 

<EPA Registration Division contact: [BeWanda Alexander, Insecticide
Branch, 703-305-7460]>

 <[BASF Corporation]>

<[EPA-HQ-OPP-2010-0234]>

<	EPA has received a pesticide petition 0F7690 from [BASF Corporation],
[26 Davis Drive, P.O. Box 13528, Research Triangle Park, North Carolina
27709-3528] proposing, pursuant to section 408(d) of the Federal Food,
Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 CFR part
180. by establishing a tolerance for residues of combined residues of
alpha-cypermethrin and cypermethrin (including zeta-cypermethrin)(
(S)-α-cyano-3-phenoxybenzyl
(1R,3R)-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropanecarboxylate and
(R)-α-cyano-3-phenoxybenzyl
(1S,3S)-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropanecarboxylate)] in
or on the raw agricultural commodity [tree nuts (group 14), dried
shelled pea and bean, except soybean (subgroup 6C), corn grain, pop
corn, sweet corn, soybeans and sugar beet roots] at [0.05] parts per
million (ppm) and commodity [succulent shelled pea and bean (subgroup
6B) and root and tuber vegetables (group 1)] at [0.1] parts per million
(ppm) and commodity [cucurbit vegetables (group 9), fruiting vegetables
(group 8), sugar beet tops and wheat grain] at [0.2] parts per million
(ppm) and commodity [citrus fruit (group 10] at [0.35] parts per million
(ppm) and commodity [cottonseed, edible podded legume vegetable
(subgroup 6A) and sorghum grain] at [0.5] parts per million (ppm) and
commodity [rice grain] at [1.5] parts per million (ppm). and commodity
[citrus dried pulp] at [1.8] parts per million (ppm) and commodity [head
and stem brassica (subgroup 5A)] at [2.0] parts per million (ppm) and
commodity [citrus oil] at [4.0] parts per million (ppm) and commodity
[leafy vegetable, except brassica (group 4)] at [10] parts per million
(ppm) and commodity [alfalfa hay] at [15] parts per million (ppm)... 
EPA has determined that the petition contains data or information
regarding the elements set forth in section 408 (d)(2) of  FDDCA;
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.>

Cypermethrin is a pyrethroid insecticide consisting of three asymmetric
carbon atoms, and therefore, 8 stereo-isomeric mixtures.  Cypermethrin
is also characterized as consisting of cis- and trans-configured
diastereo-isomeric components based on orientation around its
cyclopropane ring.  Zeta-cypermethrin and alpha-cypermethrin are
optimized stereo-isomeric mixtures of cypermethrin, each consisting of 4
major components. These zeta-cypermethrin and alpha-cypermethrin
components are the enriched trans- (alpha-S) and cis (cis2-R) isomeric
orientations of cypermethrin, respectively.  

<A. Residue Chemistry>

<	1. Plant metabolism.[The metabolism of cypermethrin in plants is
adequately understood.  Studies that have been conducted to determine
the metabolism of radiolabelled cypermethrin in various crops all
produced similar results.  The residue of concern is the parent compound
only.]>

<	2. Analytical method. [There is a practical analytical method for
detecting and measuring levels of cypermethrin in or on food with a
limit of detection that allows monitoring of food with residues at or
above the levels set in these tolerances (Gas Chromatography with
Electron Capture Detection or GC/ECD and LC/MS/MS methods are
available).]

>

<	3. Magnitude of residues. [Alpha-cypermethrin registration will cite
the applicable magnitude of the residue studies conducted for the
registration of zeta-cypermethrin.  Field trials with zeta-cypermethrin
were carried out to determine the magnitude of the residue in/on root
and tuber vegetables (group 1), leafy vegetables (group 4), head and
stem brassica (subgroup 5A), edible podded legume vegetable (subgroup
6A), succulent shelled pea and bean (subgroup 6B), dried shelled pea and
bean (subgroup 6C), fruiting vegetables (group 8), cucurbit vegetables
(group 9), citrus fruit (group 10), tree nuts (group 14), field corn,
pop corn, sweet corn, wheat grain, rice grain, sorghum, sugar beets,
soybeans, cotton and alfalfa. The number and locations of field trials
are in accordance with OPPTS Guideline 860.1500. Field trials were
carried out using the maximum label rates, the maximum number of
applications, and the minimum pre-harvest interval (PHI) for all the
crops. Detected residues of cypermethrin in all crops support the
proposed tolerances.]>

<B. Toxicological Profile>

<	1. Acute toxicity.   [Acute toxicity studies conducted with
alpha-cypermethrin show a low toxicity via the oral (category III),
dermal (category III) and inhalation (category IV) exposure routes.  
Alpha-cypermethrin is not irritating to the eyes and is not a skin
sensitizer.  However, it is mildly irritating to the skin.  The acute
toxicity of alpha-cypermethrin EC formulation is attenuated following
acute exposures via inhalation and dermal routes.  The EC formulation is
a skin and eye irritant, mild skin sensitizer and has moderate toxicity
via oral exposure route. ]>

<	2. Genotoxicty.  [Alpha-cypermethrin was negative for inducing
mutations in both in vitro Ames and an in vitro CHO/HGPRT locus
mammalian cell mutation assays.   Alpha-cypermethrin caused no increase
in the incidence of chromatid or chromosome aberrations or polyploidy in
bone marrow cells following per os in-vivo exposure to Wistar rats. 
Similarly, Alpha-cypermethrin did not increase the frequency of
chromatid gaps, chromatid breaks or total chromatid aberrations in rat
liver (RL4) cell cultures.  >Alpha-cypermethrin did not produce any
detectable DNA single-strand damage using alkaline elution profiles of
liver DNA.  

From the all available data on alpha-cypermethrin, it can be concluded
that this compound is non-mutagenic in tests with Salmonella
typhimurium, Saccharomyces cerevisiae, and in-vivo and in-vitro tests
with rat liver cells for the induction of chromosome aberration and
production of DNA single-strand damage.  Overall, the weight of the
evidence demonstrates that alpha-cypermethrin is not genotoxic. ]

	3. Reproductive and developmental toxicity.  [The reproductive and
developmental toxicity of alpha-cypermethrin was investigated in a
2-generation rat reproduction study as well as in rat and rabbit
developmental toxicity studies. The test substance in these studies was
either alpha-cypermethrin or zeta-cypermethrin – the same racemic
pyrethroid mixture with similar enantiomeric composition.

In the rat multigeneration study conducted with zeta-cypermethrin,
another related pyrethroid racemate mixture, the test substance was
administered via diet at levels of 0, 7.5, 25, 100, 375 or 750 ppm,
equivalent to 0, 0.5, 1.8, 7, 27 or 45 mg/kg/day.  Clinical signs of
neurotoxicity and isolated incidences of mortality were observed in the
parental animals at the top dose of 45 mg/kg/day.  An increased
incidence of pup mortality was also seen at 45 mg/kg/day.  At 27
mg/kg/day, decreased body weight gain, especially during lactation, and
increased relative brain weights were observed in male and female adult
animals.  Decreased body weight gain during lactation was also seen
among offspring at 27 mg/kg/day.  The NOAEL for parental and systemic
toxicity was 100 ppm, equivalent to 7 mg/kg body weight per day. 
Similarly, the NOAEL for offspring toxicity was 100 ppm, equivalent to 7
mg/kg/day.

Developmental toxicity studies, via gavage exposures, were conducted in
rats and rabbits with alpha-cypermethrin.  In these studies, there was
no evidence of teratogenicity in animals treated during the phase of
organogenesis. 

In rabbits (0, 3, 15 or 30 mg/kg/day via gavage in corn oil vehicle),
reduced maternal food consumption and body weights were observed at 30
mg/kg/day; no treatment-related effects on fetal weights were observed. 
The NOAEL for maternal toxicity and embryotoxicity was 15 mg/kg/day and
30 mg/kg/day, respectively.  There were no indications for
teratogenicity.

Administration of alpha-cypermethrin via gavage at 0, 3, 9, or 18
mg/kg/day to pregnant rats during fetal organogenesis (gestational days
6-15) elicited maternal toxicity at the two top doses, characterized by
changes in clinical conditions and reduction in food consumption and
body weight gain. Due to marked clinical signs of toxicity the dose
level of 18 mg/kg/ day was lowered to 15 mg/kg/day on day 10 of
gestation.  Females at 18 or 15 mg/kg/day showed unsteady gait,
piloerection, and other signs of maternal toxicity. Slight body weight
reductions were also seen in the females at 9 mg/kg/day. A slight
reduction in fetal weights was observed at these dose levels (9, 15/18
mg/kg/day) in concert with maternal toxicity.  There was no indication
for teratogenicity. The NOAEL for maternal and fetal toxicity was 9
mg/kg/day.

In the rat developmental toxicity study, the maternal and developmental
NOAEL was 9 mg/kg/day.  For rabbits, the NOAEL for systemic toxicity was
15 mg/kg/day, and the NOAEL for developmental toxicity was 30 mg/kg/day,
the highest dose tested. ]

<	4. Subchronic toxicity. [A similar toxicity profile was observed
across rats, mice and dogs following subchronic exposure to
alpha-cypermethrin. These profiles are mostly related to the mode of
action of alpha-cypermethrin and include effects on the neuromuscular
system.  Typical indicator effects for this mode of action were observed
and included tremors, gait abnormalities, decreased motor activity and
increased salivation.  Surviving animals recovered within 3 -7 days. 
The short term and reversible nature of these neurotoxic effects is in
line with studies showing that type II pyrethroids such as
alpha-cypermethrin can cause exaggerated pharmacological effects at high
dose levels that do not result in histopathologic lesions on nervous
system tissues.

In rats, clinical signs characteristic for pyrethroid neurotoxicity were
observed in short-term toxicity studies (4-6 weeks) at ≥800 ppm.
Clinical signs were more pronounced in males and included high stepping,
splayed gait, abasia and hypersensitivity. Further observed effects
comprised decreased food intake and body weights, and some hematological
findings at ≥400 ppm.  The NOEL was 200 ppm, equivalent to 10
mg/kg/day.  After dietary administration at 540 ppm for 90 days,
abnormal gait with splayed hind limbs in male rats and decreased food
intake and body weights were observed. No other treatment-related
effects occurred during the course of this study.  The NOEL was 60 ppm,
equivalent to 3 mg/kg/day.

 after dietary administration of alpha-cypermethrin at ≥800 ppm for 4
weeks. The death of two animals and neurological signs of toxicity were
associated with administration of alpha-cypermethrin at 1200 or 1600
ppm.  The NOEL was 400 ppm, equivalent to 57 mg/kg/day.  In a 90-day
dietary exposure toxicity study in mice, un-groomed coat, hair loss and
encrustations on the dorsal surface, reduced body weights, and increased
aspartate aminotransferase activity were observed at 250 ppm.   The NOEL
was <50 ppm, equivalent to <7.1 mg/kg/day, based on hair loss seen at
the lowest dose tested.

In dogs, clinical signs including body tremors, head nodding, ataxia,
agitation, lip licking, subdued behavior and high stepping gait were
observed at the top dose level (270 ppm) of a 90-day dietary toxicity
study. No other treatment-related effects were observed after
administration of alpha-cypermethrin to dogs.  The NOEL was 90 ppm,
equivalent to 2.25 mg/kg/day.

The neurotoxic potential of alpha-cypermethrin was studied following
acute oral exposure in the rat.  The subchronic neurotoxicity potential
of alpha-cypermethrin was also investigated in the rat, using
zeta-cypermethrin as a surrogate test material.

In the acute neurotoxicity study, no deaths or adverse clinical or
pathological treatment-related effects were observed after oral
administration of alpha-cypermethrin at 4 mg/kg body weight. At 20 and
40 mg/kg body weight, clinical signs of neurotoxicity (including
abnormal gait, piloerection, hunched posture, and diarrhea), and
significant differences to the controls in functional observation
battery tests were observed, with females exhibiting reduced
susceptibility.  The NOEL was 4 mg/kg.

No evidence of increased neurotoxicity was observed in the subchronic
neurotoxicity study with zeta-cypermethrin. Clinical signs of toxicity
were similar to acute exposure and included decreased motor activity,
decreased body weight gains and food consumption.  The NOAEL was 5 and
31 mg/kg/day in males and females, respectively.  Overall, the
neurotoxic effects elicited by alpha-cypermethrin were reversible. ] 

>

<	5. Chronic toxicity.  [The results of long-term oral exposure studies
indicate that alpha-cypermethrin is not carcinogenic in mice or rats. 
At high doses in long term oral exposure studies with rats, mice and
dogs, observations demonstrate evidence of slight neurologic signs and
decreased body weight gains.  This is consistent with the mechanism of
action of alpha-cypermethrin on the peripheral and central nervous
system, through interactions with sodium channels.  The NOAEL in the
mouse oncogenicity study was 30 ppm, equivalent to 3 mg/kg body
weight/day in males and 3.5 mg/kg body weight/day in females.  In the
rat chronic/oncogenicity study, the NOAEL was 100 ppm, equivalent to 5
mg/kg body weight/day in males and females.   In a chronic (1-year) dog
study, the NOAEL was 60 ppm, equivalent to 2 mg/kg/day in males and 2.2
mg/kg/day in females. ]>

<	6. Animal metabolism. [The metabolism of cypermethrin in animals is
adequately understood.  Cypermethrin is rapidly absorbed, distributed,
and excreted in rats when administered orally.  Biotransformation is
principally governed by hydrolytic and oxidation reactions. ] >

<	7. Metabolite toxicology [No metabolites of toxicological concern were
identified with alpha-cypermethrin. ]>

<	8. Endocrine disruption. [No specific tests have been conducted with
alpha-cypermethrin to determine whether the chemical may have an effect
in humans that is similar to an effect produced by a naturally occurring
estrogen or other endocrine effects.  However, there were no significant
findings in other relevant toxicity studies (e.g., sub-chronic and
chronic toxicity, developmental toxicity and multi-generation
reproductive studies) which would suggest that alpha-cypermethrin
produces any endocrine disruption. ]

>

<C. Aggregate Exposure>

<	1. Dietary exposure. [Exposure assessments were conducted to evaluate
the potential risk due to acute and chronic dietary exposure of the U.S.
population and sub-populations to residues of Alpha-Cypermethrin. 
Alpha-cypermethrin is an isomer of cypermethrin.  Zeta-cypermethrin is
also an isomer of cypermethrin.  When the EPA conducted the risk
assessment for zeta-cypermethrin (November 27, 2007, D335224,  Dennis
McNeilly), EPA included all uses for cypermethrin and zeta-cypermethrin
together in the exposure and risk assessment because of the close
similarity in toxicity and chemical characteristics.   The EPA exposure
and risk assessment for alpha-cypermethrin will be approached similarly
and the exposure assessment and risk evaluation will include the uses
from all three active ingredients (cypermethrin, zeta-cypermethrin,
alpha-cypermethrin).  Alpha-cypermethrin will not be registered on any
crops where zeta-cypermethrin or cypermethrin are not currently
registered.  However, alpha-cypermethrin will not be registered on all
the current crops registered with zeta-cypermethrin or cypermethrin. 
Also, the application rate and seasonal maximum rate for
alpha-cypermethrin will be less than cypermethrin and zeta-cypermethrin.
  This analysis includes all the current existing tolerances for
cypermethrin/zeta-cypermethrin 40 CFR 180.418.   ]>

<Food. [

.  

Acute Dietary Exposure Assessment

The EPA conducted a highly refined probabilistic acute dietary exposure
assessment in the “Reregistration Eligibility Decision for
Cypermethrin (revised 01/14/2008)” using PDP data, percent crop
treated information and processing factors.  This refined acute dietary
exposure estimates are applicable to alpha-cypermethrin.  The only
difference between alpha-cypermethrin and cypermethrin are in the acute
population adjusted dose (aPAD).  The aPAD for cypermethrin is based on
a NOAEL of 10 mg/kg bw/day with a 100x uncertainty factor and a 1x FQPA
SF to give a aPAD of 0.1 mg/kg bw/day. The aPAD for alpha-cypermethrin
is based on a NOAEL of 4 mg/kg bw/day with a 100x uncertainty factor and
a 1x FQPA SF to give a aPAD of 0.04 mg/kg bw/day.   

In the cypermethrin assessment, the most highly exposed population
subgroup was children 1-2 years old at 6.1% of the aPAD at the 99.9th
percentile of exposure.   The aPAD for cypermethrin is 0.1 mg/kg bw/day
and an exposure of 6.1% aPAD is a food exposure of 0.0061 mg/kg bw/day. 
Using the same acute food exposure for alpha-cypermethrin,  the most
highly exposed population subgroup was children 1-2 years old at 15.3 %
of the aPAD at the 99.9th percentile of exposure.   The results of the
analysis show that the estimated food exposures are well below the
Agency's level of concern (< 100% aPAD).  

Chronic Dietary Exposure Assessment

The chronic dietary exposure estimates cited in this document are from
the most recent dietary assessment conducted for
zeta-cypermethrin/cypermethrin by EPA (November 5, 2007, D335224, Dennis
McNeilly).  In this dietary assessment, EPA used anticipated residues,
crop treated factors, residue data from PDP.  For commodities without a
registered use or tolerance for cypermethrin/zeta-cypermethrin, EPA
assumed these commodities would be treated in a food handling
establishment (100% treated) and an anticipated residues of ½ the LOD
(0.05 ppm) was assumed for all these commodities.   

Alpha-cypermethrin registration will cite all the environmental fate
studies done for the registration of zeta-cypermethrin and cypermethrin.
 Therefore, the drinking water assessment conducted for the
zeta-cypermethrin assessment is used for this alpha-cypermethrin
exposure assessment.   The chronic surface water value used in this
assessment is 0.013 ppb (February 8, 2007, D334937, J. Melendez).

The chronic Population Adjusted Dose (cPAD) used for U.S. population and
all sub-populations is 0.015 mg/kg bw/day. This endpoint is based on the
NOAEL value of 1.5 using a FQPA safety factor of 1.  The most highly
exposed population sub-group was children 1-2 years of age which
utilized 10.0 % cPAD.  The results of the chronic dietary assessment are
presented in Table1. 

Table 1. Results for Alpha-Cypermethrin Chronic Dietary Exposure
Analysis including Food and Drinking Water Exposure.  

Population	Exposure Estimate	%cPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population	0.000454	3.0

All Infants (< 1 year old)	0.000943	6.3

Children (1-2 years old)	0.001496	10.0

Children (3-5 years old)	0.001176	7.8

Children (6-12 years old)	0.00063	4.2

Youth (13-19 years old)	0.000286	1.9

Adults (20-49 years old)	0.000333	2.2

Adults (50+ years old)	0.000415	2.8

Females (13-49 years old)	0.000344	2.3



The results of the analysis show that for all populations, the exposures
are below a level of concern (< 100% cPAD).  ]>

<Drinking water. 

[ Alpha-cypermethrin will not be registered on any crops where
zeta-cypermethrin or cypermethrin are not currently registered. 
However, alpha-cypermethrin will not be registered on all the current
crops registered with zeta-cypermethrin or cypermethrin.  

Alpha-cypermethrin registration will cite all the environmental fate
studies done for the registration of zeta-cypermethrin and cypermethrin.
 Therefore, the drinking water assessment conducted for the
zeta-cypermethrin assessment is used for this alpha-cypermethrin
exposure assessment.   The acute surface water value used in this
assessment is   1.0 ppb (February 8, 2007, D334937, J. Melendez).   The
chronic surface water value used in this assessment is 0.013 ppb
(February 8, 2007, D334937, J. Melendez).  The acute and chronic
groundwater EDWC value is 0.0036 ppb (February 8, 2007, D334937, J.
Melendez).  

Acute Aggregate Exposure and Risk (food and water)

The aggregate acute risk including exposure of Alpha-Cypermethrin from
food and water are done for the most highly exposure subpopulation,
children 1-2 years old.  The food exposure is 0.0061 mg/kgbw/day and the
drinking water exposure using a EDWC of 1.00 ppb is 0.000199 mg/kg
bw/day   The combined exposure is 0.006299 mg/kgbw/day which accounts
for 15.7% of the aPAD.  The results demonstrate that there are no safety
concerns for any subpopulation based on the proposed uses and the
results meet the FQPA standard of reasonable certainty of no harm.   

Short- and Intermediate-Term Aggregate Exposure and Risk (food, water,
and residential)

Short- and intermediate-term aggregate risk assessments include chronic
exposure from food, water, and exposure from residential uses.  The
exposure values used in this aggregate assessment are from the recent
human health assessment for Zeta-cypermethrin conducted by EPA (D.
McNally, November 27, 2007, D344749).  BASF will cite the data from
zeta-cypermethrin for the alpha-cypermethrin registration.  The short-
and intermediate-term endpoint is 7.4 mg/kg bw/day.  The aggregate
assessment was conducted for the most highly exposure population group,
children 1-2 years old.  The highest residential oral exposure for
children 1-2 was for hand-to-mouth activity from indoor surfaces
following crack and crevice treatment.  This is the highest residential
oral exposure so it is protective for all other scenarios.  The highest
dermal residential exposure for children 1-2 years old occurred from the
indoor treatment of hard wood and carpets.  This dermal exposure is
protective for all other scenarios.  The short- and intermediate-term
aggregate exposure for children 1-2 is shown in Table 2.  

Table 2.  Aggregate Short- and Intermediate-term Aggregate Exposure for
Children 1-2 years old.  

Food exposure (mg/kg bw/day)	MOE	Oral carpet (mg/kg bw/day)	MOE	Dermal
Carpet (mg/kg bw/day)	MOE	Aggregate MOE

0.001496	4947	0.01111	666	0.0336	220	160



The assessment shows that the short- and intermediate-term aggregate
exposure is below the EPA level of concern.     

Chronic Aggregate Exposure and Risk (food and water)

The aggregate chronic risk including exposure of Alpha-Cypermethrin from
food and water are shown in Table 1. The results demonstrate there are
no safety concerns for any subpopulation based on the proposed uses and
the results meet the FQPA standard of reasonable certainty of no harm. 

]>

<	2. Non-dietary exposure. [The residential exposure cited in this
assessment is based on the most recent exposure assessment cited for
cypermethrin / zeta-cypermethrin (D. McNally, November 27, 2007,
D344749).   The residential post-application incidental oral exposure
MOE’s range from 190 to 960,000 which exceed the target MOE of 100
(D334263; Nov. 29, 2006, Zeta-cypermethrin: Revised Human Health risk
assessment).  The combined exposure to toddlers following home lawn
application, hand to mouth, object to mouth, and incidental soil
ingestion was 2,600 which greatly exceeds the target MOE.  The dermal
exposure for adults is not assessed because there is no dermal NOAEL
selected for adults.  The dermal exposure for toddlers was determined
and the calculated MOEs were all greater than the target MOE (D.
McNally, November 27, 2007, D344749).  This assessment shows that there
are no levels of concern which are exceeded from the residential uses.]>

<D. Cumulative Effects>

<	["Section 408(b)(2)(D)(v) requires that, when considering whether to
establish, modify, or revoke a tolerance, the Agency consider
“available information'' concerning the cumulative effects of a
particular pesticide's residues and “other substances that have a
common mechanism of toxicity." Alpha-cypermethrin is a member of the
pyrethroid class of pesticides. Although all pyrethroids alter nerve
function by modifying the normal biochemistry and physiology of nerve
membrane sodium channels, EPA is not currently following a cumulative
risk approach based on a common mechanism of toxicity for the
pyrethroids.  Although all pyrethroids interact with sodium channels,
there are

multiple types of sodium channels and it is currently unknown whether
the pyrethroids have similar effects on all channels. Nor do we have a
clear understanding of effects on key downstream neuronal function e.g.,
nerve excitability, nor do we understand how these key events interact
to produce their compound-specific patterns of neurotoxicity.  There is
ongoing research by the EPA's Office of Research and Development and
pyrethroid registrants to evaluate the differential biochemical and
physiological actions of pyrethroids in mammals. When available, the
Agency will consider this research and make a determination of common
mechanism as a basis for assessing cumulative risk.]

>

<E. Safety Determination>

<	1. U.S. population. [Based on this risk assessment, BASF concludes
that there is a reasonable certainty that no harm will result to the
general population from the aggregate exposure to Alpha-cypermethrin
from the proposed uses.]>

<	2. Infants and children. [Based on this risk assessment, BASF
concludes that there is a reasonable certainty that no harm will result
to infants or children from the aggregate exposure to Alpha-cypermethrin
from the proposed uses.]>

<F. International Tolerances>

"

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CODEX maximum residue levels established for cypermethrin residues in
many different crop and crop groups.  JMPR considered the residue trials
for alpha-cypermethrin, zeta-cypermethrin and cypermethrin collectively.
 Codex maximum residue levels have been established in the following
crops:

Leafy vegetables			0.7	Edible offal, mammalian		0.05

Pome fruits				0.7	Meat, from mammals		2.0

Stone fruits				2.0	Poultry meat				0.05

Roots and tubers			0.01	Eggs					0.01

Fruiting vegetables, cucurbits	0.07	Milks					0.05

Legume vegetables			0.7	Milk fats 				0.5

Pulses					0.05

Dry bean				0.05

Brassica				1.0

Leafy vegetables			0.7

Citrus fruits				2.0

Cereal grains				0.3

Corn, sweet				0.05

Oilseed				0.1

Eggplant				0.03

Okra					0.5

Onion bulb				0.01

Bell pepper				0.1

Non-bell pepper			2.0

Pimentos				0.1

Sugar beet 				0.1

Sugar cane				0.2

Tomato				0.2]>

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