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EPA Registration Division contact: Laura Nollen, (703) 305-7390

Interregional Research Project Number 4 (IR-4)

Petition Number 0E7723

EPA has received a pesticide petition, PP # 0E7723, from IR-4, 500 College Road East, 

Suite 201W, Princeton, NJ 08540, proposing, pursuant to section 408(d) of the Federal Food, 

Drug, and Cosmetic Act, 21 U.S.C. 346a(d), to amend 40 CFR 180.598 by establishing a 

tolerances for residues of novaluron, N-[[[3-chloro-4-[1,1,2-trifluoro-2-

trifluoromethoxy)ethoxy]phenyl]amino]carbonyl]-2,6-difluorobenzamide, in or on corn, sweet, 

kernals plus cob with husks removed at 0.05 parts per million (ppm); corn, sweet, forage at 20

ppm; and corn, sweet, stover at 50 ppm, and to increase the established livestock tolerances 

for residues of novaluron in or on milk from 1.0 to 1.5 ppm, and milk fat from 20 to 35 ppm, 

respectively. 

Makhteshim-Agan of North America, Inc., 4515 Falls of Neuse Road, Raleigh, NC 

27609, is the manufacturer and basic registrant of novaluron. Makhteshim-Agan of North 

America, Inc., prepared and summarized the following information in support of the subject 

pesticide petition for novaluron. EPA has determined that the petition contains data or 

information regarding the elements set forth in section 408(d)(2) of the FFDCA. However, EPA 

has not fully evaluated the sufficiency of the submitted data at this time or whether the data 

supports 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 range. The Limit of Quantitation 

(LOQ) for the method in K+CWHR, forage and stover was calculated to be 0.040, 0.052 and 
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0.049 ppm, respectively. The lowest level of method validation (LLMV) for novaluron in corn 

forage, stover and K+CWHR was 0.05 ppm. 

3. Magnitude of Residues

Fourteen field trials were conducted with Rimon 0.83 EC in sweet corn at the supported 

use pattern of five foliar applications at a maximum rate of 12 fl. oz product/A, or 0.088 lb ai/A 

at 7-day intervals (for a total seasonal rate of 60 fl. oz of Rimon 0.83EC), and a PHI of 1 day 

covering NAFTA and PMRA Growing Regions 1 (2 trials), 2 (1 trial), 3 (1 trial), 5 (5 trials), 5B (1

trial), 7A (1 trial), 10 (1 trial), 11 (1 trial), and 12 (1 trial) during the 2007 season. Measured 

novaluron residues taken at 1 day PHI range from less than 0.05 ppm in kernals plus cob with 

husk removed (K+CWHR), 0.35 ppm to 15.03 ppm in forage, and 0.35 ppm to 52.06 ppm in 

stover. The proposed tolerances for corn, sweet (K+CWHR) are 0.05 ppm, forage 20 ppm, and 

stover 50 ppm based on the MRL calculator.

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 greater than 5.15 mg/l. In rabbits, novaluron is not a skin irritant, but it is 

a mild eye irritant. Novaluron is not a sensitizer in guinea pigs.

2. Genotoxicity

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 (NOAEL) in 

males was 1,000 ppm (74.2 mg/kg/day) and in females it was $12,000 ppm (1,009.8 

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. 
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4. Subchronic Toxicity

Rats, mice and dogs all show the same toxicologic 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 determined to be 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 NOEL was determined to be 10 mg/kg/day.

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, 20,000 ppm (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 levels 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 
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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 14C(U)] novaluron 

is recovered in the feces. When the diflurophenyl 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 diflurophenyl 

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 diflurophenyl moiety of the molecule. Nearly all the metabolites are formed at a level 

of 1% or less of the applied dose. They 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. For drinking water assessment the soil degradates, 

chlorophenyl urea and chloroaniline will be included besides the parent, novaluron. 

8. Endocrine Disruption

 

No special studies investigating potential estrogenic or other endocrine effects of 
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novaluron have been conducted. However, inspection of in-life data from toxicology studies 

does not indicate that novaluron is 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, there 

is no evidence to suggest that novaluron has an adverse effect on the endocrine system. 

C. Aggregate Exposure

1. Dietary Exposure

Tolerances have been established (40 CFR 180.598) for the residues of novaluron, in or 

on the following raw agricultural commodities: Apple, wet pomace at 8.0; Brassica, head and 

stem, subgroup 5A at 0.5 ppm; cattle, fat at 11 ppm; cattle, fat at 11 ppm; cattle, kidney at 1.0 

ppm; cattle, liver at 1.0 ppm; cattle, meat at 0.60 ppm; cattle, meat byproducts, except liver and 

kidney at 0.60 ppm; cotton, gin byproducts at 30 ppm; cotton, undelinted seed at 0.60 ppm; egg 

at 0.05 ppm; fruit, pome, group 11 at 2.0 ppm; goat, fat at 11 ppm; goat, kidney at 1.0 ppm; 

goat, liver at 1.0 ppm; goat, meat at 0.60 ppm; goat, meat byproducts except liver and kidney at 

0.60 ppm; hog, fat at 0.05 ppm; hog, meat at 0.01 ppm; hog, meat byproducts at 0.01 ppm; 

horse, fat at 11 ppm; horse, kidney at 1.0 ppm; horse, liver at 1.0 ppm; horse, meat at 0.60 

ppm; horse, meat byproducts, except liver and kidney at 0.60 ppm; milk at 1.0 ppm; milk, fat at 

20 ppm; poultry, fat at 0.40 ppm; poultry, meat at 0.03 ppm; poultry, meat byproducts at 0.04

ppm; sheep, fat at 11 ppm; sheep, kidney at 1.0 ppm; sheep, liver at 1.0 ppm; sheep, meat at 

0.60 ppm; sheep, meat byproducts, except liver and kidney at 0.60 ppm, sugarcane, cane at 

0.50 ppm; vegetables, tuberous and corn, subgroup 1C at 0.05 ppm; vegetable, fruiting, group 

8 at 1.1 parts per million (ppm); vegetable, cucurbit, group 9 at 0.25 ppm; berry, low growing, 

subgroup 13-07G at 0.50 ppm; cocona at 1.1 ppm; eggplant, African at 1.1 ppm; eggplant, pea 

at 1.1 ppm; eggplant, scarlet at 1.1 ppm; goji berry at 1.1 ppm; huckleberry, garden at 1.1 ppm; 

martynia at 1.1 ppm; naranjilla at 1.1 ppm; okra at 1.1 ppm; roselle at 1.1 ppm; sunberry at 1.1 

ppm; tomato, bush at 1.1 ppm; tomato, currant at 1.1 ppm; tomato, tree at 1.1 ppm; bean, 

snap, succulent at 0.60 ppm; bean, dry at 0.20 ppm; and Swiss chard at 12 ppm.

This assessment estimated the chronic dietary exposures associated with the proposed use of 

novaluron on sweet corn in addition to all pending and registered crops. EPA is presently 

reviewing MANA’s petition (PP# 0F7708) concerning the pending tolerances of novaluron in or 

on all food commodities in food handling establishments (FHE), where food products are held, 

processed or prepared, as well as the pending tolerance of novaluron in or on grain sorghum, 

which are also included in this dietary exposure assessment. In this assessment, average 

residues from field trials were used for most food crops and anticipated residues were 

estimated for meat, milk, poultry and eggs. The exceptions were sweet corn (K+CWHR), 

cotton seed commodities (other than cotton gin byproducts) and dried plums (prunes), for which

tolerance-level residues were assumed. For the proposed FHE use, an estimated residue of 

0.005 ppm (1⁄2 LOQ) was assumed only for each food without a tolerance representing EPA’s 

approach for including FHE tolerances in chronic dietary assessments. Market projections 

concerning the percent crop treated for all crops were used to produce a conservative yet 

refined estimate of chronic dietary exposures.

i. Food
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a. 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 negligible.

b. Chronic Dietary Exposure. A chronic dietary risk assessment was conducted using 

the Dietary Exposure Evaluation Model (DEEM) software with the Food Commodity Intake 

Database (DEEM-FCIDTM Version 2.16), which incorporates consumption data derived from the 

1994 - 1998 USDA Continuing Surveys of Food Intake by Individuals (CSFII). The assessment 

included all uses (existing, pending and proposed), assuming provided percent crop treated 

estimates at market maturity. A dietary exposure assessment conducted with the assumption of 

100% crop treated is quite conservative, even when average residues from field trials are 

assumed. In order to produce a more accurate estimate of exposures, a refined assessment 

using best estimates of the percent crop treated at market maturity for all registered, pending 

and proposed commodities has been conducted assuming the following percent crop treated 

estimates at market maturity: cucurbits (18%), fruiting vegetables (14%), low growing berries 

(12%), dry beans (16%), snap beans (12%), Swiss chard (15%), grain sorghum (1%), stone 

fruit (20%), bushberries (15%), leafy brassica vegetables (20%), turnip greens (15%), apples 

(30%), pears (50%), head and stem brassica (30%), tuberous and corm vegetables (18%), 

cotton (12%), sugarcane (28%), and sweet corn (12%). These percent crop treated numbers 

provide a more refined estimate of potential chronic dietary exposures to novaluron. 

Concerning the pending FHE use, all eligible food items are assumed to have novaluron 

residues (i.e., 100% crop treated is assumed for all foods for which the FHE tolerance is 

applicable).

Anticipated residues in animal tissues (i.e., meat and milk) were calculated using 

standard methodology based on recent guidance for calculating the maximum reasonably 

balanced diets (MRBD) consisting of multiple treated feed items. Average residues in animal 

feed items were used in all calculations, with the exception of cotton seed commodities (seed, 

meal, hulls), for which the tolerance (0.6 ppm) was used. 

The chronic population adjusted dose (cPAD) for novaluron is 0.011 mg/kg/day, based 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, including drinking water, for the general U.S. population is 

0.000746 mg/kg/day, or 6.8% of the cPAD. These chronic dietary exposure estimates account 

for 4.5% to 24.1% of the cPAD. The most highly exposed subpopulation, children aged 1 to 2 

years, has an estimated total novaluron exposure of 0.002649 mg/kg/day, which corresponds to 

24.1% of the cPAD. Chronic dietary exposures less than 100% of the cPAD are not of 

concern. The total chronic dietary exposures associated with all pending, registered and 

proposed uses of novaluron accounts for less than the cPAD (0.011 mg/kg/d), and therefore is 

of no concern. Thus, exposures associated with the proposed use of novaluron on sweet corn, 

in addition to all current pending and registered uses are not of concern.

c. Novaluron was classified as “not likely to be carcinogenic to humans.''. Therefore, a 

quantitative cancer risk assessment was not conducted.

ii. Drinking Water
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a. Acute Exposure. Since no acute dietary endpoint was determined, MakhteshimAgan of North America, Inc., concludes there is reasonable certainty of no harm from acute 

drinking water exposure.

Chronic Exposure. Novaluron residues in drinking water were included in the dietary exposure 

assessment. Since there are currently insufficient monitoring data to characterize novaluron 

residues in drinking water, modeling approaches were used to estimate chronic concentrations 

in surface and ground water. The residues of concern in drinking water are novaluron and its 

chlorophenyl urea and chloroaniline degradates. The Agency used screening level water 

exposure models in the dietary exposure analysis and risk assessment for novaluron and its 

degradates in drinking water, as reported in the January 27, 2010, Federal Register Notice

(EPA–HQ–OPP–2009–0273; FRL–8807–2). The Pesticide Root Zone Model/Exposure 

Analysis Modeling System (PRZM/EXAMS) was used for parent novaluron in surface water, 

and the First Index Reservoir Screening Tool (FIRST) for chlorophenyl urea and chloroaniline 

degradates in surface water, the Screening Concentration in Ground Water (SCI-GROW) 

model for novaluron, chlorophenyl urea and chloroaniline in ground water. The estimated 

drinking water concentrations (EDWCs) of novaluron, chlorophenyl urea, and chloroaniline for 

chronic exposures for non-cancer assessments are 0.76 parts per billion (ppb), 0.89 ppb and 

2.6 ppb, respectively, for surface water and for ground water 0.0056 ppb, 0.0045 ppb and 

0.0090 ppb, respectively. The highest drinking water concentrations were estimated for surface 

water. Of the three EDWC values for surface water, the chronic EDWC for the terminal 

metabolite, chloroaniline, is the highest (assuming 100% molar conversion from parent to 

aniline). This estimate is based on the total annual application rate of 0.96 lb ai/A on apples. 

The proposed sweet corn use has a total annual application rate of 0.4 lb ai/A, and all other 

uses have total annual application rates of 0.24 lb ai/A, so the estimated drinking water residue 

for the use on apples will continue to be the highest and most conservative value. Therefore, 

the drinking water residue estimated by EPA for the use on apples (2.6 ppb) was used as the 

worst case in this assessment.

2. Non-Dietary Exposure

Novaluron’s proposed use for the following residential non-dietary sites: Indoor and outdoor 

control of roaches, and crickets for spot, crack and crevice treatments, is presently under 

review by the Agency. Based on EPA’s Standard Operating Procedures for Residential 

Exposure Assessments, the residential post-application exposures to novaluron residues from 

crack and crevice applications were taken into consideration as the worst-case scenario at the 

maximum dilute application rate of 0.25% novaluron, where short- and intermediate-term 

residential post-application exposures resulted in acceptable Margins of Exposures (MOEs),

and a clear indication of reasonable certainty of no harm. 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

To Makhteshim-Agan of North America’s Inc., knowledge, there are currently no 

available data or other reliable information indicating that any toxic effects produced by 

novaluron would be cumulative with those of other chemical compounds; thus only the potential 
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risks of novaluron have been considered in this assessment of its aggregate exposure.

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. A chronic aggregate risk assessment was 

performed based on potential exposure from food and drinking water, considering all existing 

and proposed uses. Short- and intermediate-term aggregate risk assessments were performed 

based on potential exposure from food and drinking water from existing uses, as well as the 

proposed spot, crack and crevice, and outdoor perimeter uses. No cancer aggregate risk 

assessment was conducted because novaluron has not been shown to be carcinogenic. 

The chronic dietary exposure, including drinking water, for the general U.S. population is 

0.000746 mg/kg/day, or 6.8% of the cPAD. The chronic dietary exposures account for 4.5% to 

24.1% 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) is 0.002649 mg/kg/day,

utilizing 24.1% of the cPAD. In view of these assessments, Makhteshim-Agan of North 

America Inc., concludes that there is reasonable certainty that no harm will result from the 

proposed use of novaluron on sweet corn.

 Concerning the aggregate assessment from all potential sources of exposure (food, 

water, crack and crevice post-application), it has been demonstrated that the aggregate MOEs 

associated with the existing and proposed uses of novaluron do not exceed the Agency’s level 

of concern. Based on these assessments, Makhteshim-Agan of North America Inc., concludes 

that novaluron does not pose a risk due to short- and intermediate-term aggregate exposure.

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. 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). Thus, the chronic population 

adjusted dose (cPAD) is considered 0.011 mg/kg/day. The DEEM analysis regarding the 

aggregate chronic exposure calculations utilizes less than 24.1% 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 
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to novaluron residues associated with existing and proposed uses including the proposed use 

of novaluron on sweet corn. 

F. International Residue Limits

At present, no Canadian, Mexican, or CODEX maximum residue limits (MRLs) are 

established for novaluron on sweet corn. Therefore, international harmonization is not an issue 

at this time.