summary of the toxicological endpoints for thiamethoxam used for 
human risk assessment is shown in the Table of this unit .

          Summary of Toxicological Dose and Endpoints for Thiamethoxam for Use in Human Risk Assessment
----------------------------------------------------------------------------------------------------------------
                                          Dose Used in Risk
                                             Assessment,          Special FQPA SF and
          Exposure/Scenario                Interspecies and       Level of Concern for   Study and Toxicological
                                         Intraspecies and any       Risk Assessment              Effects
                                         Traditional FQPA, SF
----------------------------------------------------------------------------------------------------------------
Acute Dietary (All Populations         NOAEL = 34.5 mg/kg/day   Special FQPA SF = 1X     Rat Developmental
 including females 13-50 years of      SF = 100X..............  aPAD = acute RfD          Neurotoxicity study
 age, infants and children)            Acute RfD = 0.35 mg/kg/   Special FQPA.           LOAEL = 298.7 mg/kg/day
                                        day.                    SF = 0.35 mg/kg/day....   based on delayed
                                                                                          sexual maturation in
                                                                                          male pups, and reduced
                                                                                          brain morphometric
                                                                                          measurements.
----------------------------------------------------------------------------------------------------------------

[[Page 34405]]

 
Chronic Dietary (All populations)      NOAEL= 1.2 mg/kg/day     Special FQPA SF = 1X     2-Generation
                                       SF = 100X..............  cPAD = chronic RfD/       Reproduction study
                                       Chronic RfD = 0.012 mg/   Special FQPA SF =       LOAEL = 1.8 mg/kg/day
                                        kg/day.                  0.012 mg/kg/day.         based on increased
                                                                                          incidence and severity
                                                                                          of tubular atrophy in
                                                                                          testes of F1
                                                                                          generation males.
                                                                                         2-Generation
                                                                                          Reproduction study
                                                                                         LOAEL = 3 in males
                                                                                          based on sperm
                                                                                          abnormalities in F1
                                                                                          males. No LOAEL was
                                                                                          determined for
                                                                                          females.
----------------------------------------------------------------------------------------------------------------
Incidental Oral (All durations)        NOAEL = 8.23 mg/kg/day   LOC for MOE = 100        90-day Dog study
                                                                 (Residential)           LOAEL= 32 (males) 33.9
                                                                                          (females) mg/kg/day
                                                                                          based on slightly
                                                                                          prolonged prothrombin
                                                                                          times and decreased
                                                                                          plasma albumin and A/G
                                                                                          ratio (both sexes);
                                                                                          decreased calcium
                                                                                          levels and ovary
                                                                                          weights and delayed
                                                                                          maturation in the
                                                                                          ovaries (females);
                                                                                          decreased cholesterol
                                                                                          and phospholipid
                                                                                          levels, testis
                                                                                          weights,
                                                                                          spermatogenesis, and
                                                                                          spermatic giant cells
                                                                                          in testes (males).
----------------------------------------------------------------------------------------------------------------
Dermal (All durations) (Adults)        Oral study               LOC for MOE = 100        2-Generation
 (Residential)                         NOAEL= 1.2 mg/kg/day      (Residential)            Reproduction study
                                        (dermal absorption                               LOAEL = 1.8 mg/kg/day
                                        rate = 5%).                                       based on increased
                                                                                          incidence and severity
                                                                                          of tubular atrophy in
                                                                                          testes of F1
                                                                                          generation males.
                                                                                         2-Generation
                                                                                          Reproduction study
                                                                                          (46402904)
                                                                                         LOAEL = 3 in males
                                                                                          based on sperm
                                                                                          abnormalities in F1
                                                                                          males. No LOAEL was
                                                                                          determined for
                                                                                          females.
----------------------------------------------------------------------------------------------------------------
Dermal (All durations) (Infants/       Dermal study             LOC for MOE = 100        Rat 28-Day Dermal
 children 1-6 years old)               NOAEL = 60 mg/kg/day      (Residential)            Toxicity study
 (Residential)                          (dermal absorption                               LOAEL = 250 (females)
                                        rate = 5%.                                        mg/kg/day based on
                                                                                          increased plasma
                                                                                          glucose, triglyceride
                                                                                          levels, and alkaline
                                                                                          phosphatase activity
                                                                                          and inflammatory cell
                                                                                          infiltration in the
                                                                                          liver and necrosis of
                                                                                          single hepatocytes in
                                                                                          females.
----------------------------------------------------------------------------------------------------------------
Inhalation (All durations)             Oral study               LOC for MOE = 100        2-Generation
 (Residential)                         NOAEL = 1.2 mg/kg/day     (Residential)            Reproduction study
                                        (inhalation absorption                           LOAEL = 1.8 mg/kg/day
                                        rate = 100%).                                     based on increased
                                                                                          incidence and severity
                                                                                          of tubular atrophy in
                                                                                          testes of F1
                                                                                          generation males.
                                                                                         2-Generation
                                                                                          Reproduction study
                                                                                          (46402904)
                                                                                         LOAEL = 3 in males
                                                                                          based on sperm
                                                                                          abnormalities in F1
                                                                                          males. No LOAEL was
                                                                                          determined for
                                                                                          females.
----------------------------------------------------------------------------------------------------------------
Cancer (oral, dermal, inhalation)       ``Not Likely to be Carcinogenic to Humans'' based on convincing evidence
                                         that a non-genotoxic mode of action for liver tumors was established in
                                          the mouse and that the carcinogenic effects are a result of a mode of
                                           action dependent on sufficient amounts of a hepatotoxic metabolite
                                          produced persistently. Quantification of cancer risk is not required.
----------------------------------------------------------------------------------------------------------------

C. Exposure Assessment

    1. Dietary exposure from food and feed uses. In evaluating dietary 
exposure to thiamethoxam, EPA considered exposure under the petitioned-
for tolerances as well as all existing thiamethoxam tolerances in (40 
CFR 180.565). EPA assessed dietary exposures from thiamethoxam in food 
as follows:
    For both acute and chronic exposure assessments EPA combined 
residues of clothianidin coming from thiamethoxam with residues of 
thiamethoxam per se. As discussed above, thiamethoxam's major 
metabolite is CGA-322704, which is also the registered active 
ingredient clothianidin. There is available information indicating that 
thiamethoxam and clothianidin have different toxicological effects in 
mammals and should be assessed separately, however, these exposure 
assessments for this action incorporated the total residue of 
thiamethoxam and clothianidin to estimate dietary exposure. This 
aggregation of thiamethoxam and clothianidin began with the initial 
assessment of thiamethoxam, prior to the requested registration of 
clothianidin as an active ingredient, and is being maintained in this 
action for historical purposes. In future assessments, as time and 
resources allow, the EPA will provide a rationale for the separate 
analysis of risks coming from thiamethoxam and clothianidin, and will 
conduct separate evaluations of exposure and risk for each chemical. 
The combining of these residues, as was done in these assessments, 
results in highly

[[Page 34406]]

conservative estimates of dietary exposure and risk.
    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. In estimating acute dietary 
exposure, EPA used food consumption information from the USDA 1994-1996 
and 1998 Nationwide Continuing Surveys of Food Intake by Individuals 
(CSFII). As to residue levels in food, EPA assumed maximum residues of 
thiamethoxam and clothianidin observed in the thiamethoxam field 
trials. It was also assumed that 100% of crops with registered or 
requested uses of thiamethoxam are treated.
    ii. Chronic exposure. In conducting the chronic dietary exposure 
assessment EPA used the food consumption data from the USDA 1994-1996 
and 1998 Nationwide CSFII. As to residue levels in food, EPA assumed 
maximum residues of thiamethoxam and clothianidin observed in the 
thiamethoxam field trials. It was also assumed that 100% of crops with 
registered or requested uses of thiamethoxam are treated.
    A complete listing of the inputs used in these assessments can be 
found in the document titled Thiamethoxam Acute and Chronic Aggregate 
Dietary and Drinking Water Exposure and Risk Assessments for FIFRA 
Section 3 Registration available in the docket established by this 
action EPA-HQ-OPP-2006-0523.
    iii. Cancer. A quantitative cancer exposure assessment is not 
necessary because EPA concluded that thiamethoxam is ``Not Likely to be 
Carcinogenic to Humans'' based on convincing evidence that a non-
genotoxic mode of action for liver tumors was established in the mouse 
and that the carcinogenic effects are a result of a mode of action 
dependent on sufficient amounts of a hepatotoxic metabolite produced 
persistently. Therefore, the Agency concluded that thiamethoxam is not 
expected to pose a carcinogenic risk and an exposure assessment 
pertaining to cancer risk is not necessary.
    2. Dietary exposure from drinking water. Thiamethoxam is expected 
to be persistent and mobile in terrestrial and aquatic environments. 
These fate properties suggest that thiamethoxam has a potential to move 
into surface water and shallow ground water.
    The Agency lacks sufficient monitoring data to complete a 
comprehensive dietary exposure analysis and risk assessment for 
thiamethoxam in drinking water. Because the Agency does not have 
comprehensive monitoring data, drinking water concentration estimates 
are made by reliance on simulation or modeling taking into account data 
on the environmental fate characteristics of thiamethoxam. Further 
information regarding EPA drinking water models used in pesticide 
exposure assessment can be found at https://www.epa.gov/oppefed1/models/
water/index.htm.
    Based on the Pesticide Root Zone Model/Exposure Analysis Modeling 
System (PRZM/EXAMS) and Screening Concentrations in Groundwater (SCI-
GROW) models, the estimated environmental concentrations (EECs) of 
thiamethoxam for acute exposures are estimated to be 12.26 parts per 
billion (ppb) for surface water and 7.94 ppb for ground water. The EECs 
for chronic exposures are estimated to be 1.29 ppb for surface water 
and 7.94 ppb for ground water.
    The registrant has conducted small-scale prospective ground water 
studies in several locations in the U.S. to investigate the mobility of 
thiamethoxam in a vulnerable hydrogeological setting. A review of those 
data shows that generally residues of thiamethoxam as well as CGA-
322704 are below the limit of quantitation (0.05 ppb). When 
quantifiable residues are found, they are sporadic and at low levels. 
The maximum observed residue levels from any monitoring well were 1.0 
ppb for thiamethoxam and 0.73 ppb for CGA-322704. These values are well 
below the modeled estimates summarized above, indicating that the 
modeled estimates are, in fact, protective of what actual exposures are 
likely to be.
    Modeled estimates of drinking water concentrations were directly 
entered into the dietary exposure model. For both the acute and chronic 
assessments the acute EEC of 12.26 ppb (0.0123 ppm) was used as a 
worst-case estimate of exposure via drinking water.
    3. From non-dietary exposure. The term ``residential exposure'' is 
used in this document to refer to non-occupational, non-dietary 
exposure (e.g., for lawn and garden pest control, indoor pest control, 
termiticides, and flea and tick control on pets).
    Thiamethoxam is registered for use on turfgrass on golf courses, 
residential lawns, commercial grounds, parks, playgrounds, athletic 
fields, landscapes, interiorscapes and sod farms. Thiamethoxam is 
applied by commercial applicators only. Therefore, exposures resulting 
from homeowner applications were not assessed. However, entering areas 
previously treated with thiamethoxam could lead to exposures for adults 
and children. As a result, risk assessments have been completed for 
postapplication scenarios. Short-term exposures (1 to 30 days of 
continuous exposure) may occur as a result of activities on treated 
turf. There are no use patterns for thiamethoxam that indicate 
intermediate-term (1 to 6 months of continuous exposure) or chronic 
non-dietary exposures are likely to occur.
    Dermal exposures were assessed for adults and children. Oral non-
dietary ingestion exposures (i.e. soil ingestion, and hand-/object-to-
mouth) were assessed for children as well. Since all postapplication 
scenarios occur outdoors the potential for inhalation exposure is 
negligible and therefore does not require an inhalation exposure 
assessment. For purposes of this assessment exposure from residential 
lawns is used to represent the worst case scenario for both dermal and 
oral postapplication exposure.
    Postapplication dermal exposure resulting from contact with treated 
turf was assessed using the HED Standard Operating Procedures for 
Residential Exposure and a chemical-specific turf transfer residue 
(TTR) study.
    4. Cumulative effects from substances with a common mechanism of 
toxicity. Section 408(b)(2)(D)(v) of the 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.''
    Thiamethoxam is a member of the neonicotinoid class of pesticides 
and produces, as a metabolite, another neonicotinoid, clothianidin. 
Structural similarities or common effects do not constitute a common 
mechanism of toxicity. Evidence is needed to establish that the 
chemicals operate by the same, or essentially the same sequence of 
major biochemical events (EPA, 2002). Although clothianidin and 
thiamethoxam bind selectively to insect nicotinic acetylcholine 
receptors (nAChR), the specific binding site(s)/receptor(s) for 
clothianidin, thiamethoxam, and the other neonicotinoids are unknown at 
this time. Additionally, the commonality of the binding activity itself 
is uncertain, as preliminary evidence suggests that clothianidin 
operates by direct competitive inhibition, while thiamethoxam is a non-
competitive inhibitor. Furthermore, even if future research shows that 
neonicotinoids share a common binding activity to a

[[Page 34407]]

specific site on insect nicotinic acetylcholine receptors, there is not 
necessarily a relationship between this pesticidal action and a 
mechanism of toxicity in mammals. Structural variations between the 
insect and mammalian nAChRs produce quantitative differences in the 
binding affinity of the neonicotinoids towards these receptors, which, 
in turn, confers the notably greater selective toxicity of this class 
towards insects, including aphids and leafhoppers, compared to mammals. 
While the insecticidal action of the neonicotinoids is neurotoxic, the 
most sensitive regulatory endpoint for thiamethoxam is based on 
unrelated effects in mammals, including effects on the liver, kidney, 
testes, and hematopoietic system. Additionally, the most sensitive 
toxicological effect in mammals differs across the neonicotinoids 
(e.g., testicular tubular atrophy with thiamethoxam; mineralized 
particles in thyroid colloid with imidaclopid). Thus, there is 
currently no evidence to indicate that neonicotinoids share common 
mechanisms of toxicity, and EPA is not following a cumulative risk 
approach based on a common mechanism of toxicity for the 
neonicotinoids. 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 the policy statements 
concerning common mechanism determinations and procedures for 
cumulating effects from substances found to have a common mechanism 
released by EPA's Office of Pesticide Programs on EPA's website at 
https://www.epa.gov/pesticides/cumulative/.

D. Safety Factor for Infants and Children

    1. In general. Section 408 of FFDCA provides that EPA shall apply 
an additional (10X) tenfold 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 data base 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. In applying 
this provision, EPA either retains the default value of 10X when 
reliable data do not support the choice of a different factor, or, if 
reliable data are available, EPA uses a different additional FQPA 
safety factor value based on the use of traditional uncertainty/safety 
factors and/or special FQPA safety factors, as appropriate.
    2. Prenatal and postnatal sensitivity. In the developmental 
studies, there is no evidence of increased quantitative or qualitative 
susceptibility of rat or rabbit fetuses to in utero exposure to 
thiamethoxam. The developmental NOAELs are either higher than or equal 
to the maternal NOAELs. The toxicological effects in fetuses do not 
appear to be any more severe than those in the dams or does. In the rat 
developmental neurotoxicity study, there was no quantitative evidence 
of increased susceptibility.
    There is evidence of increased quantitative susceptibility for male 
pups in both 2-generation reproductive studies. In one study, there are 
no toxicological effects in the dams whereas for the pups, reduced 
bodyweights are observed at the highest dose level, starting on day 14 
of lactation. This contributes to an overall decrease in bodyweight 
gain during the entire lactation period. The reproductive effects in 
males appear in the F1 generation in the form of increased incidence 
and severity of testicular tubular atrophy (see developmental/
reproductive section). These data are considered to be evidence of 
increased quantitative susceptibility for male pups (increased 
incidence of testicular tubular atrophy at 1.8 mg/kg/day) when compared 
to the parents (hyaline changes in renal tubules at 61 mg/kg/day; NOAEL 
is 1.8 mg/kg/day).
    In the more recent 2-generation reproduction study, the most 
sensitive effect was sperm abnormalities at 3 mg/kg/day (the NOAEL is 
1.2 mg/kg/day) in the F1 males. This study also indicates increased 
susceptibility for the offspring for this effect.
    Although there is evidence of increased quantitative susceptibility 
for male pups in both reproductive studies, NOAELs and LOAELs were 
established in these studies and the Agency selected the NOAEL for 
testicular effects in F1 pups as the basis for risk assessment. The 
Agency has confidence that the NOAEL selected for risk assessment is 
protective of the most sensitive effect (testicular effects) for the 
most sensitive subgroup (pups) observed in the toxicological 
database.Due to the finding of quantitative sensitivity in the 
reproduction studies, the EPA conducted a degree of concern analysis to 
assess the residual uncertainties for prenatal and/or postnatal 
susceptibility. The Agency concluded that there is low concern for an 
increased susceptibility in the young given:
    i. There was no increased sensitivity (qualitative or quantitative) 
in the rat developmental, rabbit developmental and rat developmental 
neurotoxicity studies; and
    ii. There was a clear NOAEL identified for the effects in pups in 
the rat reproduction studies where sensitivity was seen; and
    iii. The Agency selected this NOAEL as the basis for risk 
assessment.
    3. Conclusion. The final rule published in the Federal Register of 
January 5, 2006 (https://www.epa.gov/fedrgstr/EPA-PEST/2005/January/Day-
05/p089.htm) reported that the EPA had determined that the 10X special 
safety factor to protect infants and children should be retained for 
thiamethoxam based on the following factors: Effects on endocrine 
organs observed across species; the significant decrease in alanine 
amino transferase levels in the companion animal studies and in the dog 
studies; the mode of action of this chemical in insects (interferes 
with the nicotinic acetyl choline receptors of the insect's nervous 
system); the transient clinical signs of neurotoxicity in several 
studies across species; and the suggestive evidence of increased 
quantitative susceptibility in the rat reproduction study.
    Since that determination the EPA has received and reviewed a 
Developmental Neurotoxicity (DNT) study in rats and an additional 
Reproduction study in rats. Taking the results of these studies into 
account, EPA has determined that reliable data show that it would be 
safe for infants and children to reduce the FQPA safety factor to 1X. 
That decision is based on the following findings:
    i. The toxicity database for thiamethoxam is complete.
    ii. For the reasons discussed above, there is low concern for an 
increased susceptibility in the young.
    iii. Although there is evidence of neurotoxicity after acute 
exposure to thiamethoxam at doses of 500 mg/kg/day including drooped 
palpebral closure, decrease in rectal temperature and locomotor 
activity and increase in forelimb grip strength, no evidence of 
neuropathology was observed. These effects occurred at doses at least 
14-fold and 416-fold higher than the doses used for the acute, and 
chronic risk assessments, respectively; thus, there is low concern for 
these effects since it is expected that the doses used for regulatory 
purposes would be protective of the effects noted at much higher doses.
    iv. There are no residual uncertainties identified in the exposure 
databases. The dietary food exposure assessments were performed based 
on assumption that the maximum residues of thiamethoxam and 
clothianidin observed in the thiamethoxam field

[[Page 34408]]

trials were remaining on crops. Although there is available information 
indicating that thiamethoxam and clothianidin have different 
toxicological effects in mammals and should be assessed separately, the 
residues of each have been combined in these assessments to ensure that 
the estimated exposures of thiamethoxm do not underestimate actual 
potential thiamethoxam exposures. An assumption of 100% crop treated 
was made for all foods evaluated in the assessments. For both the acute 
and chronic assessments the acute EEC of 12.26 ppb (0.0123 ppm) was 
used as a worst-case estimate of exposure via drinking water. Compared 
to the results from small-scale prospective ground water studies where 
the maximum observed residue levels from any monitoring well were 1.0 
ppb for thiamethoxam and 0.73 ppb for CGA-322704, the modeled estimates 
are protective of what actual exposures are likely to be. Similarly 
conservative Residential SOPs as well as a chemical-specific turf 
transfer residue (TTR) study were used to assess post-application 
exposure to children as well as incidental oral exposure of toddlers. 
These assessments will not underestimate the exposure and risks posed 
by thiamethoxam.

E. Aggregate Risks and Determination of Safety

    Safety is assessed for acute and chronic risks by comparing 
aggregate exposure to the pesticide to the acute population adjusted 
dose (aPAD) and chronic population adjusted dose (cPAD). The aPAD and 
cPAD are calculated by dividing the LOC by all applicable uncertainty/
safety factors. For linear cancer risks, EPA calculates the probability 
of additional cancer cases given aggregate exposure. Short-, 
intermediate, and long-term risks are evaluated by comparing aggregate 
exposure to the LOC to ensure that the margin of exposure (MOE) called 
for by the product of all applicable uncertainty/safety factors is not 
exceeded.
    1. Acute risk. Using the exposure assumptions discussed in this 
unit for acute exposure, the acute dietary exposure from food and water 
to thiamethoxam will occupy 3% 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 exposure to 
thiamethoxam from food and water will utilize 42% of the cPAD for 
children 1-2 years old, the population group with greatest exposure. 
Based on the use patterns proposed, chronic residential exposure to 
residues of thiamethoxam is not expected.
    3. Short-term risk. Short-term aggregate exposure takes into 
account residential exposure plus chronic exposure to food and water 
(considered to be a background exposure level).
    Thiamethoxam is currently registered for use that could result in 
short-term residential exposure and the Agency has determined that it 
is appropriate to aggregate chronic food and water and short-term 
exposures for thiamethoxam. The level of concern for the margin of 
exposure (MOE) is 100 for all residential uses (i.e., MOEs less than 
100 indicate potential risks of concern). Using the exposure 
assumptions described in this unit for short-term exposures, EPA has 
concluded that food, water, and residential exposures aggregated result 
in aggregate MOEs of 730 through 2,800 for all exposure scenarios 
(dermal exposures, and oral non-dietary ingestion) for infants, 
children and adults.
    4. Intermediate-term risk. Intermediate-term aggregate exposure 
takes into account residential exposure plus chronic exposure to food 
and water (considered to be a background exposure level). There are no 
use patterns for thiamethoxam that indicate intermediate-term (1 to 6 
months of continuous exposure) exposures are likely to occur.
    5. Aggregate cancer risk for U.S. population. The Agency has 
classified thiamethoxam as not likely to be a human carcinogen based on 
convincing evidence that a non-genotoxic mode of action for liver 
tumors was established in the mouse and that the carcinogenic effects 
are a result of a mode of action dependent on sufficient amounts of a 
hepatotoxic metabolite produced persistently. Thiamethoxam is not 
expected to pose a cancer risk.
    6. 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 thiamethoxam residues.

IV. Other Considerations

A. Analytical Enforcement Methodology

    Adequate enforcement methodology (high-performance liquid 
chromatography/ultraviolet (HPLC/UV) or mass spectrometry (MS) 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; e-mail address: residuemethods@epa.gov.

B. International Residue Limits

    There are no CODEX or Mexican maximum residue limits (MRLs) for 
thiamethoxam. A number of Canadian MRLs exist for this chemical and are 
in accord with U.S. tolerances. The new/revised tolerances established 
by this rule have been derived using the NAFTA Tolerance Harmonization 
Spreadsheet.

C. Response to Comments

    Several comments were received from a private citizen objecting to 
establishment of these tolerances. The Agency has received similar 
comments from this commenter on numerous previous occasions. Refer to 
Federal Register 70 FR 37686 (June 30, 2005), 70 FR 1354 (January 7, 
2005), 69 FR 63096-63098 (October 29, 2004) for the Agency's response 
to these objections. In addition, the commenter noted several adverse 
effects seen in animal toxicology studies with thiamethoxam and claims 
because of these effects no tolerance should be approved. EPA has 
found, however, that there is a reasonable certainty of no harm to 
humans after considering these toxicological studies and the exposure 
levels of humans to thiamethoxam.

V. Conclusion

    Based upon review of the data supporting and use of the NAFTA 
Tolerance Harmonization Spreadsheet the EPA has determined that 
tolerance levels for the following crops should be changed as follows: 
Artichoke, globe from 0.40 ppm to 0.45 ppm; caneberry subgroup 13-A 
from 0.30 ppm to 0.35 ppm; grape from 0.15 ppm to 0.20 ppm; brassica, 
head and stem, subgroup 5-A from 1.0 ppm to 4.5 ppm; brassica, leafy 
greens, subgroup 5-B from 2.0 ppm to 3.0 ppm; and vegetable, leafy, 
except brassica from 2.0 ppm to 4.0 ppm. EPA has also determined that a 
separate tolerance for grape juice is not needed since any residues in 
grape juice are not expected to exceed the grape tolerance of 0.20 ppm. 
Therefore, tolerances are established for the combined residues of 
thiamethoxam [3-[(2-chloro-5-thiazolyl)methyl]tetrahydro-5-methyl- N -
nitro-4H-1,3,5-oxadiazin-4-imine and its metabolite [N-(2-chloro-
thiazol-5-ylmethyl)-N'-methyl-N'-nitro-guanidine] on artichoke, globe 
at 0.45 ppm; barley, grain at 0.30 ppm; barley, hay at 0.40 ppm; 
barley, straw at 0.40 ppm; brassica, head and stem, subgroup 5-A at 
4.5; brassica, leafy greens, subgroup

[[Page 34409]]

5-B; caneberry subgroup 13-A at 0.35 ppm; grape at 0.20 ppm; grape, 
raisin at 0.30 ppm; hop, dried cone at 0.10 ppm; and vegetable, leafy 
except brassica, group 4 at 4.0 ppm.

VI. Statutory and Executive Order Reviews

    This final rule establishes a tolerance under section 408(d) of 
FFDCA 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 rule has been 
exempted from review under Executive Order 12866, this rule is not 
subject to Executive Order 13211, 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 section 408(d) of FFDCA, 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 section 
408(n)(4) of FFDCA. 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 6, 
2000) do not apply to this rule. In addition, This 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) (Public Law 
104-4).
    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), Public Law 104-113, section 12(d) (15 U.S.C. 272 
note).

VII. Congressional Review Act

    The Congressional Review Act, 5 U.S.C. 801 et seq., generally 
provides that before a rule may take effect, the agency promulgating 
the rule must submit a rule report to each House of the Congress and to 
the Comptroller General of the United States. 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 this final rule in the Federal 
Register. This final rule 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: June 6, 2007.
Lois Rossi,
Director, Registration Division, Office of Pesticide Programs.

0
Therefore, 40 CFR chapter I is amended as follows:

PART 180--AMENDED

0
1. The authority citation for part 180 continues to read as follows:

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

0
2. Section 180.565 is amended as follows:
0
i. In paragraph (a) by alphabetically adding commodities to the table;
0
ii. In paragraph (a) by revising the entries for Barley, grain; Barley, 
hay and Barley, straw in the table;
0
iii. In paragraph (b) by removing the entries for Artichoke, globe; 
Bean, dry , seed; Bean, succulent; and Hops in the table.
    The amendment read as follows:


Sec.  180.565  Thiamethoxam; tolerances for residues.

    (a) * * *

------------------------------------------------------------------------
                                                              Parts per
                         Commodity                             million
------------------------------------------------------------------------
Artichoke, globe...........................................         0.45
Barley, grain..............................................         0.30
Barley, hay................................................         0.40
Barley, straw..............................................         0.40
                                * * * * *
Brassica, head and stem, subgroup 5-A......................          4.5
Brassica, leafy greens, subgroup 5-B.......................          3.0
                                * * * * *
Caneberry subgroup 13-A....................................         0.35
                                * * * * *
Grape......................................................         0.20
Grape, raisin..............................................         0.30
                                * * * * *
Hop, dried cones...........................................         0.10
                                * * * * *
Vegetable, leafy, except brassica, group 4.................          4.0
------------------------------------------------------------------------

* * * * *
[FR Doc. E7-11794 Filed 6-21-07; 8:45 am]
BILLING CODE 6560-50-S