Sponsored jointly by FAO and WHO


    Joint meeting of the
    FAO Panel of Experts on Pesticide Residues
    in Food and the Environment
    and the
    WHO Expert Group on Pesticide Residues
    Rome, 6-15 October 1980



    This pesticide was evaluated by the 1979 Joint Meeting (FAO, 1980).
    Data were not submitted in sufficient time to allow an estimation
    of an ADI for man and consideration was deferred.  In the absence
    of toxicological evaluations, guideline levels for residues found
    in crops following good agricultural practice were reported.  The
    present monograph addendum considers all the available
    toxicological information submitted to the Meeting.

    Special explanatory note

    Phenothrin is a chrysanthemic acid ester of 3-phenoxybenzyl
    alcohol. Four stereoisomers of phenothrin can be derived from the
    chirality of the cyclopropane ring at the C1 and C3 positions. 
    The nomenclature does not prescribe the ratio of isomers but rather
    the ratio of isomers is a function of synthesis or purification of
    the technical product.  It is critical to note the isomeric ratio
    in the product used in supervised residue trials and in
    toxicological studies.

    Among the four isomeric esters (d:1, cis: trans), both
    1-isomers show little insecticidal activity.  In addition, the
    d-cis isomer appears to be less effective as an insecticide than
    the d-trans.  Thus, the d-trans is the isomeric molecule of
    choice for insecticidal activity.

    Phenothrin is the racemic mixture (+)cis, trans molecules
    containing a 20:80 isomeric ratio.  An additional compound
    (Sumithrin(R)) is the registered trademark for the (d+) cis,
    trans (20:80) preparation.  Thus Sumithrin(R) is a purified
    component of the technical phenothrin.



    Absorption, distribution and excretion

    Studies on the metabolic fate of phenothrin (the d, 1 trans,
    cis 80:20 3 phenoxybenzyl chrysanthemate active ingredient) have
    not been reported.  However, studies on the metabolic fate of one
    of the isomeric components of phenothrin, the d-trans
    chrysanthemic acid ester of 3-phenoxybenzyl alcohol, have been
    performed in rats.  14C-d-trans-phenothrin was orally
    administered to male rats at a dosage of 200 mg/kg body weight. 
    The isomer was rapidly absorbed, translocated in the body, and
    excreted predominantly in the urine. In the faeces, up to 9% of the
    phenothrin isomer was excreted unchanged.

    Within three hours of administration, maximum body burdens were
    recorded in all tissues examined.  Within 12 hours, these levels
    had diminished to values representing about 50% of the maximum
    residue found, and within 24 hours the vast majority of
    radioactivity had been excreted from the body.  Excretion is
    extremely rapid.  Within three hours, approximately 40% of the
    orally administered radioactivity had been excreted and all
    radioactivity was recovered within 48 hours (Miyamoto et al,


    Based upon in vivo studies with the d-trans-phenothrin, the
    metabolic fate appears to follow that observed with several other
    pyrethroid esters.  Phenothrin is hydrolysed to the 3-phenoxybenzyl
    alcohol, which in turn is oxidised to 3-phenoxybenzoic acid and
    other metabolites.  The major degradation pattern of both cis and
    trans isomers can be seen in Figure 1.  In contrast to the
    trans isomer, both in vivo and in vitro studies confirm
    that the cis-phenothrin is metabolised at a less rapid rate and
    yields a larger proportion of ester metabolites.  There exists a
    substantial difference between the two isomers in the rate of
    hydrolysis as observed by in vitro studies. Based upon both
    in vivo and in vitro data, it appears that hydrolytic
    cleavage at the ester is probably the major pathway of
    biodegradation of phenothrin although oxidative metabolism of the
    cis isomer portion would be expected to yield a somewhat
    different pattern of metabolites, some of which appear to contain
    an intact ester moiety (Miyamoto et al, 1974; Casida et al,
    1979; Soderlund and Casida, 1977; Suzuki et al, 1976, Suzuki and
    Miyamoto, 1978).

    Individual isomers (d-cis and d-trans) of phenothrin were
    formulated as a dust or an emulsified concentrate and applied
    orally or dermally to rats.  The dermal exposure was for 24 hours. 
    Following oral administration, the isomers of phenothrin were
    eliminated from the body primarily in urine and faeces within 6
    days.  With the cis-isomer the major reaction products were
    oxidative metabolites and ester hydrolytic products.  With the
    trans-isomer the major metabolites were hydrolytic products.  The
    data confirmed earlier work both in vivo and in vitro,
    which had demonstrated a similar reaction with these isomers. 
    Following dermal administration, the major quantity of the applied
    dose was recovered from the intact skin.  The emulsifiable
    concentrate was found to penetrate the skin to a greater degree
    than the dust formulation and a substantial difference was noted
    with absorption of individual isomers (the cis-isomer penetrated
    more rapidly than the trans).  As with oral administration the
    absorbed dose was rapidly eliminated from the body.

    Once in the body, the isomers were metabolised in a similar manner
    irrespective of the initial route of entry.  With the cis-isomer,
    the major metabolic reactions were oxidative at the cis and
    trans-positions of the isobutenyl group; at the trans-position
    of the gem-dimethyl group of the cyclopropane ring; at the
    4'-position of the alcohol moiety; and slightly at the 2'-position;

    additionally, cleavage of the ester bound occurred.  In contrast, 
    hydrolytic cleavage of the ester bond was the most prominent 
    reaction of the trans-isomer, occurring some 5 times faster 
    than with the cis-isomer. Hydroxylation at 4'-position occurred 
    to the same degree as with the cis-isomer.  The qualitative 
    metabolic course followed that identified in Figure 1 (Kaneko, H. 
    et al, 1980).

    Biochemical aspects

    A carboxyesterase has been isolated and purified from rat liver
    microsomes.  This carboxyesterase was found to hydrolyse
    trans-phenothrin faster than the cis isomers and may account in
    part for the reduced mammalian toxicity of the trans isomers.  In
    contrast to the increased hydrolytic rate observed with
    trans-phenothrin, the cis-phenothrin was found to be oxidised
    at a more rapid rate by mouse liver microsomal preparations.  These
    data may explain the difference in toxicity noted between the cis
    and trans isomers of several of the pyrethroid esters (Suzuki and
    Miyamoto, 1978; Soderland and Casida, 1977; Casida et al, 1979).

    FIGURE 1


    Special Pharmacological studies

    A series of pharmacological studies were performed with the
    d-isomer of phenothrin (Sumithrin(R)).  These studies reported the
    pharmacological action of this pyrethroid on respiration, blood
    pressure, and a series of tests representative of effects on the
    peripheral and central nervous system.  Sumithrin(R) was emulsified
    (Sorpol(R) 1200 and/or Tween(R) 80) and either diluted with
    physiological saline or used directly.  The following series of
    in vitro and in vivo studies were performed: spasmolytic
    activity on isolated ileum from male guinea pigs; spontaneous
    contractions of isolated uterus from rats; contractions of a
    neuromuscular preparation of phrenic nerve-diaphgram of rats;
    respiration, nictitating membrane and blood pressure of male cats
    administered Sumithrin(R) intravenously; contractile force, blood
    pressure, and heart rate of dogs administered Sumithrin(R)
    intravenously; the anticonvulsive activity following induced
    convulsion or seizures in mice; the effects on muscular relaxation
    activity in mice; coordinative movement in mice;
    hexabarbital-induced sleeping time in mice; spontaneous activity in
    mice; body temperature of male rats; and electroencephalogram in
    male cats.

    Sumithrin(R) did not show any pharmacological activity in any of
    the in vitro and/or in vivo experiments listed above.  A
    tentative arousal response in the electroencephalogram of cats
    intravenously administered a dose of 4 mg/kg body weight was
    recorded.  Several other synthetic pyrethroid esters have been
    shown to induce this arousal response in the EEG pattern of cats
    (Hare et al, 1974).

    Special studies on neurotoxicity

    Groups of rats exposed by inhalation to the d-isomer of phenothrin
    (Sumithrin(R)) at concentration of up to an including 3,760 mg/m3
    for four hours showed no adverse effects as a result of exposure.
    Examination of the sciatic nerve for possible myelin degeneration
    or axon disruption did not reveal any such occurrence (Kohda et
    al, 1977).

    Groups of rats were administered Sumithrin(R) orally for five
    consecutive days at a dosage level of 5,000 mg/kg/day.  Mortality
    was observed and toxic signs of poisoning were noted in several of
    the animals.  Toxic signs of poisoning rapidly disappeared at the
    conclusion of the treatment.  Three days after treatment, all
    animals were sacrificed and histopathological examination of
    sciatic nerve was carried out to determine whether changes had
    occurred.  Clinically, there were no toxic signs of poisoning as
    evidenced by leg weakness or ataxia.  Histological examination
    revealed minute changes in axon and myelin, characterised by very

    slight axonal swelling, axonal disintegration, and/or demyelination.  
    There were similar occurrences in the control animals and it was 
    suggested that the small changes observed were not due to the 
    administration of Sumithrin(R).  It was considered that oral 
    administration of Sumithrin(R) at excessively high doses does 
    not induce a neurotoxic effect as has been observed with several 
    other pyrethroid esters (Okuno, et al, 1978; FAO, 1980).

    Special studies on mutagenicity

    The host-mediated assay was conducted with phenothrin and
    individual isomers of phenothrin in male mice using S.
    typhimurium-G46 as an indicator strain.  Groups of six male mice
    were administered phenothrin orally, twice, at 24-hour intervals at
    dosage rates of 0, 500, or 1500 mg/kg/dose.  Additionally, the
    d-trans and d-cis isomers were administered at dosage levels of
    250 and 90 mg/kg respectively.  A positive control of
    dymethylnitrosamine (50 mg/kg) was used. Immediately after
    administration of the chemical, the tester strain (S.
    typhimurium) was administered into the abdominal cavity.  This
    was removed three hours later, cultured and examined for mutation
    frequency.  There was no increase in reversion frequency observed
    with phenothrin or its isomers although the positive control was
    found to give an increased reversion rate.

    The potential mutagenicity of phenothrin was investigated using
    various bacterial test systems including the Reo-Assay (repair
    test) with Bacillus subtilis and Salmonella typhimurium

    At dose levels ranging from 0 to 10 mg/disc/plate, phenothrin did
    not induce an increase of the growth inhibition zone of the
    microorganisms, while mytomycin C showed a substantially larger
    inhibition zone.  A negative control gave results similar to that
    obtained with phenothrin.

    Mutation induction studies (the standard "Ames test") with various
    strains of E. coli and Salmonella typhimurium (TA1535,
    TA1537, TA1538, TA98 and TA100) with and without metabolic
    activation enzymes, were performed.  Phenothrin and its individual
    isomers, at dose levels up to 10 mg per plate, with or without
    hepatic drug metabolising enzymes, showed negative results in this
    standard mutagenicity assay.  Phenothrin and its individual isomers
    alone and following metabolic activation, caused no increase in the
    mutation rate.  Positive controls employed during the course of the
    study gave significant numbers of revertants (Shirasu et al,
    1977; Suzuki and Miyamoto, 1975).  Under the conditions of these
    bioassays, phenothrin and its individual d-cis and d-trans
    isomers are not mutagenic.

    Special studies on teratogenicity

    Groups of pregnant New Zealand rabbits (17 rabbits per group) were
    administered phenothrin orally at dosage levels of 0, 3, 10 or 30

    mg/kg from day 6 to 18 of gestation.  All animals were sacrificed
    on day 29 of gestation and the young obtained by caesarean section
    were examined.

    Does treated with phenothrin at the highest dosage level exhibited
    a loss in body weight during gestation.  There was no mortality
    observed in the study.  There was a slight decrease in the number
    of live young obtained from does treated with 30 mg/kg.  Changes in
    other reproductive/teratogenic parameters did not show a
    dose-response relationship and were not believed to be induced as
    a result of phenothrin administration.  At 30 mg/kg, there was a
    slight reduced foetal weight which was not accompanied by changes
    in survival rate or in the occurrence of external or internal

    There was no apparent teratogenic effect of phenothrin as observed
    by apparent gross internal or external somatic abnormalities and by
    examination for foetal skeletal development following prenatal
    exposure.  Treatment of pregnant albino rabbits during the period
    of  foetal organogenesis did not induce abnormal foetal
    development.  At the high dosage level, possible foetal and/or
    maternal toxicity was observed.

    Groups of pregnant rabbits (15 dose/group) were administered
    Sumithrin(R)) at dosage levels of 0, 10, 100 or 1000 mg/kg/day from
    day 6 through 18 of gestation.  All does were sacrificed on day 29
    or day 30 and caesarean section was performed to remove the foetus. 
    Following caesarean section, one half of the pups were maintained
    for 24 hours to evaluate survival.

    There were no abnormalities observed in the maternal parameters
    (including: body weight, food consumption, clinical observations,
    and necropsy) or on foetal data (including: implantation sites,
    corpora lutea, resorptions sites and live or dead foetuses).  Data
    on foetal weight and condition were normal.  Data on foetal
    survival and from internal and external examinations for
    abnormalities showed no significant effects of administration of
    Sumithrin(R) during gestation (Rutter, 1974).

    The teratogenic potential of Sumithrin(R) was examined in mice. 
    Groups of pregnant mice (17-18 mice/group) were orally administered
    Sumithrin(R) emulsified in 0.1% Tween(R) 80 at dosage levels of 0,
    30, 300 or 3000 mg/kg from day 7 to 12 of gestation.  A separate
    group of mice (7 mice per group) receiving dosage levels of 0, 300
    or 3000 mg/kg were utilized in the study to evaluate postnatal
    effects.  On day 18 of gestation, mice were sacrificed and pups
    delivered by caesarean section.  The second group of mice were
    allowed to deliver naturally and the young were maintained for 29

    There were no adverse effects of the administration of Sumithrin(R)
    with respect to maternal and embryo well-being as evidenced by
    maternal growth, foetal mortality and external and internal
    examination of foetuses for teratogenic or embryotoxic effects.

    Sumithrin(R) was neither teratogenic nor embryotoxic in mice at
    dosage levels up to and including 3000 mg/kg (Nakamoto et al,

    Special studies on reproduction

    Groups of rats (8 male and 16 female Charles River rats/group) were
    fed phenothrin in the diet at dosage levels of 0, 200, 600, or 2000
    mg/kg and subjected to a standard three-generation, two-litter per
    generation reproduction study.  Data were reported on the
    significant reproductive indices (mating index, fecundity index,
    male fertility index, female fertility index and the incidence of
    parturition).  The first litters obtained were examined for
    physical abnormalities at birth and for the numbers of viable and
    stillborn pups of each litter. Records of survival were made at 1,
    4, 12, and 21 days after birth and a final examination was made at
    weaning.  Litters were reduced to 10 pups on the fifth day of
    lactation.  Following weaning, the parental females were mated and
    the procedure was repeated to obtain a second generation.  Eight
    males and 16 females of the second generation were selected at
    weaning as parental animals for a succeeding generation.

    Gross examination of tissues and organs was performed on the second
    litters of all generations.  A complete microscopic examination was
    conducted on five male and five female animals from the control and
    high dose group of the second litter from each generation.  In
    addition, gross and histopathologic examination was conducted on 10
    animals of each sex of the final litter of the third generation.

    There was no significant mortality or complications with respect to
    parental animals over the course of the study.  Although there were
    sporadic changes in some of the reproductive data during the three
    parental generations, the reproductive parameters showed no
    significant, dose-related adverse effects attributable to
    phenothrin. Gross and microscopic findings suggested no adverse
    effect as a result of dietary phenothrin and it was concluded that
    phenothrin had no effect on reproduction in a standard,
    three-generation reproduction study in rats (Takatsuka et al,

    Acute toxicity

    The acute toxicity in male and female rats and mice is extremely
    low. The LD50 was greater than 5,000 mg/kg body weight when
    phenothrin was administered orally, subcutaneously, or by
    intraperitoneal injection. An intravenous LD50 in rats was reported
    to range from 452 to 492 mg/kg and in mice ranged from 354 to 405
    mg/kg.  There were no sex differences noted in acute toxicity

    Signs of poisoning were noted rapidly following the intravenous
    administration of phenothrin.  The signs of poisoning include:
    fibrillation, tremor, slow respiration, salivation, lacrimation,
    ataxia, and paralysis.  The signs of poisoning, evident at one-half
    to one hour following administration, were rapidly diminished
    spontaneously to the point where, at 24 hours, there were no signs
    of toxicity (Segawa, 1976).

    The LC50 following a four-hour inhalation exposure was determined
    to be greater than 1,210 mg/kg3 for phenothrin with both rats and
    mice (Kohda et al, 1979).  With Sumithrin an LC50 exceeds 3,760
    mg/m3 for a 4-hour acute exposure (Kohda, et al, 1977).

    Acute oral toxicity of metabolites of phenothrin

    Chemical                 Species       LD50 (mg/kg)
    3-phenoxybenzyl alcohol    rat            1330
    3-phenoxybenazldehyde      rat             600

    Acute intraperitoneal toxicity of several phenothrin metabolites in

    Chemical                               Male         Female
    3-phenoxybenzyl alcohol                371           424
    3-(4'-hydroxyphenoxy)benzyl alcohol    750-1000      750-1000
    3-(2'-hydroxyphenoxy)benzyl alcohol    876           778

    3-phenoxybenzoic acid                  154           169
    3-(4'-hydroxyphenoxy)benzoic acid      783           745
    3-(2'-hydroxyphenoxy)benzoic acid      859           912
    3-phenoxybenzaldehyde                  415           416

    (These data on phenothrin metabolites were originally reported in
    the toxicological review of permethrin, see FAO, 1980).

    Short-term studies


    Groups of rats (15 male and 15 female rats per group) were exposed
    to phenothrin by inhalation at concentrations of 0, 43 or 220
    mg/m3 for four weeks.  The animals were exposed for five
    consecutive days per week with an exposure period of four hours per
    days.  Phenothrin, dissolved in deodorised kerosene, was
    aerosolised and admitted to the exposure chamber after larger sized
    particles were removed.  The range of particle size to which the
    animals were exposed was not reported. However, the concentration
    of the phenothrin in the chamber was measured.

    At the conclusion of the four-week treatment interval, 10 animals
    of each sex of each group were sacrificed.  Haematological
    examinations, clinical chemistry examinations, and gross and

    microscopic examinations of selected tissues and organs were 
    performed on all animals sacrificed at the conclusion of the study.  
    In addition, groups of five animals of each sex were maintained 
    and examined for gross pathological changes three weeks after 
    completion of the exposure.

    There was no mortality or evidence of acute poisoning observed in
    any of the animals.  Data on body weight, haematology and clinical
    chemistry parameters, and gross and microscopic examinations of
    tissues and organs showed that subchronic exposure to concentration
    of phenothrin up to 220 mg/m3 for four weeks did not result in any
    adverse toxicological effect (Kohda et al, 1979).

    Long-term studies


    Groups of mice (50 male and 50 female Swiss white mice/group) were
    fed phenothrin in the diet at dosage levels of 0, 300, 1,000 or
    3,000 mg/kg for 18 months in a standard carcinogenicity study.  The
    mice were examined daily for clinical signs of toxicity and
    mortality.  The animals were weighed once at the initiation of the
    study and monthly thereafter.  At the conclusion of the study,
    haematologic and clinical-blood chemistry studies were performed
    using 10 mice of each sex from each dosage group.  At the
    conclusion of the 18-month feeding trial, all mice were sacrificed
    for gross and microscopic examination of tissues and organs. 
    Statistical evaluation of the data was performed to identify group

    There was no mortality, and clinical signs of poisoning were not
    significant in the study.  Growth, as evidence by body weight of
    males fed 3,000 mg/kg, was slightly depressed throughout the major
    portion of the study.  Haematologic values were normal.  Clinical
    chemistry parameters were normal (with the exception of a
    statistically significant elevation in SGPT activity in females;
    the increase was not dose-dependant and was not present in males
    and additionally, as the data from the female control group
    appeared to be significantly lower than that observed in the male
    control group, it is believed that the statistically significant
    difference in the SGPT activity is not attributable to phenothrin
    in the diet).  Gross examination of tissues and organs at the
    conclusion of the study showed an increased liver weight at the
    high-dose level in both males and females.  There were no other
    gross pathological findings.

    Microscopic examination of liver revealed no unusual findings
    associated with the enlargement.  In lungs of mice, congestion was
    observed.  In addition, amyloidosis in alveoli was found in all
    groups in a dose-dependant manner.  The two highest dose groups
    showed a statistically significant difference from control values
    with respect to this occurrence.  There was no significant increase
    in neoplasm associated with the presence of phenothrin in the diet
    (Murakami et al, 1980).  Based on this bioassay phenothrin is not
    carcinogenic to the mouse.


    Groups of rats (50 male and 50 female rats per group) were fed
    phenothrin in the diet at dosage levels of 0, 200, 600, 2,000 or
    6,000 mg/kg for two years.  Animals were examined weekly for the
    first 13 weeks and at monthly intervals thereafter.  Food
    consumption data were reported for these same intervals. 
    Ophthalmological examinations, haematological studies, clinical
    chemistry studies, and urinalyses were performed at periodic
    intervals over the course of the study.  At the conclusion of the
    study, all animals were sacrificed and examined for gross
    abnormalities.  Extensive microscopic examinations were conducted
    on a variety of tissues and organs and where gross lesions were
    observed.  All data were statistically analyzed to evaluate
    significant intergroup differences.

    There were no abnormal clinical behaviourial problems associated
    with this study.  The survival rate of all animals of all groups
    was similar to that of controls and there were no effects of
    phenothrin on mortality.  Growth, as evidenced by body-weight
    reduction, was significantly affected at 6,000 mg/kg in both males
    and females.  The growth of males, while significantly reduced
    during the early parts of the experiment, was not substantially
    different from that of the controls after the first four months. 
    Body weights of females fed 6,000 mg/kg were slightly lower than
    the controls throughout the study.  Food consumption was observed
    to be slightly less in the high-dose male and female animals but
    was not consistently different from control animals in any of the
    other dose groups.  Ophthalmological examinations revealed some
    abnormalities, all of which appeared to be age-related changes. 
    There were no significant haematological differences.  An increase
    in SGPT activity in the 6,000 mg/kg male group was significantly
    different than controls.  There were no differences observed with
    females.  Urinalysis values were normal throughout the study.


    A group of eight male human volunteers were administered
    Sumithrin(R) (d-phenothrin) dermally at a dose of 32 mg/kg/day for
    3 consecutive days.  There were no signs of toxicity or dermal
    irritation.  Blood biochemistry and haematology parameters were
    normal and dermal absorption was slight as blood levels of
    d-phenothrin isomers were below the level of analytical detection
    0.006 mg/kg).  The daily dosages used in this dermal study ranged
    from 0.67 mg/kg body weight to 0.44 mg/kg body weight with no
    adverse effects noted (Hashimoto et al, 198O).



    Phenothrin, the chrysanthemic acid ester of 3-phenoxybenzyl
    alcohol, a synthetic pyrethroid used as an insecticide, is a

    mixture of cis and trans racemates, usually with a 
    cis:trans ratio of 20:80.

    Phenothrin is rapidly absorbed, distributed, metabolized and
    excreted from the body and the metabolic fate of the molecule has
    been well defined.  Phenothrin has a very low order of acute
    toxicity.  At very high doses, phenothrin exhibited central nervous
    system effects as noted with several other pyrethroids.  Axon and
    myelin degeneration were not demonstrated following acute treatment
    with phenothrin.

    Phenothrin is not mutagenic in microbial or mammalian tests, is not
    teratogenic and was found to have no effect on rat reproduction in
    a standard three-generation bioassay.

    Long-term studies in both the rat and the mouse showed phenothrin
    to have a low order of toxicity.  There was no carcinogenic
    potential in either rat or mouse.

    In a human volunteer study no adverse effects were reported when
    people were exposed dermally to Sumithrin(R) (also known as
    phenothrin) a mixture enriched in the (1R)-cis and (1R)-trans
    isomers but still with a cis:trans ratio of 20:80.

    Adequate data were presented to allocate a temporary ADI for man on
    the basis of no-effect levels observed in long-term studies in the
    rat and mouse.  A temporary ADI was suggested, since all long-term
    studies were in rodent species and the dog has been noted to be a
    species that has shown greater sensitivity to other pyrethroids. 
    Further studies on the dog were therefore required.  Additionally,
    further studies on the metabolic fate of phenothrin are desirable
    in order to confirm the rapid nature of its degradation and
    elimination from the body. Observations in man are valuable in
    assessing the overall hazards associated with this new class of

    Level causing no toxicological effect

    Mouse:  300 mg/kg in the diet equivalent to 45 mg/kg bw/day
    Rat:    2,000 mg/kg in the diet equivalent to 100 mg/kg bw/day

    Estimate of temporary acceptable daily intake for man

    0-0.2 mg/kg bw/day


    Since a temporary ADI has been allocated the existing guideline
    levels should be replaced by temporary MRLs.


    Required (by 1984)

    1. A two-year dog study.


    1. Additional metabolism data with phenothrin technical product.
    2. Further observations in man with phenothrin.


    Casida, J.E., Gaughan, L.C. and Ruzo, L.O. Comparative Metabolism
    of Pyrethroids derived from 3-Phenoxybenzyl and
    alpha-Cyano-3-phenoxybenzyl Alcohols. Advances in Pesticide
    Science, Ed. by Geisebühler, H., Brooke, G.T., and Kearney, P.C.
    Pergamon Press, London, Part 2, p. 182-89.

    Hara, Y., Miyagishi, A., Ohtuska, M., Asami, Y., Kurokawa, H. and
    Miyamoto, J. Pharmacological Study of Sumithrin(R): Effects of
    Respiration, Blood Pressure, and Peripheral Central Nervous
    Systems. (1974) Unpublished report from Sumitomo Chemical Co.,
    submitted to the World Health Organization by Sumitomo Chemical Co.

    Hashimoto, S., Okano, S., Yamada, H. and Miyamoto, J. Human
    volunteer study with d-phenothrin powder. (1980) Unpublished report
    from Sumitomo Chemical Co., submitted to the World Health
    Organization by Sumitomo Chemical Co.

    Hiromori, T., Koyama, Y., Okuno, Y., Arai, M., Ito, N. and
    Kiyamoto, J. Two-year Chronic Toxicity Study of S-2539 in Rats.
    (1980) Unpublished report from Sumitomo Chemical Co. of a study
    performed by Industrial Bio-Test Laboratories, Inc. validated by
    Sumitomo Chemical Co. and submitted to the World Health
    Organization by Sumitomo Chemical Co.

    Kaneko, H., Ohkawa, H. and Miyamoto, J. Absorption and Metabolism
    of Dermally Applied d-phenothrin in Rat. (1980) Unpublished report
    from Sumitomo Chemical Co., submitted to the World Health
    Organization by Sumitomo Chemical Co.

    Kohda H., Nishimoto K., Kadota, K. and Miyamoto, J. Acute and
    Subacute Inhalation Toxicity Studies of S-2539 Forte in Rats and
    Mice. (1979) Unpublished report from Sumitomo Chemical Co.,
    submitted to the World Health Organization by Sumitomo Chemical Co.

    Kohda H., Okuno Y., Kadota, K. and Miyamoto, J. Acute Inhalation
    Toxicity of d-phenothrin (S-2559 Forte) in Rats. (1977)
    Unpublished report from Sumitomo Chemical Co., submitted to the
    World Health Organization by Sumitomo Chemical Co.

    Ladd, R., Smith, P.S., Jenkins, D.H., Kennedy, G.L., jr.,
    Kinoshita, F.K. and Keplinger, M.L. Teratogenic Study with S-2539
    in Albino Rabbits. (1976) Unpublished report from Industrial
    Bio-Test Laboratories, submitted to the World Health Organization
    by Sumitomo Chemical Co.

    Miyamoto, J., Suzuki, T. and Nakae, C. Metabolism of Phenothrin of
    3-Phenoxybenzyl d-trans Chrysanthemumate in Mammals. Pestic.
    Biochem. Physiol. 4: 438-450.

    Murikami, J., Ito, S., Okuno, Y., Arai, M., Ito, N. and Miyamoto,
    J. Eighteen-month Chronic Oral Toxicity and Tumorigenicity Study of
    S-2539 in Mice. (1980) Unpublished report from Sumitomo Chemical
    Co. of a study performed by Industrial Bio-Test Laboratories, Inc.
    validated by Sumitomo Chemical Co. and submitted to the World
    Health Organization by Sumitomo Chemical Co.

    Nakamoto, N., Kato, T. and Miyamoto, J. Teratogenicity Study of
    S-2539 Forte in Mice. (1973) Unpublished report from Sumitomo
    Chemical Co. submitted to the World Health Organization by Sumitomo
    Chemical Co.

    Okuno Y., Kadota and Miyamoto, J. Neurotoxicity Study of
    d-Phenothrin (S-2539 Forte(R)) in Rats by Repeated Oral
    Administration. (1978) Unpublished report from Sumitomo Chemical
    Co., submitted to the World Health Organization by Sumitomo
    Chemical Co.

    Rutter, H.A. Teratogenicity Study in Rabbits: S-2539 Forte. (1974)
    Unpublished report from Hazleton Laboratories Inc., submitted to
    the World Health Organization by Sumitomo Chemical Co.

    Segawa, T. Acute Toxicity Study of S-2539 in Rats and Mice. (1976)
    Unpublished report from Hiroshima University School of Medicine,
    submitted to the World Health Organization by Sumitomo Chemical Co.

    Shirasu, Y., Morishita, M. and Kato, K. Mutation Test of S-2539 on
    Bacteria. (1974) Unpublished report from The Institute of
    Environmental Toxicology, submitted to the World Health
    Organization by Sumitomo Chemical Co.

    Soderland, D.M. and Casida, J.E. Effects of Pyrethroid Structure on
    Rates of Hydrolysis and Oxidation by Mouse Liver Microsomal
    Enzymes. Pestic. Biochem. Physio. 7: 391-401.

    Suzuki, H. and Miyamoto, J. Mutagenicity of Some Synthetic
    Pryethroids in Bacterial Test Systems. (1975) Unpublished report
    from Sumitomo Chemical Co., submitted to the World Health
    Organization by Sumitomo Chemical Co.

    Suzuki, T. and Miyamoto, J. Purification and Properties of
    Pyrethroid Carboxyesterase in Rat Liver Microsome. Pestic. Biochem.
    Physio. 8: 186-98.

    Suzuki, T., Ohno, N. and Miyamoto, J. New Metabolites of (+)-cis
    Fenothrin, 3-Phenoxybenzyl, (+)-cis Chrysanthemumate, in Rats. J.
    Pesticide Sci. 1: 151-52.

    Tekatsuka, M., Okuno, Y., Suzuki, T., Kadota, T., Yasuda, M. and
    Miyamoto, J. Three-generation reproduction study of S-2539 in rats.
    Unpublished report from Industrial Bio-Test Laboratories, validated
    by Sumitomo Chemical Co. and submitted to the World Health
    Organization by Sumitomo Chemical Co.


    See Also:
       Toxicological Abbreviations
       Phenothrin (Pesticide residues in food: 1979 evaluations)
       Phenothrin (Pesticide residues in food: 1984 evaluations)