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 
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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: 

- Avocado: A total of 6 field trials were conducted in NAFTA Regions. 

- Carrot: A total of 8 field trials were conducted in NAFTA Regions. 

- Bean: A total of 6 field trials were conducted in NAFTA Regions.

- 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 
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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
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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 14C(U)] novaluron is recovered in the feces. When the difluorophenyl ring of the 

molecule is labeled, the recovered 14C 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-chloro4-(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 
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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 
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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
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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 intermediateterm 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
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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.