PESTICIDE RESIDUES IN FOOD - 1981
Sponsored jointly by FAO and WHO
EVALUATIONS 1981
Food and Agriculture Organization of the United Nations
Rome
FAO PLANT PRODUCTION AND PROTECTION PAPER 42
pesticide residues in food:
1981 evaluations
the monographs
data and recommendations
of the joint meeting
of the
FAO panel of experts on pesticide residues
in food and the environment
and the
WHO expert group on pesticide residues
Geneva, 23 November-2 December 1981
FOOD AND AGRICULTURE ORGANIZATION OF THE UNITED NATIONS
Rome 1982
FENVALERATE
Explanation
Fenvalerate was first evaluated in 1979, when a temporary
acceptable daily intake was established and temporary maximum residue
limits were recommended for many raw agricultural commodities to cover
treatments applied both pre-harvest and post-harvest.*
A request was made for further information on the potential
bioaccumulation of fenvalerate and/or its metabolites; observations in
occupationally exposed humans; an additional dominant lethal assay to
confirm previous data; the occurrence and fate of photo-decomposition
products; residues in citrus, berry fruits, beans and several other
crops for which data were limited; studies on the level and fate of
fenvalerate residues in stored products, especially raw grain and
products derived therefrom.
Information on several of these items has become available,
together with further data from supervised field trials on a number of
additional crops, provided by Canada and by several manufacturers of
fenvalerate. These were evaluated by the Meeting.
DATA FOR THE ESTIMATION OF ACCEPTABLE DAILY INTAKE
BIOCHEMICAL ASPECTS
Absorption, distribution, biotransformation and excretion
In the 1979 JMPR concern was expressed over the potential for
bioaccumulation of fenvalerate in mammals. However, it has already
been shown (Ohkawa et al 1979) that 14C-fenvalerate labelled at the
acid or alcohol moiety, administered singly or consecutively, was
eliminated substantially completely and fairly rapidly from the animal
body, with a very limited retention in adipose tissue. The cyano-
fragment of the molecule was rather persistent in several tissues of
rats and mice, notably skin and hair, which is not toxicologically
significant, as this is one of the excretion processes of the cyano-
group in the body. Also, tissue residues of fenvalerate reached a
plateau within 3 weeks of dietary administration; the results indicate
the maximum build-up in the tissues during feeding and no further
increase of the tissue contents even by subsequent administration of
the compound. These findings would suggest that there is no
appreciable bioaccumulation of fenvalerate and/or its metabolites by
longer administration of the compound (Miyamoto 1981).
* See Annex II for FAO and WHO documentation.
Cow
Fenvalerate was fed to two Holstein cows and its excretion in
milk and faeces determined (Wszolek et al 1980). One animal was fed
pure fenvalerate at the 5 ppm level and the other at the 15 ppm level
based on a daily ration of 22.7 kg for 4 days. (This amounted to a
total dose of 0.454 and 1.362 g of the insecticide, respectively.)
Total excretion of fenvalerate in milk amounted to 0.44% and 0.64% of
the total dose for the cows fed, respectively 5 and 15 ppm of the
compound. Substantially more of the fenvalerate was eliminated in the
faeces, possibly about 25% of the dose. Although metabolites of
fenvalerate were not sought, it is possible that hydrolysis of the
carboxy ester linkage may occur, with resultant excretion of the
corresponding acid and conjugates of the alcohol in urine and faeces.
Bovine urinary excretion and rumen decomposition of fenvalerate
and a metabolite have also been studied (Wszolek et al 1981). Grain
containing 10 ppm of fenvalerate was fed to a catheterized, lactating
Holstein cow, one portion per day for four days. (This amounted to a
total dose of 0.908 g of fenvalerate.) Intact fenvalerate was not
detected in the urine excreted by the cow during the 10-day feeding
study.
A major metabolite, 4-chloro-alpha-(1-methylethyl)-benzene acetic
acid, was not unambiguously identified in the urine. About 0.02% or
less of the administered dose of fenvalerate was excreted in the
urine, based on the total volume of urine collected during the study
(about 290 liters). Although 4-chloro-alpha-(1-methylethyl)-benzene
acetic acid was not identified in the urine, it was calculated that an
upper limit of about 20% of the fenvalerate could be accounted for by
possible excretion of this acid in urine.
No significant degradation of fenvalerate was detected when
rumen was incubated with fenvalerate in vitro. Any degradation of the
insecticide was believed to occur further along in the cows' digestive
system. Additionally, significant amounts of fenvalerate may
accumulate in tissues and organs which were not analysed (Wszolek
et al 1981).
Rat
The metabolic fate of fenvalerate and its insecticidally active
isomer (2S,alpha RS), labelled with 14C in three positions, was
studied by Okhawa et al (1979) in male Sprague-Dawley rats following
a single oral dose or 5 consecutive daily doses. Figure 1 illustrates
the metabolic pathways for fenvalerate in male rats. This figure
includes the products obtained from the CO-, C-alpha- and CN-labelled
fenvalerate, CO-labelled Cl-V acid [(S)-2(4-chlorophenyl)isovaleric
acid], K14CN and KS14CN. As fenvalerate (a mixture of the four
optical isomers) and S-fenvalerate(the ester derived from racemic
alpha-cyano-3-phenoxybenzyl alcohol and C-Cl-V acid) showed similar
patterns of 14C excretion, tissue residues, and the amount of the
excreted metabolites, both compounds are likely to be metabolized.
A small part of the oral dose of fenvalerate was excreted in the
faeces without metabolism. The metabolism of fenvalerate and the (S)
acid ester isomer was rapid, and the acid moiety and the aromatic
portion of the alcohol moiety was almost completely eliminated from
the body within several days. The CN group of the alcohol moiety was
rapidly converted, mainly to thiocyanate, which was retained
relatively longer in selective tissues, including skin and hair.
Fenvalerate and the (S)-acid isomer yielded two faecal ester
metabolites, which resulted from hydroxylation at the 4,'- and
2'-phenoxy positions. Other significant metabolites were
3-phenoxybenzoic acid and its hydroxy derivatives (free and conjugate)
from the alcohol-labelled compound, 3-(4-chlorophenyl) isovaleric acid
and its hydroxy derivatives (free, lactones and conjugates) from the
acid-labelled compound, and thiocyanate and CO2 from the CN-labelled
compounds. There were no apparent differences in the patterns of
14C-excretion and tissue residues between fenvalerate and the
(S)-acid isomer.
TOXICOLOGICAL STUDIES
Acute toxicity
The acute oral LD50 for rat of fenvalerate dissolved in DMSO is
451 mg/kg and in aqueous suspension 3 200 mg/kg. The acute dermal
LD50 for rat and rabbit is >5 000 mg/kg and 2 500 mg/kg,
respectively.
Long-term studies
Rat
A group of 50 male and 50 female Sprague-Dawley rats was fed a
dietary concentration of 1 000 ppm fenvalerate (SD-43775 Technical,
98% purity) for two years. A concurrent group of 50 male and 50 female
rats received basal diet only. This study was designed to complement
an earlier Sprague-Dawley rat study with dietary concentrations of 0,
1, 5, 25 and 250 ppm fenvalerate for two years (Gordon and Weir 1978).
Body weight gain was reduced in the 1 000 ppm treated group compared
to control. Six male rats of the treatment group developed transitory
weakness of the hind limbs during weeks 3 and 4 of the study.
Mortality and food consumption were not affected by compound
administration. No compound-related changes were seen in the
parameters of clinical chemistry, haematology and urinalysis. Organ
weight of the treated group was similar to control. As body weight
gain was significantly decreased in the treated rats, the organ/body
weight ratio was significantly greater (p<0.05) in the treated males
for brain, liver, heart, spleen and testes, and in the treated females
for brain, kidneys, liver, spleen and heart, when compared to control
values. Five of the treated males developed skin lesions, typified by
localized hair loss and oozing, slowly-healing sores. Although the
etiology of these lesions is unknown, these were judged unrelated to
treatment with the test material. Histopathological examination of
incurrent and terminal kill animals revealed a variety of lesions
common to this strain of rat. Neoplasms of the pituitary gland
occurred to the extent of 59% and 67% in both control and treated
animals, respectively. The majority of mammary neoplasms in the female
rats were benign fibroepithelial lesions. The total incidence of
mammary neoplasms (malignant and benign) in the female rats was
similar between control and treated animals. Statistical analyses did
not reveal an effect of the test material on mammary glands. Sarcomas
of a spindle cell type were observed in the subcutis and dermis of 5
of 51 treated males. These lesions occurred in the cervical region,
hind limb, thorax, perianal area and right axilla. Although similar
lesions were not found in these locations of male control rats, one
control rat had a large mass involving its neck, shoulder and head,
and an intrathoracic mass. The former was diagnosed as a fibroma, but
the latter was diagnosed as a spindle cell sarcoma. This spindle cell
sarcoma was reported separately from other spindle cell sarcomas. The
pathologist of this study reviewed original tissue sections from
Sprague-Dawley rats of similar origin housed under similar conditions
at Litton Bionetics for five other chronic studies, in order to obtain
appropriate historical control data. In control male rats of two
studies, sarcomas consistent with this diagnosis of spindle cell
sarcoma were found; 2 of 102 male control rats of LBI Project 20541
(previous fenvalerate study, Gordon and Weir 1978) and 1 of 50 male
control rats of LBI Project No. 20823. A review by Shell of
unpublished literature revealed that in a 2-year study with Sprague-
Dawley CD rats, spindle cell sarcomas were found in 3 of 48 male
control rats (Piccirillo and Voelker 1978). The historical incidence
of spindle cell sarcomas ranged widely from 0 to 6%, indicating the
variable spontaneous incidence of this type lesion. The term "spindle
cell sarcoma" encompasses a number of malignant mesenchymal neoplasms
that are difficult and sometimes impossible to diagnose definitively
and includes such entities as fibrosarcoma, neurofibrosarcoma,
malignant fibrous histiocytoma, liposarcoma, osteosarcoma, etc. The
above definition of spindle cell sarcoma is too broad, as it may
include other types of sarcoma that can be properly diagnosed and
therefore can be separated from among the above spindle cell sarcomas.
A pathologist carefully examined the slides of the subcutaneous
sarcomas (Ito 1981). The spindle cell sarcomas found in 5 of 51 males
were divided into 4 malignant mesenchymal neoplasms, based on the re-
examination. Therefore, the incidence of each sarcoma was very low
(one of 51 males or 2 of 51 males). Although the study pathologist
stated that the carcinogenic effects were equivocal, but not clearly
negative, with respect to these sarcomas, it was concluded that the
presence of spindle cell sarcomas in the treated males was not related
to compound administration (Gordon 1979).
The incidence of spindle cell sarcomas was analysed statistically
in the life-time feeding study in rats of SD-43775 technical
(fenvalerate) by Litton bionetics. Although using the chi-square with
Yates' correction did not reveal any significance in incidence of the
spindle cell sarcomas between control and 1 000 ppm groups, slightly
higher incidence of the tumours was seen in the treated male group.
The relationships between possible tumourigenicity of fenvalerate and
occurrence of the sarcoma are discussed (as above) in the following
comment.
As noted above, the historical incidence of spindle cell sarcoma
ranged from 0 to 6%, as described in the study report and the attached
comment of Shell Development Company. Therefore, the incidence of the
treated male group (10%) is not so high when compared to the
historical incidence.
The spindle cell sarcoma, as also noted above, encompasses a
number of malignant mesencymal neoplasms that are composed of spindle-
shaped cells. The sarcomas occur in various types of tissues:
connective tissue in subcutis and submucosa, periosteum, fascia, blood
vessels, uterus, etc. The classification method by the above criteria
of spindle cell sarcoma is not currently being used by most
pathologists. At present, the tumour is usually diagnosed on the basis
of the tissue of origin. The histopathological examination of a tumour
must be conducted by using the latest method of tumour classification.
In this study different types of tumour might be diagnosed as the same
type (spindle cell sarcoma) owing to the inappropriate method of
tumour classification.
Therefore, the tumours must be properly diagnosed on the basis
of careful observation. To obtain the proper findings, the slides of
the subcutaneous sarcomas sent from Litton Bionetics were examined
histopathologically. The following results were obtained in the
re-examination:
Animal No. Area Findings
7188 Cervical subcutis Malignant schwannoma or
and mammary gland Leiomyosarcoma
7213 Left hind limb Malignant mesencymoma
7224 Thorax Fibrosarcoma
7227 Right axillary area Malignant amelanotic melanoma
823- Left perianal area Malignant amelanotic melanoma
Although it was difficult to evaluate exactly the findings, owing
to severe cellular atypia, four types of sarcoma were identified and
the incidence of each sarcoma become very low (1 of 51 males or 2 of
51 males). These low incidences are comparable to that of the control
group. From the result of the re-examination, these sarcomas are not
considered to be related to ingestion of fenvalerate and are naturally
occurring tumours (Ito 1981).
Groups of 80 male and 80 female Wistar rats were fed dietary
concentrations of fenvalerate (Sumitomo 55602 technical, purity 93.4%)
0, 50, 150, 500 and 1 500 ppm for 104 (males) or 119 (females) weeks.
Although the apparent dose-related decrease in mortality was observed
in weeks 64 and 68, owing to respiratory disease that spread more
rapidly in the control than in the treated rats, final mortality of
the treated groups was comparable to that of the control group. Body
weight gains of males from the 500 and 1 500 ppm groups and females
from the 1 500 ppm group were probably affected, although it was
difficult to evaluate exactly the male data, owing to higher initial
body weight of control males. No compound-related or consistent
adverse effects were observed on clinical signs, blood biochemistry,
urinalysis and ophthalmology. On histopathological examination, non-
neoplastic changes due to exposure to fenvalerate were noticed in
spleen, lymph nodes, liver and adrenals. Giant cell infiltration was
observed in these organs. In spleen and liver, giant cell infiltration
was clearly found at 1 500 ppm. The same change in lymph nodes and
adrenals was observed at 500 and 1 500 ppm. In mesenteric lymph nodes,
reticuloendothelial cell proliferation was also found to be dose
related, and the incidence was higher at 500 ppm and 1 500 ppm than at
the lower doses and in the control groups. Although the incidence of
testicular tumours appears to be dose-related, their incidence was as
follows: control 28%, 50 ppm 47%, 150 ppm 35%, 500 ppm 75%, 1,500 ppm
69%. The incidence of interstitial cell tumours was statistically
significantly higher at 50, 500 and 1 500 ppm than in the respective
controls (the procedure used was chi-square with the Yates correction,
but no p values were furnished). In females, uterine and mammary
tumours were observed in all groups. However, no significant
difference was observed between the control and the treated groups.
Incidences of other tumours of the treated groups were comparable to
those of the control. Thus, there was no evidence of carcinogenic
response, and the dietary no-effect level of fenvalerate was found to
be 150 ppm (equivalent to 6.7 mg/kg/day for males and 7.3 mg/kg/day
for females) (Arai et al 1981a).
Mouse
Groups of 50 male and 50 female B6C3F1 mice were fed dietary
concentrations of 10, 50, 250 and 1 250 ppm fenvalerate (SD-43775,
purity 98%) for 2 years. Two groups of control mice, 50 per sex per
group, received basal diet only. Mortality was significantly increased
and body weight gain was significantly decreased in male and female
mice in the 1 250 ppm treatment group. Mean body weight of female mice
in the 250 ppm group was also significantly lower than controls after
the 60th week of feeding. Serum albumin was decreased and serum
glutamic-oxaloacetic transaminase was increased in the 1 250 ppm mice
examined. No other effects on haematology or clinical chemistry were
observed in the study. For some organs, mean organ weights and
organ/body weight ratios were statistically different from controls.
However, these changes were not consistent in the treatment groups,
i.e. not dose-related (Johnston 1979). The number and type of
histologically diagnosed neoplasms in mice fed 10, 50, 250 or 1 250
ppm fenvalerate in the diet for 2 years was not statistically
significant when compared to the incidence of neoplasms in mice fed
the untreated control diet only. Lymphoreticular and lung neoplasms
were common in both control and treated animals. The only non-
neoplastic pathology induced by dietary administration of less than
1 250 ppm fenvalerate was multifocal granulomata. In female mice, this
lesion was present in mesenteric lymph nodes, liver and spleen at
dosage levels of 250 and 1 250 ppm. In male mice, 1 250 ppm
fenvalerate induced multifocal granulomata in mesenteric lymph nodes,
other visceral and peripheral lymph nodes, liver and spleen. Less
severe granulomatous lesions were present in mesenteric lymph nodes of
male mice administered 50 and 250 ppm fenvalerate. The dietary no-
effect level of fenvalerate was found to be 10 ppm for males or 50 ppm
for females (equivalent to 1.7 mg/kg/day for males and 11.0 mg/kg/day
for females) (McCullough and Gelatly 1979).
Groups of 50 male and 50 female ddY mice were fed dietary
concentrations of 0, 10, 30, 100 and 300 ppm fenvalerate (55602
technical, purity 91.4%) for 87 (females) and 91 (males) weeks.
Additional groups of 10 male and 10 female ddY mice were fed the same
concentrations and were sacrificed at 12th month. This study is
supplementary to the previous test (Suzuki et al 1977) and was
intended to establish a no-effect level. No treatment-related effects
were detected by clinical observations, including mortality, body
weight, food consumption, water intake, ophthalmological examination
and urinalysis. Slight reductions of erythrocyte counts in 100 and
300 ppm groups of male and slightly lower haemoglobin concentration in
the 300 ppm female group were observed, and glutamic-pyruvic
transaminase activity of 300 ppm female group was slightly increased
at termination. No noteworthy changes were obtained in other
examination on clinical biochemistry and haematology. No treatment-
related effects were detected in organ and organ/body weight ratio,
except that a slightly higher organ/body weight ratio of adrenals was
obtained in the 300 ppm female group at the 12th month. Gross
observations did not show any adverse effects. In histopathological
examinations of the life-span feeding group, dose-related changes were
noticed in spleen, liver and lymph nodes. In spleen, giant cell
infiltration was found at 300 ppm. In mandibular lymph node, giant
cell infiltration and/or large histiocytic cell filled with brown
pigment were found dose-relatedly, and the incidence was higher at
100 ppm and 300 ppm than at the lower doses and the control group. In
mesenteric lymph nodes, giant cell infiltration and/or reticulum cell
proliferation was found at 100 ppm and 300 ppm, and the incidence of
reticulum cell proliferation was higher at 300 ppm than at the lower
doses and controls. In the liver, giant cell infiltration and
granuloma were dose-relatedly noticed in the 300 ppm group of both
sexes and in the 100 ppm and 300 ppm groups of females. Large
histiocytic cells filled with brown pigment were observed in the liver
of the 100 ppm and 300 ppm male groups with higher incidence. The
granulomatous changes, which were noticed in the 12 month interim
groups, were comparable in their severity to the findings of the life-
span groups, but the incidence was higher in 100 ppm and 300 ppm
groups than in the life-span groups. This implies that the
granulomatous changes are not progressive on longer feeding of the
compound. With regard to neoplastic changes, various types of
epithelial or non-epithelial cell tumours were found. However, the
incidence of all these tumours was not different between the control
and the treated groups. The incidence of single, multiple, benign and
malignant tumours were not different among the groups and/or not dose-
related. Thus the compound was not carcinogenic in ddY mouse when
fed from 5 weeks old to about end of life span, and the dietary
no-effect level of fenvalerate was found to be 30 ppm (equivalent
to 3.48 mg/kg/day for males and 4.29 mg/kg/day for females) (Arai
et al 1981b,c).
An additional feeding study was conducted to examine
reversibility of the granulomatous changes in mouse liver, spleen and
mesenteric lymph node, in which mice of ddY strain were kept on a diet
containing 0, 1 000 and 3 000 ppm fenvalerate for 6 weeks, followed by
rearing on the control diet. Histopathological examination was
conducted periodically. The granulomatous changes in liver, lymph node
and spleen, which had been observed immediately and/or shortly after
termination of the administration of fenvalerate, were lower in
incidence as well as less in severity after 6 months of the recovery
phase. Although these granulomatous changes were still observed at 12
months of the recovery phase, the incidence and severity were clearly
reduced. Therefore, it was concluded that the granulomatous changes
are not progressive and are reversible in nature (Ito et al 1980).
Special studies on mutagenicity
Dominant lethal assay
In the dominant lethal assay in male mice mentioned in the 1979
JMPR evaluation, the weekly mean values for total implants and early
foetal deaths were analysed by a two-way analysis of variance. The
value for total implants were analysed untransformed. Since the
variate for early foetal deaths (EFD) was considered to follow a
Poisson distribution, the data were transformed to square roots of EFD
+ 0.375 to achieve normality. Based on these statistical analyses,
female mice mated to males dosed with 100 mg/kg fenvalerate showed a
statistically significant reduction in foetal implants at week 2
(p <0.05) and an increase in early foetal deaths at week 4
(p <0.05). The conclusion was that these appeared to be isolated
random events, not following any consistent or time-related pattern,
and were not considered to be of biological significance (Miyamoto
1981).
The significant changes of these parameters, even in one specific
week, might sometimes imply the effects of the compound. The raw data
were analysed by using another statistical method proposed by the US
Food and Drug Administration recently (Green et al 1976). According
to the method, the t-test was utilized to determine significant
differences between average number of implantations per pregnant
female, for each treatment, compared with the control value. Dead
implantations per total implantations were computed for each female
and transformed to the Freedman-Tukey arc-sine. The t-test was then
utilized to compare each treatment value of the proportion of dead
implantations with the control value. No statistical significances are
observed in the number of total implantations at any weeks for any
treatment groups. Also, no significant higher values of transformed
proportion of early foetal deaths were observed in any treatment
groups at any intervals. The percentage of early foetal deaths per
total implantations in this study was further analysed by using the
Mann-Whitney U-test, which was employed by some investigators (Soats
and Sheridan 1977; Teramoto et al 1980). No statistical
significances are shown in any mean proportions, including the value
of the 100 mg/kg group at week 4, which was significant in the
original statistical analyses.
From these findings, it was concluded that fenvalerate did not
cause dominant lethals in the mouse study (Miyamoto 1981).
Special studies on exposure in humans
To date, no reports are available in which exposure of humans to
a known level (not necessarily to high levels) of fenvalerate has been
suggested. During several years of usage of fenvalerate, no incidence
of human intoxication resulting in any noteworth effects including
neurological disruption, has been reported (Miyamoto 1981).
However, note should be made of a Swedish study of the
occupational exposure to three products containing synthetic
pyrethroids, which have been used in forestry to protect conifer
seedlings against the large brown pine weevil (Hylobuis abietis)
(Kolmodin-Hedman et al 1981). Fenvalerate was used in one product
and permethrin in two products containing a mixture of trans/cis
isomers in proportions 60/40 and 75/25, respectively. A high frequency
of symptoms was reported in connection with the use of fenvalerate
which led to a withdrawal of the product for use in forestry. Some
symptoms were also reported in groups exposed to permethrin. For
example, in interviews carried out with 139 planters, irritative
symptoms of the skin and upper respiratory tract were reported in 73%
of users for fenvalerate, 63% for permethrin (trans/cis 75/25) and 33%
for permethrin (trans/cis 60/40), respectively (Kolmodin-Hedman
et al 1981).
Transient facial sensory symptoms following exposure to synthetic
pyrethroids (e.g. cypermethrin, permethrin, fenvalerate and
fenpropathrin) in some workers has been reported. Of 23 workers
exposed to synthetic pyrethroids, 19 had experienced one or more
episodes of abnormal facial sensation developing between 30 min to 3 h
after exposure and persisting for 30 min to 8 h. There were no
abnormal neurological signs and electrophysiological studies of the
arms and legs were normal. It was concluded that the symptoms are most
likely to be due to transient lowering of the threshold of sensory
nerve fibres or sensory nerve endings following exposure of the facial
skin to pyrethroids, similar to the phenomena that have been described
following exposure of animal nerves to pyrethroids.
Skin sensations experienced by those handling cypermethrin or
other pyrethroids are believed to arise by repetitive firing of
sensory nerve terminals in the skin. It is said to be a strictly local
effect that may occur as soon as the pyrethroid concentration on or in
the skin reaches a certain level and is not considered as a sign of
general intoxication (provided the pyrethroid does not reach the blood
in any significant concentration). A possibility exists, however, that
repeated occurrences of intense repetitive firing can perhaps
eventually lead to dysfunction of sensory nerve terminals and sense
organs and finally to degeneration of sensory nerve fibres.
Special studies on pesticide interactions
Esterases play a major role in the detoxification of many
pyrethroid insecticides (Abernathy and Casida 1973; Jao and Casida
1974a; Soderlund and Casida 1977a). Some inhibitors of "pyrethroid
esterases" serve as synergists for pyrethroid toxicity to insects and
mammals (Abernathy et al 1973; Jao and Casida 1974b; Soderlund and
Casida 1977b). Currently, the major use of pyrethroids is in cotton
protection, where the crops may also be treated with esterase
inhibitors (e.g., organophosphorus and methyl carbamate compounds).
The evaluation of several insecticides used on cotton for
possible effects in altering the metabolism, toxicity and persistence
of pyrethroids has been reported (Gaughan et al 1980). Profenofos,
EPN [O-ethyl-O-(4-nitrophenyl)phenylphosphonothioate] and DEF
(S,S,S-tributylphosphorotrithioate) administered intraperitoneally to
mice at 25 mg/kg strongly inhibited the liver microsomal esterase(s)
that hydrolyse fenvalerate and increased the i.p. toxicity of
fenvalerate >25 fold.
RESIDUES IN FOOD
RESIDUES RESULTING FROM SUPERVISED TRIALS
Many residue trials have been conducted since 1979 to provide
additional data on residues in citrus, berry fruits and beans,
together with information on new crops including fruits, vegetables,
cereals and oilseeds. Tables 1 through 12 contain reports submitted to
the Meeting by Shell (1980a,b). These trials confirm the previous
data, which indicated that the compound was not systemic and the
residues declined with a half-life of about one to two weeks.
Oilseeds
Trials on peanuts have been carried out in the USA. The residues
in whole nuts were less than 0.1 mg/kg, when fenvalerate was applied
at rates of up to 0.45 kg a.i./ha (Table 1). It was shown that
residues in the meat did not exceed the detection limit of 0.01 mg/kg
and that the shells carried almost all the residues found in the whole
nuts. The residues in hay and vines ranged from 1.0 to 17 mg/kg, at
treatment rates of up to 0.45 kg a.i./ha. These findings confirmed the
evaluations made in 1979.
Leafy and stem vegetables
Trials have been conducted in the USA and Canada on lettuce,
spinach, celery and brassica vegetables, such as broccoli, Brussel
sprouts, cabbage, cauliflower and rapeseed. The residues were
generally less than 1 mg/kg 7 days after treatment at rates ranging
from 0.05 to 0.45 kg/ha (Table 2). In cabbage, the maximum residue
7 days or more after treatment was 4.3 mg/kg where the application
rate was 0.45 kg/ha. When lettuce was treated at rates of up to
0.45 kg/ha and harvested 7 days after treatment, the maximum residue
was 4.3 mg/kg, and 1.7 mg/kg at an application rate of 0.45 and
0.22 kg/ha, respectively. These figures are regarded as statistical
outlines. In spinach, the residues 7 days after 0.056 to 0.11 kg/ha
treatment exceed 2 mg/kg and the residues decreased to below 1 mg/kg
after 12 days. The data were insufficient to judge the validity of
these levels.
Fruiting vegetables
Residue trials for fruiting vegetables, such as cucumbers,
watermelon, cantaloupe, honeydew melon, squash, bell peppers, pumpkins
and tomatoes, were carried out mostly in the USA. The maximum residues
were generally below 1 mg/kg 3 days or later after treatment at rates
ranging from 0.05 to 0.45 kg/ha (Table 3). When tomatoes were treated
at a rate of 0.45 kg/ha and harvested 7 days after treatment, the
maximum residue of 1.8 mg/kg was found. These data provide a basis for
estimating maximum residue levels.
TABLE 1. Fenvalerate Residues on Peanuts
Application Residues (mg/kg) at intervals (days) after appl.
Crop part Country/Year No. Rate EC Formulation
(kg a.i./ha) (%) 0 7 14 21 28
Whole USA 1976 4 0.11 30 0.03 (10d)
0.22 0.03 (10d)
1979 3 0.22 30 0.02
0.45 0.03
1978 2 0.45 <0.01
1979 3 0.22 0.02
3 0.22 0.09 0.10 0.05 0.02 0.04
3 0.22 0.01
0.45 0.06
1980 3 0.22 <0.01(25d)
Nut meats 1979 3 0.22 <0.01
0.45 <0.01
3 0.22 <0.01
3 0.22 <0.01 <0.01 <0.01 <0.01 <0.01
3 0.22 <0.01
0.45 <0.01
1980 3 0.22 <0.01
Vines 1979 3 0.22 5.0
0.45 5.4
3 0.22 3.7
3 0.22 5.8
0.45 14
1980 3 0.22 0.5
Hay 1976 4 0.11 2.9(10d)
0.22 1.0(10d)
0.45 6.9(10d)
1978 2 0.45 2.6
3 0.22 17 15 9.9 5.3 6.9
TABLE 2. Fenvalerate Residues on Leafy and Stem Vegetables
Applications Residues (mg/kg) at intervals (days) after application
Crop Country Year EC
No. Rate Formulation
(kg a.i./ha) (%) 0 1 3 7 10 14
Cabbage USA 1978 6 0.22 30 0.02(21d)
0.45 <0.01(21d)
1980 8 0.22 30 4.3
0.45 10.6
8 0.22 0.41
0.45 0.64
8 0.22 5.6 0.94 1.2 2.4 0.90
0.45 11.8 1.1 1.4 4.3 0.8
8 0.22 0.18
0.45 0.25
Canada 1979 3 0.07 30 0.33 0.18 0.04
7 0.07 0.06
5 0.07-0.15 30 0.20 0.21 0.16
4 0.10 0.02 0.01 0.01
Lettuce USA 1979 7 0.11 30 0.23
0.22 0.49
0.45 0.75
7 0.22 0.85
7 0.22 0.02
0.45 0.05
0.22 1.7
0.45 3.0
7 0.22 3.9 5.3 1.8 0.59
0.45 1.4 3.6 0.54 4.3
TABLE 2. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country Year EC
No. Rate Formulation
(kg a.i./ha) (%) 0 1 3 7 10 14
1980 8 0.22 2.2 1.04(2d)
5 0.22 0.96 0.54(2d)
0.45 3.2 1.4 (2d)
5 0.20 2.3(15d)
4 0.22 2.8(18d)
3 0.13-0.21 1.4(18d)
4 0.1 -0.22 2.7
4 0.11-0.21 9.6(21d)
Netherlands 1977 1 0.075 (14d) (32d)
1 0.075 (0.25-2.25) (0.16-0.67)
1.46 0.44
0 1 3 7 14 21 28
Lettuce Canada 1979 4 0.07 30 <0.01(2d) <0.01
1978 6 0.07 <0.01
Cauliflower USA 1977 6 0.11 30 0.11
0.22 0.33
6 0.05 0.06
0.11 0.10
1980 8 0.22 0.29 0.29
0.45 0.54 0.54
Canada 1978 3 0.07 0.20 0.25 0.02
TABLE 2. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country Year EC
No. Rate Formulation
(kg a.i./ha) (%) 0 1 3 7 14 21 28
Celery USA 1979 15 0.22 1.7
0.45 3.5
15 0.22 2.8
0.45 5.1
15 0.22 0.41
198o 15 0.22 30 3.5
Canada 1978 11 0.07 0.04
1979 7 0.07 0.24 0.14
Broccoli USA 1978 4 0.22 30 1.37 0.54 0.06 0.02 <0.01
0.45 2.63 1.31 0.15 <0.01 <0.01
1980 8 0.22 0.61
0.45 0.66
0.22 0.37
0.45 0.97
Canada 1979 2 0.05 1.0 0.78 0.09
Brussels
sprouts Canada 1978 6 0.05 30 0.10
6 0.07 0.10
7 0.07 0.25 0.12
Spinach USA 1978 4 0.056 30 3.3
0.11 7.5
1979 2 0.084 0.13(12d) <0.01
0.11 0.78(12d) <0.01
TABLE 2. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country Year EC
No. Rate Formulation
(kg a.i./ha) (%) 28 48 53 70 106
Rape Canada 1979 2 0.03 30 <0.01
3 0.03 30 <0.01
2 0.03 <0.01
3 0.03 <0.01
1978 1 0.10 30 0.11(42d) <0.01
2 0.10 0.11<42d)
Chinese
cabbage Netherlands 1977 1 0.050 30 (0.24-0.50) (0.19-0.24)
0.35 (7d) 0.22 (14d)
1977 1 0.045 30 (0.02-0.04)
0.03
1 0.045 30 <0.01
TABLE 3. Fenvalerate Residues on Fruiting Vegetables
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year
No. Rate EC Formulation
(kg a.i./ha) (%) 0 1 3 7 10 14
Cucumber USA 1977 2 0.11 30 0.09 0.02 0.01 <0.01 <0.01
0.22 0.26 0.12 0.08 <0.01 <0.01
1978 4 0.11 <0.01 <0.01 <0.01
0.22 0.03 0.02 <0.01
2 0.45 0.03 0.01 0.02
1979 5 0.22 30 0.04
1980 5 0.22 30 0.06
5 0.22 o.14
0.45 0.59
5 0.22 0.26
0.45 0.69
Watermelon
(whole) USA 1979 5 0.22 30 0.23
0.45 0.29
5 0.22 0.05 0.03 0.01 0.02
0.45 0.31 0.20 0.15 0.18
1980 5 0.22 20 <0.01
0.45 0.02
5 0.22 0.06
5 0.22 0.08
5 0.22 0.15
0.45 0.26
5 0.22 0.41
0.45 0.42
TABLE 3. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year
No. Rate EC Formulation
(kg a.i./ha) (%) 0 1 3 7 10 14
Watermelon
(pulp) 1979 5 0.22 30 0.03
0.45 0.01
5 0.22 <0.01 <0.01 <0.01 <0.01
0.45 0.01 <0.01 <0.01 <0.0l
Watermelon
(peel) 1979 5 0.22 30 0.35
0.45 0.37
5 0.22 0.10 0.04 0.06 0.02
0.45 0.47 0.22 0.30 0.18
0 3 7 10 14
Cantaloupe
(whole) USA 1977 2 0.11 30 0.12 0.10 0.11 0.03
0.22 0.25 0.10 0.09 0.06
1979 5 0.22 30 0.13
0.45 0.14
5 0.22 0.10
0.45 0.14
6 0.22 0.07
0.45 0.18
1980 5 0.22 30 0.05
5 0.22 0.06
0.45 0.17
Cantaloupe
(peel) 1977 2 0.11 30 0.37 0.38 0.37 0.04
0.22 0.37 0.30 0.41 0.13
TABLE 3. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year
No. Rate EC Formulation
(kg a.i./ha) (%) 0 3 7 10 14
Cantaloupe
(pulp) 1977 2 0.11 30 <0.01 <0.01 <0.01 0.02
0.22 <0.01 0.01 <0.01 <0.01
Honeydew melon 1980 5 0.22 30 0.10
Squash USA 1980 5 0.22 20 0.23
5 0.22 0.20
0.45 0.27
5 0.22 0.04
5 0.22 0.03
0.45 0.07
5 0.22 0.05
0.45 0.07
5 0.22 0.21
0.45 0.42
5 0.22 0.03
0.45 0.04
5 0.22 0.03
0.45 0.12
5 0.22 0.02
0.45 0.02
TABLE 3. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year
No. Rate EC Formulation
(kg a.i./ha) (%) 0 1 2 3 5
Bell pepper USA 1980 7 0.22 20 0.05
0.45 0.09
7 0.22 0.33
0.45 2.57
7 0.22 1.02
0.45 1.03
7 0.22 0.07 0.05 0.05 0.18 0.07
0.45 0.13 0.02 0.10 0.05 0.03
7 0.22 0.49
7 0.22 1.1
0.45 2.0
Pumpkin USA 1980 5 0.22 30 0.05
0.45 0.09
0 5 7 13 20
Tomato USA 1977 3 0.05 30 0.03 0.02 0.02 0.02 0.02
0.11 0.07 0.04 0.03 0.02 0.01
0.22 0.10 0.10 0.07 0.04 0.04
3 0.05 0.02 0.03 0.03 0.01(14d) 0.02(21d)
0.11 0.06 0.05 0.03 0.03(14d) 0.03(21d)
0.22 0.08 0.11 0.05 0.05(14d) 0.04(21d)
2 0.11 0.41 0.19 0.11 0.10(14d) 0.04(21d)
0.22 0.12 1.35 0.59 0.24(14d) <0.01(21d)
1978 5 0.22 0.10 0.03 0.02(14d)
0.45 0.14 0.03 0.02(14d)
TABLE 3. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year
No. Rate EC Formulation
(kg a.i./ha) (%) 0 5 7 13 20
1979 10 0.22 30 0.14(whole)
0.45 0.23(whole)
10 0.22 0.67
0.45 1.8
10 0.22 0.11
0.45 0.30
10 0.22 0.10(whole)
0.06(puree) 0.07(wet pulp)
0.56(dry pulp)
9 0.22 0.37 0.39(4d) 0.34 0.31(14d) 0.26(21d)
10 0.22 0.12
1980 10 0.22 20 0.26(1d) 0.62
0.45 0.52(1d) 1.4
10 0.22 0.37(1d)
0.45 0.97(1d)
10 0.22 0.14(1d) 0.09
1979 8 0.11 0.35(3d)
0.22 0.66(3d)
0.45 0.72(3d)
TABLE 3. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year
No. Rate EC Formulation
(kg a.i./ha) (%) 0 1 2 3 7
Tomato
Canada 1979 1 0.07 30 0.09
2 0.07 0.28 0.18
1978 2 0.15 whole 1.60 1.00 0.80
pulp <0.01 <0.01 <0.01
1 0.15 whole 0.22 0.26 0.15 0.10
pulp <0.01 <0.01 <0.01 <0.01
Japan 1979 2 0.3 20 whole 1.31 1.10 0.62
3 whole 1.31 1.30 0.78
2 0.2 whole 0.06 0.07 0.10
3 whole 0.18 0.09 0.07
Netherlands 1977 1 0.112 (0.13-0.20)
0.17
1 0.225 (0.17-0.31)
0.24
Root and tuber vegetables
Residue data on sugarbeets were obtained from trials in the USA.
The maximum residue of 0.03 mg/kg was found in roots 21 days after the
last of two treatments at a rate of 0.44 kg/ha. In other trials, the
residues were at or below the detectable limit (0.01 mg/kg) (Table 4).
In beet tops, the maximum residue observed was 8.5 mg/kg 21 days after
treatments of 0.45 kg/ha. Numerous trials on the residue in potatoes
showed that no residues above the limit of detection (0.01 mg/kg) were
found in potatoes harvested 0 to 21 days after application (except one
sample which contained 0.06 mg/kg.).
Alfalfa
Residue data on alfalfa were obtained from trials in the USA
where a single treatment was made at rates of up to 0.22 kg/ha. The
maximum residues on green alfalfa of 3.8 mg/kg was found 6 days after
an application rate of 0.22 kg/ha (Table 5). The residues on dry
alfalfa were about 3 times higher than those on green alfalfa.
Legume vegetables
Residue data are available from the USA, Canada and Mexico on
legume vegetables, including green beans, soybeans, peas and
chickpeas. Residues in green beans were generally less than 1.0 mg/kg
3 days or more after treatment at rates of up to 0.45 kg/ha (Table 6).
One trial in which 0.45 kg/ha was applied gave the maximum residue of
2.0 mg/kg 7 days after treatment. Residues in soybeans were less than
0.1 mg/kg 1 day or later after treatment. The maximum residue of 0.07
mg/kg was found 21 days after treatment at 0.45 kg/ha. In peas, the
residues did not exceed 0.1 mg/kg and the pods carried almost all the
residues found in peas with pods.
Pome and stone fruits
Trials have been carried out on apples, pears, peaches and
cherries in USA, Canada and Japan. In apples, following application at
rates up to 1.12 kg/ha, the residues were less than 2.0 mg/kg 0 day or
later after treatment, except in a trial in the USA where 2.2 mg/kg
was found 42 days after 4 treatments at 0.67 kg/ha (Table 7). In
pears, the residues generally did not exceed 2 mg/kg 14 days after
treatment, except in one trial in the USA where the maximum residue of
4.3 mg/kg was found 20 days after the second of 2 applications of
0.45 kg/ha. This was judged to be an exceptional case.
Peaches were treated at rates of 0.1 to 3.4 kg/ha. At the
application rates of 1.0 kg/ha or below, the residues were generally
less than 1 mg/kg even when the treatment was made immediately before
harvest. The maximum residue was 4.3 mg/kg 14 days after the last of 5
applications at a rate of 0.9 kg/ha. As the recommended and approved
TABLE 4. Fenvalerate Residues on Root and Tuber Vegetables
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year
No. Rate EC Formulation
(kg a.i./ha) (%) 0 3 5 7 10 13 21
Sugarbeet roots USA 1978 3 0.11 20 0.01
tops 4.21
roots 0.22 0.01
tops 4.43
roots 0.45 0.02
tops 8.52
roots 2 0.22 <0.01
tops 0.10
roots 0.45 0.03
tops 0.54
Potato whole USA 1978 7 0.22 20 <0.01
pulp <0.01
peel 0.03
whole 0.45 0.02
pulp <0.01
peel 0.03
whole, pulp,
peel 1979 7 0.22 20 <0.01
whole, pulp,
peel 7 0.22 <0.01
whole, pulp,
peel 7 0.22 20 <0.01(8d)
0.45 <0.01
7 0.22 20 <0.01
7 0.22 20 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01
0.45 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01
6 0.022 30 0.06
Canada 1978 3 0.15 30 <0.01
4 0.15 30 <0.01
Carrot Canada 1979 7 0.07 30 <0.01 <0.01
TABLE 5. Fenvalerate Residues on Alfalfa
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year
No. Rate EC Formulation
(kg a.i./ha) (%) 0 1 3 7 14 24
Green USA 1976 1 0.05 30 0.30 0.34 0.40 0.51 0.20 0.12
0.11 0.74 0.90 0.88 0.96 0.53 0.43
0.22 1.9 1.7 2.0 1.7 1.3 0.70
1977 1 0.11 2.0(25d) 0.31(50d) 0.03(81d) <0.01 (116d)
1978 1 0.0065 30 0.27
0.014 0.78
0.028 0.80
1980 1 0.22 30 3.8(6d)
Dry USA 1976 1 0.05 30 1.3 1.2 1.1 0.92 0.71
0.11 2.4 2.3 2.1 2.1 1.6
0.22 5.8 5.5 5.9 5.4 3.1
1977 1 0.11 30 0.50(36d) 0.64(61d) 0.02(92d) 0.03(127d)
1980 1 0.11 30 6.9
0.22 12.0
1 0.22 30 12(20d)13(67d)
TABLE 6. Fenvalerate Residues on Legume Vegetables
Applications Residues (mg/kg) at intervals (days) after
Crop Country/Year EC application
No. Rate Formulation
(kg a.i./ha) (%) 0 3 5 7 10 14 21
Green beans USA 1976 3 0.11 30 0.17
0.22 0.26
0.45 0.67
5 0.11 0.03
0.22 0.05
4 0.11 0.04
0.22 0.07
1978 4 0.11 0.10 0.13 0.09 0.10
0.22 0.18 0.12 0.11 0.18
1979 4 0.11 0.03
1978 4 0.22 1.1 0.55 0.57 0.47 0.70
0.45 2.4 2.0 1.0 0.76 1.1
1980 4 0.22 0.26
0.45 0.47
4 0.22 0.73(4d)
1978 7 0.22 0.18(16d)
0.45 0.29(16d)
Dry beans 1978 3 0.22 <0.01
0.44 <0.01
4 0.055 <0.01
0.22 0.02
1977 3 0.11 0.02 0.01 <0.01 <0.01
0.22 0.04 0.01 0.02 0.02
0.45 0.03
1979 4 0.22 <0.01
0.45 0.02
5 0.22 <0.01
0.45 <0.01
4 0.22 <0.01
TABLE 6. (con't)
Applications Residues (mg/kg) at intervals (days) after
Crop Country/Year EC application
No. Rate Formulation
(kg a.i./ha) (%) 1 3 7 14 21 28
Soybeans USA 1978 4 0.055 30 <0.01(20d)
0.11 <0.01(20d)
0.22 0.02(20d)
0.45 0.02(20d)
1979 4 0.22 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01
4 0.22 <0.01
0.45 0.01
4 0.22 0.03
0.45 0.03
4 0.22 0.03
0.45 0.07
4 0.22 0.03
Japan 1980 3 0.2 20 0.015 0.030(35d)
3 0.18 0.005 <0.005(34d)
Dry peas USA 1978 1 0.22 30 0.03
o.45 0.05
1979 4 0.22 0.12
0.45 0.19
4 0.22 0.05
0.45 0.12
2 0.055 0.12(24d)
0.11 0.18(24d)
0.22 0.59(24d)
4 0.055 <0.01
0.11 0.02
0.22 0.03
TABLE 6. (con't)
Applications Residues (mg/kg) at intervals (days) after
Crop Country/Year EC application
No. Rate Formulation
(kg a.i./ha) (%) 0 1 3 7 10 23
Peas succulent USA 1978 3 0.22 30 <0.01(Pods 0.22)
(peas) 0.45 <0.01 (0.27)
1 0.22 0.02
0.45 0.07
1979 4 0.22 0.01(0.46)
0.44 0.01(1.01)
4 0.22 0.05(3.6) 0.04(3.1) 0.05(2.9) 0.06(1.9) 0.02(0.91)
0.45 0.09(9.7)
Peas succulen USA 1980 2 0.22 0.59
(peas a pods) 0.44 1.16
2 0.22 0.46
0.44 1.1
2 0.22 0.90
0.44 1.17
2 0.22 0.20(pods)
0.44 0.42(pods)
2 0.22 0.06
Chickpea Mexico 1979 1 0.105 30 <0.01(0.21)
(seeds) 1 0.15 <0.01(0.47)
1 0.21 <0.01(0.70)
1 0.30 <0.01(1.0)
(seeds & pods)
TABLE 7. Fenvalerate Residues on Pome and Stone Fruits
Applications Residues (mg/kg) at intervals (days) after
Crop Country/Year EC application
No. Rate Formulation
(kg a.i./ha) (%) 0 3 15 20 33 65 187
Apples
whole USA 1978 1 0.34 30 <0.01
peeled <0.01
peel <0.01
whole 1 0.28 <0.01 (174d)
peeled <0.01 (174d)
peel <0.01 (174d)
whole 4 0.34 0.51(42d)
peeled <0.01(42d)
peel 3.4 (42d)
whole 0.67 2.2 (42d)
peeled 0.03(42d)
peel 7.3 (42d)
whole 7 0.56 0.56(21d)
peeled 0.03(21d)
peel 1.5 (21d)
whole 1.12 0.92(21d)
peeled 0.06(21d)
peel 2.6 (21d)
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after
Crop Country/Year EC application
No. Rate Formulation
(kg a.i./ha) (%) 0 3 15 20 33 65 187
whole 1977 8 0.28 0.86 0.89 0.46 0.6
peeled 0.02 0.01 <0.01 0.01
peel 4.0 1.5 2.0 1.5
whole 0.56 1.1 1.6 0.85 0.78
peeled 0.04 0.02 0.01 0.01
peel 5.0 5.3 5.1 3.6
whole 1979 5 0.56 0.54
peeled 0.01
peel 1.4
whole 1.12 0.46
peeled <0.01
peel <0.1
whole 1977 4 0.11 0.22(29d)
peeled <0.01(29d)
peel 1.9 (29d)
whole 0.22 0.54(29d)
peeled <0.01(29d)
peel 3.3 (29d)
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after
Crop Country/Year EC application
No. Rate Formulation
(kg a.i./ha) (%) 0 14 21 30 35
whole USA 1979 9 0.67 30 0.78 0.64 0.67 0.88 0.77
whole 9 0.34 0.67
peeled 0.05
peel 3.8
whole 0.45 1.1
peeled 0.04
peel 9.9
whole 0.67 1.1
peeled 0.14
peel 13.0
whole 1977 10 0.056 0.35(20d) 0.37
peeled <0.01(20d) <0.01
peel 2.1 (20d) 2.6
whole 0.11 0.63(20d) 0.61
peeled <0.01(20d) 0.01
peel 3.7 (20d) 2.6
whole 1979 9 0.15 0.84
whole 0.28 1.6
whole 9 0.56 0.71
whole 1.12 1.2
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after
Crop Country/Year EC application
No. Rate Formulation
(kg a.i./ha) (%) 3 42 56 70 84 112
whole Canada 1979 1 0.14 30 <0.01
whole 1 0.14 <0.01
whole 4 0.14 0.08
pulp <0.01
whole 8 0.14 0.45 0.40(7d)
pulp 0.05 0.08(7d)
whole 1978 1 0.07 <0.01
whole 1 0.07 <0.01
whole 8 0.07 0.20
pulp <0.01
whole 8 0.07 0.28
pulp <0.01
whole 8 0.15 0.30
pulp <0.01
whole 8 0.15 0.72
pulp 0.02
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after
Crop Country/Year EC application
No. Rate Formulation
(kg a.i./ha) (%) 0 3 15 20 33 65 187
whole Japan 1980 2 0.5 20 0.450(45d) 0.338(60d) 0.344(75d)
whole 4 0.600(45a) 0.378(60d) 0.500(75d)
whole 2 0.5 0.328(45d) 0.256(60d) 0.234(VSd)
whole 4 0.605(45a) 0.555(60d) 0.498(75d)
28 83 114 135 147 161
Pear
whole USA 1977 1 0.17 30 0.20(36d)
peeled <0.01(36d)
peel 0.56(36d)
whole 0.34 0.27(36d)
peeled <0.01(36d)
peel 1.0 (36d)
whole 1978 1 0.11 <0.01(118d)
peeled <0.01(118d)
peel <0.01(118d)
whole 2 0.11 <0.01(118d)
peeled <0.01(118d)
peel <0.01(118d)
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after
Crop Country/Year EC application
No. Rate Formulation
(kg a.i./ha) (%) 28 83 114 135 147 161
whole 1 0.22 <0.01(118d)
peeled <0.01(118d)
peel <0.01(118d)
whole 1 0.34 <0.01
peeled <0.01
peel <0.01
whole 0.17 <0.01
peeled <0.01
peel <0.01
whole 0.084 <0.01
peeled <0.01
peel <0.01
whole 2 0.34 0.12(62d)
peeled <0.01(62d)
peel 0.32(62d)
whole 1 0.34 <0.01 <0.01
peeled <0.01 <0.01
peel <0.01 <0.01
whole 2 0.34 <0.01(89d)
whole 5 0.34 0.26
peeled <0.01
peel 2.0
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year EC (Days)
No. Rate Formulation
(kg a.i./ha) (%) 28 83 114 137
whole USA 1979 4 0.45 30 0.58
peeled 0.02
peel 2.2
whole 0.9 0.75
peeled 0.02
peel 3.5
whole 4 0.45 0.93(21d)
whole 0.9 0.78(21d)
whole 3 0.45 0.15
peeled <0.01
peel 0.50
whole 0.9 0.03
peeled <0.01
peel 0.14
whole 3 0.45 0.04(86d)
peeled <0.01(86d)
peel 0.20(86d)
whole 0.9 0.05(86d)
peeled <0.01(86d)
peel 0.19(86d)
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year EC (Days)
No. Rate Formulation
(kg a.i./ha) (%) 28 83 114 137
whole 2 1.8 0.08
peeled 0.01
peel 0.37
whole 4 0.45 0.47
whole 0.9 0.58
whole 3 0.45 0.02(114d)
whole 0.9 0.04(114d)
whole 3 0.45 0.01
peeled <0.01
peel 0.03
whole 1979 0.9 0.03
peeled <0.01
peel 0.05
whole 4 0.45 <0.01(35d)
whole 0.9 0.01(35d)
(Days)
1 7 14 20 31 82 100
whole 2 0.06 30 0.90 0.57 0.48 0.36
whole 0.11 1.1 1.0 1.1 0.68
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year EC (Days)
No. Rate Formulation
(kg a.i./ha) (%) 1 7 14 20 31 82 100
whole 0.22 2.1 1.3 1.7 1.5
whole 0.45 4.1 2.6 3.5 4.3
whole 4 0.45 0.7 (28d)
peeled 0.01(28d)
peel 3.2 (28d)
whole 0.9 0.80(28d)
peeled <0.01(28d)
peel 3.4 (28d)
whole 3 0.45 0.04
whole 0.9 0.05
whole 4 0.67 0.18
peeled 0.01
peel 1.0
whole 4 0.45 0.84(29d)
whole 0.9 1.1 (29d)
whole 1.8 1.7 (29d)
whole 1 0.45 <0.01(140d)
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year EC (Days)
No. Rate Formulation
(kg a.i./ha) (%) 1 7 14 20 31 82 100
whole 0.9 <0.01(140d)
whole 3 0.45 0.06(77d)
whole 0.9 0.11(77d)
whole 2 0.45 <0.01(132d)
whole 0.9 <0.01(132d)
whole 4 0.45 0.39
whole 0.9 0.87
whole 4 0.45 0.73
whole 0.9 1.5
whole 2 0.45 <0.01(119d)
whole 0.9 <0.01(119d)
whole 3 0.45 0.01(97d)
whole 0.9 0.03(97d)
whole 3 0.45 0.03(110d)
whole 0.9 0.02(110d)
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after application
Crop Country/Year EC (Days)
No. Rate Formulation
(kg a.i./ha) (%) 1 4 7 35 84
whole Canada 1978 4 0.03 30 <0.01
whole 2 0.07 <0.01
whole 1979 3 0.004% 0.23 0.22 0.15
pulp <0.01 <0.01 <0.01
1 7 14 21 28 63
Pear
Bartlett Canada 1978 2 0.065 E.C. 0.02
2 0.125 E.C. 0.07
1979 1 0.125 E.C. 0.090 0.029
2 0.125 E.C. 0.243 0.118
3 0.125 E.C. 0.348
Pear
Bartlett Canada 1978 1 0.125 E.C. 0.085 0.130 0.100
1 0.125 E.C. 0.115 0.195 0.170
whole 1 0.125 E.C. 0.170 0.210 0.140
whole 1 0.125 E.C. 0.275 0.185 0.165
peel 1 0.125 E.C. 1.34 0.71 1.14
pulp 1 0.125 E.C. 0.005 0.005 0.005
TABLE 7. (con't)
Applications Residues (mg/kg) at intervals (days) after
Crop Country/Year EC application
No. Rate Formulation
(kg a.i./ha) (%) 1 7 14 21 28 63
whole 1 0.250 E.C. 0.515 0.595 0.275
whole 1 0.250 E.C. 0.490 0.620 0.260
whole 1 0.250 E.C. 0.405 0.395 0.260
peel 1 0.250 E.C. 3.23 3.19 2.06
pulp 1 0.250 E.C. 0.013 0.012 0.009
Anjou 1 0.125 E.C. 0.085
Anjou 1 0.250 E.C. 0.225
0 3 7 14 30 126
Peach
whole USA 1978 3 0.45 30 0.65(21d)
pulp 0.03(21d)
peel 3.4(21d)
whole 0.9 2.2(21d)
pulp 0.06(21d)
peel 5.4(21d)
whole 2 0.11 0.05(35d)
pulp <0.01(35d)
peel 0.22(35d)
whole 0.22 0.11(35d)
pulp