products containing synthetic pyrethroids are often described by pest
control operators and community mosquito management bureaus as “safe as
chrysanthemum flowers.” While pyrethroids are a synthetic version of an
extract from the chyrsanthemum plant, they were chemically engineered to
be more toxic with longer breakdown times, and are often formulated with
synergists, increasing potency and compromising the human body’s ability
to detoxify the pesticide.
are Synthetic Pyrethroids?
pyrethroids are synthesized derivatives of naturally occurring pyrethrins,
which are taken from pyrethrum, the oleoresin extract of dried
chrysanthemum flowers (the term “pyrethrum” is often used as a generic
term to describe either natural pyrethrins or synthetic pyrethroids). The
insecticidal properties of pyrethrins are derived from ketoalcoholic
esters of chrysanthemic and pyrethroic acids. These acids are strongly
lipophilic and rapidly penetrate many insects and paralyze their nervous
system (Reigart et al., 1999). Both pyrethrins and synthetic pyrethroids
are sold as commercial pesticides used to control pest insects in
agriculture, homes, communities, restaurants, hospitals, schools, and as a
topical head lice treatment. Various formulations of these pesticides are
often combined with other chemicals, known as synergists, to increase
potency and persistence in the environment.
chemically and toxicologically similar, pyrethrins are extremely sensitive
to light, heat and moisture. In direct sunlight, half-lives that can be
measured in hours. However, the pyrethroids, the synthetic analogues of
naturally occurring pesticides, were developed to capture the effective
insecticidal activity of this botanical insecticide, with increased
stability in light, yielding longer residence times (Gosselin et al.,
and Health Effects
have irritant and/or sensitizing properties. They are not easily absorbed
through the skin, but are absorbed through the gut and pulmonary membrane.
Tests of some pyrethroids on laboratory animals reveal striking
neurotoxicity when administered by injection or orally. Systemic toxicity
by inhalation and dermal absorption is low. The acute toxicity, calculated
ranges from low to high, depending on the specific formulation. Low
toxicity is attributed to two factors: limited absorption of some
pyrethroids, and rapid biodegradation by mammalian liver enzymes (ester
hydrolysis and oxidation). Insects, without this liver function, exhibit
greater susceptibility to the chemicals (Reigart et al., 1999).
interfere with the ionic conductance of nerve membranes by prolonging the
sodium current. This stimulates nerves to discharge repeatedly causing
hyper-excitability in poisoned animals. The World Health Organization
explains that 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. The main systems for metabolism
include breakage of the ester bond by esterase action and oxidation at
various parts of the molecule. Induction of liver microsomal enzymes has
also been observed (WHO, 1999).
and symptoms of poisoning by pyrethroids may take several forms. Because
of the similarities to crude pyrethrum, pyrethroids may act as dermal and
respiratory allergens. Exposure to pyrethroids has resulted in contact
dermatitis and asthma-like reactions. Persons, especially children, with a
history of allergies or asthma are particularly sensitive, and a strong
cross-reactivity with ragweed pollen has been recognized. Severe
anaphylactic (allergic) reactions with peripheral vascular collapse and
respiratory difficulty are rare. Other symptoms of acute toxicity due to
inhalation include sneezing, nasal stuffiness, headache, nausea,
incoordination, tremors, convulsions, facial flushing and swelling, and
burning and itching sensations. The most severe poisonings have been
reported in infants, who are not able to efficiently break down
pyrethroids (ETN, Pyrethroids, 1994). With orally ingested doses, nervous
symptoms may occur, which include excitation and convulsions leading to
paralysis, accompanied by muscular fibrillation and diarrhea (ETN,
Pyrethroids, 1994). Death in these cases is due to respiratory failure.
Symptoms of acute exposure last about 2 days.
Disruption and Breast Cancer
pyrethroids have also been linked to disruption of the endocrine system,
which can adversely affect reproduction and sexual development, interfere
with the immune system and increase chances of breast cancer. Pyrethroids
contain human-made, or xenoestrogens, which can increase the amount of
estrogen in the body (Garey et al., 1998). When tested, certain
pyrethroids demonstrate significant estrogenicity and increase the levels
of estrogen in breast cancer cells (Go et al., 1999). Because increased
cell division enhances the chances for the formation of a malignant tumor
in the breast, artificial hormones, like those found in pyrethroids, may
increase breast cancer risk (PCBR, 1996). Some pyrethroids are classified
by EPA as class C (possible human) carcinogens.
and the Environment
the development of the synthetic pyrethroids was heralded with claims of
selective toxicity to insects, both pyrethroids and pyrethrins are
extremely toxic to aquatic organisms, including fish such as the bluegill
and lake trout, with LC50
values less than 1.0 parts per billion. These levels are similar to those
for mosquito, blackfly and tsetse fly larvae, often the actual target of
the pyrethroid application. Lobster, shrimp, mayfly nymphs and zooplankton
are the most susceptible non-target aquatic organisms (Mueller-Beilschmidt,
1990). The nonlethal effects of pyrethroids on fish include damage to the
gills and behavioral changes.
are moderately toxic to birds, with most LD50
values greater than 1000 mg/kg. Birds can also be indirectly affected by
pyrethroids, because of the threat to their food supply. Waterfowl and
small insectivorous birds are the most susceptible (Mueller-Beilschmidt,
1990). Because pyrethroids are toxic to all insects, both beneficial
insects and pests are affected by pyrethroid applications. In some cases,
predator insects may be susceptible to a lower dose than the pest,
disrupting the predator-prey relationship.
Residues / Persistence
mentioned before, pyrethroids are designed to breakdown more slowly than
the naturally occurring pyrethrins. While pyrethrins, extremely sensitive
to light, heat and moisture, break down in a few hours, the synthetic
pyrethroids are stable and persist in the environment much longer. With a
few exceptions, pyrethroids break down most quickly in direct sunlight,
usually just a few days after application, with a few exceptions. However,
in areas with limited sunlight, such as grain silos and subway tunnels,
pyrethroids can persist for months. For more specific breakdown times see
the sections below on bifenthrin, cypermethrin, deltamethrin, fenvalerate,
permethrin, resmethrin and sumithrin.
pyrethroids and pyrethrins are often formulated with oils or petroleum
distillates and packaged in combination with synergists, such as piperonyl
butoxide (PBO) and n-octyl bicycloheptene dicarboximide (Gosselin et al.,
1984). Synergists are added to increase the potency of the pesticide. A
range of products from repellants to foggers to pediculicides (lice
killers) to garden sprays contain synergists. Many formulations of
synthetic pyrethroids, including ScourgeTM
used along the East Coast
for mosquito control to combat the West Nile Virus, contain the synergist
inhibits important liver enzymes responsible for breakdown of some toxins,
including the active ingredients of pesticides. Specifically, it has been
shown to inhibit hepatic microsomal oxidase enzymes in laboratory rodents
and interfere in humans. Because these enzymes act to detoxify many drugs
and other chemicals, a heavy exposure to an insecticidal synergist may
make a person temporarily vulnerable to a variety of toxic insults that
would normally be easily tolerated. Symptoms of PBO poisoning include
anorexia, vomiting, diarrhea, intestinal inflammation, pulmonary
hemorrhage and perhaps mild central nervous system depression. Repeated
contact may cause slight skin irritation. Chronic toxicity studies have
shown increased liver weights, even at the lowest doses, 30 mg/kg/day.
While not considered a carcinogen by EPA, animal studies have shown
hepatocellular carcinomas, even treatments as low as 1.2% (Takahashi et
is an off-white to pale tan waxy solid, characterized by its slightly
sweet smell. As a Restricted Use Pesticide, bifenthrin may only be
purchased or applied by certified applicators or persons under the direct
supervision of a certified applicator. EPA has registered bifenthrin for
use on greenhouse ornamentals and cotton. Studies show bifenthrin to be
relatively insoluble in water. Its half-life in soil can range anywhere
from 7 days to 8 months depending on the soil type and the amount of air
in the soil (ETN, Bifenthrin, 1995). Bifenthrin is one of a few synthetic
pyrethroids that are relatively stable in direct sunlight. EPA has
classified products containing bienthrin as toxicity class II (I = most
toxic, IV = least toxic), and the word WARNING must appear on all product
is moderately toxic to mammals when ingested (oral rat LD50
= 54 to 70 mg/kg), and like all pyrethroids affects the central nervous
system. Symptoms of poisoning include incoordination, tremor, salivation,
vomiting, diarrhea, and irritability to sound and touch (ETN Bifenthrin,
1995). Although bifenthrin does not cause inflammation or irritation on
human skin, it can cause a tingling sensation, lasting about 12 hours. A
study on laboratory mice shows that bifenthrin causes gene mutation in
white blood cells (ETN, Bifenthrin, 1995). EPA classifies bifenthrin as a
Class C (possible human) carcinogen (EPA, 1997). Of concern in the
environment, bifenthrin is very highly toxic to fish, crustaceans, other
aquatic animals and bees, and is moderately toxic to birds. Scientists are
particularly concerned about possible bioaccumulation in birds.
one of a handful of light-stable synthetic pyrethroids, is registered to
control cockroaches, fleas and other indoor pests in homes, restaurants,
hospitals, schools and food processing plants, and also in agriculture to
control pests on cotton, fruits and vegetables. About 90% of the
cypermthrin manufactured worldwide is used to combat pests feeding on
cotton crops (WHO, 1989). Depending on the specific product formulation,
EPA classifies pesticides containing cypermethrin as toxicity class II or
III (I = most toxic, IV = least toxic) and must display the word WARNING
or CAUTION on the labels. Compared to other pyrethroids, cypermethrin is
relatively stable, with a half-life of 8 – 16 days in direct sunlight.
In soil, studies have shown the half-life to be as long as 8 weeks, and in
water as long as 100 days (ETN, Cypermethrin, 1996). After treatments in
the home, cypermethrin persists for about three months (Wright et al.,
is considered to be moderately toxic (oral male rat LD50
= 187 to 326 mg/kg, dermal rat LD50
= 1600 mg/kg) and like all pyrethroids, affects the central nervous system
(ETN, Cypermethrin, 1996). Symptoms of cypermethrin poisoning in humans
include numbness, burning, loss of bladder control, vomiting,
incoordination, seizures, coma and death. In California, cypermethrin is
the fourth most common cause of pesticide-related illness in pest control
operators. EPA classifies cypermethrin as a class C (possible human)
carcinogen (EPA, 1997). Studies in laboratory animals have shown exposure
to cypermethrin to cause reproductive effects, including abnormal sperm
and disruption of sex hormones (Cox, 1996). Cypermethrin should not be
applied near water, because it is very toxic to fish and other aquatic
is pyrethroid insecticide that kills insects on contact and through
digestion. It works by paralyzing the insects’ nervous system and
therefore giving a quick knock-down effect. It is used commonly to control
caterpillars on apples, pears and hops, and for the control of aphids,
mealy bugs, scale insects, and whiteflies on glasshouse cucumbers,
tomatoes, peppers, potted plants, and ornamentals (ETN, Deltamethrin,
1995). It is also registered for use on livestock and for public health
uses. Depending on the product formulation, deltamethrin pesticides may
range in toxicity from EPA toxicity class I to class III (I = most toxic,
IV = least toxic), bearing the words DANGER-POISON, WARNING or CAUTION on
the label (PANNA, 2000). Deltamethrin products may be general or
Restricted Use Pesticides. Most deltamethrin products persist from one to
two weeks in the environment, with shorter times in direct sunlight (ETN,
produces different signs of poisoning than other pyrethroids. When exposed
to deltamethrin, mammals exhibit typical type II motor symptoms, which
include a writhing syndrome in rodents, as well as copious salivation. The
acute oral LD50 in male rats has been reported as low as 128
mg/kg to greater than 5,000 mg/kg depending on the carrier and conditions
of the study (ETN, Deltamethrin, 1995). Some studies have shown
deltamethrin to cause skin irritation. Especially characteristic of
deltamethrin poisoning is rolling convulsions. The sequence of the signs
of poisoning is clearly defined, progressing from chewing, salivation, and
pawing to rolling convulsions, tonic seizures, and death (ETN,
Deltamethrin, 1995). In humans, symptoms of poisoning include ataxia,
convulsions leading to muscle fibrillation and paralysis, dermatitis,
edema, diarrhea, dyspnea, headache, hepatic microsomal enzyme induction,
irritability, peripheral vascular collapse, rhinorrhea, serum alkaline
phosphatase elevation, tremors, vomiting and death due to respiratory
failure. Deltamethrin is a suspected endocrine disruptor. Deltamethrin is
also toxic to fish, aquatic organisms, amphibians and bees.
is registered for use on a wide array of crops including cotton, soybeans,
corn, vegetables, apples, peaches, pears and nuts, as well as a
termiticide and insect repellent. Fenvalerate was first formulated for
agricultural use in 1974, but was approved as a termiticide in 1987, as an
alternative to the voluntarily cancelled cyclodiene termiticides. During
the late 1980’s, fenvalerate received national press coverage due to
over 200 dog and cat poisonings, including 26 deaths, following the use of
a product containing fenvalerate in combination with DEET, a common insect
repellant. EPA classifies fenvalerate products as toxicity class II (I =
most toxic, IV = least toxic), and include the word WARNING on all product
labels. Some formulations are Restricted Use Pesticides, and may only be
purchased or applied by certified applicators or persons under the direct
supervision of a certified applicator. The half-life of fenvalerate ranges
from 15 days to 3 months in soil, 21 days in water and 2-4 weeks on
is considered to be moderately toxic (oral rat LD50
= 486 mg/kg). Symptoms of poisoning through direct contact include
dizziness, burning and itching (which is worsened by sweating and
washing), blurred vision, tightness in the chest, and convulsions. When
ingested by laboratory animals, symptoms of poisoning include muscle
incoordination, tremors, convulsions, nerve damage, and weight loss.
Fenvalerate is a strong eye irritant and a suspected endocrine disruptor (PANNA,
2000). Sweden has banned the chemical for use in forestry following health
related complaints from workers. Studies have found that immediate
application of vitamin E to exposed areas can lessen the painful effects.
Fenvalerate is extremely toxic to bees and fish, and is slightly toxic to
to 1978, permethrin was registered for use on cotton crops only. During
the early 1980’s registration was expanded to include use on livestock
and poultry, eggs, vegetables and fruit. Today uses also include lice
treatments and urban/suburban pest control. Permethrin resembles
pyrethrins chemically, but is chlorinated to increase its stability. There
are four isomeric forms, two cis and two trans of technical permethrin.
Although the acute toxicity of the mixture (oral rat LD50
> 5000 mg/kg, oral mouse LD50
= 500) is less than that of natural pyrethrins, the cis-isomer is
considerably more toxic (oral mouse LD50
= 100), and in rats, the metabolites of the cis-isomer are more persistent
biologically. (The cis and trans isomers differ in the spatial arrangement
of the atoms.) Product formulations of permethrin can vary greatly in
isomeric content. Compared to other pyrethroids, permethrin is very
stable, even when exposed to ultraviolet light. Permethrin is strongly
absorbed to soil and other organic particles, with half-lives in soil of
up to 43 days. When used as a termiticide, permethrin can persist up to 5
receives an EPA toxicity class rating of II or III (I = most toxic, IV =
least toxic), and carries either the word WARNING or CAUTION on its label,
depending on the formulation. While it is not extremely toxic to humans,
there are numerous reports of transient skin, eye and respiratory
irritation. Like all pyrethroids, permethrin is a central nervous system
poison. Workers and researchers report tingling in face and hands, and
some report allergic reactions. Based on studies demonstrating
carcinogenicity, EPA ranks permethrin as a class C, or possible human
carcinogen (U.S. EPA, 1997). Other studies have shown effects on the
immune system, enlarged livers and at high doses, decreased female
fertility and endocrine disruption. Permethrin is extremely toxic to
aquatic life, bees and other wildlife. It should not be applied in crops
or weeds where foraging may occur (ETN, Permethrin, 1996).
Raid Flying Insect KillerTM)
is used for control of flying and crawling insects in homes, greenhouses,
processing plants, commercial kitchens, airplanes and for public mosquito
control. Resmethrin is considered slightly toxic to humans and is rated
EPA toxicity class III (I = most toxic, IV = least toxic), bearing the
word CAUTION on its label. The oral rat LD50
is about 2500 mg/kg. Although resmethrin has a very short half-life (under
an hour in direct sunlight), it persists much longer in soil with a
half-life of 30 days (ETN, Resmethrin, 1996). Resmethrin breaks down into
a smelly byproduct, phenylacetic acid, which binds strongly to textiles
and dissipates slowly, smelling of urine.
is absorbed rapidly and distributed to all tissues including the brain.
Skin absorption is low, although it should be noted that some individuals
manifest allergic responses including dermatitis, asthma, runny nose and
watery eyes after initial contact. In laboratory animals, chronic toxicity
studies have shown hypertrophy of the liver, proliferative hyperplasia and
benign and cancerous liver tumors. EPA reviewers noted slight, but
significant, increases in the number of offspring born dead and decreased
viability, which they thought might be secondary to trans placental
toxicity. Tests for neurotoxicity have been negative, but it is a
suspected endocrine disruptor (PANNA, 2000). Resmethrin is extremely toxic
to fish, other aquatic life and bees. The domestic manufacturer of
resmethrin, Penick Company, will not identify the inert ingredients in its
product, but recommends that it is not sprayed on paint, plastic or
varnished surfaces, and that treatment of living areas or areas with large
amounts of textiles be avoided.
has been registered for use since 1975. It is used to control adult
mosquitoes and as an insecticide in transport vehicles, commercial,
industrial and institutional non-food areas, in homes, gardens,
greenhouses and on pets. Chemically, it is an ester of chrysanthemic acid
and alcohol. It is a combination of two cis and two trans isomers.
Sumithrin is slightly toxic and is rated EPA toxicity class IV (I = most
toxic, IV = least toxic) bearing the word CAUTION on its label. The oral
is greater than 5,000 mg/kg, and the LC50
for inhalation is greater than 1210 mg/m3.
Sumithrin degrades rapidly, with a half-life of 1-2 days under dry, sunny
conditions. Under flooded conditions, the half-life increases to 2-4 weeks
for the trans isomer and 1-2 months for the cis isomer. In grain silos,
with no sunlight and little air circulation, most of the product still
remains after one year (WHO, 1990).
of acute sumithrin poisoning include hyperexcitability, prostration, slow
respiration, salivation, tremor, ataxia and paralysis. Chronic feeding
studies resulted in increased liver weights in both males and females. In
rat studies, sumithrin was completely excreted in 3-7 days (WHO, 1990).
Studies have shown that sumithrin is an endocrine disruptor, demonstrating
significant estrogenicity and increases the level of estrogen in breast
cancer cell, suggesting that sumithrin may increase the risk of breast
cancer (Go et al., 1999).
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