Document ID: EPA-HQ-OPP-2010-0471-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2010-06-23T04:00Z

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 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. 

		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.

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 (½ 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

		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

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.

 

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 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 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.

 

 

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