FENVALERATE
Human Health Effects:
Evidence for Carcinogenicity:
Evaluation: No data were available from studies in humans. There is inadequate evidence
for the carcinogenicity of fenvalerate in
experimental animals. Overall evaluation: Fenvalerate
is not classifiable as to its carcinogenicity to humans (Group 3).
Human Toxicity Excerpts:
One notable form of toxicity associated with synthetic pyrethroids has been a cutaneous
paresthesia observed in workers spraying esters containing alpha-cyano substituent
(deltamethrin, cypermethrin, fenvalerate). The
paresthesia developed several hours following exposure, being described as a stinging or
burning sensation on the skin which, in some cases, progressed to a tingling and numbness,
the effects lasting some 12 to 18 hours.
Treatment is supportive, and most casual exposures require only decontamination.
Topical vitamin E may ameliorate the parethesias that accompany contact with synthetic
pyrethroids containing an alpha-cyano group (eg fenvalerate,
cypermethrin, flucythrinate).
Fenvalerate can induce numbness, itching,
tingling, and burning sensations in exposed workers, which develop after a latent period
of approximately 30 min, peak by 8 hours, and disappear within 24 hours.
Among 23 workers exposed to synthetic pyrethroids, including fenvalerate,
19 experienced one or more episodes of abnormal facial sensation. Developing between 30
min and 3 hr after exposure and persisting for 30 min to 8 hr. However, there were no
abnormal neurological signs, and electrophysiological studies showed normal responses in
the arms and legs. The symptoms were most likely due to transient lowering of the
threshold of sensory nerve fibers or sensory nerve endings following exposure of the
facial skin to pyrethroids.
Selected individuals who had worked extensively with fenvalerate
in the delta region of the Mississippi and Alabama, USA, were interviewed and examined.
They had, on some occasions, noted paraesthesia associated with exposure to /fenvalerate/. The cutaneous sensation was described as
a stinging or burning, which progressed to numbness in approximately one third of the
exposed workers. The sensation typically began a number of hours after contact, peaked in
the evening, and rarely was present the following morning. The intensity of the sensation
varied according to the type and extent of exposure. Clinical signs of inflammation such
as edema or vesiculation were not apparent. Erythema was present in a few individuals but
this was difficult to distinguish from sunburn. Several environmental factors were found
to affect the cutaneous sensation associated with fenvalerate
exposure.
Despite early reports of negative findings, fenvalerate
produced local irritant symptoms in 73% of plant nursery workers handling treated
seedlings. Tingling or burning sensations were also described after accidental splashing
of the facial skin with fenvalerate. A study of
human volunteers who were exposed to fenvalerate
applied to the ear lobe reported that paresthesia (ie, numbness combined with irritating
abnormal sensation) could be experienced in severe cases. The threshold application
appeared to be less than 10 ug/sq cm. All reports agree that the sensation appears after a
latent period of about 30 min and persists for 0.5-24 hr, depending on severity.
Clinical manifestations of 573 cases of acute pyrethroid poisoning are reviewed. The
cases occurred in 14 provinces in China and involved 325 patients exposed to deltamethrin,
196 to fenvalerte, 45 to cypermethrin, and seven to other pyrethroid compounds. Of the 573
cases, 229 were of occupational origin resulting from inappropriate handling of the
chemicals such as spraying with higher concentrations than allowed, sustaining longer
exposure durations than recommended, spraying against the wind, clearing stoppage of
sprays by mouth and hands, spraying closer than every row of crops, or not wearing
personal protective equipment. Those occupationally exposed patients experienced initial
burning or itching sensations of the face within a few minutes of exposure or dizziness
developing at 4 to 6 hours after exposure. Half of those occupationally exposed
experienced abnoral facial sensations such as burning, itching, or tingling sensation
which were exacerbated by sweating and washing with warm water. These symptoms disappeared
several hours to 1 day after exposure. Systemic symptoms included dizziness, 60.6 percent;
headache, 44.5 percent; nausea, 59.7 percent; anorexia, 45 percent; and fatigue, 26
percent. Vomiting occurred in 16 percent of those who were occupationally exposed. Other
symptoms included chest tightness, 13.1 percent; parasthesia, 11.89 percent; palpitation,
13.1 percent; blurred vision, 7 percent; and increased sweating, 6.7 percent. Coarse
muscular fasciculations developed in large muscles of extremities in the more serious
cases. In those suffering from convulsions, seizures could arise up to 30 times a day for
the first week. Blood tests revealed leukocytosis in 15 percent. Treatment consisted of
symptomatic and supportive therapy including gastric lavage. Most recovered in 6 days.
Mitotic process disturbance by fenvalerate, a
pyrethroid insecticide, was investigated in human peripheral blood lymphocyte cultures by
analyzing C-mitosis frequency. Cell cultures were established from whole heparinized blood
from two healthy donors. After incubation for 48 hr, cells were incubated for 24 hr in 2
to 50 ug/ml fenvalerate, or without fenvalerate (control). One hundred metaphases per
concn were examined for both complete and partial C-mitosis. The frequency of C-mitosis
was reported as 18 and 24% for control, 17 and 38% for incubation with 2 ug/ml, 52 and 48%
for 4 ug/ml, 61 and 60% for 10 ug/ml, 99 and 90% for 20 ug/ml, 74 and 97% for 40 ug/ml, 70
and 98% for 5 ug/ml, and 100% (both samples) for the positive control 0.01 ug/ml
demecolcine. Fenvalerate results were highly
significant (0.001) by the chi square test at all concn except 2 ug/ml. Mitotic arrest was
confirmed by absence of anaphase and telophase figures. Results were in good agreement
with previous long term, low dose studies in rats. C-mitosis disruption was considered a
cytological indicator of normal spindle function inhibition or disruption.
Clinical manifestations of 573 cases of acute pyrethroid poisoning are reviewed. The
cases occurred in 14 provinces in China and involved 325 patients exposed to deltamethrin,
196 to fenvalerate, 45 to cypermethrin, and
seven to other pyrethroid compounds. Of the 573 cases, 229 were of occupational origin
resulting from inappropriate handling of the chemicals such as spraying with higher concn
than allowed, sustaining longer exposure durations than recommended, spraying against the
wind, clearing stoppage of sprays by mouth and hands, spraying closer than every other row
of crops, or not wearing personal protective equipment. Those occupationally exposed
patients experienced initial burning or itching sensations of the face within a few
minutes of exposure o dizziness developing at 4 to 6 hr after exposure. Half of those
occupationally exposed experienced abnormal facial sensations such as burning, itching, or
tingling sensations which were exacerbated by sweating and washing with warm water. These
symptoms disappeared several hours to 1 day after exposure. Systemic symptoms included
dizziness, 60.6%; headache, 44.5%; nausea, 59.7%; anorexia, 45%; and fatigue, 26%.
Vomiting occurred in 16% of those who were occupationally exposed. Other symptoms included
chest tightness, 13.1%; parasthesia, 11.89%; palpitation, 13.1%; blurred vision, 7%; and
increased sweating, 6.7%. Coarse muscular fasciculations developed in large muscles of
extremities in the more serious cases. In those suffering from convulsions, seizures could
arise up to 30 times a day for the first week. Blood tests revealed leukocytosis in 15%.
Treatment consisted of symptomatic and supportive therapy including gastri lavage. Most
recovered in 6 days. Four cases were detailed for illustrative purposes.
Clastogenic effects in peripheral lymphocytes of cotton field workers who were exposed
to different pesticides were studied. All the cells were grown in RPMI 1640 medium for 48
and 72 hr. The type of aberrations observed in the exposed group are gaps, breaks,
dicentrics, exchanges, rings and polyploidy. The frequency of total chromosomal
aberrations increased significantly in male pesticide applicators when compared to
controls. A significant decrease in mitotic index was observed in the exposed group as
compared to the control group. The 48 hr cultures showed high incidence of chromosomal
aberrations and low mitotic index when compared to 72 hr cultures. The difference in
chromosomal aberrations between 48 and 72 hr cultures was not significant. 24 out of 26
individuals showed ill health effects such as severe giddiness and nervous disorders.
The ability of the pyrethroid insecticide, fenvalerate,
to induce mitotic micronuclei was investigated in cultured human lymphocytes. Human
lymphocyte cultures were prepared by adding heparinized whole blood from healthy donors to
chromosome medium supplemented with fetal calf serum, antibiotics, and glutamine.
Cytochalasin-B, to block cytokinesis, and fenvalerate
(10, 20, 40, 50 ug/ml) were added to the cultures simultaneously. At 72 hr, the cultures
were centrifuged for determination of micronucleus frequency. The proportion of
cytokinesis block cells was reduced in the presence of fenvalerate
in a concn dependent manner. Fenvalerate induced
a significant increase in the frequency of micronuclei, indicating clastogenic and/or
aneugenic activity. The authors conclude that the findings complement previous data on the
genotoxicity of fenvalerate in human
lymphocytes.
Synthetic pyrethroids are neither cutaneous sensitizers nor irritants. Although these
compounds do not cause signs of inflammation (edema, erythema, vesiculation), they do
produce paresthesias after contact. Typically, symptoms begin several hours after
cutaneous exposure, peak in the evening, and resolve by the following day. /Synthetic
pyrethroids/
Contact allergy from pyrethroids ... has not been observed. /Pyrethroids/
The allergenic properties of pyrethroids /with early pyrethrum preparations/ are marked
in comparison with other pesticides. Many cases of contact dermatitis and respiratory
allergy have been reported. Persons sensitive to ragweed pollen are particularly prone to
such reactions. Preparations containing synthetic pyrethroids are less likely to cause
allergic reactions than are the preparations made from pyrethrum powder. /Pyrethroids/
There have been very few systemic poisonings of humans by pyrethroids. /Pyrethroids/
Pyrethroids are not cholinesterase inhibitors. /Pyrethroids/
Extraordinary absorbed doses may rarely cause incoordination, tremor, salivation,
vomiting, diarrhea, and irritability to sound and touch. /Pyrethroids/
Some pyrethroid (eg, deltamethrin, fenvalerate,
cyhalothrin, lambda-cyhalothrin, flucythrinate, and cypermethrin) may cause a transient
itching and/or burning sensation in exposed human skin. /Synthetic pyrethroids/
Mitotic process disturbance by fenvalerate, a
pyrethroid insecticide, was investigated in human peripheral blood lymphocyte cultures by
analyzing C-mitosis frequency. Cell cultures were established from whole heparinized blood
from two healthy donors. After incubation for 48 hr, cells were incubated for 24 hr in 2
to 50 ug/ml fenvalerate, or without fenvalerte
(control). One hundred metaphases per concentration were examined for both complete and
partial C-mitosis. The frequency of C-mitosis was reported as 18 and 24% for control, 17
and 38% for incubation with 2 ug/ml, 99 and 90% for 20 ug/ml, 74 and 97% for 40 ug/ml, 70
and 98% for 5 ug/ml, and 100% (both samples) for the positive control 0.01 ug/ml
demecolcine. Fenvalerate results were highly
significant (0.001) by the chi square test at all concentrations except 2 ug/ml. Mitotic
arrest was confirmed by absence of anaphase and telophase figures. Results were in good
agreement with previous long term, low dose studies in rats. C-mitosis disruption was
considered a cytological indicator of normal spindle function inhibition or disruption.
...
Skin, Eye and Respiratory Irritations:
Fenvalerate as technical Pydrin
is mildly irritating to the skin, but the emulsifiable concentrate is corrosive.
Eye, skin irritant.
One notable form of toxicity associated with synthetic pyrethroids has been a cutaneous
paresthesia observed in workers spraying esters containing alpha-cyano substituent
(deltamethrin, cypermethrin, fenvalerate). The
paresthesia developed several hours following exposure, being described as a stinging or
burning sensation on the skin which, in some cases, progressed to a tingling and numbness,
the effects lasting some 12 to 18 hours.
Immediately irritating to the eye. /Pyrethrins/
The chief effect from exposure ... is skin rash particularly on moist areas of the
skin. ... May irritate the eyes.
Medical Surveillance:
Initial medical screening: Employees should be screened for history of certain medical
conditions ... which might place the employee at increased risk from /pyrethroid/
exposure. Chronic respiratory disease: In persons with chronic respiratory disease,
especially asthma, the inhalation of /pyrethroids/ might cause exacerbation of symptoms
due to its sensitizing properities. Skin disease: /Pyrethroids/ can cause dermatitis which
may be allergic in nature. Persons with pre-existing skin disorders may be more
susceptible to the effects of this agent. Any employee developing the above-listed
conditions should be referred for further medical examination. /Pyrethrum/
Probable Routes of Human Exposure:
Occupational exposure to fenvalerate occurs
through dermal contact and inhalation of dust and sprays, especially to workers applying
the compound as an insecticide(1). Exposure to fenvalerate
can occur during its production and application and, at much lower levels, from
consumption of foods containing residues(2).
Air concns of fenvalerate at the breathing
zone of workers spraying fenvalerate insecticide
on cotton was 0.06-1.98 ug cu m(1); dermal exposure ranged from 4.71 to 141.61 ug/cu cm on
forearms, hands, legs and feet(1). At a fenvalerate
packing plant in China, workers were reported to be exposed to 12-55 ug/cu m in the air,
with resulting skin contact(2).
Body Burden:
Urine concns of fenvalerate of workers
spraying fenvalerate insecticide on cotton was
0.01-1.98 ug/collection interval (3-12 hr) for a period up to 72 hr after spraying(1).
Average Daily Intake:
Based upon results of the US FDA's 1990 Total Diet Study, estimated human exposure to fenvalerate from food is as follows(1): 6-11 month old
child: 0.0101 ug/kg/day; 14-16 yr old male: 0.0061 ug/kg/day; 60-65 yr old female: 0.0092
ug/kg/day(1).
Emergency Medical Treatment:
Emergency Medical Treatment:
| EMT Copyright Disclaimer: |
| Portions of the POISINDEX(R) database are provided here for general
reference. THE COMPLETE POISINDEX(R) DATABASE, AVAILABLE FROM MICROMEDEX, SHOULD BE
CONSULTED FOR ASSISTANCE IN THE DIAGNOSIS OR TREATMENT OF SPECIFIC CASES. Copyright
1974-1998 Micromedex, Inc. Denver, Colorado. All Rights Reserved. Any duplication,
replication or redistribution of all or part of the POISINDEX(R) database is a violation
of Micromedex' copyrights and is strictly prohibited. The following Overview, *** PYRETHRINS ***, is relevant for this HSDB record chemical. |
| Life Support: |
o This overview assumes that basic life support measures
have been instituted.
|
| Clinical Effects: |
SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
o The mammalian toxicity of natural pyrethrins is
generally low. Very young children are perhaps more
susceptible to poisoning because they may not hydrolyze
the pyrethrum esters efficiently. In humans, allergic
reactions are the main toxic manifestations of
pyrethrin exposure.
1. Pyrethrum and the pyrethrins produce typical type I
motor symptoms in mammals. Severe type I poisoning
may include the following signs in humans:
Severe fine tremor
Marked reflex hyperexcitability
Sympathetic activation
Paresthesia (dermal exposure)
o DERMAL - These compounds are not primary irritants.
The chief effect, however, from exposure is dermatitis.
The usual lesion is a mild erythematous dermatitis with
vesicles, papules in moist areas, and intense pruritus;
a bulbous dermatitis may also occur. Pyrethrins can
cause allergic dermatitis and systemic allergic
reactions.
o INHALATION is the major route of exposure, with airway
irritation as the primary toxic effect. Following
inhalation, a stuffy, runny nose and scratchy throat
are common. Hypersensitivity reactions including
wheezing, sneezing, shortness of breath and
bronchospasm may be noted.
o OCULAR - Eye exposures may result in mild to severe
corneal damage that generally resolves with
conservative care.
o Piperonyl butoxide and other compounds are often added
to pyrethrin insecticides as synergists and may
contribute to toxicity.
o Synthetic pyrethroids, which are related to pyrethrins,
are covered in a separate management.
HEENT
0.2.4.1 ACUTE EXPOSURE
o A stuffy, runny nose and scratchy throat following
inhalational exposure may be noted.
o Eye exposures may result in mild to severe corneal
damage, decreased visual acuity and periorbital edema.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Hypotension and tachycardia, associated with
anaphylaxis, may occur.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Hypersensitivity reactions characterized by
pneumonitis, cough, dyspnea, wheezing, chest pain, and
bronchospasm may occur. Rare cases of respiratory
failure and cardiopulmonary arrest have been reported.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o Paresthesias, headaches, and dizziness are common.
Massive exposure may result in hyperexcitability and
seizures, but this is rare.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Nausea, vomiting and abdominal pain commonly occur and
develop within 10 to 60 minutes following ingestion.
DERMATOLOGIC
0.2.14.1 ACUTE EXPOSURE
o Irritant and contact dermatitis may develop. Erythema
which mimics sunburn has also been noted after
prolonged repeated exposure.
ENDOCRINE
0.2.16.1 ACUTE EXPOSURE
o Type I motor symptoms following severe poisoning may
result in sympathetic activation.
IMMUNOLOGIC
0.2.19.1 ACUTE EXPOSURE
o Sudden bronchospasm, swelling of oral and laryngeal
mucous membranes, and anaphylactoid reactions have been
reported after pyrethrum inhalation. Hypersensitivity
pneumonitis characterized by cough, shortness of
breath, chest pain, and bronchospasm may be noted.
GENOTOXICITY
o Pyrethrum is not mutagenic in bacterial reversion tests
(Ray, 1991).
|
| Laboratory: |
o Pyrethrin plasma levels are not clinically useful or
readily available.
o Monitor for allergic responses such as asthma or contact
dermatitis.
|
| Treatment Overview: |
ORAL EXPOSURE
o There is no specific antidote for pyrethrin poisoning.
Treatment is symptomatic and supportive and includes
monitoring for the development of hypersensitivity
reactions with respiratory distress. Provide adequate
airway management when needed. Gastric decontamination
is usually not required unless the pyrethrin product is
combined with a hydrocarbon.
o ALLERGIC REACTION: MILD: antihistamines with or
without epinephrine. SEVERE: oxygen, aggressive
airway management, antihistamines, epinephrine (ADULT:
0.3 to 0.5 mL of a 1:1000 solution subcutaneously;
CHILD: 0.01 mL/kg; may repeat in 20 to 30 min),
corticosteroids, ECG monitoring, and IV fluids.
INHALATION EXPOSURE
o INHALATION: Move patient to fresh air. Monitor for
respiratory distress. If cough or difficulty breathing
develops, evaluate for respiratory tract irritation,
bronchitis, or pneumonitis. Administer oxygen and
assist ventilation as required. Treat bronchospasm with
beta2 agonist and corticosteroid aerosols.
EYE EXPOSURE
o DECONTAMINATION: Irrigate exposed eyes with copious
amounts of tepid water for at least 15 minutes. If
irritation, pain, swelling, lacrimation, or photophobia
persist, the patient should be seen in a health care
facility.
DERMAL EXPOSURE
o DECONTAMINATION: Remove contaminated clothing and wash
exposed area thoroughly with soap and water. A
physician may need to examine the area if irritation or
pain persists.
o Vitamin E topical application is highly effective in
relieving paresthesias.
|
| Range of Toxicity: |
o The minimal lethal dose of pyrethrum is not established,
but is probably in the range of 10 to 100 grams.
o Hypersensitivity reactions may be noted, especially
following a chronic dermal or inhalation exposure.
Patients with underlying asthma may be predisposed to
severe bronchospastic reactions after exposure.
|
Antidote and Emergency Treatment:
Treatment is supportive, and most casual exposures require only decontamination.
Topical vitamin E may ameliorate the paresthesias that accompany contact with synthetic
pyrethroids containing an alpha-cyano group (e.g., fenvalerate,
cypermethrin, flucythrinate). /Synthetic pyrethroids/
DO NOT ADMIN OR INSTILL MILK, CREAM, OR OTHER SUBSTANCES CONTAINING VEGETABLE OR ANIMAL
FATS, WHICH ENHANCE ABSORPTION OF LIPOPHILIC SUBSTANCES, SUCH AS ... PYRETHROIDS. DIAZEPAM
(VALIUM (R)), 5-10 MG IN ADULT, 0.1 MG/KG IN CHILDREN, GIVEN ORALLY OR SLOWLY IV, SHOULD
CONTROL NERVOUSNESS & TREMORS IN RARE CASES ... AFTER EXTRAORDINARY EXPOSURE TO ...
PYRETHROIDS. /PYRETHRUM, PYRETHRINS, PYRETHROIDS, AND PIPERONYL BUTOXIDE/
To minimize absorption of pyrethrins and piperonyl butoxide following ingestion,
gastric lavage should be performed immediately and saline cathartics administered.
Treatment of overdosage mainly involves symptomatic and supportive care. /Pyrethrins/
Skin contamination should be removed by washing with soap and water. If irritant or
paresthetic effects occur, treatment by a physician should be obtained. Because /vapor
exposure/ of pyrethroid apparently accounts for paresthesia affecting the face, strenuous
measures should be taken (ventilation, protective face mask and hood) to avoid vapor
contact with the face and eyes. Vitamin E Oil preparations (dl-alpha tocopheryl acetate)
are uniquely effective in preventing and stopping the paresthetic reaction. They are safe
for application to the skin under field conditions. Corn oil is somewhat effective, but
possible side effects with continuing use make it less suitable. Vaseline is less
effective than corn oil and zinc oxide actually worsens the reaction. /Pyrethroids/
Eye contamination should be treated immediately by prolonged flushing of the eye with
copious amounts of clean water or saline. If irritation persists, professional
ophthalmologic care should be obtained. ... Extraordinary measures should be taken to
avoid eye and skin contamination with this product. Should accidental eye contamination
occur, expert ophthalmologic care should be obtained after flushing the eye free of the
chemical with copious amounts of clean water. /Pyrethroids/
Ingestion of pyrethroid insecticide presents relatively little risk. However, if large
amounts have been ingested, empty the stomach by intubation, aspiration, and lavage. Based
on observations in laboratory animals, large ingestions of either allethrin, cismethrin, fenvalerate or deltamethrin would be the most likely
to generate neurotoxic manifestations. /Pyrethroids/
If only small amounts of pyrethroid have been ingested, or if treatment has been
delayed, oral administration of activated charcoal and cathartic probably represents
optimal management. /Pyrethroids/
Animal Toxicity Studies:
Evidence for Carcinogenicity:
Evaluation: No data were available from studies in humans. There is inadequate evidence
for the carcinogenicity of fenvalerate in
experimental animals. Overall evaluation: Fenvalerate
is not classifiable as to its carcinogenicity to humans (Group 3).
Non-Human Toxicity Excerpts:
Exposure to fenvalerate is likely to cause
central nervous system stimulation with symptoms of nervousness, anxiety, salivation,
tremors and convulsions. Nerve damage was observed in rats given high doses.
... Low toxicity to mammals. ... 24 Month feeding/oncogenic (rat) study demonstrated
that fenvalerate is not oncogenic.
... Toxic to wildlife and extremely toxic to fish. Highly toxic to bees exposed to
direct treatment on blooming crops and weeds.
Rats fed fenvalerate at 2000 mg/kg diet for
8-10 days showed typical signs of acute intoxication. Reversible morphological changes in
the sciatic nerve were observed in rats administered fenvalerate
at 3000 mg/kg diet. Histopathological changes in sciatic nerves were also observed in rats
and mice treated with a single oral dose of fenvalerate
at lethal or sublethal levels.
Hens administered fenvalerate orally at 1000
mg/kg per day for 5 days did not show any clinical or morphological signs of delayed
neurotoxicity.
When groups of ddY mice (35-47 of each sex per group) were administered fenvalerate in the diet for 78 wk at levels of 0, 100,
300, 1000, or 3000 mg/kg, mortality occurred at the highest dose level. Hyperexcitability
was observed at 1000 mg/kg or more, and body weight was depressed at 3000 mg/kg over the
18 mo period and at 1000 and 3000 mg/kg over the first 3 mo. A variety of hematological
parameters were affected at 3 mo, predominantly at the highest dose level, but no
hematological changes were observed at the end of the study. Several biochemical changes
suggestive of hepatotoxicity were observed at 3 mo and at termination of the study in the
300, 1000, and 3000 mg/kg groups. There were gross changes in several organ weights and in
organ to body weight ratios, predominantly in the liver. Microscopic examination revealed
changes in the liver, mesenteric lymph nodes, and kidney. Dose dependent granulomatous
changes were observed in the liver and/or mesenteric lymph nodes in all treatment groups.
At the 3 mo interim sacrifice multiple small necrotic foci in liver and changes in the
epithelial cells of the proximal convoluted tubules were noted at the two highest dose
levels. There were no indications in this study of tumorigenicity or carcinogenicity as a
result of fenvalerate administration.
Fenvalerate has also been examined for its
mutagenic potency with the Ames test in Salmonella typhimurium (TA1535, TA1538, TA98, and
TA100), using dose levels of up to 1 mg/plate both with and without a metabolic enzyme
system. Fenvalerate was non-mutagenic in these
tests. It was also tested using hepatic metabolic enzyme systems prepared from various
PCB-treated animals (three strains of rats, six strains of mice and the Syrian golden
hamster). At dose levels of up to 1 mg/plate, fenvalerate
was non-mutagenic.
Groups of pregnant ICR mice (32-33 per group) were orally administered fenvalerate at dose levels of 0, 5, 15, or 50 mg/kg
per day on days 6 to 15 of gestation. Groups of 20 mice were sacrificed on day 18, and the
fetuses were removed and examined for visceral and skeletal abnormalities. The remaining
dams were allowed to deliver naturally and the young were maintained until weaning to
evaluate postnatal deficits. Additionally two male and two female weanlings from each dam
were maintained for 8 weeks and mated to investigate their reproductive potential.
Although toxic signs were noted in the dams at the highest dose level, there was no
significant mortality. Examination of the fetuses revealed no external, visceral, or
skeletal abnormalities. Treatment of the dams with fenvalerate
did not affect the reproductive performance of the offspring.
When groups of six male and six female rats were fed fenvalerate
in the diet at a concentration of 2000 mg/kg for 8 to 10 days, all the animals showed
typical signs of acute intoxication such as ataxia, tremors, and hyperexcitability.
Histopathological examinations did not reveal any adverse effects of fenvalerate
on the sciatic nerve.
the type II pyrethroids /including fenvalerate/
produce a complex poisoning syndrome and act on a wide range of tissues. They give sodium
tail currents with relatively long time constants, which may be the reason for their
ability to act on the whole range of excitable tissues. Type II poisoning in rats involves
progressive development of nosing and exaggerated jaw opening similar to that seen in
response to an irritant placed on the tongue, salivation which may be profuse, increasing
extensor tone in the hind limbs causing a rolling gait, incoordination progressing to a
very coarse tremor, choreoform movements of the limbs and tail often precipitated by
sensory stimuli, generalized choreoathetosis (writhing spasms), tonic seizures, apnea, and
death. At lower doses more subtle repetitive behavior is seen. In dogs, similar symptoms
are seen but salivation and upper airway hypersecretion and gastrointestineal symptoms are
more prominent.
Rats receiving 2000 ppm in their diet for 90 days died, but others receiving 1500 ppm
for 15 mo showed typical motor symptoms but did not die. Rats showing severe motor
symptoms developed axonal swelling and demyelination in the sciatic nerve. These changes
appeared to be reversible.
Fenvalerate has no teratogenic or mutagenic
activity.
In both rats and dogs fed 500-1000 ppm fenvalerte, granulomatous changes and giant cell
infiltration were seen in the liver. These were, however, a foreign body response to
deposition of crystals of the cholesterol 2-(4-chlorophenyl)-isovalerate ester in the
liver. The esters are formed by microsomal carbaryl esterases and are highly specific for fenvalerate.
Field and laboratory toxicity tests were conducted on the grass shrimp, Palaemonetes
pugio, to evaluate the usefulness of laboratory testing in estimating mortality from fenvalerate exposure associated with agricultural
runoff. The study examined an integrated approach for assessing the impacts of fenvalerate on estuarine fauna, using 96 hr static
renewal and 6 hr pulsed-dose laboratory toxicity tests and in situ toxicity tests. The
laboratory toxicity tests with fenvalerate gave
96 hr LC50 values ranging from 0.007 to 0.071 ug/l and 6 hr pulsed dose LC50 values
ranging from 0.100 to 0.130 ug/l. Comparisons of the results of two field toxicity tests
with laboratory-derived LC50 values showed good agreement between field and laboratory
toxicity data. The variation betweenfield and laboratory toxicity tests may have been due
to the limitations of the water sampling regime used in characterizing the pesticide
exposure during the field toxicity tests. These comparisons suggest that combination of
laboratory and field toxicity testing is required to estimate the actual field mortality
from fenvalerate exposure associated with
agricultural runoff. Future studies should include composite water sampling and more
frequent discrete sampling methods to better characterize field exposure regimes.
Fenvalerate is a widely used pesticide, which
has been shown recently to be nonmutagenic. Its carcinogenicity was studied in a long term
experiment in inbred C57B1/6 mice given 0, 40 and 80 mg/kg body wt fenvalerate
(99% pure) by gavage on 5 days/wk for 104 wk. Survival was decreased especially among
females receiving the high dose. Exposure to fenvalerate
resulted in a slight increase in the incidence of liver cell tumors over that in controls
only in male mice receiving the high dose. No significant difference in the incidence of
other types of tumors was observed in treated groups when compared with controls. Fenvalerate induced microgranulomas occurred
concomitantly in the liver, spleen and lymph nodes of male and female mice, but their
overall incidence did not increase with dose. In a separate experiment, groups of SJL/ola
female mice were administered two different samples of fenvalerate
(92% and 99% pure) once per week for 12 wk. In animals that received 92% pure compound,
the latent period for induction of lymphomas was shortened and their incidence increased,
when compared with the group receiving 99% pure fenvalerte and with controls.
Pure, microcosm-cultured populations of benthic copepods were established from pristine
or pesticide impacted Spartine marsh creeks and used as efficient bioassay groups to
assess lethal and sublethal effects of sediment bound pesticide residues. Naturally
weathered sediments contaminated with the synthetic pyrethroid insecticide fenvalerate were collected by traps moored in a tidal
creek receiving major pesticide laced runoff from an agricultural watershed, and used as
dosing material. Silty sediments with fenvalerate
residues reaching 100 ppb were traped and then diluted with uncontaminated sediments to
achieve an exposure range of 0, 25, 50 adn 100 ppb (i.e. no dilution). Despite a broad
database showing extreme sensitivity to water solubilized fenvalerate
by many marine invertebrates fishes, a 7 day exposure to sediment bound residues as high
as 100 ppb caused no significant mortality for any life stages (i.e. nauplii, copepodites
or adults) of the benthic harpacticoid copepods Microarthridion littorale or
Paronychocamptus wilsoni, and no mortality for adults of enhydrosoma propinquum. However,
sediment bound residues as low as 25 ppb significantly depressed egg production (50-100%
reduction) and mean clutch sized (40-100% reduction) of fertile Microarthridion littorale
and Paronychocamptus wilsoni. If sedimenting fenvalerate
depresses copepod reproduction in the field, then lowered recruitment of new individuals
will lead inevitably to a decline in population growth.
Effects of pyrethroids suggestive of tumor promoting acitivity were investigated. An in
vivo assay was used to measure enhancement of nitrosodiethylamine induced enzyme altered
foci in Sprague-Dawley rat liver due to fenvalerate.
During the first week of fenvalerte adminstration, most rats demonstrated transient
neurotoxic effects including hind limb incoordination and tremor. Slight decreases in body
weight gains during the period of tumor promotion were noted in rats receiving 57 mg/kg
per day. No lesions related to fenvalerate
administration were noted in hematoxylin and eosin stained liver sections. Rats given fenvalerate at 75 mg/kg per day for 10 wk after
partial hepatectomy and nitrosodiethylamine injection had significantly more
gamma-glutamyl-transpeptidase positive foci per cubic centimeter of liver tissue compared
to rats given only vehicle during the promotion phase. Slightly but nonsignificantly
elevated foci incidence was noted in rats receiving 25 mg/kg per day of fenvalerate.
Rats receiving fenvalerate only had no or only a
few small gamma-glutamyl-transpeptidase positive hepatocyte foci. Total volume of
gamma-glutamyl-transpeptidase foci was significantly increased in rats given either high
dose fenvalerate or phenobarbital but was only
marginally elevated with low dose fenvalerate. Fenvalerate, cypermethrin, deltamerthrin, permethrin,
and the fenvalerate metabolite
p-chlorphenylisovaleric acid were tested in-vitro for inhibition of intercellular gap
junctional communication in Chinese hamster lung fibroblasts (V79 cells). At non-cytotoxic
levels, only fenvalerate and
p-chlorophenylisovaleric acid were active at inhibiting V79 cell metabolic cooperation. It
was concluded that fenvalerate shows activities
suggestive of potential tumor promotion.
This review presents data on the impacts of pyrethroid insecticides on nontarget
aquatic invertebrates. Toxicological information on both photolabile and photostable
pyrethroids against insects and mammals has been evaluated. A detailed analysis is also
provided on the contamination of aquatic habitats by pyrethroids through direct,
purposeful use in pest control, and indirect routes such as spray drift, run-off and
erosion processes. Based on laboratory data, some of the photostable and more effective
compounds could be ranked in order of decreasing toxicity to nontarget species as:
permethrin = fenvalerate < cypermethrin <
deltamethrin. In field studies, depending and their use pattern in agricultural,
silvicultural and public health pest control programs, nontarget aquatic insects such as
Ephemeroptera, Odonata, Plecoptera, Hemiptera, Coleoptera and Trichoptera, and crustacean
groups such as Cladocera, Ostracoda, Copepoda, Amphipoda, Isopoda and Decapoda, were more
severely affected by exposure to pyrethroids than other invertebrates. In most of these
cases, however, the population recovery of affected species to pretreatment levels was
noticed within weeks to months after application. Moreover, the impact of these transient
effects of pyrethroids on nontarget fauna resulted in short-term reductions in the
populations of dependent fish species in aquatic ecosystems.
Two synthetic pyrethroids namely fenvalerate
and decamethrin were evaluated for their subchronic dermal toxicity against male albino
rats weighing from 120-125 g. The backs of the animals were clipped free of hair and each
group received a daily dose of 40 ul fenvalerate
and 5 ul decamethrin/kg for two weeks, five consecutive days per week. The animals were
kept under observation for two more weeks. The results showed a significant fall in
hemoglobin content and a decrease in the number of red blood cells accompanied with an
increase in the level of serum bilirubin as indication of some degree of liver function
failure. An increase in the circulating leukocytes was a common finding during the
toxicity course. The results revealed an increase in blood urea levels and a temporary
increase in blood glucose. The activity of whole blood acetylcholinesterase was also
affected. No significant changes were detected after gross examination of the internal
organs.
Certain natural toxins and environmental agents have been found to act on nerve
membrane ionic channels in a highly specific manner. For example, the puffer fish poison,
tetrodotoxin, blocks the sodium channel without affecting its gating mechanism. The sodium
channel is also the major target site of the pyrethroid and DDT insecticides. Patch clamp
single channel recording experiments with cultured neuroblastoma cells have revealed that
individual sodium channels are kept open much longer in the presence of the pyrethroid
tetramethrin than in control. This effect accounts for a marked prolongation of sodium
current by tetramethrin observed in giant axons. The prolonged sodium current increases
the depolarizing after potential which in turn generates repetitive after discharges. The
symptoms of pyrethroid poisoning in animals can be explained on this basis. Only a very
small fraction of sodium channels, less than 1%, needs to be modified by pyrethroids to
produce the symptoms of poisoning. Fenvalerate,
a cyano-containing type II pyrethroid, prolongs the sodium channel open time much more
drastically than tetramethrin. This causes a persistent depolarization of the membrane,
which in turn blocks conduction.
The transmitter activated ion channels are known to be important target sites of a
variety of therapeutic and toxic agents. The gamma-aminobutyric acid activated chloride
channel has been shown to be modulated by general anesthetics, alcohols, and the
pyrethroid, cyclodiene and lindane insecticides. The general anesthetics halothane,
enflurane and isoflurane greatly augmented the gamma-aminobutyric acid activated current
before desensitization took place, and suppressed it after desensitization at clinically
relevant concn equivalent to 1-2 minimum alveolar concn. The stimulating effect appears to
be a mechanism of general anesthesia. It seems that general anesthetics have a specific
affinity for the gamma-aminobutyric acid receptor channel complex. Ethanol also augmented
the gamma-aminobutyric acid activated peak chloride current with little or no effect on
the desensitized sustained current. Longer chain alcohols n-butanol, n-hexanol, n-octanol,
and n-decanol also exerted the same type of effect, with the potency and efficacy
increasing with lengthening of the carbon chain. The gamma-aminobutyric acid receptor
channel complex has also been shown to be an important target site of certain
insecticides. The type II pyrethroids deltamethrin and fenvalerate
augmented the gamma-aminobutyric acid activated peak chloride current when applied
concurrently with gamma-aminobutyric acid, but the effect was diminished as the
pyrethroids were applied for long periods of time prior to gamma-aminobutyric acid
application. The latter effect might explain the controversy in the literature regarding
the pyrethroid action on the gamma-aminobutyric acid system. The type I pyrethroid
allethrin suppressed the gamma-aminobutyric acid activated peak chloride current when
co-applied with gamma-aminobutyric acid. Both types of pyrethroids suppressed the
N-methyl-d-aspartate-induced current. Lindane and the cyclodienes dieldrin, endrin,
heptachlor-epoxide, and isobenzan suppressed the gamma-aminobutyric acid activated
chloride current. These effects can account for the convulsant action of lindane and the
cyclodienes.
To characterize the behavioral effects of pyrethroid (fenvalerate)
and organochlorine (endosulfan) insecticides, the effect of acute exposure to these agents
on behavioral despair and forced locomotor activity responses in albino mice was studied.
In the behavioral despair model, the time for which the animals remained immobile, and in
the forced locomotor activity model, the ability of the mice to stay on a moving rod, was
studied in control and treatment groups. The effect of pretreatment with drugs affecting
cholinergic (physostigmine), GABAergic (thiosemicarbazide), dopaminergic and noradrenergic
(alpha-methyl-p-tyrosine) and serotonergic (p-chlorophenylalanine) transmission was
studied to investigate which neurotransmitters are involved in the behavioral effects of
these compounds. Physostigmine and thiosemicarbazide further decreased the duration of
immobility in fenvalerate-treated mice, while
p-chlorophenylalanine antagonized the decrease in immobility duration caused by fenvalerate. alpha-Methyl-p-tyrosine pretreatment did
not have any effect. Physostigmine, thiosemicarbazide, p-chlorophenylalanine and
alpha-methyl-p-tyrosine pretreatments significantly decreased the time the animals stayed
on the rota rod. Physostigmine, thiosemicarbazide and alpha-methyl-p-tyrosine
significantly enhanced the effects of endosulfan on the rota rod, while in the forced
swimming test, only alpha-methyl-p-tyrosine was found to potentiate the effects of
endosulfan. PCPA pretreatment lter the response of endosulfan in either of the models
studied.
Toxicosis attributable to fenvalerate and
N,N-diethyl-m-toluamide exposure was suspected in 2 cats. Clinical signs of toxicosis
developed within 4 to 6 hr of dermal application of the pesticide. Clinical signs of
toxicosis seen in both cats included hypersalivation, ataxia, and depression. In addition,
seizures were seen in 1 cat. Both cats died. Analysis of skin, kidney/urine, liver, and
brain tissues confirmed the presence of fenvalerate
and N,N-diethyl-m-toluamide. The pyrethroid fenvalerate
and the insect repellent N,N-diethyl-m-toluamide are used for the control of fleas and
ticks on cats. Suspected fenvalerate/N,N-diethyl-m-toluamide
toxicosis in cats is associated with tremors, hypersalivation, ataxia, vomiting,
depression, and seizures.
The effect of systemic treatment of a synthetic pyrethroid insecticide, fenvalerate was examined in adult female rats at
different doses ie, 5, 10, 20 mg/kg body wt by gavage for 21 consectuive days on regional
brain levels of noradrenaline, dopamine, their acid metabolites: dihydroxyphenylacetic
acid and homovanillic acid by HPLC-EC system. Rsults demonstrate pronounced inhibition of
noradrenaline, dopamine, homovanillic acid dihydroxyphenylacetic acid levels in several
brain regions which were neither dose related nor region specific.
An attempt was made to study the genotoxic effect of fenvalerate
in the mouse in vivo test system using bone marrow chromosome aberration, micronucleus and
sperm abnormality assays. For metaphase analyses three dose levels of the test chemical
(100, 150, or 200 mg/kg) were given to Swiss mice, 10 to 12 weeks old. With the 200 mg/kg
dose level, three routes of administration were employed, ip, oral and sc. For chronic
treatment, five equal subdivisions of the highest acute dose were injected ip at intervals
of 24 hr and the mice sacrificed at 130 hr after the first injection. The results
indicated a variety of cytogenetic effects. A small and insignificant increase was noted
in the frequency of chromosome aberrations with dose. Maximum aberrations were noted 24 hr
after chemical treatment. An insignificant increase in chromosomal aberrations over
control in the sc route of chemical administration may have been caused by a slo rate of
chemical absorption from dermal tissue. The higher incidence of chromatid separations in
most of the test cases suggests that fenvalerate
has the ability to induce malsegregation. The occurrence of chromatid separations may be
an important observation as it relates to aneuploidy. The frequency of micronucleated
cells was greater with higher doses. The induction of chromosome and chromatid type
deletions, exchanges and micronuclei in the bone marrow cells of mice indicated
clastogenic as well as spindle poisoning actions.
Fenvalerate @ 10.12 and20 mg/kg (eg, 1/20 and
1/10th LD50 respectively) had no effect on learning process, retrieval of memory and
permanent memory traces /in rats/.
This investigation explored the behavioral and neurochemical toxicity of perinatal oral
exposure to Ambush (Type I) and Pydrin (Type
II), two pyrethroid formulations. Thirty six female rats were mated and exposed to various
pyrethroid formulations by oral gavage from the first gestational day until their pups
(culled to 8/litter) were 12 days old. Six mothers were exposed daily to one of the
following treatments: corn oil control, corn oil+96% xylene, 1.25 mg/kg Pydrin
(pesticidal ingredient fenvalerate), 0.125 mg/kg
Pydrin, 4.0 mg/kg Ambush (pesticidal ingredient
permethrin), or 0.4 mg/kg Ambush. Behavioral evaluations of locomotor activity, muscular
coordination and passive avoidance learning were conducted on half of the pups from each
litter (N = 24 pups/treatment condition). The other pups were sacrificed, brains were
removed and sectioned into frontal cortex, hippocampus, caudate, and cerebellum for
neurochemical assessment. The monoamines DA, DOPAC, 5-HIAA, 5-HT and HVA levels were
determined and the amino acids aspartate, glutamate, glutamine, glycine, GABA, and taurine
were determined for each of the brain regions. Gestational duration was shortened by
exposure to the high doses of Pydrin and Ambush
but only pups from the 4.0 mg/kg Ambush group were significantly lighter. No physical
malformations were observed in pups from any of the treatment conditions, although the
high Pydrin exposure condition resulted in a 4%
death rate. Behavioral changes were seen for both locomotor activity and muscular
coordination. The shape of across-session habituation of locomotion was different for the
xylene and corn oil and the high dose Ambush groups. Both groups were less active on day 1
and more active on days 2 and 3 than the other pups. The high doses of Ambush and Pydrin produced slower intrasession habituation.
Muscular coordination was improved slightly following low dose exposure to both pesticides
and reduced following high dose exposures. Regional brain weights were normal for the
cortex, cerebellum and caudate but the hippocampus was 64% heavier for pups treated with
4.0 mg/kg Ambush. Amino acid determinations indicated that the cerebellum was most
affected where glutamate, glutamine, aspartate and taurine were reduced following xylene
or pyrethroid exposure. The biogenic amine transmitter 5-HT was reduced in several brain
regions following pyrethroid exposures. These data suggest that levels of Ambush and Pydrin as low as the LD50/10,000 can alter behavior
and neurotransmitter functioning.
The kinetic variations in the morphology of the alveolar cells in bronchoalveolar
lavage fluid from male Sprague-Dawley rats exposed to fenvalerate
suspension by a single intratracheal instillation were observed with a scanning electron
microscope. The results showed that fenvalerate
suspension did not induce lung injury at a dose of 0.19 mg/kg, caused a mild alveolitis at
a dose of 0.93 mg/kg and led to the lung parenchyma injury at a dose of 4.7 and/or 23.3
mg/kg. The injury on the cellular membranes of pulmonary alveolar macrophages mainly
revealed the appearances of pores in different sizes, pits in varied shapes and the uneven
distribution of the cell ruffling (or cytoplasmic prominence), and even the disolution or
death of lots of pulmonary alveolar macrophages. In addition, the conspicuous increases in
polymorphonuclear neutrophils, monocytes, lymphocytes, type II pneumocytes, ciliated cells
and RBC, and a number of cell aggregation could be seen. The above mentioned responses of
the lung injury took place following 30 min of exposure, reached their peak about 4-24 hr
after exposure, and returned t the normal state about 4 day later. The findings of present
study provide the cellular morphological bases for the probe into the toxicity mechanisms
of fenvalerate on the lung and for the
formulation of the hygienic standards in the production and application of fenvalerate.
These compounds /including fenvalerate and
cypermethrin/ are generally very toxic to crustaceans and fish in laboratory bioassays.
These compounds /including fenvalerate and
cypermethrin/ are generally very toxic to crustaceans and fish in laboratory bioassays.
Synthetic pyrethroids are neuropoisons acting on the axons in the peripheral and
central nervous systems by interacting with sodium channels in mammals and/or insects. A
single dose produces toxic signs in mammals, such as tremors, hyperexcitability,
salivation, choreoathetosis, and paralysis. ... At near-lethal dose levels, synthetic
pyrethroids cause transient changes in the nervous system, such as axonal swelling and/or
breaks and myelin degeneration in sciatic nerves. They are not considered to cause delayed
neurotoxicity of the kind induced by some organophosphorus compounds. /Synthetic
prethroids/
Extreme doses /of pyrethroids/ have caused convulsions in laboratory animals.
/Pyrethroids/
Synthetic pyrethroids have been shown to be toxic for fish, aquatic arthropods, and
honeybees in laboratory tests. But, in practical usage, no serious adverse effects have
been noticed because of the low rates of application and lack of persistence in the
environment. The toxicity of synthetic pyrethroids in birds and domestic animals is low.
/Synthetic pyrethroids/
The Type II /poisoning/ syndrome, also known as the "CS syndrome," is
produced by those esters containing the alpha-cyano substituent and elicits intense
hyperactivity, incoordination, and convulsions in cockroaches, whereas rats display
burrowing behavior, coarse tremors, clonic seizures, sinuous writhing (choreoathetosis),
and profuse salivation without lacrimation; hence the term CS (choreoathetosis/salivation)
syndrome. /Pyrethroid esters containing the alpha-cyano substituent/
The in vitro effects of pyrethroids on the mitogenic responsiveness of murine splenic
lymphocytes to concanavalin A and lipopolysaccharide were determined. Allethrin was the
most potent inhibitor, with effective concn in the range of 1X10-6 to 1.5X10-5 M. The
results support the possibility of immune suppression by pyrethroid exposure.
/Pyrethroids/
Following absorption through the chitinous exoskeleton of arthropods, pyrethrins
stimulate the nervous system, apparently by competitively interfering with cationic
conductances in the lipid layer of nerve cells, thereby blocking nerve impulse
transmissions. Paralysis and death follow. /Pyrethrins/
Non-systemic insecticide with contact action. Causes paralysis initially, with death
occurring later. Has some acaricidal activity. /Pyrethrins/
Non-Human Toxicity Values:
LD50 Rat oral 451 mg/kg
LD50 Rat percutaneous > 5000 mg/kg
LD50 Rat oral 3200 mg/kg /technical pydrin
suspended in water/
LD50 Rat oral 1-3 g/kg /technical grade/
LD50 Rabbit dermal 1-3 g/kg /technical grade/
LC50 Rat inhalation > 101 g/cu m/4 hr
LD50 Rat oral 200 mg/kg
LC50 Pimephales promelas (fathead minnow) 5.14 mg/l/96 hr (confidence limit 4.89- 5.40
mg/l), flow-through bioassay with measured concentrations, 25.5 deg C, dissolved oxygen
7.4 mg/l, hardness 45.5 mg/l calcium carbonate, alkalinity 41.6 mg/l calcium carbonate,
and pH 7.3.
Ecotoxicity Values:
LC50 Rainbow trout 0.0036 mg/1/96 hr /Conditions of bioassay not specified/
LC50 Salmo salar (Atlantic salmon) 1 ug/l/96 hr, juvenile /Conditions of bioassay not
specified/
LC50 Pimephales promelas (fathead minnow) 0.42 mg/l/96 hr (confidence limit 0.39-0.46
mg/l), flow-through bioassay with measured concentrations, 24.5 deg C, dissolved oxygen
7.3 mg/l, hardness 44.8 mg/l calcium carbonate, alkalinity 40.9 mg/l calcium carbonate,
and pH 7.8.
EC50 Pimephales promelas (fathead minnow) 0.04 mg/l/96 hr (confidence limit 0.36-0.44
mg/l), flow-through bioassay with measured concentrations, 24.5 deg C, dissolved oxygen
7.3 mg/l, hardness 44.8 mg/l calcium carbonate, alkalinity 40.0 mg/l calcium carbonate,
and pH 7.8. Effect: loss of equilibrium.
LC50 Pimephales promelas (fathead minnow) 5.14 mg/l/96 hr (confidence limit 4.89-5.40
mg/l), flow-through bioassay with measured concentrations, 25.5 deg C, dissolved oxygen
7.4 mg/l, hardness 45.5 mg/l calcium carbonate, alkalinity 41.6 mg/l calcium carbonate,
and pH 7.3. Effect: Loss of equilibrium.
LC50 Rainbow trout technical grade 76.0 ppb active ingredient/24 hr (static test)
LC50 Rainbow trout formulated product 21.0 ppb active ingredient/24 hr (static test)
LD50 Mallard oral 9932 mg/kg
LC50 Bobwhite quail dietary > 10000 ppm
LC50 Mallard dietary 5500 ppm /Conditions of bioassay not specified/
LC50 Bluegill sunfish fish 0.42 ppb/96 hr /Conditions of bioassay not specified/
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
Fenvalerate undergoes hydroxylation to give
2'- or 4'- hydroxylated phenoxy esters and hydrolysis to give 3-phenoxybenzoic acid and
its hydroxy derivatives (free and conjugates), 3-(4-chlorophenyl)-isovaleric acid and its
hydroxy derivatives (free, lactones, and conjugates), thiocyanate, and CO2.
The fate of fenvalerate in rats and mice has
been studied using fenvalerate radiolabelled in
the acid moiety or benzyl or cyano groups. The administered radioactivity, except that of
the cyano-labelled compounds, is readily excreted (up to 99% in 6 days). The major
metabolic reactions are ester cleavage and hydroxylation at the 4' position. Various
oxidative and conjugation reactions that lead to a complex mixture of products have been
shown to occur. When studies were carried out with fenvalerate
radiolabelled in the cyano group, elimination of the radioactive dose was less rapid (up
to 81% in 6 days). The remaining radioactivity was retained mainly in the skin, hair, and
stomach as thiocyanate. A minor, but very important, metabolic pathway is the formation of
a lipophilic conjugate of (2R)-2-(4-chlorophenyl)isovalerate. This congugate, which is
implicated in the formation of granuloma, has been detected in the adrenals, liver
mesenteric lymph nodes of rats, mice, and some other species.
Despite its lack of a cyclopropane ring in the acid, fenvalerate
is rapidly metabolized in rats by ester cleavage and hydroxylation, as are the more
traditional pyrethroids.
Studies with permethrin, cypermethrin and fenvalerate
have established that rates of metabolism and elimination in rainbow trout are
significantly lower than those reported for birds and mammals. Comparatively low lethal
brain pyrethroid concn and nonneural aspects of pyrethroid intoxication in fish suggest
that variations in toxicodynamics are also crucial in evaluating pyrethroid selectivity.
Using tracer technique of (14)C isotope, toxicokinetics of fenvalerate
was studied in rats and mice. The results strongly suggested the existence of distinct
differences between species in mammals in the metabolism of (14)C fenvalerate.
The absorption and elimination of (14)C fenvalerate
in the blood of mice following single intragastric administration was faster than that of
the rats. The plasma and brain of animal have greater affinity for (14)C-fenvalerate.
The absorption of fenvalerate was faster and the
biological half-time was longer in brain. (14)C-fenvalerate
and its metabolites were mainly eliminated through urine and fenvalerate
can partially be stored in the skin and the hair of animal.
On a single oraldose or five consecutive oral doses of (14)C-esfenvalerate or (14)C-fenvalerate labeled in the acid moiety to 13-day
pregnant rats at rates of 2.5 and 10 mg/kg/day, respectively, the maternal blood and
placenta generally showed higher (14)C levels as compared with the fetus and amniotic
fluid. Both compounds and their metabolites did not transfer readily from the maternal
blood to the fetus, the amount of (14)C transferred being less than 0.07% of the dose.
There were no substantial differences in the fetal (14)C level and the transfer ratio
((14)C tissue level/(14)C maternal blood level) between both labeled preparations. Major
(14)C-compounds in the fetus, maternal blood and placenta were the parent compounds,
CPIA[2-(4-chlorophenyl)isovaleric acid] and CPIA-hydroxylated derivatives and there was no
qualitative difference in metabolic fates between the two compounds, except that a trace
amount of CPIA-cholesterol ester [cholesteryl (2R)-2-(4-chlorophenyl)isovalerate] was
detected in the maternal blood and placenta only with fenvalerate.
CPIA-cholesterol ester did not seem to transfer from the maternal blood to the fetus.
Overall, esfenvalerate and fenvalerate seem to
behave in the same manner as far as placental transfer was concerned.
The metabolic pathways for the breakdown of the pyrethroids vary little between
mammalian species but vary somewhat with structure. ... Essentially, pyrethrum and
allethrin are broken down mainly by oxidation of the isobutenyl side chain of the acid
moiety and of the unsaturated side chain of the alcohol moiety with ester hydrolysis
playing and important part, whereas for the other pyrethroids ester hydrolysis
predominates. /Pyrethrum and pyrethroids/
The relative resistance of mammals to the pyrethroids is almost wholly attributable to
their ability to hydrolyze the pyrethroids rapidly to their inactive acid and alcohol
components, since direct injection into the mammalian CNS leads to a susceptibility
similar to that seen in insects. Some additional resistance of homeothermic organisms can
also be attributed to the negative temperature coefficient of action of the pyrethroids,
which are thus less toxic at mammalian body temperatures, but the major effect is
metabolic. Metabolic disposal of the pyrethroids is very rapid, which means that toxicity
is high by the intravenous route, moderate by slower oral absorption, and often
unmeasureably low by dermal absorption. /Pyrethroids/
FASTEST BREAKDOWN IS SEEN WITH PRIMARY ALCOHOL ESTERS OF TRANS-SUBSTITUTED ACIDS SINCE
THEY UNDERGO RAPID HYDROLYTIC & OXIDATIVE ATTACK. FOR ALL SECONDARY ALCOHOL ESTERS
& FOR PRIMARY ALCOHOL CIS-SUBSTITUTED CYCLOPROPANECARBOXYLATES, OXIDATIVE ATTACK IS
PREDOMINANT. /PYRETHROIDS/
Pyrethrins are reportedly inactivated in the GI tract following ingestion. In animals,
pyrethrins are rapidly metabolized to water soluble, inactive compounds. /Pyrethrins/
Synthetic pyrethroids are generally metabolized in mammals through ester hydrolysis,
oxidation, and conjugation, and there is no tendency to accumulate in tissues. In the
environment, synthetic pyrethroids are fairly rapidly degraded in soil and in plants.
Ester hydrolysis and oxidation at various sites on the molecule are the major degradation
processes. /Synthetic pyrethroids/
Absorption, Distribution & Excretion:
Poorly absorbed through rabbit skin.
Elimination from body fat is slow, with a half-life of 7-10 days; elimination from
brain is less slow, with a half-life of 2 days (Marei et al., 1982), presumably due to the
more effective perfusion of brain and the presence of esterases in brain tissue.
Dermal penetration of pesticides. Compound: Fenvalervate; species: mouse; Application
site: dermal; solvent: acetone; Penetration parameter: 9%, 2 hr; Method: patch. /From
table/
In mammals, following oral administration, fenvalerate
is rapidly metabolized. Up to 96% is excreted in the feces within 6-14 days.
An in vivo rainbow trout (Salmo gairdneri) preparation was used to evaluate the gill
uptake and toxicokinetics of (3)H fenvalerate
((R,S)-alpha-cyano-3- phenoxybenzyl (R,S)-2-(4-chlorophenyl)-3-methylbutyrate), a
synthetic pyrethroid insecticide. Fish were exposed to technical grade fenvalerate
(0.28 or 23 ng/l) or an emulsifiable-concentrate formulation (16 ng/l) for 36 to 48 h. No
significant effects of emulsifiers or fenvalerate
concentration on uptake were observed. The overall mean gill uptake efficiency was
determined to be 28.6%. Following 8 hr to 48 hr depuration periods, carcass and bile
contained 80 to 90 percent and 10 to 20 percent of the gill-absorbed doses, respectively.
Analysis of biliary metabolites indicated that the glucuronide of 4'-HO-fenvalerate
was the only significant degradation product. Results from the present study suggest that
efficient gill uptake does not explain the extreme sensitivity of fish to fenvalerate. Rather, a low rate of biotransformation
and excretion may play a significant role in the susceptibility of rainbow trout to the
synthetic pyrethroid insecticides.
Using tracertechnique of (14)C isotope, toxicokinetics of fenvalerate
was studied in rats and mice. The results strongly suggested the existence of distinct
differences between species in mammals in the metabolites of (14)C fenvalerate.
The absorption and elimination of (14)C fenvalerate
in the blood of mice following single intragastric administration was faster than that of
the rats. The plasma and brain of animals have greater affinity for (14)C fenvalerate. The absorption of fenvalerate
was faster and the biological half-time was longer in brain. (14)C Fenvalerate
and its metabolites were mainly eliminated through urine and fenvalerate
can partially be stored in the skin and the hair of animals.
/PYRETHROIDS/ READILY PENETRATE INSECT CUTICLE AS SHOWN BY TOPICAL LD50 TO PERIPLANETA
(COCKROACH) ... /PYRETHROIDS/
WHEN RADIOACTIVE PYRETHROID IS ADMIN ORALLY TO MAMMALS, IT IS ABSORBED FROM INTESTINAL
TRACT OF THE ANIMALS & DISTRIBUTED IN EVERY TISSUE EXAMINED. EXCRETION OF
RADIOACTIVITY IN RATS ADMIN TRANS-ISOMER: DOSAGE: 500 MG/KG; INTERVAL 20 DAYS; URINE 36%;
FECES 64%; TOTAL 100%. /PYRETHROIDS/
Pyrethrins are absorbed through intact skin when applied topically. When animals were
exposed to aerosols of pyrethrins with piperonyl butoxide being released into the air,
little or none of the combination was systemically absorbed. /Pyrethrins/
Although limited absorption may account for the low toxicity of some pyrethroids, rapid
biodegradation by mammalian liver enzymes (ester hydrolysis and oxidation) is probably the
major factor responsible. Most pyrethroid metabolites are promptly excreted, at least in
part, by the kidney. /Pyrethroids/
Biological Half-Life:
Elimination from body fat is slow, with a half-life of 7-10 days; elimination from
brain is less slow, with a half-life of 2 days (Marei et al., 1982), presumably due to the
more effective perfusion of brain and the presence of esterases in brain tissue.
Mechanism of Action:
In intact locusts and neuromuscular preparations of locusts, fenvalerate
caused (a) prolonged firing in the crural nerve without associated muscle contractions;
(b) sustained muscle contractions; and (c) a block of neurally evoked muscle contractions
at low concentrations (1x10-8 to 1x10-5 mol/l). However, fenvalerate
did not cause repetitive firing and after-discharges with associated muscle contractions.
The fenvalerate steroisomers with an (S)
configuration in the alcohol moiety are more active pharmacologically and toxicologically
than those with the (R) configuration or the racemate (R,S). It is also apparent that
steroisomers with the (S) configuration in the acid moiety are more active than those with
the (R) configuration or the racemate (R,S).
Phosphoinositide breakdown in guinea pig cerebral cortical synaptoneurosomes induced by
the Type-I pyrethroids allethrin, resmethrin, and permethrin, and the Type-II pyrethroid
deltamethrin and fenvalerate were investigated
with various receptor agonists as well as sodium channel blockers and agents.
Phosphoinositide breakdown was determined from inositol-phosphate formation by tritiated
inositol labeled synaptoneurosomes. All five pyrethroids dose dependently induced
phosphoinositide breakdown. Type II pyrethroids exhibited higher potency and deltamethrin
was more efficacious than the Type I pyrethroids. Five uM tetrodotoxin, a blocker of
voltage dependent sodium channels, partially inhibited deltamethrin (85 percent) and fenvalerate (60 percent) responses but not allethrin
or resmethrin. Fenvalerate induced stimulation
of phosphoinositide was additive with stimulation elicited by the receptor agonists
carbamylcholine (1 mM) and norepinephrine (1000 uM) but less than additive with the sodium
channel agents batrachotoxin, pumiliotoxin-B, and scorpion venom. Allethrin (100 uM) was
less than additive with receptor agonists or sodium channel agents and actually
significantly inhibited response to scorpion venom. Effects for 100 uM allethrin with
either fenvalerate or deltamerthrin were not
different from allethrin alone. Ten uM allethrin slightly decreased response to 10 to 100
uM deltamethrin. The local anesthetic dibucaine, a sodium channel activation inhibitor,
completely blocked deltamethrin induced phosphoinositide breakdown but was much less
effective in inhibiting allethrin response. It appears likely that Type I pyrethroids
induce phosphoinositide breakdown through a mechanism other than sodium channel activation
while Type II pyrethroids act in a manner analogous to other sodium channel agents.
Eight different synthetic pyrethroids were examined to determine their effects on the
excitability of hippocampal granule cells in urethane anesthetized rats. A paired stimulus
approach was used. All eight prolonged the depression of granule cells excitability that
follows stimulation of their major synaptic input, the perforant path. The magnitude of
this effect depended upon the class to which the pyrethroid belonged. Type I pyrethroids
(those primarily producing tremor) prolonged the depression of granule cell excitability
for shorter periods than did type II pyrethroids (those primarily producing salivation and
choreoathetosis) or pyrethroids producing a mixed type of intoxication. No overlap was
found between groups. To determine whether the difference observed between type I and type
II pyrethroids was the result of an infelicitous selection of doses, cismethrin (type I)
was tested over a dose range of 1.5-24 times the conscious rat iv LD50. Even at the
highest dose, the prolongation remained well below that produced by type II pyrethroids.
The effect of deltamethrin was shown to be consistent with the production or potentiation
of a surmountable inhibitory response. This action of deltamethrin was antagonizable by
mephenesin and lidocaine, but not by picrotoxin or halothane. The type of effect, its time
course, and the anatagonism data suggest that type II pyrethroids enhance inhibition in
the dentate gyrus. This action does not appear to be mediated by GABA receptors.
The transmitter activated ion channels are known to be important target sites of a
variety of therapeutic and toxic agents. The GABA activated chloride channel has been
shown to be modulated by general anesthetics, alcohols, and the pyrethroid, cyclodiene and
lindane insecticides. The general anesthetics halothane, enflurane and isoflurane greatly
augmented the GABA activated current before desensitization took place, and suppressed it
after desensitization at clinically relevant concn equivalent to 1-2 minimum alveolar
concn. The stimulating effect appears to be a mechanism of general anesthesia. It seems
that general anesthetics have a specific affinity for the GABA receptor-channel complex.
Ethanol also augmented the GABA activated peak chloride current with little or no effect
on the desensitized sustained current. Longer chain alcohols n-butanol, n-hexanol,
n-octanol, and n-decanol also exerted the same type of effect, with the potency and
efficacy increasing with lengthening of the carbon chain. The GABA receptor-channel
complex has also been shown to be an important target site of certain insecticides. The
type II pyrethroids deltamethrin and fenvalerate
augmented the GABA activated peak chloride current when applied concurrently with GABA,
but the effect was diminished as the pyrethroids were applied for long periods of time
prior to GABA application. The latter effect might explain the controversy in the
literature regarding the pyrethroid action on the GABA system. The type I pyrethroid
allethrin suppressed the GABA activated peak chloride current when co-applied with GABA.
Both types of pyrethroids suppressed the N-methyl-d-aspartate induced current. Lindane and
the cyclodienes dieldrin, endrin, heptachlor epoxide, and isobenzan suppressed the GABA
activated chloride current. These effects can account for the convulsant action of lindane
and the cyclodienes.
The synthetic pyrethroids delay closure of the sodium channel, resulting in a sodium
tail current that is characterized by a slow influx of sodium during the end of
depolarization. Apparently the pyrethroid molecule holds the activation gate in the open
position. Pyrethroids with an alpha-cyano group (e.g., fenvalerate)
produce more prolonged sodium tail currents than do other pyrethroids (e.g., permethrin,
bioresmethrin). The former group of pyrethroids causes more cutaneous sensations than the
latter. /Synthetic pyrethroids/
Interaction with sodium channels is not the only mechanism of action proposed for the
pyrethroids. Their effects on the central nervous system have led various workers to
suggest actions via antagonism of gamma-aminobutyric acid (GABA)-mediated inhibition,
modulation of nicotinic cholinergic transmission, enhancement of noradrenaline release, or
actions on calcium ions. Since neurotransmitter specific pharmacological agents offer only
poor or partical protection against poisoning, it is unlikely that one of these effects
represents the primary mechanism of action of the pyrethroids, and most neurotransmitter
release is secondary to increased sodium entry. /Pyrethroids/
The symptoms of pyrethrin poisoning follow the typical pattern of nerve poisoning: (1)
excitation, (2) convulsions, (3) paralysis, and (4) death. The effects of pyrethrins on
the insect nervous system closely resemble those of DDT, but are apparently much less
persistent. Regular, rhythmic, and spontaneous nerve discharges have been observed in
insect and crustacean nerve-muscle preparations poisoned with pyrethrins. The primary
target of pyrethrins seems to be the ganglia of the insect central nervous system although
some pyrethrin-poisoning effect can be observed in isolated legs. /Pyrethrins/
Electrophysiologically, pyrethrins cause repetitive discharges and conduction block.
/Pyrethrins/
The interaction of a series of pyrethroid insecticides with the sodium channels in
myelinated nerve fibers of the clawed frog, Xenopus laevis, was investigated using the
voltage clamp technique. Of 11 pyrethroids, 9 insecticidally active cmpd induced a slowly
decaying sodium tail current on termination of a step depolarization, whereas the sodium
current during depolarization was hardly affected. /Pyrethroids/
The biochemical process by which various pyrethroid insecticides alter membrane-bound
ATPase activities of the squid nervous system was examined. Of the 5 ATP-hydrolyzing
systems tested, only Ca(2+)-stimulated ATPase activities were clearly affected by the
pyrethroids. The natural type /I/ pyrethroid, allethrin, primarily inhibits Ca-ATPase
activity. /Pyrethroids/
Mode of action of pyrethrum & related cmpd has been studied more in insects &
in other invertebrates than in mammals. This action involves ion transport through the
membrane of nerve axons &, at least in invertebrates & lower vertebrates, it
exhibits a negative temperature coefficient. In both of these important ways & in many
details, the mode of action of pyrethrin & pyrethroids resembles that of DDT.
Esterases & mixed-function oxidase system differ in their relative importance for
metabolizing different synthetic pyrethroids. The same may be true of the constituents of
pyrethrum, depending on strain, species, & other factors. /Pyrethrins and pyrethroids/
The interactions of natural pyrethrins and 9 pyrethroids with the nicotinic
acetylcholine (ACh) receptor/channel complex of Torpedo electronic organ membranes were
studied. None reduced (3)H-ACh binding to the receptor sites, but all inhibited
(3)H-labeled perhydrohistrionicotoxin binding to the channel sites in presence of
carbamylcholine. Allethrin inhibited binding noncompetitively, but (3)H-labeled imipramine
binding competitively, suggesting that allethrin binds to the receptor's channel sites
that bind imipramine. The pyrethroids were divided into 2 types according to their action:
type A, which included allethrin, was more potent in inhibiting (3)H-H12-HTX binding and
acted more rapidly. Type B, which included permethrin, was less potent and their potency
increased slowly with time. The high affinities that several pyrethroids have for this
nicotinic ACh receptor suggest that pyrethroids may have a synaptic site of action in
addition to their well known effects on the axonal channels. /Pyrethrins and Pyrethroids/
... Pyrethroid esters /containing the alpha-cyano substituent/ produce an even longer
delay /than those lacking the substituent/ in sodium channel inactivation, leading to a
persistent depolarization of the nerve membrane without repetitive discharge, a reduction
in the amplitude of the action potential, and an eventual failure of axonal conduction and
a blockade of impulses. /Pyrethroid esters containing the alpha-cyano substituent/
The primary target site of pyrethroid insecticides in the vertebrate nervous system is
the sodium channel in the nerve membrane. Pyrethroids without an alpha-cyano group
(allethrin, d-phenothrin, permethrin, and cismethrin) cause a moderate prolongation of the
transient increase in sodium permeability of the nerve membrane during excitation. This
results in relatively short trains of repetitive nerve impulses in sense organs, sensory
(afferent) nerve fibers, and, in effect, nerve terminals. On the other hand the
alpha-cyano pyrethroids cause a long lasting prolongation of the transient increase in
sodium permeability of the nerve membrane during excitation. This results in long-lasting
trains of repetitive impulses in sense organs and a frequency-dependent depression of the
nerve impulse in nerve fibers. The difference in effects between permethrin and
cypermethrin, which have identical molecular structures except for the presence of an
alpha-cyano group on the phenoxybenzyl alcohol, indicates that it is this alpha-cyano
group that is responsible for the long-lasting prolongation of the sodium permeability.
Since the mechanisms responsible for nerve impulse generation and conduction are basically
the same throughout the entire nervous system, pyrethroids may also induce repetitive
activity in various parts of the brain. The difference in symptoms of poisoning by
alpha-cyano pyrethroids, compared with the classical pyrethroids, is not necessarily due
to an exclusive central site of action. It may be related to the long-lasting repetitive
activity in sense organs and possibly in other parts of the nervous system, which, in a
more advance state of poisoning, may be accompanied by a frequency-dependent depression of
the nervous impulse. /Synthetic pyrethroids/
Pyrethroids also cause pronounced repetitive activity and a prolongation of the
transient increase in sodium permeability of the nerve membrane in insects and other
invertebrates. Available information indicates that the sodium channel in the nerve
membrane is also the most important target site of pyrethroids in the invertebrate nervous
system. /Synthetic pyrethroids/
In the electrophysiological experiments using giant axons of cray-fish, the Type II
pyrethroids retain sodium channels in a modified continuous open state persistently,
depolarize the membrane, and block the action potential without causing repetitive firing.
/Pyrethroids type II/
Diazepam, which facilitates GABA reaction, delayed the onset of action of deltamethrin
and fenvalertae, but not permethrin and allethrin, in both the mouse and cockroach.
Possible mechanisms of the Type II pyrethroid syndrome include action at the GABA receptor
complex or a closely linked class of neuroreceptor. /Pyrethroids type II/
Interactions:
The ability of 3 mg/kg/day diazepam to alter the neurobehavioral and neurochemical
consequences of perinatal exposure to Ambush and Pydrin
was examined. Seventy-two pregnant female rats served as subjects. Half of the subjects
were treated with diazepam and the other half were treated with the vehicle via
subcutaneous osmotic pumps for 33 days starting on gestational day 1 Each group was
further divided into six gavage treatment groups: corn oil, corn oil + 96% xylene, 1.25 or
0.125 mg/kg Pydrin, and 4.0 or 0.4 mg/kg Ambush.
Behavioral evaluations were conducted on half the pups in each litter and the other pups
were used for the neurochemical assays. Behavioral evaluations included locomotor
activity, screen testing, and passive avoidance learning. Brains for neurochemical
analysis were extracted and sectioned into frontal cortex, caudate, hippocampus and
cerebellum. Neurochemical assays assessed levels of DA, DOPAC, 5-HIAA, 5-HT, HVA,
aspartate, glutamate, glutamine, glycine, GABA, and taurine. Diazepam treatment did
produce some neurotoxicity in the control pups but diazepam exposure did reverse
elevations in amino acid levels in the cerebellum produced by both pyrethroids. In
addition diazepam reversed the pyrethroid effects on activity and muscular coordination.
These diazepam effects were not specific to Type I or Type II pyrethroids.
This investigation explored the behavioral and neurochemical toxicity of perinatal oral
exposure to Ambush (Type I) and Pydrin (Type
II), two pyrethroid formulations. Thirty-six female rats were mated and exposed to various
pyrethroid formulations by oral gavage from the first gestational day until their pups
(culled to 8/litter) were 12 days old. Six mothers were exposed daily to one of the
following treatments: corn oil control, corn oil+96% xylene, 1.25 mg/kg Pydrin
(pesticidal ingredient fenvalerate), 0.125 mg/kg
Pydrin, 4.0 mg/kg Ambush (pesticidal ingredient
permethrin), or 0.4 mg/kg Ambush. Behavioral evaluations of locomotor activity, muscular
coordination and passive avoidanc learning were conducted on half of the pups from each
litter (N = 24 pups/treatment condition). The other pups were sacrificed, brains were
removed and sectioned into frontal cortex, hippocampus, caudate, and cerebellum for
neurochemical assessment. The monoamines DA, DOPAC, 5-HIAA, 5-HT and HVA levels were
determined and the amino acids aspartate, glutamate, glutamine, glycine, GABA, and taurine
were determined for each of the brain regions. Gestational duration was shortened by
exposure to the high doses of Pydrin and Ambush
but only pups from the 4.0 mg/kg Ambush group were significantly lighter. No physical
malformations were observed in pups from any of the treatment conditions, although the
high Pydrin exposure condition resulted in a 4%
death rate. Behavioral changes were seen for both locomotor activity and muscular
coordination. The shape of across-session habituation of locomotion was different for the
xylene and corn oil and the high dose Ambush groups. Both groups were less active on day 1
and more active on days 2 and 3 than the other pups. The high doses of Ambush and Pydrin produced slower intrasession habituation.
Muscular coordination was improved slightly following low dose exposure to both pesticides
and reduced following high dose exposures. Regional brain weights were normal for the
cortex, cerebellum and caudate but the hippocampus was 64% heavier for pups treated with
4.0 mg/kg Ambush. Amino acid determinations indicated that the cerebellum was most
affected where glutamate, glutamine, aspartate and taurine were reduced following xylene
or pyrethroid exposure. The biogenic amine transmitter 5-HT was reduced in several brain
regions following pyrethroid exposures. These data suggest that levels of Ambush and Pydrin as low as the LD50/10,000 can alter behavior
and neurotransmitter functioning.
Following the administration of a single or repeated doses of dimethoate, carbaryl, and
fenvalerate, the activities of
tryptophan-2,3-dioxygenase, indoleamine-2,3-dioxygenase, kynurenine, kynureninase,
kynurenine-transaminase, and pyridoxal-phosphokinase were determined in the liver, kidney
and lung of male Wistar rats. Treatment consisted of 10% of the median lethal dose of each
insecticide given orally for the single dosing investigations and 5% of the median lethal
dose was given orally for 5 consecutive days as repeated doses. Weight losses in both body
and organ were noted only after repeated dose of dimethoate. Significant decreases in the
activity of kynurenine-3-hydroxylase, kynurenine-2-oxoglutarate-transaminase,
kynurenine-pyruvate-transaminase, and pyridoxal-phosphokinase were noted following
repeated administration of dimethoate. Carbaryl in repeated doses caused significant
decreases in the activity of apo-tryptophan-2,3-dioxygenase,
kynurenine-2-oxoglutarate-transaminase, kynurenine-pyruvate-transaminase, and
serine-glyoxylate-transaminase. An inhibition was noted in tryptophan-2,3-dioxygenase
following external addition of insecticides at different concn to an incubation mixture.
Other enzymes demonstrated no change in their activities following this treatment.
/Pyrethroid/ detoxification ... important in flies, may be delayed by the addition of
synergists ... organophosphates or carbamates ... to guarantee a lethal effect. ...
/Pyrethroid/
Piperonyl butoxide potentiates /insecticidal activity/ of pyrethrins by inhibiting the
hydrolytic enzymes responsible for pyrethrins' metabolism in arthropods. When piperonyl
butoxide is combined with pyrethrins, the insecticidal activity of the latter drug is
increased 2-12 times /Pyrethrins/
At dietary level of 1000 ppm pyrethrins & 10000 ppm piperonyl butoxide ...
/enlargement, margination, & cytoplasmic inclusions in liver cells of rats/ were well
developed in only 8 days, but ... were not maximal. Changes were proportional to dosage
& similar to those produced by DDT. Effects of the 2 ... were additive. /Pyrethrins/
Pharmacology:
Therapeutic Uses:
MEDICATION (VET): ectoparasiticide
Pyrethrins with piperonyl butoxide are used for topical treatment of pediculosis(lice
infestations). Combinations of pyrethrins with piperonyl butoxide are not effective for
treatment of scabies (mite infestations). Although there are no well-controlled
comparative studies, many clinicians consider 1% lindane to be pediculicide of choice.
However, some clinicians recommend use of pyrethrins with piperonyl butoxide, esp in
infants, young children, & pregnant or lactating women ... . If used correctly, 1-3
treatments ... are usually 100% effective ... Oil based (eg, petroleum distillate)
combinations ... produce the quickest results. ... For treatment of pediculosis, enough
gel, shampoo, or solution ... should be applied to cover affected hair & adjacent
areas ... After 10 min, hair is ... washed thoroughly ... treatment should be repeated
after 7-10 days to kill any newly hatched lice. /Pyrethrins/
Interactions:
The ability of 3 mg/kg/day diazepam to alter the neurobehavioral and neurochemical
consequences of perinatal exposure to Ambush and Pydrin
was examined. Seventy-two pregnant female rats served as subjects. Half of the subjects
were treated with diazepam and the other half were treated with the vehicle via
subcutaneous osmotic pumps for 33 days starting on gestational day 1 Each group was
further divided into six gavage treatment groups: corn oil, corn oil + 96% xylene, 1.25 or
0.125 mg/kg Pydrin, and 4.0 or 0.4 mg/kg Ambush.
Behavioral evaluations were conducted on half the pups in each litter and the other pups
were used for the neurochemical assays. Behavioral evaluations included locomotor
activity, screen testing, and passive avoidance learning. Brains for neurochemical
analysis were extracted and sectioned into frontal cortex, caudate, hippocampus and
cerebellum. Neurochemical assays assessed levels of DA, DOPAC, 5-HIAA, 5-HT, HVA,
aspartate, glutamate, glutamine, glycine, GABA, and taurine. Diazepam treatment did
produce some neurotoxicity in the control pups but diazepam exposure did reverse
elevations in amino acid levels in the cerebellum produced by both pyrethroids. In
addition diazepam reversed the pyrethroid effects on activity and muscular coordination.
These diazepam effects were not specific to Type I or Type II pyrethroids.
This investigation explored the behavioral and neurochemical toxicity of perinatal oral
exposure to Ambush (Type I) and Pydrin (Type
II), two pyrethroid formulations. Thirty-six female rats were mated and exposed to various
pyrethroid formulations by oral gavage from the first gestational day until their pups
(culled to 8/litter) were 12 days old. Six mothers were exposed daily to one of the
following treatments: corn oil control, corn oil+96% xylene, 1.25 mg/kg Pydrin
(pesticidal ingredient fenvalerate), 0.125 mg/kg
Pydrin, 4.0 mg/kg Ambush (pesticidal ingredient
permethrin), or 0.4 mg/kg Ambush. Behavioral evaluations of locomotor activity, muscular
coordination and passive avoidanc learning were conducted on half of the pups from each
litter (N = 24 pups/treatment condition). The other pups were sacrificed, brains were
removed and sectioned into frontal cortex, hippocampus, caudate, and cerebellum for
neurochemical assessment. The monoamines DA, DOPAC, 5-HIAA, 5-HT and HVA levels were
determined and the amino acids aspartate, glutamate, glutamine, glycine, GABA, and taurine
were determined for each of the brain regions. Gestational duration was shortened by
exposure to the high doses of Pydrin and Ambush
but only pups from the 4.0 mg/kg Ambush group were significantly lighter. No physical
malformations were observed in pups from any of the treatment conditions, although the
high Pydrin exposure condition resulted in a 4%
death rate. Behavioral changes were seen for both locomotor activity and muscular
coordination. The shape of across-session habituation of locomotion was different for the
xylene and corn oil and the high dose Ambush groups. Both groups were less active on day 1
and more active on days 2 and 3 than the other pups. The high doses of Ambush and Pydrin produced slower intrasession habituation.
Muscular coordination was improved slightly following low dose exposure to both pesticides
and reduced following high dose exposures. Regional brain weights were normal for the
cortex, cerebellum and caudate but the hippocampus was 64% heavier for pups treated with
4.0 mg/kg Ambush. Amino acid determinations indicated that the cerebellum was most
affected where glutamate, glutamine, aspartate and taurine were reduced following xylene
or pyrethroid exposure. The biogenic amine transmitter 5-HT was reduced in several brain
regions following pyrethroid exposures. These data suggest that levels of Ambush and Pydrin as low as the LD50/10,000 can alter behavior
and neurotransmitter functioning.
Following the administration of a single or repeated doses of dimethoate, carbaryl, and
fenvalerate, the activities of
tryptophan-2,3-dioxygenase, indoleamine-2,3-dioxygenase, kynurenine, kynureninase,
kynurenine-transaminase, and pyridoxal-phosphokinase were determined in the liver, kidney
and lung of male Wistar rats. Treatment consisted of 10% of the median lethal dose of each
insecticide given orally for the single dosing investigations and 5% of the median lethal
dose was given orally for 5 consecutive days as repeated doses. Weight losses in both body
and organ were noted only after repeated dose of dimethoate. Significant decreases in the
activity of kynurenine-3-hydroxylase, kynurenine-2-oxoglutarate-transaminase,
kynurenine-pyruvate-transaminase, and pyridoxal-phosphokinase were noted following
repeated administration of dimethoate. Carbaryl in repeated doses caused significant
decreases in the activity of apo-tryptophan-2,3-dioxygenase,
kynurenine-2-oxoglutarate-transaminase, kynurenine-pyruvate-transaminase, and
serine-glyoxylate-transaminase. An inhibition was noted in tryptophan-2,3-dioxygenase
following external addition of insecticides at different concn to an incubation mixture.
Other enzymes demonstrated no change in their activities following this treatment.
/Pyrethroid/ detoxification ... important in flies, may be delayed by the addition of
synergists ... organophosphates or carbamates ... to guarantee a lethal effect. ...
/Pyrethroid/
Piperonyl butoxide potentiates /insecticidal activity/ of pyrethrins by inhibiting the
hydrolytic enzymes responsible for pyrethrins' metabolism in arthropods. When piperonyl
butoxide is combined with pyrethrins, the insecticidal activity of the latter drug is
increased 2-12 times /Pyrethrins/
At dietary level of 1000 ppm pyrethrins & 10000 ppm piperonyl butoxide ...
/enlargement, margination, & cytoplasmic inclusions in liver cells of rats/ were well
developed in only 8 days, but ... were not maximal. Changes were proportional to dosage
& similar to those produced by DDT. Effects of the 2 ... were additive. /Pyrethrins/
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Fenvalerate's use as a contact insecticide in
agriculture, in public health programs, in homes and gardens, and on cattle releases the
compound directly to the environment in sprays, dusts, concentrates and other routes of
application. Fenvalerate is a mixture of four
stereo-isomer of which esfenvalerate is the most biologically active. If released to the
atmosphere, fenvalerate will degrade rapidly in
the vapor phase by reaction with photochemically produced hydroxyl radicals (estimated
half-life of 10 hr). If released to soil or water, fenvalerate
can degrade through biodegradation, photodegradation and aqueous hydrolysis. Screening
studies have suggested that biodegradation is the primary route of degradation.
Photodegradation may become the major degradation route on terrestrial surfaces (soil,
plants, etc) or shallow waters exposed to sunlight. Aqueous hydrolysis may become
important when the medium pH exceeds 8. Fenvalerate
is not expected to leach in soil. In aquatic ecosystems, fenvalerate
is expected to partition from the water column to sediment and suspended matter. Fenvalerate is reported to have half-lives of 1 to 18
days on soil surfaces, 15 days to 3 months within soil systems, 8 to 14 days on plants,
and 4 to 15 days in natural water. Occupational exposure to fenvalerate
occurs through dermal contact and inhalation of dust and sprays, especially to workers
applying the compound as an insecticide. (SRC)
Probable Routes of Human Exposure:
Occupational exposure to fenvalerate occurs
through dermal contact and inhalation of dust and sprays, especially to workers applying
the compound as an insecticide(1). Exposure to fenvalerate
can occur during its production and application and, at much lower levels, from
consumption of foods containing residues(2).
Air concns of fenvalerate at the breathing
zone of workers spraying fenvalerate insecticide
on cotton was 0.06-1.98 ug cu m(1); dermal exposure ranged from 4.71 to 141.61 ug/cu cm on
forearms, hands, legs and feet(1). At a fenvalerate
packing plant in China, workers were reported to be exposed to 12-55 ug/cu m in the air,
with resulting skin contact(2).
Body Burden:
Urine concns of fenvalerate of workers
spraying fenvalerate insecticide on cotton was
0.01-1.98 ug/collection interval (3-12 hr) for a period up to 72 hr after spraying(1).
Average Daily Intake:
Based upon results of the US FDA's 1990 Total Diet Study, estimated human exposure to fenvalerate from food is as follows(1): 6-11 month old
child: 0.0101 ug/kg/day; 14-16 yr old male: 0.0061 ug/kg/day; 60-65 yr old female: 0.0092
ug/kg/day(1).
Artificial Pollution Sources:
Fenvalerate's use as a contact insecticide in
agriculture, in public health programs, in homes and gardens, and on cattle(1) releases
the compound directly to the environment in sprays, dusts, concentrates and other routes
of application(SRC).
Environmental Fate:
TERRESTRIAL FATE: The primary route of fenvalerate
degradation within most soil systems is probably biodegradation. The results of various
screening studies conducted in both non-sterile and sterilized soils have indicated that
microbial activity was the primary route of disappearance(1-3). The results of various
field and laboratory tests have demonstrated that fenvalerate
is essentially immobile in soil and will not leach appreciably(4-6). Fenvalerate
is reported to have half-lives of 1 to 18 days on soil surfaces, 15 days to 3 months
within soil systems and 8 to 14 days on plants(7). A review of available literature
determined that the average soil half-life of fenvalerate
is about 50 days(8). The US Dept of Agric's Pesticide Properties Database reports a fenvalerate soil half-life of 35 days(9). Enhanced
degradation on soil surfaces is probably due to photodegradation via sunlight(10-11,SRC).
Measured alkaline hydrolysis rates(12) suggest that hydrolysis may become an important
fate process in moist soil systems where the pH is greater than 8(SRC).
Soil degradation studies using 14-C labelled fenvalerate
have identified the following fenvalerate
metabolites(1-2): phenoxybenzoic acid, 3-(4-hydroxyphenoxy)benzoic acid, 4'-OH-fenvalerate, CONH2-fenvalerate,
and 4-chloro-alpha-(1-methylethyl)benzene acetic acid(1-2); at the end of 12 months,
evolved 14-CO2 accounted for 50.5% of applied radioactivity which indicated extensive
metabolite degradation(1-2).
AQUATIC FATE: Fenvalerate can degrade in the
aquatic environment through biodegradation photodegradation and aqueous hydrolysis. The
results of various screening studies conducted in both non-sterile and sterilized water
systems have indicated that microbial activity was a primary route of disappearance
(half-lives of 14 to 34 days)(1-3). Photodegradation studies have demonstrated that
sunlight can be an important fate process(4-5), and could even be the major fate process
in shallow waters with intense sunlight(SRC). Measured alkaline hydrolysis rates(6)
suggest that hydrolysis may become an important fate process in water systems where the pH
is greater than 8(SRC). Based upon water-sediment sorption studies(7), fenvalerate
can be expected to partition from the water column to sediment and suspended matter(SRC). Fenvalerate's estimated Henry's Law constant indicates
that volatilization from water is not an important fate process(SRC). The half-life of fenvalerate in natural water has been reported to
range from 4 to 15 days(8).
ATMOSPHERIC FATE: Based upon a reported vapor pressure of 2.8X10-7 mm Hg at 25 deg
C(1), fenvalerate can exist in both the vapor
and particulate-phases in the ambient atmosphere(2,SRC). It will degrade rapidly in the
vapor phase by reaction with photochemically produced hydroxyl radicals with an estimated
half-life of about 10 hr(3,SRC). Particulate-phase fenvalerate
and aerosols released to air during spray applications of fenvalerate
insecticide will be removed from air physically by dry and wet deposition(SRC).
Environmental Biodegradation:
In a laboratory study using sediment and seawater collected from a salt marsh near
Escambia County, FL, fenvalerate was observed to
have a half-life of about 34 days(1); however, when the media was sterilized, fenvalerate showed no appreciable degradation after 28
days of incubation(1), thus suggesting that degradation was occurring through biotic
means(SRC). In degradation tests using an activated sludge inoculum, the aerobic and
anaerobic degradation rates of fenvalerate were
50-72% faster than in sterile controls(2); addition of a glucose medium to cometabolize
the non-sterile flasks resulted in a 6-fold increase in the degradation rate under aerobic
conditions(2). The aerobic (semi-open system, activated sludge inocula) and anaerobic
(serum bottle technique) biodegradation rates of fenvalerate
were determined in tests using both inoculated and non-inoculated (control)
experiments(3); the biodegradation half-life was determined to be 13 days under both
aerobic and anaerobic conditions(3).
In soil degradation studies using a mineral and an organic soil, 92-98% of applied fenvalerate disappeared after an 8-week incubation
period(1); in sterile soil controls, only 6-17% of applied fenvalerate
disappeared suggesting that the disappearance was primarily due to biotic processes(1).
The results of a soil degradation study in a sandy loam soil (both natural and sterilized)
indicated that the soil disappearance was predominantly by microbial activity(2). In
seawater and seawater-sediment microcosm studies, the half-life of fenvalerate
was determined to be 14-17 days in non-sterile systems and 33-41 days in sterile systems
suggesting a presence of microbial activity(3).
Environmental Abiotic Degradation:
The rate constant for the vapor phase reaction of fenvalerate
with photochemically produced hydroxyl radicals has been estimated to be 3.76X10-11 cu
cm/molecule-sec at 25 deg C which corresponds to an atmospheric half-life of about 10
hours at an atmospheric concn of 5X10+5 hydroxyl radicals per cu cm(1,SRC). In a seawater
solution study, fenvalerate had an 8 day
half-life when exposed to sunlight, but a half-life greater than 14 days under no-sunlight
conditions(2). Photodegradation of one isomer of fenvalerate
(s,s-isomer) on thin films of intact soil, clay minerals and humic acid was examined by
irradiation with a xenon lamp (wavelengths > 300 nm)(3); in all cases, irradiation
increased the degradation rates of fenvalerate
as follows (half-life in days with light -- half life in days in dark)(3): upland soil
(100.0 - - 138.2), kaolinite (7.8 -- 391.2), montmorillonite (68.3 -- 553.4), humic acid
(80.6 -- 150.8); the dominant photodegradation reactions were hydration of the cyano group
and ether cleavage in the alcohol moiety(3).
Fenvalerate in various solutions (hexane,
methanol, acetonitrile-water) degraded rapidly (16-18 min half-lives) when exposed to
strong laboratory irradiation of > 290 nm(1); thin films of fenvalerate
on glass exhibited an initial photodegradation half-life of 4 days when exposed to
sunlight(1). The alkaline hydrolysis rate constant fenvalerate
(optical isomer) in 1:1 dioxane water at 25 deg C was measured as 0.182 L/mol-sec(2) which
corresponds to respective half-lives of 440 days, 44 days and 4.4 days at pHs of 7, 8 and
9(SRC); the alkaline hydrolysis rate constant in 1:1 dioxane water at 20 deg C was
measured as 0.149 L/mol-sec(2).
Environmental Bioconcentration:
In a 28 day laboratory study, steady-state BCFs of 4700 and 570 were measured in
eastern oysters (Crassostrea virginica) and sheepshead minnow (Cyprinodon variegatus),
respectively(1). A BCF of 1100 was measured for one isomer of fenvalerate
(s,s-isomer) in carp in a 24 hr renewal exposure following 7 days of exposure(1). In a 30
day aquatic ecosystem study, fenvalerate BCFs of
100 for fish, 491 for snails and 412 for algae were measured(1); relatively low residues
in the organisms were attributed to metabolism, especially by the fish(1).
Soil Adsorption/Mobility:
In undisturbed soils with >2% organic matter, fenvalerate
has been shown to be immobile(1); in a field study at an onion field in Ontario, Canada
conducted between 1980 and 1982, most of the applied fenvalerate
remained in the upper third of 15 cm soil cores(1). In 6-hr water-sediment sorption tests,
32% of added fenvalerate sorbed to a clay
sediment while 84% of applied fenvalerate sorbed
to a silty-clay sediment(2); 4% sorbed to sand(2); based upon measured isotherms and
organic carbon content(2), the Koc values for fenvalerate
in the silty-clay and clay sediments are log 4.04-4.22(2); the US Dept of Agric's
Pesticide Properties Database reports a fenvalerate
Koc of 3.72(6); according to a suggested classification scheme(3), these estimated Koc
values suggest that fenvalerate is immobile in
soil(SRC). In a field study near New Delhi, India, fenvalerate
did not leach below a 7.5 cm depth(4). Under saturated flow conditions in soil column
leaching studies, fenvalerate was found to be
essentially immobile(5).
Volatilization from Water/Soil:
The Henry's Law constant for fenvalerate can
be estimated to be 1.19X10-7 atm-cu m/mole at 25 deg C using a structure estimation
method(1,SRC). This value of Henry's Law constant indicates that fenvalerate
is essentially non-volatile from water(2); therefore, volatilization from water will not
be important(SRC). During a laboratory metabolism study, volatilization of fenvalerate from activated sludge, sediment or soil
was less than 0.1%(3).
Effluent Concentrations:
Water collected from exterior washings of an airplane used for spray applications of fenvalerate insecticide contained fenvalerate
concns of 0.004-0.02 mg/L(1); fenvalerate concns
in rinses of the spray tanks were 53-528 mg/L in the first rinse, 3.15-25.2 mg/L in the
second rinse and 0.32-1.80 mg/L in the third rinse(1).
Food Survey Values:
According to compiled results of the US Food and Drug Administration's pesticide
residue monitoring programs (including the Total Diet Study) for fiscal years 1978-1986, fenvalerate has been detected as a pesticide residue
in American foods(1,2); the frequency of occurrence or concns of fenvalerate
detected were not reported(SRC). During a 5-yr period from 1982-1986, the US FDA's Los
Angeles District Laboratory analyzed 19,581 samples of domestic and imported food and feed
commodities for pesticide residues(3); fenvalerate
was detected in 25 samples at concns of 0.05-1.0 ppm(3). For fiscal years 1988 and 1989,
27065 food samples were collected and analyzed for pesticide residues by 10 state
laboratories (CA, NY, FL, IN, MA, MI, NC, OR, VA and WI)(4); fenvalerate
was detected in 54 samples (concns not reported)(4).
Of a total of 946 samples analyzed in the 1984-1989 Canadian national surveillance
program, 7 were found to contain fenvalerate
residues, at levels of 0.02-0.096 mg/kg(1); most were in pears (6/114 samples) and one in
lettuce (1/11 samples)(1). In Sweden, 163 of 165 samples of imported fruit and vegetables
contained residues up to 0.2 mg/kg(1); one had a residue of 0.54 mg/kg(1).
Milk Concentrations:
Two Holstein cows were treated with 0.5 g of fenvalerate
per cow in three consecutive topical treatments at 14-day intervals(1); residues in whole
milk were at a max 6 hr after treatment and declined to less than 0.2 ug/L over 21
days(1); only 0.03-0.06% of applied fenvalerate
appeared in the milk as the intact insecticide(1).
Environmental Standards & Regulations:
FIFRA Requirements:
Tolerances are established for residues of the insecticide
Cyano(3-phenoxyphenyl)methyl-4-chloro-a-(1-methylethyl) benzeneacetate in or on the
following raw agricultural commodities: Almond hulls; Almonds; Apples; Artichokes; Beans,
dried; Beans, snap; Broccoli; Blueberries; Cabbage; Caneberries; Cantaloupes; Carrots;
Cattle (fat, meat byproducts, and meat); Cauliflower; Collards; Corn, grain; Corn, fodder;
Corn, forage; Corn, sweet, kernels & cobs; Cottonseed; Cucumbers; Currants; Eggplant;
Elderberries; English walnuts; Filberts; Goats (fat, meat byproducts, and meat);
Gooseberries; Hogs (fat, meat byproducts, and meat); Honeydew melons; Horses (fat, meat
byproducts, and meat); Huckleberries; Milk; Milk, fat; Muskmelons; Peanuts; Peanut hulls;
Pears; Peas; Peas, dried; Pecans; Peppers; Potatoes; Pumpkins; Radish, roots; Radish,
tops; Sheep (fat, meat byproducts, and meat); Soybeans; Stone fruits; Sugarcane; Summer
squash; Sunflower seed; Tomatoes; Turnip roots; Turnip tops; Watermelons; and Winter
squash.
A tolerance with regional registration is established for residues of the insecticide
cyano(3-phenoxyphenyl)methyl-4-chloro-alpha-(1-methylethyl)benzeneacetate in or on the raw
agricultural commodity okra.
A food additive tolerance is established for residues of the insecticide
cyano(3-phenoxyphenyl) methyl-4-chloro-alpha-(1-methylethyl)benzeneacetate and an isomer,
(S)-cyano(3- phenoxyphenyl)methyl-(S)-4-chloro-alpha-(1-methylethyl)-benzeneacetate, as
follows: In or on all food items (other than those already covered by a higher tolerance
as a result of use on growing crops) in food-handling establishments where food products
are held, processed, or prepared.
A food additive tolerance is established for residues of the insecticide
cyano(3-phenoxyphenyl) methyl-4-chloro-alpha-(1-methylethyl)benzeneacetate as follows:
Application of cyano(3-phenoxyphenyl)methyl-4-chloro- alpha-(1-methylethyl)benzeneacetate
shall be limited to space treatment with a max of 0.5 fluid oz of a 0.05% active
ingredient soln per 1,000 cu ft of space, or as a contact spray applied as a coarse wet
spray at a max of 1 gal of a 0.2% active ingredient soln per 1,000 sq ft of surface. Food
must be removed or covered during treatment. Spray should not be applied directly to
surfaces or utensils that may come into contact with food. Food-contact surfaces and
equipment should be thoroughly cleaned with an effective cleaning compound and rinsed with
potable water before using.
To assure safe use of the additive, its label and labeling shall conform to that
registered with the USEPA, and shall be used in accordance with such label and labeling.
A regulation is established permitting residues of the insecticide
cyano(3-phenoxyphenyl)methyl 4-chloro-alpha-(1-methylethyl) benzeneacetate in or on the
following commodities: Dried apple pomace; Dried tomato pomace; Soybean hulls; Sugarcane
bagasse; and Sunflower hulls.
As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of
older pesticides to consider their health and environmental effects and make decisions
about their future use. Under this pesticide reregistration program, EPA examines health
and safety data for pesticide active ingredients initially registered before November 1,
1984, and determines whether they are eligible for reregistration. In addition, all
pesticides must meet the new safety standard of the Food Quality Protection Act of 1996.
Pesticides for which EPA had not issued Registration Standards prior to the effective date
of FIFRA, as amended in 1988, were divided into three lists based upon their potential for
human exposure and other factors, with List B containing pesticides of greater concern and
List D pesticides of less concern. Fenvalerate
is found on List B. Case No: 2280; Pesticide type: Insecticide; Case Status: OPP is
reviewing data from the pesticide's producers regarding its human health and/or
environmental effects, or OPP is determining the pesticide's eligibility for
reregistration and developing the Reregistration Eligibility Decision (RED) document.;
Active ingredient (AI): alpha-Cyano-(3-phenoxylphenyl)methyl
4-chloro-alpha-(1-methylethyl)benzeneacetate; Data Call-in (DCI) Date(s): 07/11/91,
03/03/95, 07/20/95, 10/13/95; AI Status: The producers of the pesticide has made
commitments to conduct the studies and pay the fees required for reregistration, and are
meeting those commitments in a timely manner.
Acceptable Daily Intakes:
FAO/WHO ADI: 0.02 mg/kg
OPP RfD= 0.025 mg/kg; EPA RfD= 0.025 mg/kg
State Drinking Water Guidelines:
(AZ) ARIZONA 180 ug/l
Allowable Tolerances:
Tolerances are established for residues of the insecticide
cyano(3-phenoxyphenyl)methyl-4-chloro-a-(1-methylethyl) benzeneacetate in or on the
following raw agricultural commodities: Almond hulls: 15.0 ppm; Almonds: 0.2 ppm; Apples:
2.0 ppm; Artichokes: 0.2 ppm; Beans, dried: 0.25 ppm; Beans, snap: 2.0 ppm; Broccoli: 2.0
ppm; Blueberries: 3.0 ppm; Cabbage: 10.0 ppm; Caneberries: 3.0 ppm; Cantaloupes: 1.0 ppm;
Carrots: 0.5 ppm; Cattle (fat, meat byproducts, and meat): 1.5 ppm; Cauliflower: 0.5 ppm;
Collards: 10.0 ppm; Corn, grain: 0.02 ppm; Corn (fodder and forage): 50.00 ppm; Corn,
sweet, kernels & cobs: 0.1 ppm; Cottonseed: 0.2 ppm; Cucumbers: 0.5 ppm; Currants: 3.0
ppm; Eggplant: 1.0 ppm; Elderberries: 3.0 ppm; English walnuts: 0.2 ppm; Filberts: 0.2
ppm; Goats (fat, meat byproducts, and meat): 1.5 ppm; Gooseberries: 3.0 ppm; Hogs (fat,
meat byproducts, and meat): 1.5 ppm; Honeydew melons: 1.0 ppm; Horses (fat, meat
byproducts, and meat): 1.5 ppm; Huckleberries: 3.0 ppm; Milk: 0.3 ppm; Milk, fat: 7.0 ppm;
Muskmelons: 1.0 ppm; Peanuts: 0.02 ppm; Peanut hulls: 0.10 ppm; Pears: 2.0 ppm; Peas: 1.0
ppm; Peas, dried: 0.25 ppm; Pecans: 0.2 ppm; Peppers: 1.0 ppm; Potatoes: 0.02 ppm;
Pumpkins: 1.0 ppm; Radish, roots: 0.3 ppm; Radish, tops: 8.0 ppm; Sheep (fat, meat
byproducts, and meat): 1.5 ppm; Soybeans: 0.05 ppm; Stone fruits: 10.0 ppm; Sugarcane: 2.0
ppm; Summer squash: 0.5 ppm; Sunflower seed: 1.0 ppm; Tomatoes: 1.0 ppm; Turnip roots: 0.5
ppm; Turnip tops: 20.0 ppm; Watermelons: 1.0 ppm; and Winter squash: 1.0 ppm.
A tolerance with regional registration is established for residues of the insecticide
cyano(3-phenoxyphenyl)methyl-4-chloro-alpha- (1-methylethyl)benzeneacetate in or on the
following raw agricultural commodity: Okra: 0.1 ppm.
A food additive tolerance of 0.05 ppm is established for residues of the insecticide
cyano(3-phenoxyphenyl) methyl-4-chloro-alpha-(1-methylethyl)benzeneacetate and an isomer,
(S)-cyano(3- phenoxyphenyl)methyl-(S)-4-chloro-alpha-(1-methylethyl)-benzeneacetate, as
follows: In or on all food items (other than those already covered by a higher tolerance
as a result of use on growing crops) in food-handling establishments where food products
are held, processed, or prepared.
A food additive tolerance of 0.05 ppm is established for residues of the insecticide
cyano(3-phenoxyphenyl) methyl-4-chloro-alpha-(1-methylethyl)benzeneacetate as follows:
Application of cyano(3-phenoxyphenyl)methyl-4-chloro- alpha-(1-methylethyl)benzeneacetate
shall be limited to space treatment with a max of 0.5 fluid oz of a 0.05% active
ingredient soln per 1,000 cu ft of space, or as a contact spray applied as a coarse wet
spray at a max of 1 gal of a 0.2% active ingredient soln per 1,000 sq ft of surface. Food
must be removed or covered during treatment. Spray should not be applied directly to
surfaces or utensils that may come into contact with food. Food-contact surfaces and
equipment should be thoroughly cleaned with an effective cleaning compound and rinsed with
potable water before using.
A regulation is established permitting residues of the insecticide
cyano(3-phenoxyphenyl)methyl 4-chloro-alpha-(1-methylethyl) benzeneacetate in or on the
following commodities: Dried apple pomace: 20 ppm; Dried tomato pomace: 10 ppm; Soybean
hulls: 1.0 ppm; Sugarcane bagasse: 20.0 ppm; and Sunflower hulls: 2.0 ppm.
Chemical/Physical Properties:
Molecular Formula:
C25-H22-Cl-N-O3
Molecular Weight:
419.92
Color/Form:
Clear yellow viscous liquid
Odor:
Mild chemical odor
Corrosivity:
Non-corrosive to metals.
Density/Specific Gravity:
1.17 at 23 deg C/4 deg C
Octanol/Water Partition Coefficient:
log Kow= 4.42
Solubilities:
In water at 20 deg C, < 1 mg/l. Readily soluble in most organic solvents, in
acetone, ethanol, chloroform, cyclohexanone, xylene, all > 1 kg/kg at 23 deg C.
Spectral Properties:
Index of refraction: 1.5533 at 20 deg C/D
Vapor Pressure:
1.1X10-8 mm Hg at 25 deg C
Other Chemical/Physical Properties:
Brown viscous liquid /Technical grade, 90% min fenvalerate/
Has two chiral centers giving four possible optical isomers.
Decomposes gradually between 150-300 deg C. No significant breakdown 100 hr at 75 deg
C.
Decomposes on distillation
Chemical Safety & Handling:
Skin, Eye and Respiratory Irritations:
Fenvalerate as technical Pydrin
is mildly irritating to the skin, but the emulsifiable concentrate is corrosive.
Eye, skin irritant.
One notable form of toxicity associated with synthetic pyrethroids has been a cutaneous
paresthesia observed in workers spraying esters containing alpha-cyano substituent
(deltamethrin, cypermethrin, fenvalerate). The
paresthesia developed several hours following exposure, being described as a stinging or
burning sensation on the skin which, in some cases, progressed to a tingling and numbness,
the effects lasting some 12 to 18 hours.
Immediately irritating to the eye. /Pyrethrins/
The chief effect from exposure ... is skin rash particularly on moist areas of the
skin. ... May irritate the eyes.
Fire Potential:
/Pyrethrins/ ... burn with difficulty. /Pyrethrins/
Fire Fighting Procedures:
Use carbon dioxide, foam, or dry chemical /on fires involving pyrethroids/. /Pyrethrum/
Fire-fighting: Self-contained breathing apparatus with a full facepiece operated in
pressure-demand or other positive-pressure mode. /Pyrethrum/
Extinguish fire using agent suitable for type of surrounding fire. /Pyrethrins/
Toxic Combustion Products:
Hydrogen cyanide may be formed during thermal decomposition.
Hazardous Reactivities & Incompatibilities:
Incompatible with alkaline materials.
Incompatibility: Strong oxidizers. /Pyrethrins/
... Incompatible with lime & ordinary soaps because acids & alkalies speed up
processes of hydrolysis. /Pyrethrins/
Hazardous Decomposition:
Hydrogen cyanide may be formed during thermal decomposition.
Protective Equipment & Clothing:
Protective gloves, goggles, or full face shield when handling.
Employees should be provided with and required to use dust- and splash-proof safety
goggles where /pyrethroids/ ... may contact the eyes. /Pyrethroids/
Employees should be provided with and be required to use impervious clothing, gloves,
and face shields (eight-inch minimum). /Pyrethroids/
Wear appropriate equipment to prevent: Repeated or prolonged skin contact. /Pyrethrum
and pyrethrins/
Wear eye protection to prevent: Reasonable probability of eye contact. /Pyrethrins/
Recommendations for respirator selection. Max concn for use: 50 mg/cu m: Respirator
Classes: Any chemical cartridge respirator with organic vapor cartridge(s) in combination
with a dust, mist, and fume filter. May require eye protection. Any supplied-air
respirator. May require eye protection. Any self-contained breathing apparatus. May
require eye protection. /Pyrethrins/
Recommendations for respirator selection. Max concn for use: 125 mg/cu m: Respirator
Classes: Any supplied-air respirator operated in a continuous flow mode. May require eye
protection. Any powered, air-purifying respirator with organic vapor cartridge(s) in
combination with a dust, mist, and fume filter. May require eye protection. /Pyrethrins/
Recommendations for respirator selection. Max concn for use: 250 mg/cu m: Respirator
Classes: Any chemical cartridge respirator with a full facepiece and organic vapor
cartridge(s) in combination with a high-efficiency particulate filter. Any self-contained
breathing apparatus with a full facepiece. Any supplied-air respirator with a full
facepiece. Any powered, air-purifying respirator with a tight-fitting facepiece and
organic vapor cartridge(s) in combination with a high-efficiency particulate filter. May
require eye protection. /Pyrethrins/
Recommendations for respirator selection. Max concn for use: 5,000 mg/cu m: Respirator
Class: Any supplied-air respirator with a full facepiece and operated in a pressure-demand
or other positive pressure mode. /Pyrethrins/
Recommendations for respirator selection. Condition: Emergency or planned entry into
unknown concn or IDLH conditions: Respirator Classes: Any self-contained breathing
apparatus that has a full facepiece and is operated in a pressure-demand or other positive
pressure mode. Any supplied-air respirator with a full face piece and operated in
pressure-demand or other positive pressure mode in combination with an auxiliary
self-contained breathing apparatus operated in pressure-demand or other positive pressure
mode. /Pyrethrins/
Recommendations for respirator selection. Condition: Escape from suddenly occurring
respiratory hazards: Respirator Classes: Any air-purifying, full-facepiece respirator (gas
mask) with a chin-style, front- or back-mounted organic vapor canister having a
high-efficiency particulate filter. Any appropriate escape-type, self-contained breathing
apparatus. /Pyrethrins/
Preventive Measures:
Avoid eye, skin, mouth contact.
SRP: The scientific literature supports the wearing of contact lenses in industrial
environments, as part of a program to protect the eye against chemical compounds and
minerals causing eye irritation. However, there may be individual substances whose
irritating or corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases contact lenses should not be worn.
Skin that becomes contaminated with /pyrethrum/ should be promptly washed or showered
with soap or mild detergent and water. /Pyrethrum/
Clothing contaminated with /pyrethrum/ should be placed in closed containers for
storage until provision is made for the removal of /pyrethrum/ from the clothing.
/Pyrethrum/
Respirators may be used when engineering and work practice controls are not technically
feasible, when such controls are in the process of being installed, or when they fail or
need to be supplemented. Respirators may also be used for operations which require entry
into tanks or closed vessels, and in emergency situations. /Pyrethrum/
Employees who handle /pyrethrum/ ... should wash their hands thoroughly with soap or
mild detergent and water before eating, smoking, or using toilet facilities. /Pyrethrum/
Avoid contact with skin. Keep out of any body of water. Do not contaminate water by
cleaning of equipment or disposal of waste. Do not reuse empty container. Destroy it by
perforating or crushing. /Pyrethrum/
Contact lenses should not be worn when working with this chemical. /Pyrethrins/
Workers should wash: Promptly when skin becomes contaminated. /Pyrethrins/
Work clothing should be changed daily: If it is reasonably probable that the clothing
may be contaminated. /Pyrethrins/
Remove clothing: Promptly if it is non-impervious clothing that becomes contaminated.
/Pyrethrins/
If /pyrethrins/ are not involved in a fire: keep /pyrethrins/ out of water sources and
sewers. Build dikes to contain flow as necessary. /Pyrethrins/
SRP: The scientific literature for the use of contact lenses in industry is
conflicting. The benefit or detrimental effects of wearing contact lenses depend not only
upon the substance, but also on factors including the form of the substance,
characteristics and duration of the exposure, the uses of other eye protection equipment,
and the hygiene of the lenses. However, there may be individual substances whose
irritating or corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn. In any
event, the usual eye protection equipment should be worn even when contact lenses are in
place.
Stability/Shelf Life:
More stable in acidic solution than in alkaline solution.
Pyrethrins ... /are/ stable for long periods in water-based aerosols where ...
emulsifiers give neutral water systems. /Pyrethrins/
Storage Conditions:
Store in original containers away from food stuffs, animal feed.
Pyrethrins with piperonyl butoxide topical preparations should be stored in well-closed
containers at a temperature less than 40 deg C, preferably between 15-30 deg C.
/Pyrethrins/
Cleanup Methods:
Spillages of pesticides at any stage of their storage or handling should be treated
with great care. Liquid formulations may be reduced to solid phase by evaporation. Dry
sweeping of solids is always hazardous: these should be removed by vacuum cleaning, or by
dissolving them in water, or other solvent in the factory environment. /Pesticides/
Environmental consideration - Land spill: Dig a pit, pond, lagoon, or holding area to
contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes,
or holding areas should be sealed with an impermeable flexible membrane liner./ Dike
surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk
liquid with fly ash, or cement powder. /Pyrethrins/
Environmental consideration - Water spill: If /pyrethrins/ are dissolved, apply
activated carbon at ten times the spilled amount in the region of 10 ppm or greater concn.
Use mechanical dredges or lifts to remove immobilized masses of pollutants and
precipitates. /Pyrethrins/
Disposal Methods:
Incineration would be an effective disposal procedure where permitted. If an efficient
incinerator is not available, the product should be mixed with large amounts of
combustible material and contact with the smoke should be avoided. /Pyrethrin products/
The following wastewater treatment technology has been investigated for chlorinated
pesticides: Concentration process: Resin adsorption. /Chlorinated pesticides/
The following wastewater treatment technology has been investigated for chlorinated
pesticides: Concentration process: Resin adsorption. /Chlorinated pesticides/
Group I Containers: Combustible containers from organic or metallo-organic pesticides
(except organic mercury, lead, cadmium, or arsenic compounds) should be disposed of in
pesticide incinerators or in specified landfill sites. /Organic or metallo-organic
pesticides/
Group II Containers: Non-combustible containers from organic or metallo-organic
pesticides (except organic mercury, lead, cadmium, or arsenic compounds) must first be
triple-rinsed. Containers that are in good condition may be returned to the manufacturer
or formulator of the pesticide product, or to a drum reconditioner for reuse with the same
type of pesticide product, if such reuse is legal under Department of Transportation
regulations (eg 49 CFR 173.28). Containers that are not to be reused should be punctured
... and transported to a scrap metal facility for recycling, disposal or burial in a
designated landfill. /Organic or metallo-organic pesticides/
Occupational Exposure Standards:
Manufacturing/Use Information:
Major Uses:
Highly active contact insecticide effective against a wide range of pests, including
strains resistant to organochlorine, organophosphorus, and carbamate insecticides. It
controls insects that attack leaves or fruits on various crops, including cotton, fruit,
vegetables and vines at 25-250 g ai/ha, and is persistent under various field conditions.
It is also used in public health and animal husbandry, controlling flies in cattle sheds
for 60 days at 100 mg/sq m wall, and is effective against Boophilus at 200-300 mg/l.
A broad-spectrum insecticide for use on cotton and fruit.
/For treatment of animals/ apply one or two tags per head as needed. Will aid in
control of face flies. Will control ear ticks.
Uses include control of chewing, sucking, and boring insects (particularly Lepidoptera,
Diptera, Orthoptera, Hemiptera, and Coleoptera) in fruit, vines, olives, hops, nuts,
vegetables, cucurbits, cotton, oilseed, rape, sunflowers, lucerne, cereals, maize,
sorghum, potatoes, beet, groundnuts, soya beans, tobacco, sugar cane, ornamentals,
forestry, and on non-crop land. Also used for control of flying and crawling insects in
public health situtations and in animal houses.
Insecticide /Pyrethrins/
MEDICATION (VET)
MEDICATION
Manufacturers:
Du Pont Co, Hq, 1007 Market St, Wilmington, DE 19898; (302) 774-1000, (800) 441-7515,
Du Pont Agricultural Products; Production site: Axis, AL 36505
Methods of Manufacturing:
... prepared by esterification of 3-phenoxybenzaldehyde cyanohydrin with
2-(4-chlorophenyl)isovaleroyl chloride.
... condensation of 3-phenoxy-alpha-halobenzyl cyanide with the isovaleric acid in the
presence of a base such as potassium carbonate.
General Manufacturing Information:
A synthetic pyrethroid insecticide without the usual cyclopropane ring.
/Pyrethroids/ are modern synthetic insecticides similar chemically to natural
pyrethrins, but modified to increase stability in the natural environment. /Pyrethroids/
Formulations/Preparations:
Emulsifiable concentrate, dust, granules, wettable powder.
Technical grade 90% min of fenvalerate.
An emulsifiable concentrate, marketed as Pydrin
2.4 EC Insecticide, is comprised of 32% technical Pydrin
and 68% aromatic hydrocarbon solvents and emulsifiers.
Ectrin 8%
Laboratory Methods:
Analytic Laboratory Methods:
Fenvalerate canbe determined by GLC with a
flame ionization detector (3% ov-17 glass column with temperature programming). The
detection limit is 0.054 ug/ml.
Product analysis is by HPLC or by GLC. Residues may be determined by GLC with ECD.
Pyrethrins ... in pesticide formulations are analyzed using gas chromatography equipped
with flame ionization detection. Average recovery is 98% with a precision of 0.0044-0.011.
/Pyrethrins/
... Liquid chromatography method has been developed to quantitate pyrethrins in
pesticide formulations. ... Detection was monitored at 240 nm. ... Percent coefficients of
variation ranged from 1.39 to 9.68 with the majority less than 5.00. ... /Pyrethrins/
Pyrethrins were detected in soils by gas chromatography after extraction with hexane.
/Pyrethrins/
Low level pyrethrin formulations are extracted with tetrahydrofuran and determined via
capillary gas chromatography with electron capture detection. ... Analysis of 5
formulations gave an average standard deviation of 3.3%. /Pyrethrins/
Special References:
Special Reports:
Clark JR et al; Toxicity of pyrethroids to Marine Invertebrates and Fish: A Literature
Review and Test Results with Sediment-Sorbed Chemicals. Environ Toxicol Chem 8 (5):
393-401 (1989). Data on acute and chronic toxicity of permethrin, fenvalerate,
cypermethrin, and flucythrinate to marine invertebrates and fishes are reviewed.
Miyamoto J; Environ Health Perspect 14: 15-28 (1976). Degradation, metabolism, and
toxicity of synthetic pyrethroids.
Miyamoto J, et al; Pure Appl Chem 53: 1967-2022 (1981). The chemistry, metabolism, and
residue analysis of synthetic pyrethroids.
Hutson DH; Progress in Drug Metabolism 3: 215-252 (1979). The metabolic fate of
synthetic pyrethroid insecticides in mammals.
Gammon DW; Fundam Appl Toxicol (5) 1: 9-23 (1985). Correlations between in vitro and in
vivo mechanisms of pyrethroid insecticide action.
Casida JE et al; Ann Rev Pharmacol Toxicol 23: 413-38 (1983). The mechanisms of
selective action of pyrethroid insecticide are discussed.
Papadopoulou-Mourkidou E; Residue Rev 89: 179-208 (1983). A review with many references
on analysis of allethrin & other pyrethroid insecticides.
Purdue University; National Pesticide Information Retrieval System, Fenvalerate
Fact Sheet No. 145 (1987)
WHO; Environmental Health Criteria 95: Fenvalerate
(1990)
Synonyms and Identifiers:
Related HSDB Records:
6625 [ESFENVALERATE] (isomer)
Synonyms:
S-5602
**PEER REVIEWED**
Balmark
**PEER REVIEWED**
Belmark
**PEER REVIEWED**
4-Chloro-alpha-(1-methylethyl)benzeneacetic acid cyano(3-phenoxyphenyl)methyl ester
**PEER REVIEWED**
(+)Alpha-cyano-3-phenoxybenzyl-(+)-alpha-(4-chlorophenyl)isovalerate
**PEER REVIEWED**
alpha-Cyano-3-phenoxy-benzyl alpha-(4-chlorophenyl)isovalerate
**PEER REVIEWED**
Alpha-cyano-3-phenoxybenzyl 2-(4-chlorophenyl)-3-methylbutyrate
**PEER REVIEWED**
alpha-Cyano-3-phenoxy-benzyl alpha-isopropyl-4-chlorophenylacetate
**PEER REVIEWED**
alpha-cyano-3-phenoxybenzyl isopropyl-4-chlorophenylacetate
**PEER REVIEWED**
cyano(3-Phenoxyphenyl)methyl 4-chloro-alpha-(1-methylethyl)benzeneacetate
**PEER REVIEWED**
(cyano(3-phenoxyphenyl)methyl-4-chloro-alpha-(1-methylethyl)phenylacetate)
**PEER REVIEWED**
Ectrin
**PEER REVIEWED**
EPA Shaughnessy Code: 109301
**PEER REVIEWED**
Fenkill
**PEER REVIEWED**
Phenvalerate
**PEER REVIEWED**
Pydrin
**PEER REVIEWED**
Pyridin
**PEER REVIEWED**
(RS)-alpha-cyano-3-phenoxybenzyl (RS)-2-(4-chlorophenyl)-3-methylbutyrate
**PEER REVIEWED**
Sanmarton
**PEER REVIEWED**
SD-43775
**PEER REVIEWED**
Sumibac
**PEER REVIEWED**
Sumicidin
**PEER REVIEWED**
Sumifleece
**PEER REVIEWED**
Sumifly
**PEER REVIEWED**
Sumipower
**PEER REVIEWED**
Sumitick
**PEER REVIEWED**
Sumkidin
**PEER REVIEWED**
Tirade
**PEER REVIEWED**
WL43775
**PEER REVIEWED**
Formulations/Preparations:
Emulsifiable concentrate, dust, granules, wettable powder.
Technical grade 90% min of fenvalerate.
An emulsifiable concentrate, marketed as Pydrin
2.4 EC Insecticide, is comprised of 32% technical Pydrin
and 68% aromatic hydrocarbon solvents and emulsifiers.
Ectrin 8%
Administrative Information:
Hazardous Substances Databank Number: 6640
Last Revision Date: 20010808
Last Review Date: Reviewed by SRP on 3/11/1993
Update History:
Field Update on 08/08/2001, 1 field added/edited/deleted.
Field Update on 05/16/2001, 1 field added/edited/deleted.
Complete Update on 09/12/2000, 1 field added/edited/deleted.
Complete Update on 06/12/2000, 1 field added/edited/deleted.
Complete Update on 03/13/2000, 1 field added/edited/deleted.
Complete Update on 02/08/2000, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 08/27/1999, 1 field added/edited/deleted.
Complete Update on 06/03/1998, 1 field added/edited/deleted.
Complete Update on 11/01/1997, 1 field added/edited/deleted.
Complete Update on 05/09/1997, 1 field added/edited/deleted.
Complete Update on 04/24/1997, 2 fields added/edited/deleted.
Complete Update on 03/18/1997, 2 fields added/edited/deleted.
Complete Update on 02/28/1997, 1 field added/edited/deleted.
Complete Update on 10/20/1996, 1 field added/edited/deleted.
Complete Update on 05/14/1996, 1 field added/edited/deleted.
Complete Update on 02/01/1996, 1 field added/edited/deleted.
Complete Update on 08/21/1995, 1 field added/edited/deleted.
Complete Update on 11/28/1994, 1 field added/edited/deleted.
Complete Update on 03/01/1994, 75 fields added/edited/deleted.
Record Length: 174506