Makhteshim-Agan of North America, Inc. 

PP 0F7708 

EPA has received a pesticide petition (PP # to be assigned) from Makhteshim-Agan of North 

America, Inc., 4515 Falls of Neuse Road, Raleigh, NC 27609, 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 tolerance for residues of novaluron (N-[[[3-chloro-4-[1,1,2-trifluoro-2-

trifluoromethoxy)ethoxy]phenyl]amino]carbonyl]-2,6-difluorobenzamide) in or on all food 

commodities (other than those already covered by a higher tolerance as a result of use on 

growing crops) in food handling establishments where food products are held, processed or 

prepared at 0.01 parts per million (ppm). 

Makhteshim-Agan of North America, Inc., 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). 

Concerning this petition a validation method was conducted determining residue concentrations 

of novaluron in/on butter, meat, milk, bread, lettuce and typical dinner plates serving as 

representative commodities in a simulated food-handling establishment to which novaluron was 

applied. The LOQ in butter, processed meat (turkey), milk, bread and lettuce was established as 

0.01 mg/kg (0.01 ppm), the lowest fortification concentration tested where recoveries were 

acceptable (70 to 120% with RSD < 20%). 
3. Magnitude of Residues 

In a Food Handling Establishment, novaluron was applied to the room as a typical space spray 

treatment, simulating a routine pest control treatment in the form of a fine mist (fog) at an 

exaggerated rate (3x of the maximum label rate or 38.75 mg ai/m

2

). Samples of common food 

matrices (butter, turkey lunchmeat, milk, sliced bread and lettuce) and bare vitreous china plates 

were placed into the treated room to measure direct deposition, re-deposition and decline (or 

concentration) of residues over a 12-hour sampling period. Covered and non-covered samples 

were collected 4, 8 and 12 hours after application, frozen, and sent to the analytical laboratory 

for analysis. 

The results of the proposed use of novaluron in food handling establishments demonstrate 

minimal residues on covered food items. Novaluron residues did not increase or decrease during 

the sampling period covered by the study (12 hours). Novaluron residues on uncovered foods at 

exaggerated rates (3x) ranged up to 10 ppm, whereas residues on covered food were nondetectable (<0.01 ppm), with the exception of one bread sample at a residue concentration of 

0.01 ppm. Therefore, covered food matrices and surfaces had approximately 1000X less 

novaluron than uncovered food matrices and surfaces. There was no significant re-deposition of 

novaluron residues following the initial test substance application 

In conclusion, at the maximum, nominal application rate (1x), novaluron residues are anticipated 

to be less than 0.01 ppm on food that has been covered or removed during treatment. Therefore, 

the proposed tolerance for the use of novaluron in food handling establishments should be set at 

0.01 ppm. 

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. 

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 treatmentrelated 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 

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 diflurophenyl 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 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 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. 

In addition to the existing tolerances, this Notice of Filing includes exposure assessments for 

potential residues 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 (PP# 9F7547), which is presently being reviewed by the 
Agency. The assessment is based on average residues from field trials (except cottonseed, for 

which tolerances were used), DEEM default processing factors and percent crop treated 

assumptions from previous assessments for pending and registered crops. Although lowbush 

blueberries are included in Crop Subgroup 13-07G, the anticipated residue for strawberries 

(representative crop for Subgroup 13-07G) is 0.14 ppm, whereas that for highbush blueberries 

is 1.97 ppm. Therefore, EPA has approved the tolerance for low-growing berries with lowbush 

blueberries excluded. 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. 
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 negligible. 

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-FCID

TM 

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%) and 

sugarcane (28%). These percent crop treated numbers provide a more refined estimate of 

potential chronic dietary exposures to novaluron. All eligible food items are assumed to have 

novaluron residues associated with the FHE use (i.e., 100% crop treated is assumed for all 

foods for which the FHE tolerance is applicable), representing a very conservative assessment. 

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 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. The most highly exposed subpopulation, children aged 1 to 2 years, has an estimated 

total novaluron exposure (0.001995 mg/kg/day), which corresponds to 18.1% of the cPAD. The 
estimated novaluron exposure for the general U.S. population (0.000579 mg/kg/day) 

corresponds to 5.3% of the cPAD. Residues associated with the proposed FHE use (i.e., 0.005 

ppm at 100% treatment of all foods without tolerances) contribute insignificantly to the total 

exposure. Thus, exposures associated with the FHE use, 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 

a. Acute Exposure. Since no acute dietary endpoint was determined, Makhteshim-Agan of North 

America, Inc., concludes there is reasonable certainty of no harm from acute drinking water 

exposure. 

b. 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 (SCIGROW) 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). Therefore, the drinking water concentration of 2.6 ppb was used as the worst case in 

this assessment. 

2. Non-Dietary Exposure 

Novaluron is proposed to be used for the following residential non-dietary sites: Indoor and 

outdoor control of roaches, and crickets for spot, crack and crevice treatments. Both short-and 

intermediate-term exposures are of interest because the period of residual control for novaluron 

may result in exposures over a prolonged period. Since the product will be applied only by 

professional applicators, residential handler exposures are not of concern. Residential postapplication exposures to novaluron residues from crack and crevice applications were taken into 

consideration as the worst-case scenario based on the EPA’s Standard Operating Procedures 

for Residential Exposure Assessments. 

At the maximum dilute application rate of 0.25% novaluron, 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. 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. 

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 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 

0.000579 mg/kg/day, or 5.3% of the cPAD. The chronic dietary exposures account for 3.5% to 

18.1% 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 0.001995 mg/kg/day, 

utilizing 18.1% 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 uses 

of novaluron. 

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 18.1% of the cPAD for the most 

sensitive subgroup, children 1 to 2 years old. In addition, it is evident that short-and intermediateterm 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 agricultural uses, and the proposed new uses 

associated with the proposed spot, crack and crevice, and outdoor perimeters. 

F. International Residue Limits 

There are no Canadian, Mexican, or CODEX maximum residue limits (MRLs) established for 

novaluron in or on all food commodities in food or feed handling establishments, where food or 

feed products are held, processed or prepared. Therefore, international harmonization is not an 

issue at this time.