Document ID: EPA-HQ-OPP-2014-0232-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2014-12-17T05:00Z

EPA REGISTRATION DIVISION - COMPANY NOTICE OF FILING FOR PESTICIDE PETITION 

EPA Registration Division contact: Sidney Jackson, (703) 305-7610

Interregional Research Project Number 4 (IR-4)

Pesticide Petition Number: PP# 4E8241

 EPA has received a pesticide petition (PP# 4E8241) from Interregional Research Project Number 4 (IR-4), 500 College Road East, Princeton, NJ 08540 proposing, pursuant to section 408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 CFR part 180 by establishing a tolerance for residues of  novaluron in or on the raw agricultural commodities Avocado at 0.60 parts per million (ppm), Carrot at 0.05 ppm, Bean at 0.60 ppm, Vegetable, fruiting, group 8-10 at 1.0 ppm, Fruit, pome, group 11-10 at 2.0 ppm, Cherry subgroup 12-12A at 8.0 ppm, Peach subgroup 12-12B at 1.9 ppm, and Plum subgroup 12-12C at 1.9 ppm.  In addition, the petitioner proposes based upon the establishment of new tolerances above, removal of existing tolerances at 40 CFR 180.598 on Bean, succulent, snap at 0.60 ppm, Bean,  dry, seed at 0.30 ppm, Cherry at 8.0 ppm, Fruit, pome, group 11 at 2.0 ppm, Fruit, stone, group 12, except cherry at 1.9 ppm, Vegetable, fruiting, group 8 at 1.0 ppm, cocona at 1.0 ppm, African  eggplant at 1.0 ppm, pea eggplant at 1.0 ppm, scarlet eggplant at 1.0 ppm, goji berry at 1.0 ppm, garden huckleberry at 1.0 ppm, martynia at 1.0 ppm, naranjilla at 1.0 ppm, okra at 1.0 ppm, roselle at 1.0 ppm, sunberry at 1.0 ppm, bush tomato at 1.0 ppm, currant tomato at 1.0 ppm, and  tree  tomato at 1.0 ppm.

EPA has determined that the petition contains data or information regarding the elements set forth in section 408 (d)(2) of the FDDCA; however, EPA has not fully evaluated the sufficiency of the submitted data at this time or whether the data support granting of the petition. Additional data may be needed before EPA rules on the petition.

A. Residue Chemistry

	1. Plant and Livestock metabolism. The qualitative nature of the residue of novaluron in plants is adequately understood based on acceptable plant metabolism studies reflecting its uses on apples, cabbage, cotton, and potatoes. These plant metabolism studies have demonstrated that novaluron does not metabolize and is non-systemic (does not translocate within the plant). The results observed in the plant and livestock metabolism studies show similar metabolic pathways. The residue of concern, which should be regulated, is the parent compound, novaluron only. 

	2. Analytical method. An adequate analytical enforcement method, gas chromatography/electron capture detector (GC/ECD) and a high performance liquid chromatography/ultraviolet method (HPLC/UV) for enforcing tolerances of novaluron residues in or on different matrices are available, as published in the Federal Register of January 27, 2010 (Volume 75, Number  17; FRL-8807-2).

A method validation was conducted both prior to sample analysis and concurrently with sample analysis determining that the method recoveries were in the proper range. For avocado the LOD for the method was calculated to be 0.00839 ppm and the LOQ was calculated to be 0.0252 ppm. For carrot the LOD for the method was calculated to be 0.0175 ppm and the LOQ was calculated to be 0.0524 ppm. For bean, the LOD for the method was calculated to be 0.013 ppm and the LOQ was calculated to be 0.039 ppm. For cucumber the LOD for the method was calculated to be 0.0091 ppm and the LOQ was calculated to be 0.027 ppm. The lowest level of method validation (LLMV) for these commodities was 0.05 ppm.

	3. Magnitude of residues. Residue trials were conducted to support the tolerances requested above including the following: 

   oo Avocado: A total of 6 field trials were conducted in NAFTA Regions. 
   oo Carrot: A total of 8 field trials were conducted in NAFTA Regions. 
   oo Bean: A total of 6 field trials were conducted in NAFTA Regions.
   oo Greenhouse grown cucumber: A total of 4 field trials were conducted in NAFTA Regions.

B. Toxicological Profile

	1. Acute toxicity. In an acute oral toxicity study in rats, novaluron had an LD50  >5,000 mg/kg. A dermal toxicity study in rats resulted in an LD50  greater than 2,000 mg/kg. The LC50 for acute inhalation in rats was great.er than 5.15 mg/I. In rabbits, novaluron is not a skin irritant, but it is a mild eye irritant. Novaluron is not a sensitizer in guinea pigs.

	2. Genotoxicty. The mutagenic potential of novaluron was investigated in several in vivo and in vitro studies. Results in two Ames assays, an in vivo mouse micronucleus assay, an in vitro unscheduled DNA synthesis (UDS) assay, an in vitro cell mutation assay, and an in vitro human lymphocyte clastogenicity test were negative. Novaluron is therefore considered to have no potential to induce mutagenicity.

	3. Reproductive and developmental toxicity. i. A two generation rat reproduction study was conducted with dose levels of 1,000, 4,000, and 12,000 ppm (74.2, 297.5, 894.9 mg/kg/day, and 84, 336.7, 1,009.8 mg/kg/day for males and females, respectively). Maternal and offspring toxicity was evidenced by increased absolute and relative spleen weights, whereas reproductive toxicity was observed only in males at 297.5 mg/kg/day (LOAEL) based on decreased epididymal sperm counts and increased age at preputial separation in the F1 generation. The no observed adverse effect level (NOAC) in males was 1,000 ppm (74.2 mg/kg/day) and in females it was 12,000 ppm (109.8 mg/kg/day).

ii. Teratology studies were conducted in the rat and rabbit. No treatment related mortalities were observed in either study. No effect on survival, development or growth of fetuses was noted in either species in either study. No maternal or developmental toxicity was observed up to and including the limit dose of 1,000 mg/kg/day (NOAEL). These two studies demonstrate that novaluron was not teratogenic in either rats or rabbits.

	4. Subchronic toxicity. Rats, mice and dogs all show the same toxicological response. Generally, novaluron induces small increases in methemoglobin; red cells are sequestered; and, compensatory hematopoiesis occurs. The severity of these changes is well within the physiological capacity of the animals and is judged not adverse.

Rats treated topically with novaluron in a 28-day study at 0, 75, 400 and 1,000 mg/kg/day did not show signs of systemic toxicity. Small treatment-related increases in methemoglobin were seen in both sexes at 1,000 mg/kg/day and in females at 400 mg/kg/day. The highest methemoglobin value seen in females was 1.28% compared with 0.86% in controls. Organ weights, macroscopic and microscopic examination of organs and tissues did not reveal any treatment-related changes. 

Two 13-week rat studies were conducted. In one study, doses were administered at 50, 100, 200, 400 ppm (3.52, 6.93, 13.83, 27.77 mg/kg/day and 4.38, 8.64, 17.54 and 34.39 mg/kg/day for males and females, respectively). The LOAELs from the combined results were 27.77 mg/kg/day in males based on increased occurrence of extramedullary hematopoiesis and hemosiderosis in spleen; and 8.64 mg/kg/day in females based on reduction in hemoglobin, hematocrit and RBC count; increased occurrence of extramedullary hematopoiesis and hemosiderosis in spleen and liver. The NOAEL was 4.38 mg/kg/day. 

A 13-week mouse study was conducted with dose levels of 30, 100, 1,000, 10,000 ppm (4.2, 12.8, 135.9, 1,391.9 and 4.7, 15.2, 135.6, 1,493.1 mg/kg/day, for males and females, respectively). The NOAEL was determined to be 100 ppm (12.8 and 15.2 mg/kg/day, male and females, respectively). The LOAEL was 1,000 ppm (135.9 and 135.6 mg/kg/day, males and females, respectively) based on increased body weight gain, low erythrocyte counts, and secondary splenic changes. There were no clinical treatment-related signs noted.

Two 13-week dog studies were conducted. One study resulted in an NOAEL of 100 mg/kg/day and a LOAEL of 300 mg/kg/day based on low erythrocyte counts and secondary splenic and liver changes. No clinical treatment-related signs were noted. Another study was conducted using only one dose level of 10 mg/kg/day. There were no clinical or histopathological treatment-related signs and the NOAEL was determined to be 10 mg/kg/day. Acute and subchronic neurotoxicity screening batteries were performed with novaluron in rats. Novaluron is not considered neurotoxic, since effects observed in the acute neurotoxicity study were observed at the limit dose only and were not reproduced at similar, repeated doses in the subchronic neurotoxicity study (0, 17.5/20.5, 174/207, 1752/2000 mg/kg/day Male/Female). No signs of neurotoxicity or neuropathology were observed following, repeated dosing in the subchronic neurotoxicity study in rats or in any other subchronic or chronic toxicity study in rats, mice or dogs.]

	5. Chronic toxicity. i. Chronic toxicity and oncogenicity was evaluated in the rat, mouse and dog. The rat chronic toxicity and oncogenicity was conducted with dose levels of 25, 700, 20,000ppm (1.1, 30.6, 884.2 and 1.4, 39.5, 1,113.5 mg/kg/day for males and females, respectively). The LOAEL in male and female rats was 30.6 and 39.5 mg/kg/day, respectively, based on evidence of erythrocyte damage and turnover resulting in a regenerative anemia in both sexes. The corresponding NOAEL was 25 ppm (1.1 and 1.4 mg/kg/day for male and female rats, respectively). There was no evidence of carcinogenicity in this study. A mouse chronic toxicity study was conducted with dose ·revels of 30, 450, 7,000 ppm (3.6, 53.4, 800.0 and 4.3, 63.3, 913.4 mg/kg/day for males and females, respectively). The LOAEL in male and female mice was 53.4 and 63.3 mg/kg/day, respectively, based on erythrocyte turnover due to hemoglobin oxidation and resulting in a compensated anemia. The corresponding NOAEL was 30 ppm (3.6 and 4.3 mg/kg/day for male and female mice, respectively). There was also no evidence of carcinogenicity in this study. Chronic toxicity was investigated in dogs using dose levels of 10, 100, 1,000 mg/kg/day. The NOAEL of 100 mg/kg/day was based on methemoglobin.

ii. The chronic reference dose (cRfD) of 0.011 mg/kg/day has been established on the basis of the chronic carcinogenicity study in rats. An uncertainty factor (UF) of 100 was applied to the NOAEL of 1.1 mg/kg/day for male rats deriving to the cRfD.

iii. In accordance with the EPA Draft Guidelines for Carcinogen Risk Assessment (July
1999), novaluron is classified as not likely to be carcinogenic to humans due to results of oncogenicity studies that show no evidence of carcinogenicity in rats and mice.

<	6. Animal metabolism. Metabolism studies in rats and goats were conducted with the parent material labeled in both the difluorophenyl and chlorophenyl moieties. Rats absorb little novaluron when it is administered orally. More than 90% of the dietary administered [chlorophenyl [14]C(U)] novaluron is recovered in the feces. When the difluorophenyl ring of the molecule is labeled, the recovered [14]C activity in the feces is lower but still above 75%. The difference is thought to reflect intestinal metabolism by microbial flora and the higher absorption of the difluorophenyl metabolites.

The parent molecule as well as its degradates are absorbed from the gastrointestinal tract. All parent material is metabolized either upon initial entry into the systemic circulation or, if sequestered to the fat, upon its depuration back to the systemic circulation. There is no intact novaluron found in the urine. Novaluron's high octanol-water partition coefficient is responsible for its preferential movement to fat. The half-life in fat calculated from the rat metabolism study is approximately 55 hours. 

Two groups of metabolites are formed after oral administration of novaluron. One group is typified by the aniline metabolite 3-chloro-4-(1, 1,2-trifluoro-2-trifluoromethoxyethoxy) aniline, referred to as 3-TFA. The other group of metabolites is typified by 2,6-difluorobenzoic acid is from the difluorophenyl moiety of the molecule. Nearly all the metabolites are formed at a level of 1 % or less of the applied dose. These metbolites are rapidly excreted.

The metabolism in goats and hens mimics that seen in rats.>

	7. Metabolite toxicology. Makhteshim-Agan of North America Inc., has determined that there are no metabolites of toxicological concern and therefore, no metabolites need to be included in the tolerance expression and require regulation. The residues of concern in drinking water for purpose of risk assessment are novaluron, the chlorophenyl urea degradate (1-[3-chloro-4-(1, 1,2-trifluoro-2- trifluoromethoxyethoxy)phenyl]urea), and the chloroaniline metabolite (3-chloro-4-(1, 1,2- trifluoro-2-trifluoromethoxyethoxy)aniline).

	8. Endocrine disruption. No special studies investigating potential estrogenic or other endocrine effects of novaluron have been conducted. However, inspection of in-life data from toxicology studies indicates that novaluron is not an endocrine disruptor. Specifically, endocrine organ weights (e.g., thyroid, testes, ovaries, pituitary from the two-generation study) were not adversely affected by novaluron. Milestones of sexual development were not affected by novaluron; and, reproduction was not adversely affected. Based on these observations, novaluron does not have an adverse effect on the endocrine system.

C. Aggregate Exposure

	1. Dietary exposure. For novaluron, only chronic exposures are of interest because there is no acute toxicity endpoint of concern. The dietary exposure from the recent 2013 EPA assessment for peanut and soybean considered exposure of all existing novaluron tolerances in 40 CFR 180.598. Tolerances for bean, snap, succulent, dry, seed; for vegetable, fruiting, group 8; for fruit, pome, group 11; for cherry; and for fruit, stone, group 12, except cherry have previously been established and the updates to the crop grouping is not likely to influence assessment calculations. As well, the contribution of carrot and avocado are not likely to result in dietary exposures at a level of concern for any subpopulation. The July 2013 assessment noted the following conclusions.

i. Food. Acute Dietary Exposure. No toxicological endpoint attributable to a single exposure was identified in the available toxicology studies, including the rat and rabbit developmental studies. Therefore, the acute aggregate risk is minimal.

Chronic Dietary Exposure. In conducting the chronic dietary exposure  assessment EPA used the food consumption data from the USDA under the National Health and Nutrition Examination Survey, What We Eat in America (NHANES/WWEIA), 2003-2008. As to residue levels in food, EPA incorporated average percent crop treated (PCT) data for apples, cabbage, cauliflower, cotton, pears, potatoes, strawberries, and tomatoes and utilized estimates for PCT for uses for grain sorghum and sweet corn. 100 PCT was assumed for the remaining food commodities. Anticipated residues (ARs) for meat, milk, hog, and poultry commodities were calculated based on the uses and percent crop treated for grain sorghum, sweet corn, apple and cotton; and an assumption of 100 PCT for sugarcane, aspirated grain fractions (AGF), and cowpea seed.

The chronic analysis also incorporated a half-limit of quantitation (LOQ) residues for food commodities other than those covered by a higher tolerance as a result of use on growing crops from the registered use in food and feed handling establishments. Additionally, empirical processing factors for apple juice (translated to pear and stone fruit juice), cottonseed oil, dried plums, and tomato paste and pure, and Dietary Exposure Evaluation Model (DEEM) (ver. 7.81) default processing factors for the remaining processed commodities, where provided were incorporated.

The PCT was estimated: Apples at 10%; cabbage at 10%; cauliflower at < 2.5%, cotton at < 2.5%, pears at 15%, potatoes at < 2.5%, strawberries at 35%, sweet corn at 36% and grain sorghum at 2% and tomatoes at < 1%.

The chronic population adjusted dose (cPAD) for novaluron is 0.011 mg/kg/day, upon the NOAEL of 1.1 mg/kg/day from the chronic carcinogenicity study in rats, and an UF of
100. The chronic dietary exposure (food plus drinking water) for the general U.S. population is 0.002301 mg/kg/day, or 20.9% of the cPAD. These chronic dietary exposure estimates corresponds to 14.3% to 72.4% of the cPAD (0.011 mg/kg/day). The most highly exposed subpopulation, children aged 1 to 2 years, has an estimated total novaluron exposure of 0.007963 mg/kg/day, which corresponds to 72.4% of the cPAD. Chronic dietary exposures less than 100% of the cPAD are not of concern. 

Novaluron was classified as "not likely to be carcinogenic to humans." Therefore, a quantitative cancer risk assessment is unnecessary.

ii. Drinking water. Acute Exposure. Since no acute toxicity endpoint was determined, it can be concluded there is reasonable certainty of no harm from acute drinking water exposure, and therefore, a drinking water exposure assessment is unnecessary.

Chronic Exposure. Novaluron residues in drinking water were included in the dietary exposure assessment for peanut and soybean. The residues of concern in drinking water are novaluron and its chlorophenyl urea and chloroaniline degradates. The Pesticide Root Zone Model/Exposure Analysis Modeling System (PRZM/EXAMS) for estimating parent novaluron in surface water, the Tier 1 FQPA Index Reservoir Screening Tool (FIRST) model for surface water estimates for chlorophenyl urea and chloroaniline degradates, and the Screening Concentration in Ground Water (SCI-GROW) model for novaluron, chlorophenyl urea, and chloroaniline in ground water were used. These simulation models take into account data on the physical, chemical, and fate/transport characteristics.

Based on these models, the estimated drinking water concentrations (EDWCs) of novaluron, chlorophenyl urea, and chloroaniline for chronic exposures for non-cancer assessments are estimated to be 0.41 parts per billion (ppb), 0.375 ppb, and 3.301 ppb respectively, for surface water and 0.00137 ppb, 0.00149 ppb, and 0.00658 ppb respectively for ground water.

Modeled estimates of drinking water concentrations were directly entered into the dietary exposure model. The highest 1-in-10 year annual mean surface water EDWCs were combined to estimate drinking water exposures. For chronic dietary risk assessment, the water concentration of value 4.086 ppb was used to assess the contribution to drinking water.

	2. Non-dietary exposure. Novaluron has been approved for its use in and around residences including crack & crevice, spot and outdoor perimeter uses. It can be applied at a maximum dilute concentration of 0.25% novaluron (0.02 lb ai/gal). Residents may apply the product so residential handler exposures are assessed in addition to post-application exposures. Both short- and intermediate-term post- application exposures are of interest because the period of residual control for novaluron may result in exposures over a prolonged period. However handler exposures are of interest for the short-term only. 

Due to the limited area treated in outdoor perimeter treatments, potential post-application exposure associated with perimeter treatments to negligible has generally been considered by EPA as negligible. Crack & crevice applications and spot treatments in residences can lead to potential novaluron exposures for residents in treated homes. Spot treatments will be made to storage areas, closets, around water pipes, behind/under refrigerators, etc., whereas crack & crevice applications will be made to baseboards, floors, ceilings, walls, etc.. Thus, exposure to residues is minimized by the application of sprays to areas that are generally inaccessible to residents. Post-application exposures to residues from crack & crevice applications may be taken as the worst-case scenario from among the novaluron uses because such applications may be made in areas residents occupy.

Based on EPA's updated Standard Operating Procedures for Residential Exposure
Assessments (2012), the short-term aggregate residential MOEs (food + water, residential
application and post - application) are 1,800 for adults, and 460 for children; and the intermediate-term aggregate residential MOEs are 1,200 for adults, and 420 for children, taken into consideration as the worst-case scenario the maximum dilute application rate of 0.25% novaluron {0.02 lb ai/gal). Thus, based on the crack and crevice treatment all of the route- and product-specific MOEs were greater than 100, and the aggregate MOEs were greater than 100 for all population subgroups, demonstrating a reasonable certainty of no harm.

D. Cumulative Effects

	EPA has not found novaluron to share a common mechanism of toxicity with any other substances and novaluron does not appear to produce any toxic metabolite produced by other substances. There are currently no available data or other reliable information indicating that any toxic effects produced by novaluron that would be cumulative with those of other chemical compounds.

E. Safety Determination

	1. U.S. population. No acute aggregate risk assessment was conducted because there is no toxicological endpoint attributable to a single exposure. No cancer aggregate risk assessment was conducted because novaluron has not been shown to be carcinogenic.

A chronic aggregate risk assessment was performed for the proposed peanut and soybean tolerances based on potential exposure from food and drinking water. Short- and intermediate-term aggregate risk assessments were performed based on potential exposure from food and drinking water, as well as spot, crack and crevice, and outdoor perimeter uses. The chronic dietary exposure, including drinking water, for the general U.S. population was found to be 0.002301 mg/kg/day, or 20.9% of the cPAD. The chronic dietary exposures account for 14.3% to 72.4% of the cPAD (0.011 mg/kg/day) depending on the population subgroup. The calculation for the most sensitive population subgroup (children 1 to 2 years old) was 0.007963 mg/kg/day, utilizing 72.4% of the cPAD. In view of these previous assessments, Makhteshim-Agan of North America Inc. concludes that there is reasonable certainty that no harm will result from the proposed use of novaluron with the additional uses of avocado and carrot; or the update to the noted crop groupings.

Concerning the aggregate assessment from all potential sources of exposure (food, water, residential), it has been demonstrated that the aggregate MOEs associated with the existing uses of novaluron do not exceed the Agency's level of concern. There is reasonable certainty that no harm will result to the general population or to infants and children from the additional new uses of novaluron.

	2. Infants and children. Section 408 of FFDCA provides that EPA may apply an additional safety factor for infants and children to account for prenatal and postnatal toxicity and the completeness of the database. The toxicology database for novaluron is complete including acceptable data from rat and rabbit developmental toxicity studies, and a two generation rat reproduction study that have been used to assess the potential for increased sensitivity of infants and children. The data provided no quantitative or qualitative evidence of increased susceptibility of rats or rabbits to in utero and/or postnatal exposure to novaluron. Neither maternal nor developmental toxicity was seen in the developmental studies up to the limit doses. The reproduction study demonstrated offspring and parental toxicity were similar and occurred at the same dose; reproductive effects occurred at a higher dose than the one which resulted in parental toxicity. In addition, there is no concern for developmental neurotoxicity resulting from exposure to novaluron, and a developmental neurotoxicity study is not required. Therefore, the Agency determined to reduce the FQPA Safety Factor to 1X (Federal Register of June 2, 2004; 69 FR 31013; FRL-7359-2).

With the current uses of novaluron the chronic population adjusted dose (cPAD) is determined to be 0.011 mg/kg/day and the DEEM analysis regarding the aggregate chronic exposure calculated at utilizing less than 72.4% of the cPAD for the most sensitive subgroup, children 1 to 2 years old. In addition, it is evident that short- and intermediate-term aggregate residential exposures based on the crack and crevice treatment as the worst case for post-application exposures, result in MOEs greater than 100.

Based on this information Makhteshim-Agan of North America Inc., concludes that there is reasonable certainty that no harm will result to infants and children from aggregate exposure to novaluron residues associated with existing and proposed uses of novaluron on avocado and carrot; or the update to the noted crop groupings.

F. International Tolerances

On December 8, 2010, the Federal Register published a final rule with revisions to the fruiting vegetables crop group and the pome fruit crop group. Tolerances for novaluron have previously been established for both of these crop groups, at 1.0 ppm for Vegetable, fruiting, group 8 (and also for various commodities that are now part of the updated crop group), and 2.0 ppm for Fruit, pome, group 11. The IR-4 Project proposes new tolerances for novaluron for the updated crop groups at the same levels as the current tolerances. 

At present, no Canadian, Mexican, or CODEX maximum residue limits (MRLs) are established for novaluron on avocado, carrot, or lima beans.

No Canadian or Mexican maximum residue limits (MRLs) are established for novaluron on the fruiting vegetable group 8-10, although CODEX maintains a novaluron MRL of 0.7 on "fruiting vegetables other than cucurbits and sweet corn." The residues of novaluron on tomatoes and peppers in the IR-4 studies that supported the original tolerance were <0.5 ppm, thus it is unlikely that fruiting vegetables with novaluron residues >0.7 ppm will be produced and become a trade irritant even if the current tolerance level is maintained. 

Codex maintains a novaluron MRL of 3 set on "pome fruit", however a lower US MRL will not impact exports. The residues of novaluron on pome fruit in the studies (not sponsored by IR-4) that supported the original tolerance resulted in a calculated tolerance of 2.0 ppm, thus it is extremely unlikely that pome fruit with novaluron residues >3.0 ppm will be produced and become a trade irritant even if the current tolerance level is maintained. 

Codex maintains a novaluron MRL of 7 set on "stone fruit."  On August 22, 2012, the Federal Register published a final rule with revisions to the stone fruit crop group. Tolerances for novaluron have previously been established for Cherry at 8.0 ppm and for Fruit, stone, group 12, except cherry at 1.9 ppm. The IR-4 Project proposes new tolerances for novaluron for the new Cherry subgroup 12-12A at 8.0 ppm and for the new Peach subgroup 12-12B and the new Plum subgroup 12-12C, both at 1.9 ppm.

CODEX has established an MRL of 7.0 ppm for novaluron on stone fruit. The residues of novaluron on cherries in the study (not sponsored by IR-4 but submitted with an IR-4 petition) that supported the original cherry tolerance were <4.0 ppm, thus it is extremely unlikely that cherries or other fruit in the cherry subgroup with novaluron residues >7.0 ppm will be produced and become a trade irritant even if the current tolerance level is maintained. 

The residues of novaluron on peaches and plums in the respective studies that supported the original stone fruit tolerance were <2.0 ppm, thus it is extremely unlikely that peaches, plums, or other fruit in the respective subgroups with novaluron residues >7.0 ppm will be produced and become a trade irritant even if the current tolerance level is maintained for the two new subgroups. Establishing a single tolerance for Fruit, stone, group 12-12 could change the risk calculations in a way that would be detrimental to the establishment of future tolerances for this compound, thus IR-4 has proposed the separate subgroup tolerances.