DELTAMETHRIN
Human Health Effects:
Evidence for Carcinogenicity:
Evaluation: No data were available from studies in humans. There is inadequate evidence
for the carcinogenicity of deltamethrin in
experimental animals. Overall evaluation: Deltamethrin
is not classifiable as to its carcinogenicity to humans (Group 3).
Human Toxicity Excerpts:
Clinical manifestations of 573 cases of acute pyrethroid poisoning are reviewed. The
cases occurred in 14 provinces in China & involved 325 patients exposed to deltamethrin, 196 to fenvalerate, 45 to cypermethrin,
& 7 to other pyrethroid compds. 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 & 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 4-6 hr after exposure. Half of those occupationally
exposed experienced abnormal facial sensations such as burning, itching, or tingling
sensation which were exacerbated by sweating & 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%; & 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%; & incr
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/day for the first wk. Blood tests revealed leukocytosis in 15%. Treatment
consisted of symptomatic & supportive therapy including gastric lavage. Most recovered
in 6 days.
Among plant workers dermally exposed to technical deltamethrin
or its formulations, cutaneous and mucous manifestation were observed. Initial lesions
were tenacious painful pruritus, especially observed after exposure to hot water or
perspiration, followed by a blotchy local burning sensation with blotchy erythema for
about 2 days. Thereafter, slight and regular desquamation, restricted to the contaminated
area, occurred. Cutaneous signs were sometimes accompanied by itching of the face (mainly
around the mouth) and/or rhinorrhea or lacrymation. ... No long-term or persistent effect,
or allergic diseases were reported in 70 workers, who had been exposed from 1977-87 in a deltamethrin-manufacturing and -formulating plant in
France.
A field study was carried out in the United Kingdom with three unprotected operators
& one operator wearing hood, gloves, & respirator, all of whom were involved in
orchard spraying with deltamethrin according to
normal field practice. The exposure time was 3.5 hr. No changes were found in blood cell
counts, total protein urea, alkaline phosphates, y-GT & SGOT in blood. Little deltamethrin was found in the respiratory pad & no
residues were found in the urine. There was no decr in nerve conduction velocity, but a
slight tendency to the opposite reaction. None of the operators experienced facial
sensations.
A health survey was carried out among spraymen exposed to 2.5% deltamethrin
emulsifiable concentrate in cotton fields in China. The subjects were exposed to deltamethrin at concn 0.002-24.070 ug/cu m in the air
of the respiratory zone & 0.013-0.347 ug/cm sq of skin contact. One half of the 44
sprayers complained of itching & burning sensations on their faces. A few ... red
papules also appeared on the face of one them, but no signs of acute deltamethrin
poisoning were noticed during physical exam. There were no significant differences in the
sodium, potassium, & urea contents of the serum, the sodium, potassium, ATPase, &
serotonin contents of whole blood, & the levels of 3-methyl-4-hydroxymandelic acid
& 5-hydroxy-indoleacetic acid in the urine between the subjects examined & the
controls. Deltamethrin in the urine of spraymen
was below the detection limit of 0.10 ug/litre.
Five healthy volunteers, 16-40 yr of age, were exposed to deltamethrin
during 5 days of spraying in a cotton field in India in 1981. A sixth volunteer was
engaged in mixing & loading the emulsion during the same period. Spraymen were exposed
for 7 hr/day. No one complained about any symptoms. No clinical abnormalities were
detected, particularly with respect to neurological exam (muscle power, coordination,
tremors, reflexes, & both light & deep sensations). No cardiovascular,
respiratory, or abdominal abnormalities were detected, & no skin, mucous membrane, or
eye lesions were observed during, & after cessation of exposure.
Persons exposed to deltamethrin for 7-8 yr in
production & formulation were subjected to clinical & hematological exam.
Evaluations were conducted at several plants. There were no measurable effects other than
transient irritation of cutaneous & mucous membranes, which was without sequelae.
Adequate precautionary measures such as the wearing of gloves & face masks, provided
protection from exposure.
A medical survey of agricultural workers involved in the same use & application of
emulsified concentrate (EC) & wettable powder (WP) formulations of deltamethrin
in Yugoslavia revealed no untoward symptoms of exposure, other than itching & burning
of the face, & nasal hypersecretion. Medical exam included chest X-ray, ECG, liver
function tests, neurological exam (eye tonometry, Goldman perimetry, dark adaptation
ability), kidney function tests, & whole blood & plasma cholinesterase activity.
No adverse effects were noted.
In a department producing an aerosol of the domestic Bulgarian insecticide
"Dekazol" containing 0.02, 0.04, or 0.08% deltamethrin,
severe subjective complaints of sensory irritation were found because of the high levels
of contamination of the workplace air with deltamethrin
& also dermal contamination. Skin irritation with conjunctivitis & irritation of
the respiratory system were discovered in all 25 workers. Two of them had contact
urticaria. Patch testing with 0.03% deltamethrin
showed a positive reaction in 5 out of 23 workers tested.
Three formulations of deltamethrin in
petroleum solvent were patch tested on 37 human volunteers (double blind trial against
solvent control). A dose of 20 ul of a 1% suspension in water, of a 25 g/litre
emulsifiable concentrate was put on the facial skin of each volunteer, with a randomized
distribution of control and active dilution. The duration of the irritation was short
(from some minutes to 1 hr) and the severity was described as slight by most of the
volunteers. No skin damage was reported.
An agricultural worker as a result of skin contamination with a liquid containing 5g deltamethrin/l ... developed paresthesia in the legs,
mouth, & tongue, & diarrhea. Following washing of the skin & admin of
antihistamines, he still had tingling sensations in his toes after 24 hr, but was fully
recovered after 48 hr.
Outbreaks of acute deltamethrin &
fenvalerate poisoning occurred in cotton growers in China in 1982-84. The farmers handled
the pyrethroid insecticides without taking any precautions. Skin sensations occurred in
>90% of the exposed workers. After repeated spraying in the cotton fields, the mild
cases presented severe headaches, dizziness, fatigue, nausea, & anorexia, with
transient changes in the EEG. A severe case developed muscular fasciculation, repetitive
discharges in the EMG, & frequent convulsions, which were treated with diazepam &
phenobarbital. However, in follow-up studies, all workers were found to have made complete
recovery, & the prognosis of acute pyrethroid poisoning was found to be good.
Attempted suicide by a 23-yr-old man, was reported. After oral absorption of 70 cc of a
2.5% emulsified concentrate (EC) formulation (1.75 g pure deltamethrin),
there were no neurological signs in this patient. Digestive & hepatic signs occurred,
probably due to absorption of the solvent, since determination of xylene in plasma was
positive. The patient was treated with hemodialysis, phenobarbital, lidocaine, &
provoked alkaline diuresis. Recovery followed within 48 hr.
A 13-year-old girl who ingested voluntarily 200 ml of a 2.5% emulsified concentrate
(EC) formulation (5 grams of deltamethrin), ...
lost consciousness and developed generalized muscle cramps, myosis, and tachycardia.
Treatment in hospital was as follows: gastric lavage, ... PAM; ... atropine; ... sodium
nitrite, ...sodium thiosulfate; and, lastly, high doses of diazepam. She completely
recovered in 48 hr.
One notable form of toxicity associated with synthetic pyrethroids has been a cutaneous
paresthesia observed in workers spraying esters containing alpha-cyano substituent (/eg/ deltamethrin ...). The paresthesia developed several
hr following exposure, being described as a stinging or burning sensation on the skin
which, in some cases, progressed to a tingling & numbness, the effects lasting some
12-18 hr.
Workers exposed to deltamethrin during its
manufacture over 7-8 yr experienced transient cutaneous & mucous membrane irritation
which could be prevented by use of gloves & face masks, but no other ill effects were
seen.
Workers handling deltamethrin concentrates,
especially in aromatic solvents, without adequate protection of the facial skin
experienced more severe irritation. This involved an initial painful pruritis & a
blotchy erythema & burning sensation, which persisted for several days.
An epidemiological study of the prevalence of acute pyrethroid poisoning in cotton
farmers was conducted in a cohort of 3113 cotton farmers (2230 males) from 8 villages in
Gaocheng County, People's Republic of China. Subjects were interviewed by questionnaire to
obtain information on demographic characteristics, exposure to pyrethroids or other
pesticides, symptoms of exposure, medical history, & use of protective gear. 38 male
applicators were selected for environmental & biological monitoring over a 72 hr
period starting before & continuing to 1 day after spraying. Environmental monitoring
was performed by measuring breathing zone & dermal exposures. Biological monitoring
was performed by analyzing urine samples for pyrethroids. The subjects sprayed deltamethrin & fenvalerate. Respiratory exposures
of deltamethrin & fenvalerate ranged up to
0.53 & 1.19 ug/hr, respectively. Dermal exposures to deltamethrin
& fenvalerate ranged from 0.02 to 1.56 & 1.25 to 6.42 mg/hr, respectively. Urinary
excretion of deltamethrin & fenvalerate
ranged up to 0.4 & 0.33 ug/liter, respectively. A total of 834 subjects (26.9%)
developed symptoms such as abnormal facial sensations, dizziness, headache, fatigue,
nausea, or anorexia after spraying pure pyrethroids or mixtures of pyrethroids &
organophosphates. 10 subjects who developed significant systemic symptoms, listlessness
& muscular fasciculations, were diagnosed as having acute pyrethroid poisoning. A
total of 2131 subjects had been exposed to pyrethroids previously. Of these, 696 reported
symptoms in this study. A total of 2173 subjects were not aware of the toxicity of
pyrethroids. Use of protective equipment was negligible. Contamination of the shoes &
trousers occurred in 93.1 & 65% of the subjects, respectively. It was concluded that
26.9% of the subjects have been clinically affected by exposure to pyrethroids, with
dermal contamination as a major route.
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/
Some pyrethroid (eg, deltamethrin,
fenvalerate, cyhalothrin, lambda-cyhalothrin, flucythrinate, & cypermethrin) may cause
a transient itching &/or burning sensation in exposed human skin. /Synthetic
pyrethroids/
The clinical manifestations of inhalation exposure to pyrethrins can be local or
systemic. Localized reactors confined to the upper respiratory tract include rhinitis,
sneezing, scratchy throat, oral mucosal edema, and even laryngeal mucosal edema. Localized
reaction of the lower respiratory tract include cough, shortness of breath, wheezing, and
chest pain. An asthmalike reaction occurs with acute exposures in sensitized patients.
Hypersensitivity pneumonitis characterized by chest pain, cough, dyspnea, &
bronchospasm may occur in an individual chronically exposed. /Pyrethrum and synthetic
pyrethroids/
Skin, Eye and Respiratory Irritations:
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/
Populations at Special Risk:
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. ... /Pyrethroids/
Probable Routes of Human Exposure:
Dermal exposure of deltamethrin to a pilot
applying the insecticide while flying an ultra-light aircraft was 10.8 ug/hr(1); a
ground-based flagman on duty during the aerial spraying received a dermal exposure of 25
ug/hr(1); dermal exposure to workers manually spraying deltamethrin
was 2.8-42.2 mg/hr(1); the 1000-fold exposure difference between hand-held applicators and
aerial applicators was due, in part, to work practices of the workers(1). Inhalation
exposure of workers involved in spray applications of deltamethrin
in greenhouses was measured as 5.2 ug/cu m at the time of spraying and 0.008 ug/cu m 30
min after spraying(2); dermal exposures (chest, back, arms, forearms, hands, legs) ranged
from 0.21 to 10.5 ug/100 cu cm(2). Workers packaging deltamethrin
in a small importing factory in China were reported to have been exposed to airborne
levels of 0.2-1.2 ug/cu m, with resulting skin contact(3). Air concns of deltamethrin
at the breathing zone of workers spraying deltamethrin
insecticide on cotton was 0.02-0.11 ug/cu m(4); dermal exposure ranged from 0.14 to 1.48
ug/cu cm on forearms, hands, legs and feet(4). Occupational exposure to deltamethrin
may occur through inhalation of dust particles and dermal contact with this compound at
workplaces where deltamethrin is produced or
used. Monitoring data indicate that the general population may be exposed to deltamethrin via inhalation of ambient air, ingestion
of food and dermal contact with this compound(SRC).
Body Burden:
Urine concns of deltamethrin of workers
spraying deltamethrin insecticide on cotton was
0.01-1.79 ug/collection interval (3-12 hr) for a period up to 72 hr after spraying(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/
The additives (e.g. petroleum distillate), when present, represent a greater toxic
threat to the patient than the active ingredient itself. ... Emesis should not be induced
when petroleum distillate additives are present unless the product ingested is estimated
to contain a near lethal dose (1 g/kg) of pyrethrum or pyrethrins. The alert person with
an intact gag reflex & a sublethal pyrethrum ingestion without other toxic
constituents may have emesis induced by ipecac, followed by a saline cathartic &
slurry of activated charcoal. ... Pulmonary & allergic sequelae are treated
symptomatically with airway maintenance, oxygen, & ventilatory assistance as required.
Standard drugs and management protocols may be used for treatment of bronchospasm &
anaphylaxis. Seizures are treated with diazepam. /Pyrethrum and synthetic pyrethroids/
As in animals, the "seizures" were poorly controlled by anesthetics,
phenytoin, diazepam or chlorpromazine whilst atropine was effective against the
hypersalivation and pulmonary edema.
Skin decontamination. Wash skin promptly with soap and water ... . If irritant or
paresthetic effects occur, obtain treatment by a physician. Because volatilization of
pyrethroids 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. Zinc oxide actually worsens the reaction. /Pyrethroids/
Eye contamination. Some pyrethroid compounds can be very corrosive to the eyes.
Extraordinary measures should be taken to avoid eye contamination. the eye should be
treated immediately by prolonged flushing of the eye with copious amounts of clean water
or saline. If irritation persists, obtain professional ophthalmologic care. /Pyrethroids/
Other treatments. Several drugs are effective in relieving the pyrethroid neurotoxic
manifestations observed in deliberately poisoned laboratory animals, but none has been
tested in human poisonings. Therefore, neither efficacy nor safety under these
circumstances is known. Furthermore, moderate neurotoxic symptoms and signs are likely to
resolve spontaneously if they do occur. /Pyrethroids/
Animal Toxicity Studies:
Evidence for Carcinogenicity:
Evaluation: No data were available from studies in humans. There is inadequate evidence
for the carcinogenicity of deltamethrin in
experimental animals. Overall evaluation: Deltamethrin
is not classifiable as to its carcinogenicity to humans (Group 3).
Non-Human Toxicity Excerpts:
The type II pyrethroids /including deltamethrin/
produce a complex poisoning syndrome & 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 & exaggerated jaw opening similar to that
seen in response to an irritant placed on the tongue, salivation which may be profuse,
incr extensor tone in the hind limbs causing a rolling gait, incoordination progressing to
a very coarse tremor, choreoform movements of the limbs & tail often precipitated by
sensory stimuli, generalized choreoathetosis (writhing spasms), tonic seizures, apnea,
& death. At lower doses more subtle repetitive behavior is seen. In dogs, similar
symptoms are seen but salivation & upper airway hypersecretion and gastrointestineal
symptoms are more prominent.
Pyrethroids are potent synthetic insecticides which have been increasingly employed in
recent years. Such compounds have been shown to bind covalently to hepatic proteins.
Covalent binding is often associated with toxic effects. Possible cytotoxic, cytogenotoxic
and allergenic effects could be due to covalent binding of these compounds and/or their
metabolites to endogenous macromolecules. In the present paper we examined possible
cytotoxic effects of certain pyrethroids on human lyphocytes and L 1210 lymphoblastoid
mouse cells, cytogenotoxic effects with micronuclei test and allergenic effects with
Magnusson and mast cell degranulation tests. Under our experimental conditions, the tested
compounds showed neither acute cytotoxic nor cytogenotoxic effects, though, cismethrin
presented slight antimitotic effects statistically different to those with the control.
Slight allergenic character of cismethrin, bioresmethrin and deltamethrin
was revealed by Magnusson and mast cell degranulation tests.
Non-phytotoxic
Deltamethrin dissolved in maize oil was
administered in the diet to 64 beagle dogs (8 of each sex per group) at levels of 0, 1,
10, and 40 mg/kg for 24 months. This corresponds to 0, 0.025, 0.25, and 1 mg/kg body
weight, respectively. Individual body weights and food consumption values were determined
weekly. Ophthalmoscopic, hematological, biochemical, and urinalysis examinations were
conducted during the pretest period at 6, 12, 18, and 24 months of the study. Neurological
examinations were conducted at approximately 1 year and before termination. No signs of
overt toxicity were observed in any of the dogs. Body weight and food consumption values
were similar for control and treated dogs. No compound-related effects were observed
during the ophthalmoscopic and physical examinations. Although there were some random
statistically significant differences between the control and other dose groups in the
hematological and biochemical tests, physiologically significant changes were not observed
at any interval in the study. Two treated and two control animals died during the study.
No compound-related gross or microscopic changes were observed in the surviving dogs that
were sacrificed and necropsied. Inflammatory, degenerative, and proliferative changes
described were spontaneous in nature, or related to the estrous phase of the menstrual
cycle, and unrelated to compound administration. On the basis of this study, it has been
concluded that the no-observed-effect level is 40 mg/kg diet (equivalent to 1 mg/kg body
weight per day).
DNA repair tests in Escherichia coli were conducted at dose levels of 1250, 2500, or
5000 ug deltamethrin/ml. Deltamethrin
was dissolved in dimethyl sulfoxide (DMSO) and 0.1 ml of the solution was spread on a
plate. Growth inhibition was compared between DNA repair deficient mutants (p3478 and
CM611) and wild types (W3110 and WP2). Partial precipitation of deltamethrin
from the soluton occurred when it came into contact with the aqueous bacterial growth
medium. Deltamethrin did not have any damaging
effects on DNA.
Deltamethrin was examined for its mutagenic
potential in the Ames test with 5 strains of Salmonella typhimurium (TA 1535, TA 1537, TA
1538, TA98, and TA100) and doses of 2, 10, 50, 200, 500, 1000, or 5000 ug/plate, with and
without S-9 mix (metabolic enzyme system). It was dissolved in DMSO and precipitated out
of solution at concentrations of 200 ug/plate or more. Deltamethrin
did not have any effect on the mutation rate in any of the strains at any of the
concentrations tested. ... A similar Ames test was carried out at 0.2, 2, 20, 200, or 500
ug deltamethrin/plate with microsome enzymes.
The compounds did not influence the number of revertants of the 5 strains (same as above)
of Salmonella typhimurium. Again, deltamethrin
was dissolved in DMSO and precipated out of solution at 200 ug/plate or more.
Deltamethrin was found not to be mutagenic in
V79 Chinese hamster cells, in the presence or absence of hepatocytes.
An in vivo cytogenetic test was conducted on mice (3 males and 3 females per group).
Mice were treated orally with deltamethrin in
sesame oil for 2 consecutive days at 5 or 10 mg/kg body weight. The incidence of
chromosomal aberrations in bone marrow cells or micronuclei in the polychromatic
erythrocytes of treated groups was, however, comparable to that of the control groups. No
positive controls were tested.
Deltamethrin was applied orally, once, at 15
mg/kg body weight to Swiss mice. A time-related effect on the chromosomes in bone marrow
cells was observed by killing 2 animals every 3 hr during 24 hr. The report stated that
incidences of chromatid aberrations were low and that there were no consistent
time-related trends in the distribution of the aberrations. However, the time-related
trend of aberrations was not reported. Again, no positive controls were tested.
In a micronucleus test, a single dose of deltamethrin
in corn oil was administered orally at 16 mg/kg body weight to Swiss CD-1 mice (5 of each
sex per group). No mutagenic activity was observed with deltamethrin,
whereas the positive controls, triethylenemelamine and dimethylbenzanthracene, both induce
positive responses.
A dominant-lethal assay with deltamethrin was
performed. Groups of 9-13 male mice were dosed orally at 3 mg/kg body weight in sesame oil
for 7 days or at a single dose of 6 or 15 mg/kg body weight in sesame oil, and mated with
6-18 non-treated females. There were no effects on the rates of pre- and post-
implantation losses, while the positive control, triethylene triphosphoramide (10 mg/kg
body weight), reduced pregnancies in the second and third weeks after treatment and
increased embryonic losses.
Deltamethrin in olive oil was administered
orally to female Swiss mice at single or repeated (5 times at daily intervals) doses of
1.36, 3.4, or 6.8 mg/kg per day. Bone marrow smears were prepared 6, 24, or 48 hr after
treatment. No mutagenic activity was observed with deltamethrin,
whereas the positive control, cyclophosphamide, induced a positive response.
Deltamethrin was dissolved in corn oil and
administered by gastric intubation at doses of 0, 3.0, 6.0, or 12.0 mg/kg body weight on
days 7-16 of gestation to groups of CD-1 mice. Mice were sacrificed on day 18 of
gestation. There was a dose-related (P <0.001) reduction in maternal weight gain during
pregnancy and high-dose females gained 58% less weight than the controls. There was no
dose-related mortality but dams in the high- and mid-dose groups became convulsive after
dosing. Treatment did not affect the number of implantation sites, fetal mortality, fetal
weights, or the number of sternal and caudal ossification centers. A significant (p
<0.01) dose-related increase in the occurrence of supernumerary ribs was observed. No
other dose-related skeletal or visceral anomalies were observed.
Pregnant female Swiss CD-1 SPF mice (24 per group) were given deltamethrin
dissolved in sesame oil by oral intubation at dose-levels of 0, 0.1, 1, or 10 mg/kg body
weight per day on days 6-17 of pregnancy. The animals were necropsied on day 18 of
pregnancy. The numbers of implantation sites fetal losses, and viable fetuses were not
affected by treatment. There was a dose-related decrease in mean fetal weight. Apart from
delayed ossification at all dose levels, skeletal examination revealed no abnormalities. A
teratogenic effect was not observed.
In a complementary teratology study, pregnant female Swiss CD-1 mice were given deltamethrin dissolved in sesame oil by oral
intubation at 0, 0.1, 1, or 10 mg/kg body weight per day from day 6 to day 17 of
gestation. Females were either sacrificed on day 18 of gestation or allowed to litter for
subsequent examination of pups on days 1 or 21 of lactation. The compound caused a
moderate and transient retardation of development of the fetus at the 1 and 10 mg/kg body
weight dose rate, but these effects were not observed on days 1 or 21 post-partum. There
were no teratogenic effects related to treatment.
Pregnant female Sprague-Dawley rats (24 per group) received 0, 0.1, 1, or 10 mg deltamethrin/kg body weight per day oral intubation on
days 6-18 of pregnancy. Apart from 12 females in the control and 10 mg/kg groups, which
were allowed to deliver, the dams were sacrificed and examined on day 21. There were no
effects on reproduction or on the teratogenic parameters examined, except for slightly
delayed ossification at the highest dose level.
Deltamethrin was dissolved in corn oil and
administered by gastric intubation at doses of 0, 1.25, 2.5, or 5.0 mg/kg body weight on
days 7-20 of gestation. Rats were sacrificed on day 21 of gestation. There was a dose
related reduction (P <0.01) in maternal weight gain during pregnancy, and dams in the
highdose group gained only 80% of the control value. Treatment did not affect the number
of implantation sites, fetal mortality, fetal weight, or the number of sternal and caudal
ossification centers.
Groups of 15 pregnant New Zealand White rabbits received deltamethrin
dissolved in sesame oil at levels of 0, 1, 4, or 16 mg/kg body weight per day during days
6-19 of pregnancy. Examination was carried out on day 28 of gestation. The mean fetal loss
was not dose-related. The mean fetal weight in the highest-dose group was decreased. Some
malformations (hydrocephaly, exencephaly, and thoracogastroschisis) were observed in 2
fetuses of animals at the highest dose level. In a supplementary study, pregnant rabbits
were similarly dosed with 16 mg/kg body weight per day; one fetus with spina bifida and
shortened tail was detected among 69 apparently normal fetuses. Malformations were within
the normal limits of the strain used and were not considered to be related to the
treatment, despite the occurrence at the highest dose level only.
Adult hens (10per group) were gavaged with a single dose of 0, 500, 1250, or 5000 mg deltamethrin/kg body weight suspended in corn oil or 0
or 100 mg/kg body weight dissolved in sesame oil. During 21 days, observations were made
on mortality, health, neurotoxic signs, and body weight. Deltamethrin
did not induce any clinical, macroscopic, or histological signs of delayed neurotoxicity.
Groups of 5 male and l5 female Wistar rats were administered 25 mg deltamethrin/kg
body weight in 10 mg corn oil/kg body weight. A tilting plane test was performed every
second day from day 4 to day 16 of the study. Two male rats died at 25 mg/kg. No effect
was found on the slip-angle.
The effects of deltamethrin were studied in a
rat performance test that arranged for milk delivery after every fortieth lever press. Deltamethrin (1-8 mg/kg body weight, given orally, 2
hr before the test) produced both dose-related increases in pause duration and decreases
in response rate. Deltamethrin was also studied
using a conditional flavor-aversion test. Deltamethrin
treated, trained rats displayed an aversion to saccharin that was greatest at 2 mg/kg.
To better characterize the behavioral toxicity of pyrethroid insecticides, comparisons
were made of the effects of cismethrin and deltamethrin
exposure and motor activity and the acoustic startle response in Long-Evans rats. Acute
dose-effect acute time-course, and 30-day repeated-exposure determinations of 1-hr motor
activity were made using figure-eight mazes. The acoustic startle response was measured to
a 13-kHz, 120-dB(A), 40-millisecond tone at each of 3 background white noise levels (50,
65, and 80 dB). Deltamethrin (0,2,4,6, or 8
mg/kg body weight) or cismethrin (0,6,12,18, or 24 mg/kg) were administered orally in 0.2
ml/kg corn oil. Cismethrin and deltamethrin
produced similar dose-dependent decreases in motor activity. The time course of onset and
recovery for this decreased activity was rapid (1-4 hr). No cumulative effects on motor
activity of 30-day exposure to 2 mg deltamethrin/kg
per day or 6 mg cismethrin/kg per day were found. The effects of cismethrin and deltamethrin on the acoustic startle response were
dissimilar: deltamethrin produced a
dose-dependent decrease in amplitude and an increase in latency, and cismethrin produced
an increase in amplitude and no change in latency. The differential effects of cismethrin
(Type I pyrethroids) and deltamethrin (Type II
pyrethroids) on the acoustic startle response may be related to the contrasting effects
previously shown with neurophysiological and/or neurochemical techniques.
The neurological effects of the 4 synthetic pyrethroids, resmethrin, permethrin,
cypermethrin, and deltamethrin, have been
investigated in the rat to establish whether there is a correlation between the
clinical-functional status of the animal and peripheral nerve damage, as measured
biochemically. Neuromuscular dysfunction was assessed by means of inclined plane test and
peripheral nerve damage by reference to beta-glucuronidase and beta-galactosidase activity
increases in nerve tissue homogenates from treated and control animals. A transient
functional impairment was found in animals treated with any one of the 4 pyrethroids
tested and in all cases this was greatest at the end of the 7 day dosing regimen (deltamethrin doses of 5-20 mg/kg per day in arachis
oil). Significant increases in beta-glucuronidase and beta-galactosidase activities were
found 3-4 weeks after the start of dosing, in the distal portion of the sciatic/posterior
tibial nerves from permethrin-, cypermethin-, and deltamethrin-treated
animals, but no changes were found in resmethrin-treated animals. It is concluded
therefore that there is no direct correlation between the time-course of the neuromuscular
dysfunction and the neurobiochemical changes. This suggests that these pyrethroids have at
least two distinct actions-a short-term pharmacological effect at near-lethal dose levels
and a more long-term neurotoxic effect that results in sparse axonal nerve damage.
When rats were dosed orally with a single dose of 1/2 LD50 or 3 daily doses of 1/5 LD50
deltamethrin, the activities of transferrin and
ceruloplasmin in plasma, 20 hr after dosing, were unchanged. After the single dose,
microsomal mono-oxygenase activity was increased by 87%, and after the 3 doses, it was
increased by 290%.
Non-irritating to skin, mild eye irritant (rabbits).
In 2-year feeding trials, no effect level for rats was 2.1 mg/kg diet, for mice 12
mg/kg diet, and for dogs 1 mg/kg bw. Non-mutagenic and non-teratogenic (mice, rats,
rabbits).
Rats & dogs given oral doses of 10 mg/kg/day for 13 wk showed some motor symptoms
but no fatalities & showed no pathological changes. The dogs showed diarrhea,
vomiting, & depression of the gag & patellar reflexes & hind limb placing
reaction in addition to the typical type II motor symptoms.
Rats given 15 daily oral doses of 10mg/kg (LD50) showed severe motor symptoms, but a
full neuropathological exam of the CNS showed no pathological changes.
Deltametrin has no teratogenic or mutagenic activity.
Signs of acute intoxication in rats and mice included salivation, ataxia and
choreoathetotic movements.
Deltamethrin has been tested for
carcinogenicity in one study in C57Bl/6 mice and BD-VI rats that were given up to 8 mg/kg
orally, respectively. Deltamethrin was not
carcinogenic to mice. Deltamethrin caused
unspecified thyroid adenomas in male rats given 3 mg/kg and female rats given 6 mg/kg. ...
Deltamethrin demonstrated high acute toxicity in
laboratory animals, median lethal doses of 30 to 50 mg/kg being measured. Deltamethrin has demonstrated clastogenicity in in
vivo mouse bone marrow and sperm assays. Deltamethrin
was not mutagenic in bacterial assays, but induced chromosome aberrations in plant cells.
For teratogenicity, decamethrin (1.0, 2.5 and
5.0 mg/kg) was given orally to female albino rats daily from day 6 through 15 of
gestation. The compound produced a dose-related mortality of the dam. At the highest dose
level (5.0 mg/kg), maternal weight gain and gravid uterine fetal weights were
significantly reduced. The number of implants resorption frequency, number of live fetuses
and sex ratio were unaffected at any of the dose levels used in the study. A few
incidences in minor malformation(s) like focal subcutaneous haemorrhages and retarded
growth were observed in both the treated and control groups. The only skeletal variation
was bilateral wavy ribs in one of the fetuses of dams. There were quite low incidences of
microphthalmia and hypoplastic kidney but these variations were not significant. The study
reveals that decamethrin did not produce any
serious fetotoxicity or teratogenicity in rats.
The effect of the synthetic pyrethroid insecticide deltamethrin
was investigated in mice in vivo for the induction of bone marrow chromosome aberrations
and micronuclei in bone marrow and for sperm abnormalities. Technical deltamethrin
(10, 15 and 20 mg/kg) was injected ip and the respective cells were fixed after 24 hr, 30
hr and 35 days for the observation of chromosome aberrations micronuclei and sperm
abnormalities respectively. Additionally, route-response (ip, oral and sc), time-response
(6, 24 and 48 hr) and acute-chronic (24 versus 120 hr) studies were conducted for the
induction of chromosome aberrations by the highest dose (20 mg/kg) of deltamethrin.
All the above test results showe significant increases over respective controls. Moreover,
a linear relationship was evident between the dose of deltamethrin
used and the frequencies (%) of chromosome aberrations, micronuclei or sperm
abnormalities.
The pesticide deltamethrin, a synthetic
pyrethroid, was studied for carcinogenicity in long-term experiments in mice and rats.
Mice were given deltamethrin by gavage in
arachis oil at 0, 1, 4 or 8 mg/kg body wt for 2 yr. A group of untreated controls was also
available. Rats received 0, 3 or 6 mg/kg body wt deltamethrin
in arachis oil for 2 yr. In mice, an increased incidence of lymphomas was observed in the
groups receiving 1 and 4 mg/kg body wt, but not in the group treated with 8 mg/kg body wt Deltamethrin. In rats, an increased incidence of
thyroid tumours was noted, but, no clear dose-response relationship was shown. Deltamethrin does not appear to be carcinogenic in
mice or rats, but further studies are needed on the group of compounds to which this
substance belongs.
The possibility that deltamethrin induced
tumors when given orally to inbred C57BL/6 mice and BDVI rats was investigated. Dosages
were as follows: 30 male and 30 female mice received 1.0 or 4.0 mg/kg body weight deltamethrin; 50 animals of each sex received 8.0
mg/kg deltamethrin; and 50 male and 50 female
rats received 0 3.0, or 6.0 mg/kg dose levels of deltamethrin.
All animals were treated 5 days per week for 104 wk. The experiments were terminated when
the animals were 120 wk of age. An increased incidence of lymphomas was noted in the
groups of mice receiving 1 and 4 mg/kg doses but not in the group treated with 8 mg/kg. An
increased incidence of thyroid tumors was noted in rats, with a significant increase
observed in the incidence of thyroid adenomas in males and females receiving the 3 and 6
mg/kg deltamethrin doses, respectively. However
no dose response relationship or treatment related increase in tumor incidence related to deltamethrin exposure could be indicated. It was
concluded that deltamethrin does not appear to
be carcinogenic in either mice or rats, however, further investigations are needed on the
group of compounds to which deltamethrin
belongs.
The release of (3)H neurotransmitters was used as a functional assay to assess the
actions of selected neurotoxins on the synaptosomal membranes prepared from the
invertebrate nervous systems of squid and house fly. A reproducible release of (3)H
neurotransmitter was evoked by pulsed-depolarization in the presence of elevated K+ or of
veratridine. Pretreatment with deltamethrin
resulted in a substantial enhancement of (3)H neurotransmitter release during
pulsed-depolarization. This enhanced neurotransmitter release was greatly reduced or
absent when synaptosomes of knockdown resistant house flies were examined. No enhanced
neurotransmitter release due to deltamethrin
pretreatment was apparent from any synaptosomal preparation under non-depolarizing
conditions. Under similar conditions, collaborative experiments demonstrated that deltamethrin causes a significant change in protein
phosphorylation activities which follow depolarization. The most significant change caused
by deltamethrin was the prolonged elevation of
the level of phosphorylation on a number of key synaptic proteins beyond the normal time
of their recovery to the dephosphorylated state. The most notable protein reacting to deltamethrin in this manner was calcium-calmodulin
dependent protein kinase.
The inhibitory action of synthetic pyrethroids and some chlorinated hydrocarbon
insecticides on the neural calcium-calmodulin dependent protein phosphatase, calcineurin,
was studied using one radiotracer and two colorimetric methods. It was found that all
insecticidal Type II pyrethroids (cypermethrin, deltamethrin
and fenvalerate) are potent inhibitors of isolated calcineurin from bovine brain. Their
IC50 values were approximately 1 X 10-9 to 1 X 10-11 M. By contrast, neither
noninsecticidal chiral isomers of these pyrethroids, neuroactive Type I pyrethroids nor
neuroactive chlorinated hydrocarbon insecticides showed comparable potencies against this
enzyme. To confirm the action of Type II pyrethroid in situ, isolated intact rat brain
synaptosomes were incubated with (32)P phosphoric acid and subsequently depolarized in the
presence and absence of 0.1 uM deltamethrin. As
expected, there was a sharp rise in protein phosphorylation due to the action of
calcineurin. deltamethrin caused a distinct
delay in the dephosphorylation process. The results clearly indicate that calcineurin is
specifically inhibited by Type II pyrethroids.
Effects of deltamethrin, a powerful synthetic
pyrethroid, on the protein phosphorylation activity in the intact rat brain synaptosome
during the time course of depolarization induced changes were studied. For this purpose,
depolarization was induced either by veratridine or high concentration of K+. The level of
phosphorylation on various synaptic proteins was found to quickly rise for 15 to 30 sec
and return to the resting level in about 3 min. Deltamethrin,
when given to the synaptosomes 10 min prior to depolarization, caused stimulation on this
depolarization-induced protein phosphorylation activity at > 1012 M concentration. To
find the cause for such an action of deltamethrin,
the effects of ion-channel blockers and calmodulin inhibitors on the same phosphorylation
process were studied. The inhibitory effect of a Ca2+ -channel blocker, verapamil, and a
Na+-channel blocker, tetrodotoxin, on the stimulatory action of deltamethrin
was first established. However, in neither case were their actions complete. The former
reduced the stimulatory effects of deltamethrin
on synapsin I but not on calcium and calmodulin dependent protein kinase II (CaM-Kinase
II), B50, or 38-kDa proteins. The latter could not inhibit the stimulatory action of deltamethrin on synapsin I. Even when both blocking
agents were present, the stimulatory action of deltamethrin
was apparent. The stimulatory effect of deltamethrin
on the phosphorylation rate of phosphoproteins, synapsin I, calcium-calmodulin dependent
protein kinase II and B50 was less when the entire external calcium chloride was replaced
by barium chloride in the prelabeling medium. Again, even under these conditions, the
stimulatory effect of deltamethrin was evident
on all proteins examined. In addition, the effect of calmodulin-inhibition
trifluoroperazine was tested in the same manner. This inhibitor was found to reduce the
phosphorylation on all of the tested synaptosome-proteins except protein 38 kDa, where
there was an increase in phosphorylation in the presence of deltamethrin,
especially, at 30, 60, and 180 sec of depolarization. These results indicate that (a) deltamethrin's action is not limited to calmodulin or
the sodium or the calcium channel, (b) it must stimulate the release of Ca2+ from the
intracellular storage site(s), and (c) such a stimulatory action of deltamethrin
may be recognized only when the synaptosomes are depolarized regardless of the method of
depolarization.
Two pyrethroids, bioallethrin and deltamethrin,
affect muscarinic cholinergic receptors in the neonatal mouse brain when given to suckling
mice during the period of rapid brain growth. Such early exposure to these pyrethroids can
also lead to permanent changes in the muscarinic cholinergic receptors and behavior in the
mice as adults. In the present study, male NMRI mice were given bioallethrin (0.7 mg), deltamethrin (0.7 mg), or a 20% fat emulsion vehicle
(10 ml) per kg of body wt per os once daily between the 10th and 16th postnatal day. The
mice were subjected to behavioral tests upon reaching the age of 17 days and at 4 mo.
Within 1-2 wk after the behavioral tests the mice were killed by decapitation and crude
synaptosomal fractions (P2) were prepared from the cerebral cortex, hippocampus, and
striatum. The densities of muscarinic cholinergic receptors were assayed by measuring the
amounts of quinuclidinyl benzilate specifically bound in the P2 fraction. The proportions
of high affinity and low affinity binding sites of muscarinic cholinergic receptors were
assayed in a displacement study using quinuclidinyl benzilate/carbachol. The behavioral
tests at an adult age of 4 mo indicated a significant increase in spontaneous motor
behavior in both bioallethrin and deltamethrin
treated mice. There was also a significant decrease and a tendency toward a decrease in
the density of muscarinic cholinergic receptorsin the cerebral cortex in mice receiving
bioallethrin and deltamethrin, respectively. The
proportions of high affinity and LA-binding sites of muscarinic cholinergic receptors were
not changed. This study further supports that disturbances of the cholinergic system
during rapid development in the neonatal mouse can lead to permanent changes in
cholinergic and behavioral variables in the animals as adults.
Effects of deltamethrin, a powerful
pyrethroid insecticide, on the protein phosphorylation and dephosphorylation processes
during depolarization in rat brain synaptosomes were studied by using (32)P phosphoric
acid as a starting radio-tracer and high external concentration of potassium ions or
veratridine (1 X 10-5 M) as depolarizing agents. At the onset of depolarization there was
a quick rise in phosphorylation in various synaptic proteins for about 15-30 s followed by
a gradual decline in levels of phosphorylation. The effect of deltamethrin
(1 X 10-7 M) on this system was found to be dependent on the length of preincubation of
the synaptosome with the pesticide prior to depolarization. At an early stage (0-3 min
preincubation period) it caused a modest suppression of protein phosphorylation
activities. When the period of deltamethrin
preincubation was extended to 5-20 min, however, it caused a significant increase in
protein phosphorylation throughout the depolarization period. At the alter stage of the
action of deltamethrin (eg preincubation period
of 30-40 min), deltamethrin treated synaptosomes
no longer responded to the depolarization signal to raise the level of phosphorylation on
many proteins. These results indicate that deltamethrin's
actions on the synaptic process are complex. Depending on the length of exposure, its
effects on protein phosphorylation responses in intact synaptosomes could be either
stimulatory or inhibitory. To study the cause of deltamethrin
induced synaptic block at the later stage, effects of deltamethrin
on protein kinases were studied by using lysed synaptic membranes with (gamma-(32)P)ATP. Deltamethrin was shown to inhibit
calcium-calmodulin-dependent protein phosphorylation activities at ... when given directly
to the enzyme source 10 min prior to the addition of (32)P ATP. Such an observation helps
to explain the inhibitory action of deltamethrin
on protein phosphorylation which occurs at the late stage of its action (eg preincubation
time > 20 min).
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/
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 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 and stomach action. Fast-acting.
Deltamethrin was dissolved in corn oil and
administered by gastric intubation at doses of 0, 2.5 mg/kg body weight to Sprague-Dawley
rats from day 7 of gestation to day 15 of lactation. The dams were allowed to litter and
rear their young: litters were reduced at birth to 4 males and 4 females per litter. The
pups were weighed weekly and examined for the development of eye-opening, startle reflex,
and air-righting. The litters were weaned on day 22 post-partum and the males discarded.
Weekly weighing of the females continued and at 6 weeks of age they were tested in a
circular open-field. There were no effects on parturition, litter size, or pup viability.
Weights at birth were similar for all groups, but a dose-related depression in growth was
observed during the pre-weaning period. This early diminution in pre-weaning weight
appeared to have little effect on the morphological and behavioral parameters measured.
Groups of 10 male and 20 female Charles River rats were fed deltamethrin
in the diet at 0, 2, 20, or 50 mg/kg and mated to begin a 3-generation, 2-litter (first
generation, 3 litter) standard reproduction study. Parental body weights and food
consumption were recorded during the study. After weaning of the second litter, the
surviving parent rats were sacrificed and necropsied. Five male and 5 female pups of the
F3b generation were necropsied. No changes relevant to treatment were observed in general
behavior or survival of parent rats or pups. The body weight of F0 males of the 50 mg/kg
group was decreased from week 11 onwards. There were some slight decreases in mean food
consumption of F1 male parent rats in the 50 mg/kg group. The basic reproduction indices
(fertility, gestation, lactation, viability, and litter size) were not affected by the
treatment. However, the mean pup weight in some litters, especially in the 50 mg/kg group,
was slightly decreased in comparison to the controls on day 21 lactation. Gross external
examination did not reveal any abnormalities. No gross or microscopic lesions of
treatment-related significance or significant effects on the organ weights of the F3b
generation were observed.
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, in contrast to rats, which
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/
Tissue culture experiments have shown that the dorsal root ganglion is more sensitive
to deltamethrin than the spinal cord or
peripheral nerve fibres. The morphologial alterations observed in the neuronal bodies of
the ganglia may reflect some perturbation of the ionic equilibrium (Na+ and Ca+).
Pyrethroid-induced motor symptoms, i.e., deltamethrin-induced
writhing and cismethrin-induced tremor, were studied, using a number of pharmacological
agents, in intact conscious rats and spinal rats. The results suggest that
pyrethroid-induced motor-symptoms, i.e., writhing and tremor, are mediated via a spinal
site of action, probably involving interneurons. Deltamethrin-induced
"non-motor" symptoms, i.e., increase in brain blood flow and blood glucose may
result from a supraspinal component of deltamethrin
activity. In contrast, the cardiovascular effects of deltamethrin
are mediated via a peripheral site of action.
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/
The low toxicity of pyrethroids in mammals is due largely to their rapid
biotransformation by ester hydrolysis and/or hydroxylation. /Pyrethroids/
Non-Human Toxicity Values:
LD50 Rat male oral 128 mg/kg (in vegetable oil)
LD50 Dog (male & female), oral, in capsules >300 mg/kg /Technical grade/
LD50 Dog (male & female), oral, in PEG 200 2 mg/kg /Techanical grade/
LD50 Rabbit, dermal, in PEG 400 >2000 mg/kg /Technical grade/
LD50 Rat (male), oral, in sesame oil 128 mg/kg /Technical grade/
LD50 Rat (female), oral, in sesame oil 139 mg/kg /Technical grade/
LD50 Rat (male), oral, in PEG 200 67 mg/kg /Technical grade/
LD50 Rat (female), oral, in PEG 200 86 mg/kg /Technical grade/
LD50 Rat (male adult), oral, in peanut oil 52 mg/kg /Technical grade/
LD50 Rat (female adult), oral, in peanut oil 31 mg/kg /Technical grade/
LD50 Rat (female weanling), oral, in peanut oil 50 mg/kg /Technical grade/
LD50 Rat dermal, 700 mg/kg /Technical grade/
LD50 Rat (male & female), dermal, in methylcellulose (1%) > 2940 mg/kg
/Technical grade/
LD50 Rat (female adult), dermal, in xylene > 800 mg/kg /Technical grade/
LC50 (male & female), inhalation, dust 600 mg/cu m/6 hr /Technical grade/
LD50 Mouse (male), oral, in sesame oil 33 mg/kg /Technical grade/
LD50 Mouse (female), oral, in sesame oil 34 mg/kg /Technical grade/
LD50 Mouse (male), oral, in PEG 200 21 mg/kg /Technical grade/
LD50 Mouse (female), oral, in PEG 200 19 mg/kg /Technical grade/
LD50 Mouse ip 33 mg/kg /Technical grade/
LD50 Rat female oral 139 mg/kg (in vegetable oil)
LD50 Rat oral > 5000 mg (of 5 g/l UL)/kg
LD50 Rabbit percutaneous > 2000 mg/kg
LC50 Rat inhalation 785 mg/cu m/2 hr
LD50 Rat iv 2526 mg/kg
LD50 Mouse intracerebral 26,100 ug/kg
LD50 Dog iv 3440 ug/kg
Ecotoxicity Values:
LC50 Alburnus alburnus (Bleak) (static condition) 0.69 ug/l/96 hr /Technical product/
LC50 Brachydanio rerio (Zebra fish) (flow system, static condition) 2.0 ug/l/96 hr
/Technical product/
Cyrpinus carpio (Common carp) (flow system, static condition) 1.84 ug/l /96 hr 0.86
ug/l/96 hr /Technical product/
lctalurus nebulosus (Brown bullhead) (flow system, static conditions) ug/l/96 hr
/Technical product/
LC50 Lctalurus punctatus (Channel catfish) (flow system, static condition) 0.63 ug/l/96
hr /Technical product/
LC50 Lepomis gibbosus (Pumpkinseed sunfish) (flow system, static condition) 0.58
ug/l/96 hr
LC50 Lepmois machrochirus (Bluegill sunfish) (flow system, static condition) 1.2
ug/l/96 hr
LC50 Rhodeus sericeus amarus (static condition) 1.12 ug/l/96 hr
LC50 Salmo gairdneri (Rainbow trout) (flow system, static conditions) 0.39 ug/l/96 hr
LC50 Salmo salar 1.97 ug/l/96 hr
LC50 Sarotherodon mossambicuse (flow system, static conditions) 3.5 ug/l/96 hr
LD50 Mallard duck oral >4640 mg/kg
LC50 Quail dietary >5620 mg/kg diet/8 day
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
Deltamethrin (1 ug) was incubated at 37 deg C
for 30 min with each of the following mouse microsome preparations; a) tetraethyl
pyrophosphate (TEPP)-treated microsomes (no esterase and oxidase activity); b) normal
microsomes (esterase acivity); c) TEPP-treated microsomes plus NADPH (oxidase activity);
and d)normal microsomes plus NADPH (esterase plus oxidase activity). Deltamethrin
was more rapidly metabolized under the oxidase system than under the esterase system. The
major site of ring hydroxylation was 4'-position and the secondary site was the
5-position. The trans methyl group was an important site of hydroxylation of the esters
and cis methyl oxidation was evident in the metabolites of the cleaved acid moiety. The
preferred sites of hydroxylation were as follows; trans of dimethyl group, 4'-position in
the phenol group, and cis of the dimethyl group was equal to the 5-position in the phenoxy
group. Cleavage of deltamethrin to cyanohydrin
may result from both esterase and oxidase enzyme activities, since larger amounts of the
cleaved products were evident in the oxidase system. ... However, at a much higher
(approximately 35-fold) concentration of deltamethrin
than that in the above study, it was not detectably hydrolysed. ... Deltamethrin
was hydrolysed by esterases in the blood, brain, kidney, and stomach of mice yielding
PBald and PBacid.
In a metabolic study, (14)C-deltamethrin was
administered orally to lactating dairy cows at the rate of 10 mg/kg body weight per day
for 3 consecutive days. It was poorly absorbed and mainly eliminated in the feces as
unchanged deltamethrin. Only 4-6% of the
administered (14)C was eliminated in the urine, and 0.42-1.62% was secreted in the milk.
The radiocarbon contents of various tissues were generally very low with the exception of
those of the liver, kidney, and fat, which were higher. Deltamethrin
degradation occured by cleavage of the ester bond, as already reported in rats and mice.
The enzymes responsible for the ester bond cleavage were located in cow liver homogenate,
mainly in the microsomal fraction, as seen in an in vitro study. Metabolites resulting
from ester bond cleavage further metabolized and/or conjugated, resulting in a large
number of compounds excreted in the urine. In the milk, the major identifiable
radiolabelled compound was deltamethrin.
The major metabolic pathways of deltamethrin
in mice were similar to those in rats, though there were some differences. These included
the presence of more unchanged deltamethrin in
mouse feces than in rat feces. In mouse feces, there were 4 monohydroxy ester metabolites
(2'-OH-, 4'-OH-, 5-OH-, and trans-OH-deltamethrin
and one dihydroxy metabolite (4'-OH-trans-OH- deltamethrin)
that were not found in mouse urine. Major metabolites from the acid moiety in mice were
Br2CA, trans-OH-Br2CA, and their glucuronide and sulfate conjugates. Among them,
trans-OH-Br2CA-sulfate was detected only in mice, but not in rats. Compared with rats,
much larger amounts of trans-OH-Br2CA and its conjugates were formed in mice. A major
metabolite of the alcohol moiety in mice was the taurine conjugate of PBacid in the urine,
which was not detected in rats. Generally, mice produced smaller amounts of phenolic
compounds compared with rats. Also, 3-phenoxybenzaldehyde (24) (PBald), 3-phenoxybenzyl
alcohol (PBalc), and its glucuronide, and glucuronides of 3-(4-hydroxyphenoxy)benzyl
alcohol (4'-OH-PBalc) and 5-hydroxy-3-penoxybenzoic acid (5-OH-PBacid) were found in mice,
but not in rats. When mice were given an ip dose of (14) C-deltamethrin
with or without piperonyl butoxide (PBO) and/or S,S,S-tributylphosphorotrithioate (DEF),
the same metabolites were obtained as with oral administration. However, DEF decreased the
hydrolytic products relative to the controls, while PBO decreased the oxidation products.
Sulfate of 4'-OH-PBacid accounted for about 50% of the dose, together with small
amounts of free (4%) and glucuronide forms (2%). The CN group was converted mainly to
thiocyanate and, in small amounts, to ITCA. The trans-isomer of deltamethrin
was also rapidly metabolized and yielded almost the same metabolties as deltamethrin,
though 5-OH-derivative was found in the cis-isomer, but not in the trans-isomer.
When a single oral dose of (14)C-(acid-, alcohol-, or cyano-labelled) deltamethrin
was administered to male mice at 1.7-4.4 mg/kg, the acid moiety and the aromatic portion
of the alcohol moiety were rapidly and almost completely excreted, whereaa the CN group
was excreted relatively slowly.
After oral administration to male rats at 0.64-1.60 mg/kg the major metabolic reactions
of deltamethrin /observed/ were oxidation (at
the trans methyl relative to carbonyl group of the acid moiety and the 2'-4'-, and
5-position of the alcohol moiety), cleavage of the ester linkage, and conversion of the
cyano portion to thio-cyanate and 2-iminothiazolidine-4-carboxylic acid (ITCA). These
carboxylic acid and phenol derivatives were conjugated with sulfuric acid, glycine, and/or
glucuronic acid. The major fecal metabolites were unchanged deltamethrin,
accounting for 13-21% of the dose, followed by 4'-OH-(10) and 5-OH-deltamethrin,
and a trace amount of 2'-OH-deltamethrin. Intact
deltamethrin and the 4'-OH-derivative appeared
not only as the administered S-epimer, but also in parts as the R-epimer, probably due to
artifactual racemization on exchange of the alpha-position hydrogen in methanol solution.
The metabolites from the acid moiety were mostly
3-(2,2-dibromovinyl)-2,2-dimethyl-cyclopropanecarboxlic acid (Br2CA) in free form (10% of
the dose), glucuronide (51%) and glycine (trace level) conjugates, and OH-Br2CA in free
form and glucuronide conjugate (<1%). The major metabolites of the aromatic portion of
the alcohol moiety were 3-phenoxybenzoic acid (PBacid) in free form (5%), and glucuronide
(13%) and glycine (4%) conjugates and its 4'-hydroxy derivative (4'-OH-PBacid).
3-Hydroxybenzoic acid (both free and conjugates) was detected in the excreta of hens
fed deltamethrin or fenvalerate. The diphenyl
ether cleavage of 3-phenoxybenzaldehyde is a major route, probably via 3-phenoxybenzoic
acid, in chickens.
The metabolic pathways for the breakdown of the pyrethroids vary little between
mammalian species but vary somewhat with structure. ... Essentially, pyrethrum &
allethrin are broken down mainly by oxidation of the isobutenyl side chain of the acid
moiety & of the unsaturated side chain of the alcohol moiety with ester hydrolysis
playing & 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 & alcohol
components, since direct injection into the mammalian CNS leads to a susceptibility
similar to that seen in insects. Some addtl 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 iv route, moderate by slower oral absorption, & 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/
In rats, following oral administration, elimination occurs within 2-4 days. The phenyl
ring is hydroxylated, the ester bond hydrolyzed, and the acid moiety is eliminated as the
glucuronide and glycine conjugated.
In a feeding study, deltamethrin was
administered twice daily to lactating dairy cows in portions of their daily feed at the
rate of 2 or 10 mg/kg diet for 28 consecutive days. ... Br2CA
(3-(2,2-dibromovinyl)-2,2-dimethylcyclopro-panecarboxylic acid) and PBacid
(3-phenoxybenzoic acid) were the only metabolites detected in the milk and tissues of
treated cows. In all cases, they were found at trace levels of < 0.0235 mg/l and <
0.034 mg/l, respectively. These two metabolites were also previously identified in rats
and mice as the major degradation productions of deltamethrin.
Absorption, Distribution & Excretion:
In rats, following oral administration, elimination occurs within 2-4 days. The phenyl
ring is hydroxylated, the ester bond hydrolyzed, and the acid moiety is eliminated as the
glucuronide and glycine conjugated.
Three young male human volunteers underwent a complete medical check-up one week prior
to the morning of the study. Each of them received a single dose of 3 mg of (14)C deltamethrin mixed in 1 g glucose and diluted first in
10 ml polyethylene glycol300 and again in 150 ml water. Total radioactivity was 1.8 + or -
0.9 mBq. Samples of blood, urine, saliva, and feces were taken at intervals over 5 days.
Clinical and biological examinations were performed every 12 hr during the trial and one
week after its termination. Radioactivity in the biological samples was measured with a
liquid scintillation spectrometer. The clinical and biological checks did not detect any
abnormal findings. There were no signs of side effects ... either during or after the
trial period. The maximum plasma radioactivity appeared between 1 and 2 hr after
administration of the product, and remained over the detection limit (0.2 KBq/l) during
the 48 hr. The apparent elimination half-life was between 10.0 and 11.5 hr. The
radioactivity of blood cells, as well as the saliva, was extremely low. Urinary excretion
was 51-50% of the initial radioactivity; 90% of this radioactivity was excreted during the
24 hr following absorption. The apparent half-life of urinary excretion was 10.0-13.5 hr,
which is consistent with the plasma data. Fecal elimination at the end of the observation
period represented 10-26% of the dose. The total fecal plus urine elimination was around
64-77% of the initial dose after 96 hr.
In a feeding study, deltamethrin was
administered twice daily to lactating dairy cows in portions of their daily feed at the
rate of 2 or 10 mg/kg diet for 28 consecutive days. The level of 2 mg/kg diet was the
residue level found in a recently treated pasture, whereas 10 mg/kg diet was five times
this level. Deltamethrin residues in the milk
were dose-dependent and appeared to reach a plateau between 7 and 9 days after the start
of treatment. At the high deltamethrin intake of
10 mg/kg diet, the deltamethrin residue in milk
was about 0.025 mg/l. Deltamethrin residues in
tissues were measured 1, 4, and 9 days after the last dose. At the 10 mg/kg diet intake,
very small amounts of deltamethrin residues were
found in the liver (<0.005 mg/kg), kidney )<0.002 mg/kg), and muscle (0.002-0.014
mg/kg). Residues in fat were about 0.04 mg/kg and 0.2 mg/kg for the 2 and 10 mg/kg intake,
respectively. Depletion of deltamethrin in milk
was very rapid (estimated half-life was about 1 day); while in fat (renal and
subcutaneous) the half-life was 7-9 days. Br2CA
(3-(2,2-dibromovinyl)-2,2-dimethylcyclopro-panecarboxylic acid) and PBacid
(3-phenoxybenzoic acid) were the only metabolites detected in the milk and tissues of
treated cows. In all cases, they were found at trace levels of < 0.0235 mg/l and <
0.034 mg/l, respectively. These two metabolites were also previously identified in rats
and mice as the major degradation products of deltamethrin.
In a metabolic study, (14)C-deltamethrin was
administered orally to lactating dairy cows at the rate of 10 mg/kg body weight per day
for 3 consecutive days. It was poorly absorbed and mainly eliminated in the feces as
unchanged deltamethrin. Only 4-6% of the
administered (14)C was eliminated in the urine, and 0.42-1.62% was secreted in the milk.
The radiocarbon contents of various tissues were generally very low with the exception of
those of the liver, kidney, and fat, which were higher. Deltamethrin
degradation occurred by cleavage of the ester bond, as already reported in rats and mice.
The enzymes responsible for the ester bond cleavage were located in cow liver homogenate,
mainly in the microsomal fraction, as seen in an in vitro study. Metabolites resulting
from ester bond cleavage further metabolized and/or conjugated, resulting in a large
number of compounds excreted in the urine. In the milk, the major identifiable
radiolabelled compound was deltamethrin.
The fate of (14)C-deltamethrin was examined
in Leghorn hens. When laying hens were administered 7.5 mg of (14)C-labelled deltamethrin/hen per day orally for 3 consecutive
days, about 83% and 90% of the administered (14)C was eliminated during the first 24 hr
and 48 hr after dosing, respectively. Tissue residues were generally very low with the
exception of those in the liver and kidney. Very low levels of residues were found in eggs
obtained within the first 24 h after dosing, but levels increased reaching a peak within
48 hr of the last dose. Residue levels were higher in the yolk (up to 0.6 mg/kg) than the
albumen (up to 0.2 mg/kg), which is probably related to the lipid content of yolks.
Metabolites were the same as those found in rats and mice.
The comparison between the excreted radioactivity of (14)C- deltamethrin
in rats treated by the percutaneous route and iv (controls) showed the only 3.6% of the
dosage applied on the skin was absorbed and excreted in 24 hr with 1.1% excreted during
the first 6 hr. Since rat skin is more permeable than human skin, the uptake of deltamethrin through the human skin should be
relatively weak.
After oral administration to male rats at 0.64-1.60 mg/kg, the acid and alcohol
moieties of deltamethrin were almost completely
eliminated from the body within 2-4 days. On the other hand, the cyano group was
eliminated more slowly, the total recovery during 8 days being 79% of the radiocarbon dose
(43% and 36% in the urine and feces, respectively). Tissue residues of deltamethrin
labelled with (14)C at the dibromovinyl carbon in the acid moiety and the benzylic carbon
in the alcohol moiety were generally very low, whereas residue levels in the fat were
somewhat higher (0.1-0.2 mg/kg). Residue levels of the radiocarbon derived from the cyano
group were relatively high, especially in the skin and stomach. Essentially, all the
radiocarbon in the stomach was thiocyanate. No noticable (14)CO2 was evolved from any of
the radioactive preparations, including the CN-labelled group, in contrast to the CN group
from fenvalerate, which yielded (14)CO2 in considerable amounts.
Lactating dairy cows were fed deltamethrin (2
or 10 mg/kg feed) for 28 consecutive days and deltamethrin
residues were then measured in milk and tissues. Deltamethrin
residues were higher relative to dose administered. The order of relative concentrations
of deltamethrin in tissues, measured 1, 4, and 9
days after the last dose was: renal fat > subcutaneous fat > forequarter muscle >
hindquarter muscle > liver > kidney. Depletion of deltamethrin
residues in milk was very rapid indicating that half-life of the insecticide of about 1
day. Trace amounts of deltamethrin metabolites
3-(2,2-dibromovinyl)-2,2-dimethylcyclopropane carboxylic acid (<0.0235 ppm) and
3-phenoxybenzoic acid (< 0.034 ppm) were also detected in milk and tissues of treated
cows.
/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/
The distribution of (14)C-acid-, (14)C-alcohol-, and (14)C-cyano-labelled deltamethrin and selected metabolites in the liver,
blood, cerebrum, cerebellum, and spinal cord /was studied/ after iv administration of a
toxic, but non-lethal, dose (1.75 mg/kg) to rats. Approximately 50% of the dose was
cleared from the blood within 0.7-0.8 min, after which the rate of clearance decreased.
3-Phenoxybenzoic acid (PBacid) was isolated from the blood in vivo, and was also the major
metabolite when (14)C-alcohol-labelled deltamethrin
was incubated with blood in vitro. Deltamethrin
levels in the liver peaked at 7-10 nmol/g at 5 min and then decreased to 1 nmol/g by 30
min. In contrast, peak central nervous system levels of deltamethrin
were achieved within 1 min (0.5 nmol/g), decreasing to 0.2 nmol/g at 15 min and remaining
stable until 60 min. Peak levels of deltamethrin
were not related to the severity of toxicity, though the levels of unextractable pentane
radiolabel did appear to be correlated with signs of motor toxicity.
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/
The cutaneous and gastrointestinal absorption of deltamethrin
in humans has been demonstrated after acute poisonings due to occupational overexposure or
ingestion of deltamethrin products. The presence
of a deltamethrin metabolite
(3-2,2-dibromovinyl)-2,2-dimethylcyclopropane carboxylic acid) has been reported in the
urine of people with acute deltamethrin
intoxication, confirming the absorption and metabolic degradation of this insecticide in
the human body.
Biological Half-Life:
Deltamethrin has a half-life in rat brain of
1-2 days, but it is rather more persistent in body fat, with a half-life of 5 days.
Mechanism of Action:
The lowest concentration of deltamethrin to
have an effect in crayfish stretch receptor neurons on sodium channels was 1X10-12 mol/l,
but the response of the preparation to gamma-aminobutyric acid (GABA) appeared to be
unaffected by concentrations of deltamethrin up
to 1X10-7 mol/l. Although 1X10-6 mol/l deltamethrin
had a slight effect on the GABA response of the dactyl abductor muscle, it appears that
the majority of the effects of cyano-pyrethroids in invertebrates could be accounted for
solely by their action on sodium channels.
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 CNS 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 partial
protection against poisoning, it is unlikely that one of these effects represents the
primary mechanism of action of the pyrethroids, & most neurotransmitter release is
secondary to incr sodium entry. /Pyrethroids/
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/
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 (3H)-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/
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 fenvalerate, 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/
... Type II pyrethroids /containing the alpha-cyano substituent/ extend the time
constant for inactivation by hundreds of milliseconds to seconds, causing a persistent
depolarization and a frequency-dependent conduction block in sensory and motor axons, and
prolonged repetitive firing of sensory end organs and muscle fibers. The depolarizing
action would have a dramatic effect on the sensory nervous system because such neurons
tend to discharge when depolarized even slightly, resulting in an increase in the number
of discharges. /Pyrethroid esters containing the alpha-cyano substituent/
Interactions:
Deltamethrin was hydrolysed in vitro by
esterases in blood, brain, kidney, liver, and stomach preparations of mice. Pretreatment
of mice with the oxidase inhibitor, pipronyl butoxide (PBO), or the esterase inhibitor,
S,S,S-tributylphosphorotrithoiate (DEF), delayed metabolism of intraperitoneally
administered deltamethrin. PBO or DEF made mice
more sensitive to deltamethrin.
Plasma esterases, in addition to hepatic esterases, play a role in the metabolism of deltamethrin in mammals and cause its rapid
detoxification by the oral route. In a potentiation study, a range of esterase inhibitors,
consisting mainly of organophosphorus insecticides, was given to male rats in oral doses
that inhibited 50% of the plasma cholinesterase. After 15 min, or 2 or 24 hr, an oral LD50
dose of deltamethrin EC formulation was given
which showed potentiation with azinphos ethyl, omethoate, and dichlorvos. It appears that
users must handle deltamethrin in these
combinations very carefully because of their high toxicity. Acephate, monocrotophos,
phosphamidon, parathion methyl, and the 2 controls did not act as potentiators.
The effect of deltamethrin pretreatment on
the pharmacokinetics and metabolism of antipyrine was studied in male rats. The total
plasma clearance of antipyrine was significantly decreased by deltamethrin
pretreatment (20 mg/kg and 40 mg/kg daily for 6 days prior to antipyrine administration),
while the elimination half-life at beta phase, the area under the concentration-time curve
and the mean residence time of antipyrine were significantly increased. The magnitude of
the observed changes was dose dependent. The urinary excretion of norantipyrine,
4-hydroxyantipyrine and 3-hydroxymethylantipyrine was decreased by 39%, 32% and 26%,
respectively (p <0.001) in the presence of deltamethrin.
In addition, the rate constants for formation of each of these metabolites were
significantly decreased by an average of approximatel 71%. These results suggest that deltamethrin is capable of inhibiting oxidative
metabolism, a finding which could be of clinical and toxicological significance.
The effect of deltamethrin pretreatment on
the pharmacokinetics and metabolism of antipyrine was studied in male rats. The total
plasma clearance of antipyrine was significantly decreased by deltamethrin
pretreatment (20 mg/kg and 40 mg/kg daily for 6 days prior to antipyrine administration),
while the elimination half-life at beta phase, the area under the concentration-time curve
and the mean residence time of antipyrine were significantly increased. The magnitude of
the observed changes was dose dependent. The urinary excretion of norantipyrine,
4-hydroxyantipyrine and 3-hydroxymethylantipyrine was decreased by 39%, 32% and 26%,
respectively (p < 0.001) in the presence of deltamethrin.
In addition, the rate constants for formation of each of these metabolites were
significantly decreased by an average of approximately 71%. These results suggest that deltamethrin is capable of inhibiting oxidative
metabolism, a finding which could be of clinical and toxicological significance.
There is a potential hazard in mixed intoxications by pyrethroids and organophosphate
insecticides, due to the fact that low toxicity of pyrethroids on mammals is chiefly due
to quick cleavage of molecule by esterases, which can be thwarted by esterase inhibitors.
We have developed a method in order to measure the duration and the intensity of
potentiation of deltamethrin by a variety of
organophosphate compounds. It was demonstrated that some of them (azinphos, dichlorvos,
dimethoate, fenitrothion, omethoate) induce an increase of toxicity of deltamethrin.
But, the total toxicity of association of Deltamethrin
with Dimethoate, Fenitrothion, is weak, and does not prohibit their use. Others
(methyl-parathion, acephate, phosphamidon, monocrotophos) have no such effects, even if
they have a very high intrinsic toxicity. Cholinesterase inhibitors of the carbamate group
are ineffective. It is suggested that the potentiation is mainly in relation with the
kinetic of esterase inhibition, which is different, and specific to each organophosphate
compound. So, it is essential that a specific toxicological measurement must be performed
with any different insecticide, in order to anticipate the danger of a mixed intoxication
by pyrethroids and organophosphates.
Dimethoate and omethoate, two common organophosphorus insecticides, induced a dose
related increase in the frequency of sister chromatid exchanges in human lymphocytes in
vitro (p of the regression lines less than 1). Two other common pesticides, the pyrethroid
insecticide deltamethrin and the systemic
fungicide benomyl, induced a modest increase in sister chromatid exchanges which bordered
on statistical significance (p = 0.053 and 0.055, respectively). Mixtures of the four
pesticides at total concentrations of 41.5 and 83 ug/ml (composed of 43% dimethoate, 43%
omethoate, 12% deltamethrin and 1.2% benomyl)
induced a dose-dependent increase in sister chromatid exchanges (p <0.01). The effects
of these mixtures of pesticides were variable using lymphocytes from different
individuals, although these differences did not attain statistical significance. Moreover,
low concentrations of the four pesticides that did not increase sister chromatid exchanges
significantly when tested alone, were positive for sister chromatid exchange induction
when tested as a mixture. The experiments show that sub-threshold doses of pesticides may
increase sister chromatid exchanges when present in a mixture.
/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:
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:
Deltamethrin was hydrolysed in vitro by
esterases in blood, brain, kidney, liver, and stomach preparations of mice. Pretreatment
of mice with the oxidase inhibitor, pipronyl butoxide (PBO), or the esterase inhibitor,
S,S,S-tributylphosphorotrithoiate (DEF), delayed metabolism of intraperitoneally
administered deltamethrin. PBO or DEF made mice
more sensitive to deltamethrin.
Plasma esterases, in addition to hepatic esterases, play a role in the metabolism of deltamethrin in mammals and cause its rapid
detoxification by the oral route. In a potentiation study, a range of esterase inhibitors,
consisting mainly of organophosphorus insecticides, was given to male rats in oral doses
that inhibited 50% of the plasma cholinesterase. After 15 min, or 2 or 24 hr, an oral LD50
dose of deltamethrin EC formulation was given
which showed potentiation with azinphos ethyl, omethoate, and dichlorvos. It appears that
users must handle deltamethrin in these
combinations very carefully because of their high toxicity. Acephate, monocrotophos,
phosphamidon, parathion methyl, and the 2 controls did not act as potentiators.
The effect of deltamethrin pretreatment on
the pharmacokinetics and metabolism of antipyrine was studied in male rats. The total
plasma clearance of antipyrine was significantly decreased by deltamethrin
pretreatment (20 mg/kg and 40 mg/kg daily for 6 days prior to antipyrine administration),
while the elimination half-life at beta phase, the area under the concentration-time curve
and the mean residence time of antipyrine were significantly increased. The magnitude of
the observed changes was dose dependent. The urinary excretion of norantipyrine,
4-hydroxyantipyrine and 3-hydroxymethylantipyrine was decreased by 39%, 32% and 26%,
respectively (p <0.001) in the presence of deltamethrin.
In addition, the rate constants for formation of each of these metabolites were
significantly decreased by an average of approximatel 71%. These results suggest that deltamethrin is capable of inhibiting oxidative
metabolism, a finding which could be of clinical and toxicological significance.
The effect of deltamethrin pretreatment on
the pharmacokinetics and metabolism of antipyrine was studied in male rats. The total
plasma clearance of antipyrine was significantly decreased by deltamethrin
pretreatment (20 mg/kg and 40 mg/kg daily for 6 days prior to antipyrine administration),
while the elimination half-life at beta phase, the area under the concentration-time curve
and the mean residence time of antipyrine were significantly increased. The magnitude of
the observed changes was dose dependent. The urinary excretion of norantipyrine,
4-hydroxyantipyrine and 3-hydroxymethylantipyrine was decreased by 39%, 32% and 26%,
respectively (p < 0.001) in the presence of deltamethrin.
In addition, the rate constants for formation of each of these metabolites were
significantly decreased by an average of approximately 71%. These results suggest that deltamethrin is capable of inhibiting oxidative
metabolism, a finding which could be of clinical and toxicological significance.
There is a potential hazard in mixed intoxications by pyrethroids and organophosphate
insecticides, due to the fact that low toxicity of pyrethroids on mammals is chiefly due
to quick cleavage of molecule by esterases, which can be thwarted by esterase inhibitors.
We have developed a method in order to measure the duration and the intensity of
potentiation of deltamethrin by a variety of
organophosphate compounds. It was demonstrated that some of them (azinphos, dichlorvos,
dimethoate, fenitrothion, omethoate) induce an increase of toxicity of deltamethrin.
But, the total toxicity of association of Deltamethrin
with Dimethoate, Fenitrothion, is weak, and does not prohibit their use. Others
(methyl-parathion, acephate, phosphamidon, monocrotophos) have no such effects, even if
they have a very high intrinsic toxicity. Cholinesterase inhibitors of the carbamate group
are ineffective. It is suggested that the potentiation is mainly in relation with the
kinetic of esterase inhibition, which is different, and specific to each organophosphate
compound. So, it is essential that a specific toxicological measurement must be performed
with any different insecticide, in order to anticipate the danger of a mixed intoxication
by pyrethroids and organophosphates.
Dimethoate and omethoate, two common organophosphorus insecticides, induced a dose
related increase in the frequency of sister chromatid exchanges in human lymphocytes in
vitro (p of the regression lines less than 1). Two other common pesticides, the pyrethroid
insecticide deltamethrin and the systemic
fungicide benomyl, induced a modest increase in sister chromatid exchanges which bordered
on statistical significance (p = 0.053 and 0.055, respectively). Mixtures of the four
pesticides at total concentrations of 41.5 and 83 ug/ml (composed of 43% dimethoate, 43%
omethoate, 12% deltamethrin and 1.2% benomyl)
induced a dose-dependent increase in sister chromatid exchanges (p <0.01). The effects
of these mixtures of pesticides were variable using lymphocytes from different
individuals, although these differences did not attain statistical significance. Moreover,
low concentrations of the four pesticides that did not increase sister chromatid exchanges
significantly when tested alone, were positive for sister chromatid exchange induction
when tested as a mixture. The experiments show that sub-threshold doses of pesticides may
increase sister chromatid exchanges when present in a mixture.
/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:
Deltamethrin's production and use as an
insecticide will result in its release to the environment. If released to air, a vapor
pressure of 1.5X10-8 mm Hg at 25 deg C indicates deltamethrin
will exist solely in the particulate phase in the ambient atmosphere. Particulate-phase deltamethrin will be removed from the atmosphere by
wet and dry deposition. If released to soil, deltamethrin
is expected to have no mobility based upon a Koc range from 46,000 to 1,630,000.
Volatilization from moist soil surfaces is expected to be an important fate process based
upon an estimated Henry's Law constant of 5X10-6 atm-cu m/mole. However, adsorption to
soil is expected to attenuate volatilization. Deltamethrin
is not expected to volatilize from dry soil surfaces based upon its vapor pressure.
Biodegradation is expected to be an important environmental fate process for deltamethrin, the half-life of deltamethrin
within soil has been shown to range from several weeks to over a 100 days. If released
into water, deltamethrin is expected to adsorb
to suspended solids and sediment based upon its experimental Koc range. Deltamethrin
was found to have a water column disappearance half-life of 2-4 hrs. Volatilization from
water surfaces is expected to be an important fate process based upon this compound's
estimated Henry's Law constant. Estimated volatilization half-lives for a model river and
model lake are 30 and 500 hours, respectively. However, volatilization from water surfaces
is expected to be attenuated by adsorption to suspended solids and sediment in the water
column. The volatilization from a model pond is about 7 years when adsorption is
considered. An estimated BCF of 270 suggests the potential for bioconcentration in aquatic
organisms is high. Estimated hydrolysis half-lives of 36 and 3.6 years were estimated for
pH values of 7 and 8, respectively. Occupational exposure to deltamethrin
may occur through inhalation of dust particles and dermal contact with this compound at
workplaces where deltamethrin is produced or
used. Monitoring data indicate that the general population may be exposed to deltamethrin via inhalation of ambient air, ingestion
of food and dermal contact with this compound. (SRC)
Probable Routes of Human Exposure:
Dermal exposure of deltamethrin to a pilot
applying the insecticide while flying an ultra-light aircraft was 10.8 ug/hr(1); a
ground-based flagman on duty during the aerial spraying received a dermal exposure of 25
ug/hr(1); dermal exposure to workers manually spraying deltamethrin
was 2.8-42.2 mg/hr(1); the 1000-fold exposure difference between hand-held applicators and
aerial applicators was due, in part, to work practices of the workers(1). Inhalation
exposure of workers involved in spray applications of deltamethrin
in greenhouses was measured as 5.2 ug/cu m at the time of spraying and 0.008 ug/cu m 30
min after spraying(2); dermal exposures (chest, back, arms, forearms, hands, legs) ranged
from 0.21 to 10.5 ug/100 cu cm(2). Workers packaging deltamethrin
in a small importing factory in China were reported to have been exposed to airborne
levels of 0.2-1.2 ug/cu m, with resulting skin contact(3). Air concns of deltamethrin
at the breathing zone of workers spraying deltamethrin
insecticide on cotton was 0.02-0.11 ug/cu m(4); dermal exposure ranged from 0.14 to 1.48
ug/cu cm on forearms, hands, legs and feet(4). Occupational exposure to deltamethrin
may occur through inhalation of dust particles and dermal contact with this compound at
workplaces where deltamethrin is produced or
used. Monitoring data indicate that the general population may be exposed to deltamethrin via inhalation of ambient air, ingestion
of food and dermal contact with this compound(SRC).
Body Burden:
Urine concns of deltamethrin of workers
spraying deltamethrin insecticide on cotton was
0.01-1.79 ug/collection interval (3-12 hr) for a period up to 72 hr after spraying(1).
Artificial Pollution Sources:
Deltamethrin's production and use as an
insecticide(1) is expected to result in its direct release to the environment(SRC).
Environmental Fate:
TERRESTRIAL FATE: Based on a classification scheme(1), an experimental Koc range from
46,000 to 1,630,000(2) indicates that deltamethrin
is expected to be immobile in soil(SRC). Volatilization of deltamethrin
from moist soil surfaces is expected to be an important fate process(SRC) given an
estimated Henry's Law constant of 5X10-6 atm-cu m/mole(SRC), determined from its vapor
pressure, 1.5X10-8(3), and water solubility, 2X10-3 mg/l(3). However, adsorption to soil
is expected to attenuate volatilization(SRC). Deltamethrin
is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor
pressure(3). Biodegradation is expected to be an important environmental fate process for deltamethrin. Laboratory and field studies measured deltamethrin soil half-lives of 4.9-6.9 weeks in a
sandy clay loam soil(4).
AQUATIC FATE: Based on a classification scheme(1), an experimental Koc range from
46,000 to 1,630,000(2), indicates that deltamethrin
is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water
surfaces is expected(3) based upon an estimated Henry's Law constant of 5X10-6 atm-cu
m/mole(SRC), determined from its vapor pressure, 1.5X10-8(4), and water solubility, 2X10-3
mg/l(4). According to a classification scheme(5), an estimated BCF of 270(SRC), from its
log Kow of 6.2(6) and a regression-derived equation(7), suggests the potential for
bioconcentration in aquatic organisms is high(SRC). A field study involving 4 prairie
ponds in Saskatchewan, Canada and aerial spraying found deltamethrin
half-lives of 0.6-5 hr in the surface-film formed by the spraying and an avg half-life of
14-hr in the subsurface water(8); degradation products included a cyclopropyl acid
derivative and phenoxybenzoic acid(8).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile
organic compounds in the atmosphere(1), deltamethrin,
which has a vapor pressure of 1.5X10-8 mm Hg at 25 deg C(2) will exist solely in the
particulate phase in the ambient atmosphere. Particulate-phase deltamethrin
may be removed from the air by wet and dry deposition(SRC).
Environmental Biodegradation:
AEROBIC: Laboratory and field studies measured deltamethrin
soil half-lives of 4.9-6.9 weeks in a sandy clay loam soil(1). A German laboratory study
measured a soil half-life of 110 days(2). When applied to soil (in both field and
laboratory tests) in high water volumes with a pipet, deltamethrin
exhibited initial half-lives of about 5-8 weeks(3); when applied as a spray, disappearance
was roughly 2-4 times faster(3). A half-life of 72 days was measured in an organic soil
(under laboratory conditions) over a 180-day observation period(4). Half-lives of 35 and
60 days have been reported for German sandy soil and sandy loam soil, respectively(5).
Half-lives of deltamethrin sprayed on forage,
litter, alfalfa and sweet peppers were 5.9, 17, 3.4 and 1.5-2.0 days, respectively(6-8).
Less than 50% deltamethrin remained on cotton
and beans after 4-5 days outdoors(9). In soil degradation studies using a mineral and an
organic soil, 26-48% of applied deltamethrin
disappeared after an 8-week incubation period(10); in sterile soil controls, only 0-3% of
applied deltamethrin disappeared suggesting that
the disappearance was primarily due to biotic processes(10). In a biodegradation study
using deltamethrin as a sole source of carbon
and energy and bacterial isolates from soil as inoculum, 35.7-44.4% of initial deltamethrin metabolized in one week and 59.7-72.5% in
two weeks(11); in the absence of bacterial isolates, only 3-10% of the deltamethrin
was metabolized(11). Deltamethrin's half-life
was reported to be 23 days in the Vemmenhog catchment located in Southern Sweden(12).
Activated sludge collected from a purification plant in the city of Rome, Italy was used
to biodegrade nine pesticides(13). The biodegradation of deltamethrin
was evaluated after 3, 6, and 9 hours: deltamethrin
was 51.4% degraded after 3 hours, 59.8% degraded after 6 hours and 63.4% degraded after 9
hours(13). Deltamethrin applied to alfalfa at a
concentration of 14 g/ha had a DT50 of 5.1-7.7 days and a DT90 of 24-26 days(14). Based on
a minimum detectable level of 0.03 ppm dry weight basis, it was estimated that 45-48 days
would be required to reduce the concentration of deltamethrin
to non-detectable levels(14).
Environmental Abiotic Degradation:
A base-catalyzed second-order hydrolysis rate constant of 6.1X10-3 L/mole-sec(SRC) was
estimated using a structure estimation method(1). This corresponds to half-lives of 36 and
3.6 years at pH values of 7 and 8, respectively(1). Deltamethrin
was observed to undergo direct photolysis when hexane, acetonitrile-water, or water
solutions were exposed to UV radiation >295 nm(2). In aqueous solution, the photolysis
rate increased rapidly when a 2% acetone photosensitizer was added(2). Photolysis rates
were slower in water than in hexane or acetonitrile-water(2). The photodegradation
reaction went through racemization at the alpha position in the alcohol moiety, ester
cleavage and reductive bromination(2). When cotton strips impregnated with deltamethrin were exposed to a UV lamp (simulating
midday natural sunlight) for a 24-hr period, 31-99% of the initial deltamethrin
degraded(3). The fastest degradation rates occurred on white fabric while the slowest
rates occurred on black fabric(3); addition of 2,4-dihydroxybenzophenone (a UV absorber)
reduced photodegradation rates(3). Deltamethrin,
impregnated on cloth, has been observed to degrade rapidly when exposed to sunlight(4).
The photodegradation half-life of deltamethrin
in distilled and natural water solutions exposed to sunlight was found to range from 1 to
less than 5 days(5). Deltamethrin also
photodegraded as thin-films or when sprayed on potato leaves exposed to sunlight(5). Deltamethrin disappears much more rapidly from soil
environments from surface application routes as compared to application routes that wash
it into or incorporate it into the soil(6) which indicates the importance of
photodegradation and volatilization(SRC). A field study involving 4 prairie ponds in
Saskatchewan, Canada and aerial spraying found deltamethrin
half-lives of 0.6-5 hr in the surface-film formed by the spraying and an avg half-life of
14-hr in the subsurface water(7); degradation products included a cyclopropyl acid
derivative and phenoxybenzoic acid(7). In a field study using two small ponds and
subsurface injections of deltamethrin, a water
column disappearance half-life of 2-4 hr was observed with rapid partitioning to sediment
and suspended solids (disappearance included transport, degradation and partitioning)(8);
the disappearance half-life in the sediment was 5-14 days(8); major degradation products
were cis-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropane-carboxylic acid and
3-phenoxybenzoic acid(8).
Environmental Bioconcentration:
In a static system for a 24-hr exposure period, deltamethrin
BCFs of about 200 to 1300 were measured for Daphnia magnus(1); observed BCFs decreased
with increases in dissolved organic carbon(1). BCF values of 39-303 were measured in
larvae of the midge Chronomus tentans in sand, silt or clay sediment water systems(2). In
a pond study using radio-labelled C-14 deltamethrin,
fathead minnows (Pimephales promelas) accumulated levels of extractable radioactivity
248-907 times higher than levels in the water at 24-hr after exposure although the nature
of the radioactive compounds was not provided(3). According to a classification scheme(4),
these BCF values suggest that the potential for bioconcentration in aquatic organisms is
high(SRC).
Soil Adsorption/Mobility:
The Koc of deltamethrin has been found to
range from 46,000 to 1,630,000(1). According to a classification scheme(2), this Koc range
suggests that deltamethrin is expected to be
immobile in soil. The mobility of deltamethrin
in soil was studied in soil column experiments and by soil thin-layer chromatography (TLC)
using a Hagerstown silty clay, a silty clay loam and a Tifton loamy sand(3); deltamethrin was found to be immobile in all soils
studied(3). Two hours after dissolved organic carbon (DOC) was added to water solutions of
deltamethrin, about 20% of the deltamethrin
was sorbed to the DOC(4); after 24 hr, nearly 81% was sorbed to the DOC(4). Laboratory
studies have shown that deltamethrin applied to
water surfaces or to subsurface water will partition rapidly from the water column to
suspended solids, sediment, and plants(5,6).
Volatilization from Water/Soil:
The Henry's Law constant for deltamethrin is
estimated as 5X10-6 atm-cu m/mole(SRC) determined from its vapor pressure, 1.5X10-8 mm
Hg(1), and water solubility, 2X10-3 mg/l(1). This Henry's Law constant indicates that deltamethrin is expected to volatilize from water
surfaces(3). Based on this Henry's Law constant, the volatilization half-life from a model
river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(3) is estimated as 30
hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec,
wind velocity of 0.5 m/sec)(3) is estimated as 500 hours(SRC). However, volatilization
from water surfaces is expected to be attenuated by adsorption to suspended solids and
sediment in the water column. The volatilization from a model pond is about 7 years(4)
when adsorption is considered. Deltamethrin's
Henry's Law constant indicates that volatilization from moist soil surfaces may
occur(SRC). Deltamethrin is not expected to
volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 1.5X10-8 mm Hg(1).
When insecticidal formulations of deltamethrin
are sprayed on water, they form a thin microlayer on the water's surface(5-8); the
thickness of the surface microlayer depends upon the formulation and amount of spray;
since deltamethrin is relatively insoluble in
water, its transport into subsurface waters can be slow, which has been demonstrated by
laboratory and field studies(5-8); laboratory tests have shown that deltamethrin
volatilizes rapidly from a surface microlayer with half-lives of several hours or
faster(5,6); the results of field and laboratory tests indicate that volatilization may be
the major route for disappearance of deltamethrin
sprayed on water surfaces(5,6). Laboratory tests were conducted to determine
volatilization losses of deltamethrin sprayed on
plant and soil surfaces(9); under the conditions of the experiment, evaporative losses
from lettuce, kohlrabi, green beans and summer wheat ranged from 12-71% over a 24-hr
period(9); evaporative loss from soil was 24% in 24-hr(9).
Effluent Concentrations:
In one aerial deposition study involving spray application from an airplane, peak
deposition to the ground was 0.5-1.2 ng/cu cm(1). A site 4 km from the spray area received
ground depositions as high as 0.2 ng/cu cm, although most areas outside the spray area
received insignificant deposition(1).
Sediment/Soil Concentrations:
Deltamethrin was applied at an amount of less
than 1 kg per year in 1990 and 1991 in the Vemmenhog catchment in Southern Sweden(1).
During that same time period deltamethrin was
detected in sediment samples of the Vemmenhog catchment at an average concentration of 20
ug/kg dry weight(1).
Food Survey Values:
598 samples of food were analyzed as part of the Canadian National Surveillance Program
in 1984-1989(1); 3 samples contained deltamethrin
residues (2/25 samples of apples and 1/21 of strawberries) at levels of 0.004-0.006
mg/kg(1). Deltamethrin concentrations were
measured by means of capillary gas chromatography using extraction with ethyl acetate and
dichloromethane from vegetable and fruit samples(2). Deltamethrin
concentrations ranged from 69.4 to 98.6 ppm for those samples measured with ethyl acetate
extraction(2), while concentrations ranged from 64.1 to 88.5 ppm for those samples
measured with dichloromethane extraction(2). Fruit and vegetable samples in Pakistan were
tested for pesticide residues by means of gas and thin-layer chromatography(3).
Deltramethrin was detected at the following concentrations: cucumber, 0.13 mg/kg; bitter
gourd, 1.12-1.7 mg/kg(3). Deltamethrin residues
were detected at concentrations ranging from non-detectable to 0.23 mg/kg in laboratory
pressed olive oil samples in Italy(4).
Other Environmental Concentrations:
A study was conducted to determine the ability of laundry practices used by farm
families to remove pesticides from clothing(1). After one wash, 2-18% of initial deltamethrin remained on fabrics(1); after two washes,
1-10% of initial deltamethrin remained on
fabrics(1). Cotton strips were coated with deltamethrin
and then washed in deionized water for one hr(2). After 4 washings, only 37.7% of initial deltamethrin was removed from the cotton(2).
Impregnating the cotton with various paraffin wax and oils (corn, linseed, silicone)
before coating with deltamethrin resulted in
lower percentages removed when washed (9.9-29.2% removal)(2).
Environmental Standards & Regulations:
FIFRA Requirements:
Tolerances are established for the combined residues of the pesticide chemical deltamethrin
[(1R,3R)-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylic acid
(S)-alpha-cyano-3-phenoxybenzyl ester and its major metabolites, trans deltamethrin
[(S)-alpha-cynao-m-phenoxybenzyl(1,R,3S)-3-(2,2-dibromovinyl)-2,2-dimethylcyclop
ropanecarboxylate] and alpha-R-deltamethrin
[(R)-alpha-cyano-m-phenoxybenzyl-(1R,3R)-3-(2,2-dibromovinyl)-2,2-dimethylcyclop
ropanecarboxylate] in or on the following agricultural commodities: cottonseed; cottonseed
oil; tomatoes; and tomato (products) concentrated.
A tolerance is established for residues of the insecticide deltamethrin
(1R,3R)-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylic acid
(S)-alpha-cyano-3-phenoxybenzyl ester and its major metabolites, trans deltamethrin
(S)-alpha-cynao-m-phenoxybenzyl(1,R,3S)-3-(2,2-dibromovinyl)-2,2-dimethylcyclopr
opanecarboxylate and alpha-R-deltamethrin
[(R)-alpha-cyano-m-phenoxybenzyl-(1R,3R)-3-(2,2-dibromovinyl)-2,2-dimethylcyclop
ropanecarboxylate] as follows: in or on all food/feed items (other than those covered by a
higher tolerance as a result of use on growing crops) in food/feed handling
establishments.
Acceptable Daily Intakes:
FAO/WHO ADI: 0.01 mg/kg
Allowable Tolerances:
Tolerances are established for the combined residues of the pesticide chemical deltamethrin
[(1R,3R)-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylic acid
(S)-alpha-cyano-3-phenoxybenzyl ester and its major metabolites, trans deltamethrin
[(S)-alpha-cynao-m-phenoxybenzyl(1,R,3S)-3-(2,2-dibromovinyl)-2,2-dimethylcyclop
ropanecarboxylate] and alpha-R-deltamethrin
[(R)-alpha-cyano-m-phenoxybenzyl-(1R,3R)-3-(2,2-dibromovinyl)-2,2-dimethylcyclop
ropanecarboxylate] in or on the following agricultural commodities: cottonseed, 0.04 ppm;
cottonseed oil, 0.2 ppm; tomatoes, 0.2 ppm; and tomato (products) concentrated, 1.0 ppm.
A tolerance of 0.05 ppm is established for residues of the insecticide deltamethrin
(1R,3R)-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylic acid
(S)-alpha-cyano-3-phenoxybenzyl ester and its major metabolites, trans deltamethrin
(S)-alpha-cynao-m-phenoxybenzyl(1,R,3S)-3-(2,2-dibromovinyl)-2,2-dimethylcyclopr
opanecarboxylate and alpha-R-deltamethrin
[(R)-alpha-cyano-m-phenoxybenzyl-(1R,3R)-3-(2,2-dibromovinyl)-2,2-dimethylcyclop
ropanecarboxylate] as follows: in or on all food/feed items (other than those covered by a
higher tolerance as a result of use on growing crops) in food/feed handling
establishments.
Chemical/Physical Properties:
Molecular Formula:
C22-H19-Br2-N-O3
Molecular Weight:
505.21
Color/Form:
Crystals
Colorless crystals
White or slightly beige powder
Odor:
Odorless
Melting Point:
101-102 deg C
Corrosivity:
Non-corrosive to metals
Octanol/Water Partition Coefficient:
log Kow= 6.20
Solubilities:
Acetone: 500 g/l @ 20 deg C
Sol in ethanol, acetone, dioxane.
Water solubility= < 0.002 mg/l
Acetone (500 g/l), ethanol (15 g/l), cyclohexanone (750 g/l), dioxan (900 g/l), xylene
(250 g/l), ethyl acetate.
Solubility; in cyclohexanone 750, dichloromethane 700, benzene 450, dimethyl sulphoxide
450, xylene 250, isopropanol 6 (all in g/l at 20 deg C)
In water, 0.002 mg/l @ 25 deg C
Spectral Properties:
Specific rotation: +61 deg (40 g/l benzene)
Vapor Pressure:
1.5X10-8 mm Hg @ 25 deg C
Other Chemical/Physical Properties:
The technical material produced industrially ... contains greater than or equal to 98% deltamethrin m/m (proportion by mass) and is a
colorless crystalline powder. /Technical deltamethrin/
Chemical Safety & Handling:
Skin, Eye and Respiratory Irritations:
The chief effect from exposure ... is skin rash particularly on moist areas of the
skin. ... May irritate the eyes.
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/
Hazardous Reactivities & Incompatibilities:
Incompatibility: Strong oxidizers. /Pyrethrins/
... Incompatible with lime & ordinary soaps because acids & alkalies speed up
processes of hydrolysis. /Pyrethrins/
Hazardous Decomposition:
Half life of 2.5 days (pH 9, 25 deg C)
When heated to decomp it emits toxic fumes of /hydrogen bromide, hydrogen cyanide,
nitrogen oxides/.
Protective Equipment & Clothing:
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:
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:
Extremely stable on exposure to air. Stable < or = 190 deg C. Under UV irradiation
& in sunlight, a cis-trans isomerization, splitting of the ester bond, & loss of
bromine occur. More stable in acidic media than in alkaline media.
Pyrethrins ... /are/ stable for long periods in water-based aerosols where ...
emulsifiers give neutral water systems. /Pyrethrins/
Storage Conditions:
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/
Disposal Methods:
SRP: At the time of review, criteria for land treatment or burial (sanitary landfill)
disposal practices are subject to significant revision. Prior to implementing land
disposal of waste residue (including waste sludge), consult with environmental regulatory
agencies for guidance on acceptable disposal practices.
Incineration would be an effective disposal procedure where permitted. ... /Pyrethrin
products/
Occupational Exposure Standards:
Manufacturing/Use Information:
Major Uses:
For Deltamethrin (USEPA/OPP Pesticide Code:
097805) ACTIVE products with label matches. /SRP: Registered for use in the U.S. but
approved pesticide uses may change periodically and so federal, state and local
authorities must be consulted for currently approved uses./
Insecticide
Used in agriculture and in public health programs
Deltamethrin is used to protect stored
commodities (mainly cereals, grains, coffee beans, dry beans), in forestry, and in public
health (e.g., Chagas disease control in South America, and malaria control in Central
America and on the African continent). It is also used in animals facilities and against
cattle infestation.
After an initial period when the product was mainly used on cotton, several major crops
were treated with deltamethrin from 1980 to
1987. Some 85% of the total production is used for crop protection. Within this, 45% is
used in cotton, 25% on fruit and vegetable crops, 20% on cereals, corn, and soybean, and
the remaining 10% on miscellaneous crops.
Control of many species of insect, particularly Lepidoptera, Homoptera, and Coleoptera,
in a very wide range of crops, including fruit, vines, olives, figs, vegetables, potatoes,
ornamentals, hops, maize, oilseed rape, sunflowers, oil palms, beet cotton, coffee, cocoa,
tea, rice, cereals, soya beans, lucern, tobacco, forestry, etc. Control of flying and
crawling insects in households, animal houses and stored products. Control of flies,
mosquitoes (adult and larvae), cockroaches, bedbugs, and other insects in public health.
Also used as a wood preservative, and as an animal ectoparasiticide.
Introduced commercially in 1978 to be used against a wide range of insect pests.
MEDICATION
Methods of Manufacturing:
Deltamethrin is ... /a/ pyrethroid composed
of a single isomer of 8 stereoisomers selectively prepared by the esterification of [1R,
3R or cis]-2,2-dimethyl-3-(2,2- dibromovinyl) cyclopropanecarboxylic acid with (alpha S)-
or (+)-alpha-cyano-3- phenoxybenzyl alcohol or by selective recrystallization of the
racemic esters obtained by esterification of the (1R, 3R or cis)-acid with the racemic or
[alpha R, alpha S, or alpha RS or + or -]-alcohol.
General Manufacturing Information:
Potent synthetic pyrethroid insecticide
Compatible with many insecticides and fungicides.
Contains only one of eight possible isomers.
/Pyrethroids/ are modern synthetic insecticides similar chemically to natural
pyrethrins, but modified to increase stability in the natural environment. /Pyrethroids/
Formulations/Preparations:
USEPA/OPP Pesticide Code 097805; Trade Names: DECIS,
FMC 45498, NRDC 161, Butoflin, Butox, Othrin, RU
22974, Othrine dust, striker IEC Insecticide (097805+121501).
Emulsifiable concentrate; wettable powder; ULV liquid; suspension concentrate;
granules; dustable powder, fogging concentrate.
Mixed formulations: (deltamethrin +)
heptenophos, sulphur
Domestic Bulgarian insecticide "Dekazol" /contains/ 0.02, 0.04, or 0.08% deltamethrin ... .
Laboratory Methods:
Analytic Laboratory Methods:
AOAC Method 991.03. Deltamethrin in Technical
Products and Pesticide Formulation by Liquid Chromatographic method.
Product analysis is by high performance liquid chromatography. Residues may be
determined by gas liquid chromatography with electron capture detection.
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:
Mian LS, Mulla MS; Effects of Pyrethroid Insecticides on Nontarget Invertebratesin
Aquatic Ecosystems. J Agric Entomol 9 (2): 73-98 (1992). This review presents data on the
impacts of pyrethroid insecticides on nontarget aquatic invertebrates.
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.
Synonyms and Identifiers:
Synonyms:
Butoflin
**PEER REVIEWED**
Butoss
**PEER REVIEWED**
Butox
**PEER REVIEWED**
Cislin
**PEER REVIEWED**
Crackdown
**PEER REVIEWED**
(S)-alpha-cyano-3-phenoxybenzyl(1R,3R)-3-(2,2-dibromovinyl)-2,2-dimethyl-
cyclopropanecarboxylate
**PEER REVIEWED**
(S)-alpha-Cyano-3-phenoxybenzyl-(1R)-cis-3-(2,2-dibromovinyl)-2,2-dimethyl-
cyclopropane carboxyate
**PEER REVIEWED**
[1R-[1alpha(S*),3alpha]]-cyano(3-phenoxyphenyl)methyl
3-(2,2-dibromoethenyl)-2,2-dimethylcyclopropanecarboxylate
**PEER REVIEWED**
(1R-(1-alpha(S*),3-alpha))-Cyano-(3-phenoxyphenyl)methyl-3-(2,2-dibromovinyl)-
2,2-dimethylcyclopropanecarboxylate)
**PEER REVIEWED**
Decamethrin
**PEER REVIEWED**
Decis
**PEER REVIEWED**
Dekametrin (Hungarian)
**PEER REVIEWED**
Deltamethrine
**PEER REVIEWED**
3-(2,2-Dibromoethenyl)-2,2-dimethylcyclopropanecarboxylic acid cyano(3-phenoxy-
phenyl)-methyl ester
**PEER REVIEWED**
Pesticide Code: 097805
**PEER REVIEWED**
Esbecythrin
**PEER REVIEWED**
FMC 45498
**PEER REVIEWED**
JMC 45498
**PEER REVIEWED**
NRDC 161
**PEER REVIEWED**
K-Othrin
**PEER REVIEWED**
K-Othrine
**PEER REVIEWED**
RU 22974
*PEER REVIEWED**
Formulations/Preparations:
USEPA/OPP Pesticide Code 097805; Trade Names: DECIS,
FMC 45498, NRDC 161, Butoflin, Butox, Othrin, RU
22974, Othrine dust, striker IEC Insecticide (097805+121501).
Emulsifiable concentrate; wettable powder; ULV liquid; suspension concentrate;
granules; dustable powder, fogging concentrate.
Mixed formulations: (deltamethrin +)
heptenophos, sulphur
Domestic Bulgarian insecticide "Dekazol" /contains/ 0.02, 0.04, or 0.08% deltamethrin ... .
Administrative Information:
Hazardous Substances Databank Number: 6604
Last Revision Date: 20011010
Last Review Date: Reviewed by SRP on 5/10/2001
Update History:
Complete Update on 10/10/2001, 54 fields added/edited/deleted.
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 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 06/08/1999, 7 fields added/edited/deleted.
Field Update on 06/03/1998, 1 field added/edited/deleted.
Field Update on 11/01/1997, 1 field added/edited/deleted.
Field Update on 05/09/1997, 1 field added/edited/deleted.
Complete Update on 03/17/1997, 1 field 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, 2 fields added/edited/deleted.
Complete Update on 11/21/1994, 1 field added/edited/deleted.
Complete Update on 09/08/1994, 2 fields added/edited/deleted.
Complete Update on 03/01/1994, 63 fields added/edited/deleted.
Record Length: 184986