Document ID: EPA-HQ-OPP-2010-0466-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2010-06-23T04:00Z

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-2trifluoromethoxy)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/m2). 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 non-detectable (<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 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 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 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 (½ 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-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%) 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 post-application
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 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 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.