Summary of Toxicological Studies on Acrinathrin
Market Development, AgrEvo Japan Limited(Received January 26, 1998 ; Accepted March 20, 1998)
DESCRIPTION OF THE TEST CHEMICALSAcrinathrin is a new active ingredient which belongs to the family of Synthetic
Pyrethroids and possesses high insecticidal activity against a wide range of insect
pest together with miticidal activity. It has been discovered and synthesized by Roussel
Uclaf in 1980s. In Japan, acrinathrin has been developed for application on various
crops including vegetables, fruits, tea and ornamentals as the formulation product of
the compound, ARDENT® 3% WP (acrinathrin 3% wettable powder, hereafter as WP
formulation) and was registered in 1995 as a insecticide for the control of these crops.
The chemical structure and physico-chemical properties of acrinathrin are given as
below.
Common name: Acrinathrin (BSI, draft ISO)
Chemical name: (S)-α-cyano-3-phenoxybenzyl (Z)-(1R, 3S)-2,2-dimethyl-3[2-(2,2,2-trifluoro-1-trifluoromethylethoxycarbonyl)vinyl]cyclopropanecarboxylate (IUPAC)
Structural formula:
O

CN

O

O

O

O
F3C
CF3

Molecular formula: C26H21F6NO 5
Molecular weight: 541.4
Physical state: Whitish powder
Melting point: 81.5˚CVapor pressure: 3.9 x l0-4 mPa (25˚C)
Solubility in water (mg/l at 25˚C): <0.02 mg/l
Solubility in organic solvents (g/l at 25˚C): xylene 400, toluene 550, dichloroethane
650, acetone 700, ethanol 61, n-octanol 13
Partition coefficient (n-octanol/water): log P= 5.24
Stability: Stable under heat or acidic condition, unstable under diffused light andalkaline condition
ACUTE TOXICITY STUDIESThe results of acute toxicity studies via various routes are summarized in Table 1.
In these studies via routes of oral or respiratory tract, dosing of acrinathrin technicalor WP formulation caused non-specific signs of toxicity, which were reversible during

Table l Acute toxicity studies.
Test substance Route

Formulation(3% WP)a)b)

Laboratory (year)

Rat
Mouse
Rat

M, Fa) > 5,000 Centre International deM, F > 5,000 Toxicologie ( 1987)
M, F > 2,000

Inhalation(4 hr)

Rat

LC50 (mg/l )Huntingdon ResearchMl.72 Centre Ltd. ( 1987)
F
1.21
b)
M + F 1.60

Oral

Rat
Mouse

DermalRat

M, F > 5,000 Biosafety Research
M, F > 5,000 Center, Foods, Drugs
and Pesticides (1989)
M, F > 2,000

OralTechnical

Species LD50 (mg/kg)

DermalM, F: Value each for male and female.
M+F: Value combined male and female.

the observation period of 14 day. No toxic signs were observed in dermal toxicity
studies.
Acute oral LD50 was considered to be 5000 mg/kg or more in rats and in mice.
IRRITATION STUDIES
1. Primary Eye Irritation Studies on Rabbits
A dose of 100 mg of acrinathrin technical was placed into the left eye of 6 New
Zealand White rabbits. Untreated right eye served as a control.
One hour after the instillation, slight ocular reactions were observed in all of theanimals. No ocular reactions were noted at 24, 48 and 72 hr.
Under this test conditions, acrinathrin was considered to be non-irritant.
(Centre International de Toxicologie, 1989)
A dose of 100mg of WP formulation or 0.1 ml of 1000 x diluted solution of theformulation (1 g/l water) each was instilled into the right eye of 9 New ZealandWhite rabbits consisting of 6 unwashed and 3 washed eye animals. The eyelids were
gently held together for 1 sec, then the right eye of each rabbit was washed withphysiological saline at 2-3 min after instillation. The eyes were examined after 1, 24,
48, 72 hr and after 7 and 14 days.
In the rabbits treated with the undiluted formulation, although slight to moderate
irritation was noted in the unwashed eye, the irritation reaction was reduced andrecovered to normal within shorter period in the eyes washed after installation of thetest substance compared to the unwashed eyes. In the rabbits treated with 1000 x
diluted solution of the formulation, no irritation was observed.
(Biosafety Research Center, Foods, Drugs and Pesticides, l 989)
2. Primary Dermal lrritation Studies on Rabbits
A single application of 500 mg of acrinathrin technical or WP formulation each
was applied to the clipped area of 6 New Zealand White rabbits. The test substance
was held in contact with the skin for 4 hr by a occlusive dressing.
The cutaneous reactions were observed 1 hr after the removal of the dressing andthen daily, up to 3 days. No irritation was observed in the rabbits treated withacrinathrin technical, while very slight and reversible irritation was noted in the
animals treated with WP formulation.
(Technical: Centre International de Toxicologie, 1989;
WP formulation: Biosafety Research Center, Foods, Drugs and Pesticides, 1990)
DERMAL SENSITISATION STUDIES ON GUINIA PIGS
The potential of acrinathrin technical or WP formulation to induce delayed contact
hypersensitivity were evaluated according to guinea pig Maximization method.
At any scoring time, following the removal of the occlusive dressing of the cutaneous
challenge application of each test substance, no reaction of cutaneous sensitisation
was recorded for both acrinathrin technical and WP formulation. On the other hand,
positive reactions were apparently noted in positive control group of 2,4dinitrochlorobenzen.
It was concluded, therefore, neither acrinathrin nor WP formulation have any
evidence of cutaneous sensitisation potential.
(Technical: Centre International de Toxicologie, 1993;
WP formulation: BOZO Research Center Inc., 1991 )THE DELAYED NEUROTOXICITY STUDY
Oral administration of a single dose of acrinathrin technical at a dose level of 5000
mg/kg, followed by a repeat dose after 21 days, did not produce any clinical signs ofneurotoxicity in adult hens used. This results was confirmed by histological examination,
which showed no treatment-related changes in the nerve tissue.
(Huntingdon Research Centre Ltd., 1988)
SUBCHRONIC TOXICITY STUDIES
1. Rats Study by Dietary Repeat Dose for 90 Days Followed by a 28-Day Recovery
PeriodGroup of 20 male and 20 female CD (SD) rats were fed diet containing 0, 30, 100
or 300 ppm of acrinathrin for 90 days. The animals were housed two per cage of thesame sex and the same group in metallic cages.
At doses of 100 and 300 ppm, several animals of both sexes showed skin lesions
with scabs, sores and alopecia which sometimes persisted with an itching phenomenon.
During the recovery period all of the skin lesions (except only for one female in 100
ppm group) seen in the treatment period regressed and disappeared in the high levelsof 100 ppm or more.
Overall, the mortality was not marked, except in the 300 ppm group where deaths
recorded in females could be treatment related and/or due to malnutrition. A bodyweight decrease and a reduction in food consumption each related to the concentration
were observed in both sexes of the 100 and 300 ppm groups.
Those effects were gradually reversible during the recovery period. The microscopic
examinations showed skin lesions recorded in 1 male and 1 female from the 100 ppm
group and 7 animals of 300 ppm group. Other microscopic findings observed werelymphoid deletion in the spleen and thymus in 5 females of the 300 ppm group andmedullar atrophy in 2 females of the 300 ppm group.
No other treatment related changes were observed in hematological and bloodbiochemical examinations, urinalysis and organ weight. The No Observed EffectLevel (NOEL) for this study was considered to be 30 ppm (male: 2.4 mg/kg/day;female: 3.1 mg/kg/day).
(Centre International de Toxicologie, 1988)
2. Dogs Study by Repeated Oral Dose for 90 Days Followed by a 4-Week Recovery
PeriodGroups of 8 male and 8 female Beagle dogs were dosed daily for 90 days ingelatin capsules at 0, 1, 3 and 10 mg/kg/day.
The main treatment-related clinical signs observed were vomiting and diarrhea.
They occurred sporadically and sometimes repeatedly (only for diarrhea) in almost
all the treated animals with dose-related incidence and Intensity. They did not impair
the general condition of the animal and were still present during the first day of therecovery period, but not thereafter. No deaths occurred during the study.
At 10 mg/kg/day, a slight body weight loss which did not exceed 6% in the males
and 3% in the females was recorded only in the first month of treatment.
In conclusion, acrinathrin dosed daily for 90 days at l, 3 and 10 mg/kg/day did not
induce overt signs of systemic toxicity. Except vomiting and diarrhea clinically recordedwith a dose-relationship in the treated dogs, no test substance-related changes wereseen in this study.
Under these experimental conditions, because of the slight digestive intolerance
seen at 1 mg/kg/day, a true NOEL was not clearly established; however, considering
the absence of impairment on the clinical condition of the dogs, it had been ascertainedthat 3 mg/kg/day was a true No Observed Adverse Effect Level (NOAEL).
(Centre International de Toxicologie, 1989)

3. 13 Week Complementary Toxicity Study in Dogs
This study was carried out as the complementary to the 90 day and 52-week
toxicity studies in Beagle dogs previously performed by the oral route and in gelatin
capsule. The objective of this study was to evaluate, on a clinical basis, the potential
toxicity and determine the NOEL of acrinathrin when administered daily by oralroute, capsules, to female dogs for 13 weeks at the dose levels of 0, 0.1, 0.3, 0.6, 1
and 3 mg/kg/day.
The conclusion was that no treatment-related effect on diarrhea and vomiting
could be demonstrated at any doses up to 3 mg/kg/day. No treatment-related effects
were also observed both on body weight change and food consumption.
Consequently, the digestive findings in the 90 day and 52 week studies are considered
to be of no toxicological importance at doses up to 3 mg/kg/day.
(Centre International de Toxicologie, 1994)
4. Mice Study by Dietary Repeat Dose for 8 Weeks
Group of 10 male and 10 female Swiss (CD-1) mice were fed diet containing 0, 5,
50, 150 and 450 ppm of acrinathrin for 8 weeks. The animals were housed individuallyin polycarbonate cages.
Increase of skin lesions was noted at higher dose levels of 150 and 450 ppm.
No other treatment related changes were observed in hematological and bloodbiochemical examinations and in organ weight. Some signs of cutaneous reactions
were seen in the two high dose levels.
Thus, the highest dose level for a carcinogenicity study had been ascertained aslower than 150 ppm.
(Centre International de Toxicologie, 1988)
CHRONIC TOXICITY/ONCOGENICITY STUDIESl. Combined Dietary Chronic Toxicity and Oncogenicity Study in Rat
Groups of 90 male and 90 female SD rats each were fed diet containing 0, 5, 15
and 45 ppm of acrinathrin for 104 weeks. A fourth treated group of 40 male and 40
female rats were fed diet containing highest concentration of 90 ppm of the test
substance for 104 weeks.
The highest dose for this study was ascertained to be lower than 100 ppm based on
the findings observed in the 90 day rats subchronic toxicity study; at the dose levelsof 100 and 300 ppm, acrinathrin induced signs of cutaneous toxicity and decreased
body weight gain and food consumption.
The animals were housed two per cage of the same sex and the same group insuspended wire-mesh cages.
No treatment-related clinical signs were observed. The palpable masses in animalsof both sexes of all groups did not indicate any treatment or dose-relationship, either

in frequency, time of onset, location, size or morphological type. There was nodifference in mortality between the treated and control groups and any treatment-related
effects could not be seen. No treatment-related body weight and food consumptionchanges were observed. Efficiency of food utilization was similar in control andtreated groups of both sexes. No treatment-related changes were observed in water
consumption and ophthalmological examination.
Upon hematological examination, a slight decrease in total white cell count andlymphocyte number observed in both sexes of the 15 ppm or more without a dose andtime-relationship were considered unlikely to be treatment-related.
No treatment-related changes were noted in biochemistry, urinalysis and organ
weight.
At the microscopic examination, after 52 weeks of treatment, the changes encountered
were recognized as those commonly occurring in the laboratory rat, furthermore
similar in incidence, severity and morphological character between the control andtreated animals, therefore they were considered irrelevant to the treatment.
After 104 weeks, the non-neoplastic changes encountered were commonly recorded
findings in the aged rat. In addition, these changes were of similar incidence, severity,and morphological character in control and treated animals and were considered as
not treatment-related.
All neoplastic lesions reported in all organs were recognized as those commonlyoccurring in the aged rat and showed no variations in incidence or morphologicaltypes that were considered to be related to the treatment with the test substance.
In conclusion, the oral administration by dietary mixture of the test substance for
104 weeks to rats at the dose levels of 5, 15, 45 and 90 ppm did not show any
treatment-related abnormalities in all parameters evaluated and any evidence indicating
the carcinogenic potential of the test substance.
Under conditions of this study, therefore the NOEL is considered to be 90 ppm(4.6 mg/kg/day for males and 6.1 mg/kg/day for females).
(Centre International de Toxicologie, 1991)
2. Oncogenicity Study in Mice
Groups of 50 male and 50 female Swiss (CD-1) mice were fed diet containing 0, 3,
15 and 75 ppm of acrinathrin for 78 weeks. The animals were housed individually inpolycarbonate cages.
In the highest dose group of 75 ppm, cutaneous lesions (weeping wounds andcrusts) were observed with a higher frequency and led to a poor physical condition ofsome animals.
The palpable masses found among mice of both sexes of all groups showed no
indication of treatment or dose-relationship either in frequency, time of onset, size, or
histological type.

Except the animals prematurely sacrificed for humane reasons due to severe
cutaneous lesions, the mortality rate and the factors contributing to death or prematuresacrifice showed no indication of a treatment or dose-relationship.
No changes in body weight, food consumption, hematological parameters andorgan weight which could be related to the treatment were observed.
At the macroscopic examination, only non-neoplastic lesions such as subcutaneous
swellings were observed in some animals at the highest dose of 75 ppm. The massfound in some organs at the macroscopic examination among mice of control andtreated groups, showed no indication of treatment or a dose-relationship either infrequency, size or multiplicity.
At the microscopic examination, skin ulcerations and chronic inflammations wereobserved in some animals of the highest dose of 75 ppm and were considered to betreatment-related.
The neoplastic lesions found among control and treated animals, were recognized
as those occurring commonly in mice and were not modified by treatment either inincidence, morphological type or multiplicity.
In conclusion, the oral administrations by dietary mixture of the test substance for
78 weeks to mice at the concentration of 3, 15 and 75 ppm had neither carcinogenic
potential nor caused an increase in the incidence of spontaneously occurring tumors.
The highest dose of 75 ppm induced severe skin lesions (ulceration and chronic
inflammations) among the animals with high frequency which could be treatmentrelated.
Thus, the NOEL in this study is determined to be 15 ppm (or 2.49 and 3.00
mg/kg/day in males and females, respectively).
(Centre International de Toxicologie, 1990)
3. 52 Week Oral Study in Dogs
Group of 6 male and 6 female Beagle dogs were dosed by oral route, in gelatin
capsules for 52 weeks at the levels of 0, l, 3 and l0 mg/kg/day. Control animals
received empty capsules only.
Slight to moderate, soft or liquid diarrhea were observed sporadically throughout
the study in the treated animals.
A loss of weight was observed until week 3 or 4 in both sexes treated at 10
mg/kg/day and the mean body weight of the males of this group remained inferior tothat of the other males thereafter (with a statistical significance for weeks 5 to 35 and
43 to 46), while it was similar to that of the other groups in the females.
The food consumption of the animals was not influenced by the treatment.
The ophthalmological and neurological examinations of the animals did not reveal
any test substance-related abnormality. The results of the laboratory investigations(hematology, blood chemistry and urinalysis) failed to indicate any test substance-related change.
The organ weight, macroscopic and microscopic examinations of the animals at
the end of the study did not show any abnormality which could indicate a treatment
relationship concerning the few observations made.
Based on the transient body weight loss observed until weeks 3-4, then a bodyweight retardation throughout the study for the males only, at 10 mg/kg/day, the
NOAEL in this 52 week study is considered to be 3 mg/kg/day. The animals showedoccasionally mild diarrhea with a very slight occurrence, however a clear dose response
could not be observed.
(Centre International de Toxicologie, 1990)
In conclusion, the dose of 3 mg/kg/day is confirmed to be the NOEL of acrinathrin
through above three studies in dogs.
(Centre International de Toxicologie, 1989-1994)
REPRODUCTION AND TERATOGENICITY STUDIES
1. Rat Two-Generation Study
Acrinathrin was administered to SD rats in the diet at concentrations of 0, 5, 20
and 80 ppm. After about 8 weeks of treatment, groups of 25 male and 25 female rats
from the F0 generation were paired to produce the Fl litters. Mated F0 females werethen treated during pregnancy and lactation.
The only observed clinical signs were transient cutaneous lesions in F0 adult animalsof the 20 and 80 ppm groups during the first 6 weeks of treatment; the cutaneous
lesions were not observed either in F1 pups or in Fl adult animals or F2 pups.
The treatment did not induce any effect in the reproductive parameters of bothparents and offspring. In particular, the mating and fertility indices, the length ofgestation of F1 and F2 animals as well as the birth index and viability of pups on day 4
and 21 post-partum of the F1 and F 2 litters were comparable in treated and control
groups.
In the parents, the highest dose level of 80 ppm induced a slight and transient
reduction in body weight gain and food consumption of F0 and F1 animals.
In conclusion, the NOEL in terms of reproductive performance is defined as 80
ppm corresponding to 9.4 mg/kg/day for males and 10.6 mg/kg/day for the females.
And the NOEL for parental generations is 20 ppm corresponding to 2.5 mg/kg/day
for the males and 2.8 mg/kg/day for the females.
(Centre International de Toxicologie, 1989)
2. Rat Teratology Study
Acrinathrin suspended in corn oil was administered at the dose levels of 0, 2, 6 and18 mg/kg/day to groups of 25 mated females in SD rats from days 6 to 15 ofpregnancy. On day 20 of pregnancy, females were sacrificed and fetuses were removed
by caesarean section. Litter values were determined and fetuses were subsequently

examined for external, visceral and skeletal abnormalities.
The following findings were observed:
Maternal findings: At 6 mg/kg/day or more, the body weight gain of the females
had stopped or decreased between days 9 and 15. At 18 mg/kg/day, piloerection wereobserved in high frequency and three females were found dead. At this highest doselevel, the body weight still remained lower through days 20, and furthermore thedecrease in the rate of live fetuses and the increase in the rate of fetal loss were noted.
Litter findings: At 18mg/kg/day, the mean body weight of fetuses was decreased.
The incidence of minor skeletal abnormalities was increased at the highest dose levelbut these abnormalities were essentially represented by a delay in the ossification
process. The rate of fetuses affected with external, skeletal or visceral abnormalities
was comparable between the control and the 2 and 6 mg/ kg/day groups.
In conclusion, the dose of 2 mg/kg/day was considered to be the NOEL in terms ofmaternal toxicity. The dose of 6 mg/kg/day was considered as the NOEL in terms ofembryofetal development. Acrinathrin revealed no evidence of teratogenicity even at
the highest dose level of 18 mg/kg/day. (Centre International de Toxicologie, 1988)
3. Rabbit Teratology Study
Acrinathrin suspended in corn oil was administered at the dose levels of 0, 15, 45
and 135 mg/kg/day to groups of 16 mated females in New Zealand White rabbits
from days 6 to 18 of pregnancy. On day 28 of pregnancy, females were sacrificed andfetuses were removed by caesarean section. Litter values were determined and fetuses
were subsequently examined for external, visceral and skeletal abnormalities.
The following findings were observed:
Maternal findings: At 45 mg/kg/day or more, a transient decrease in body weightgain from days 5 to 12 was observed slightly. At 135 mg/kg/day, the rate of live
fetuses was lower and the rate of fetal losses was higher. On general symptoms,
reduced food consumption and anorexia were observed animals ofthe highest doselevel.
Litter findings: The delay in ossification was observed at the highest dose of
135mg/kg/day. The rate of fetuses affected with external, skeletal, or visceralabnormalities were quite comparable between control and treated groups.
In conclusion, the dose of 15 mg/kg/day was considered to be the NOEL in termsof maternal toxicity. The dose of 45 mg/kg/day was considered as the NOEL in termsof embryofetal development. Acrinathrin revealed no evidence of teratogenlcity evenat the highest dose level of 135 mg/kg/day.
(Centre International de Toxicologie, 1988)

MUTAGENICITY STUDIESAcrinathrin has been the subject of numerous studies in the field of mutagenicity.
The possible mutagenic potential of acrinathrin has been studied at three possiblelevels of genotoxic action:(1) Detection of gene mutation(2) Detection ofchromosomal aberration (in vitro and in vivo)(3) DNA damage repair test
While a very weak positive reaction was noted only in vitro cytogenic assay with
Chinese hamster CHO cell with metabolic activation system, both in vivo cytogenic
assay and micronucleus assay were negative.
Acrinathrin was also negative in other test systems, therefore it is not consideredthat this test substance is mutagenic. All the test results are summarized in Table 2.

Table 2 Mutagenicity studies.
MethodSpecies,cell type

Concentrations Test conditionsof acrinathrin

Ames test in vitro

S. typhimurium;
100 to 5000
TA 98, 100, 1535, µg/plate
1537, 1538
E. coli, WP2uvrA

Without S-9 mix
With S-9 mix

Negative CITb)
Negative (1989)

Gene mutation
test in vitro

HPRT locus in
V79 Chinese
hamster cell

3 to 300µg/ml

Without S-9 mix
With S-9 mix

Negative CIT
Negative (1990)

Metaphasechromosome
analysis in vitro

Chinese hamster
ovary (CHO) cell

30 to 300 µM

Without S-9 mix
With S-9 mix

Negative CIT
Positivea) (1987)

Metaphasechromosome
analysis in vivo

Chinese hamsterbone marrow cell

50 to 200mg/kg
per osHamsters
sacrificed,
6, 24, 48 hr
after dosing

Negative CIT(1989)

Micronucleus
test in vivo

Swiss Cr1 mousebone marrow cell2000 mg/kg
per osMice sacrificed,
24, 48, 72 hr
after dosing

Negative CIT(1987)

DNA repair
test in vivo

E. coli ;pol A+, pol A-

50 to 5000
µg/plate

Without S-9 mix
With S-9 mix

Negative CIT
Negative (1987)a)Results Laboratory(year)

Statistically significant slightly enhanced number of aberrations was observed at the highest
level of 300 µM Which is the limit of solubility in culture medium.
b)
CIT: Centre International de Toxicologie.

RAT METHABOLISM STUDIESAbsorption, distribution, excretion and metabolism in rats were tested using [14Cbenzyl] and/or [14C-dimethyl]acrinathrin.
In the study in SD rats given by gavage at single dose of 1 mg/kg, it was measured
in plasma that Tmax is 4-6 hr and Cmax is 0.5-0.8 µg eq./ml.
At the 48 hr after dosing, 48-52% dose in bile, 33-45% dose in urine and 55-67%
dose in feces each was excreted. Thus, acrinathrin in rats was rapidly absorbed andexcreted. At the Tmax after dosing of the compound, a relatively higher concentrationof radioactivity in liver when compared to that in plasma was detected, but it was
decreased rapidly with time. There was no indication of preferential accumulation ofradioactivity in any specific tissue. Major metabolites identified in feces were unchanged
parent compound and cis-deshexafluoroisopropyl acrinathrin.
Major metabolic reactions were hydrolysis of ester bonds, oxidation of cyano-3phenoxybenbenzyl alcohol group and production of conjugates.
(Huntingdon Research Centre Ltd., 1990)
SUMMARY
The results of studies showed that acrinathrin demonstrated low mammalian toxicity
following acute oral, dermal or inhalation exposure. The results obtained support
those already known for other pyrethroids in particular the cyano-pyrethroids.
No irritation was observed in the skin and eye of rabbits treated with acrinathrin
technical, while very slight and reversible irritation was noted following treatment
with WP formulation. No ocular irritation was observed with the diluted solution of
WP formulation. Both acrinathrin technical and WP formulation were negative inskin sensitisation studies conducted by Maximization method.
Acrinathrin did not show mutagenic potential, was not oncogenic in rats and miceand did not affect reproduction of two generations in rats.
Acrinathrin exhibited no teratogenic potential in rats and rabbits.
Main effects observed in subchronic toxicity studies through chronic toxicity studies
were the decrease of body weight gain and food consumption, and skin lesions seen
at high dose levels in rats and mice dietary studies. The skin lesions persisted with anitching and scratching phenomenon due to paresthetic changes, which were considered
to be related to the pharmacological property of acrinathrin and it seems probable that
it is brought about by an action of the substance on sodium channels and depolarisationof the sensory nerves. The findings in the reproduction study indicate that the effects
are reversible and result in no permanent changes.
Through these long term studies, the overall NOAEL for acrinathrin was determined
to be 15 ppm (2.49 mg/kg/day) in the oncogenicity study in mice. ARDENT® 3% WP
was registered by Japanese MAFF in 1995 as the insecticide with miticidal activity
for various crops including vegetables, fruits, tea as well as ornamental. When usedin accordance with label directions, acrinathrin and its formulation will not adverselyaffect human health.
Contact
Market Development, AgrEvo Japan Limited, l0-33, Akasaka 4-chome Minato-ku,
Tokyo 107-0052, Japan
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