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I’m amazed yet again at the cavalier way this presumed “nature” community treats these powerful, destructive, and not fully studied neurotoxins. It’s completely out of keeping with the natural ethos.
A few studies are in order, and yes, I fully expect to get slammed by some pretty analytical but not very convincing justifications. It’s happened before…..
Permethrin undergoes its first official testing for endocrine disruption this year, after years of evidence which suggests endocrine effects.
-----------------------------
Melissa Kaplan's
Herp Care Collection
Last updated August 11, 2002
Pyrethrin and Pyrethroid Exposure Causes Adverse Reactions
Compiled by Melissa Kaplan
Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.
Soderlund DM, Clark JM, Sheets LP, Mullin LS, Piccirillo VJ, Sargent D, Stevens JT, Weiner ML. Department of Entomology, New York State Agricultural Experiment Station, Cornell University, Geneva, NY 14456, USA.
Toxicology 2002 Feb 1;171(1):3-59
The Food Quality Protection Act (FQPA) of 1996 requires the United States Environmental Protection Agency to consider the cumulative effects of exposure to pesticides having a 'common mechanism of toxicity.' This paper reviews the information available on the acute neurotoxicity and mechanisms of toxic action of pyrethroid insecticides in mammals from the perspective of the 'common mechanism' statute of the FQPA.
The principal effects of pyrethroids as a class are various signs of excitatory neurotoxicity. Historically, pyrethroids were grouped into two subclasses (Types I and II) based on chemical structure and the production of either the T (tremor) or CS (choreoathetosis with salivation) intoxication syndrome following intravenous or intracerebral administration to rodents. Although this classification system is widely employed, it has several shortcomings for the identification of common toxic effects. In particular, it does not reflect the diversity of intoxication signs found following oral administration of various pyrethroids.
Pyrethroids act in vitro on a variety of putative biochemical and physiological target sites, four of which merit consideration as sites of toxic action. Voltage-sensitive sodium channels, the sites of insecticidal action, are also important target sites in mammals. Unlike insects, mammals have multiple sodium channel isoforms that vary in their biophysical and pharmacological properties, including their differential sensitivity to pyrethroids.
Pyrethroids also act on some isoforms of voltage-sensitive calcium and chloride channels, and these effects may contribute to the toxicity of some compounds. Effects on peripheral-type benzodiazepine receptors are unlikely to be a principal cause of pyrethroid intoxication but may contribute to or enhance convulsions caused by actions at other target sites. In contrast, other putative target sites that have been identified in vitro do not appear to play a major role in pyrethroid intoxication. The diverse toxic actions and pharmacological effects of pyrethroids suggest that simple additivity models based on combined actions at a single target are not appropriate to assess the risks of cumulative exposure to multiple pyrethroids.
[Pyrethroid exposure following indoor treatments with a dog flea powder]
[Article in German] Schulze M, Helber B, Hardt J, Ehret W. Umweltmedizinisches Zentrum (Direktor: Prof. Dr. Dr. W. Ehret), Klinikum, Augsburg. Dtsch Med Wochenschr 2002 Mar 22;127(12):616-8
HISTORY: A 42 year old woman reported hair loss, gastrointestinal and non-specific symptoms. The patient has lived in a council flat and kept a dog who had been regularly treated with pyrethroid containing flea powder.
INVESTIGATIONS: The biological monitoring of pyrethroid meta-bolites in urine was performed using gas chromatography-mass spectrometry. The values at admission and follow-up after 4 weeks were highly elevated. Inspection of the flat revealed a humid and cramped dwelling.
TREATMENT: We recommended redevelopment and cleaning of the dwelling and the avoidance of ectoparasiticide use.
CONCLUSION: To our knowledge this is the first documented case of high indoor pyrethroid exposure following the use of ectoparasiticides with domestic animals. Pyrethroids can cause neurotoxic symptoms and skin irritation. There are few data concerning chronic effects. The causal connection between pyrethroid exposure and symptoms remains unclear and poses a great problem in environmental medicine.
Striatal dopaminergic pathways as a target for the insecticides permethrin and chlorpyrifos.
Karen DJ, Li W, Harp PR, Gillette JS, Bloomquis JR. Department of Entomology, Virginia Polytechnic Institute and State University, Blacksburg 24061, USA. Neurotoxicology 2001 Dec;22(6):811-7
Because insecticide exposure has been linked to both Parkinsons disease and Gulf War illness, the neurotoxic actions of pyrethroid and organophosphate insecticides on behavior and striatal dopaminergic pathways were investigated in C57BL/6 mice treated with permethrin (three i.p. doses at 0.2-200 mg/kg) or chlorpyrifos (three s.c. doses at 25-100 mg/kg) over a 2-week period. Permethrin altered maximal [3H]dopamine uptake in striatal synaptosomes from treated mice, with changes in Vmax displaying a bell-shaped curve. Uptake was increased to 134% of control at a dose of 1.5 mg/kg. At higher doses of PM (25 mg/kg), dopamine uptake declined to a level significantly below that of control (50% of control at 200 mg/kg, P < 0.01). We also observed a small, but statistically significant decrease in [3H]dopamine uptake by chlorpyrifos, when given at a dose of 100 mg/kg. There was no significant effect on the Km for dopamine transport. Evidence of cell stress was observed in measures of mitochondrialfunction, which were reduced in mice given high-end doses of chlorpyrifos and permethrin. Although cytotoxicity was not reflected in decreased levels of striatal dopamine in either 200 mg/kg PM or 100 mg/kg CPF treatment groups, an increase in dopamine turnover at 100 mg/kg CPF was indicated by a significant increase in titers of the dopamine metabolite, 3,4-dihydroxyphenylacetic acid. Both permethrin and chlorpyrifos caused a decrease in open field behavior at the highest doses tested. Although frank Parkinsonism was not observed, these findings confirm that dopaminergic neurotransmission is affected by exposure to pyrethroid and organophosphorus insecticides, and may contribute to the overall spectrum of neurotoxicity caused by these compounds.
--------------------------------
Thursday, May 1, 2003
WASHINGTON (Reuters) - Farmers who use certain pesticides seem to have a higher-than-average risk of prostate cancer, U.S. government researchers said on Thursday.
The researchers, who published their study in the American Journal of Epidemiology, confirmed other findings that show farmers have an unusually high risk of prostate cancer.
"Associations between pesticide use and prostate cancer risk among the farm population have been seen in previous studies; farming is the most consistent occupational risk factor for prostate cancer," Michael Alavanja of the National Cancer Institute (NCI), who helped lead the study, said in a statement.
Researchers at NCI and at the National Institute of Environmental Health Sciences and the Environmental Protection Agency studied 55,332 farmers and nursery workers who worked with pesticides.
Between 1993 and 1999, 566 new prostate cancers developed among the men, compared to 495 that would normally be expected in Iowa and North Carolina, the two states studied.
The risk of developing prostate cancer was 14 percent greater for the pesticide applicators compared to the general population.
One pesticide, methyl bromide, increased the risk of prostate cancer in all men.
Six others raised the risk in men with a family history of prostate cancer. They are chlorpyrifos, coumaphos, fonofos, phorate, permethrin and butylate.
More than 220,000 U.S. men will be diagnosed with prostate cancer this year, according to the American Cancer Society, and 30,000 will die of it.
The biggest risk factors for prostate cancer are age and family history. African-American men have higher rates of prostate cancer, and some evidence suggests that men who eat lots of red meat and animal fat have a higher risk.
PERMETHRIN
The insecticide permethrin (in the synthetic pyrethroid family) is widely
used on cotton, wheat, corn, alfalfa, and other crops. In addition, over 100
million applications are made annually in and around U.S. homes.
Permethrin, like all synthetic pyrethroids, is a neurotoxin. Symptoms
include tremors, incoordination, elevated body temperature, increased
aggressive behavior, and disruption of learning. Laboratory tests suggest
that permethrin is more acutely toxic to children than to adults.
The U.S. Environmental Protection Agency has classified permethrin as a
carcinogen because it causes lung tumors in female mice and liver tumors
in mice of both sexes. Permethrin inhibits the activity of the immune
system in laboratory tests, and also binds to the receptors for a male sex
hormone. It causes chromosome aberrations in human and hamster cells.
Permethrin is toxic to honey bees and other beneficial insects, fish,
aquatic insects, crayfish, and shrimp. For many species, concentrations of
less than one part per billion are lethal. Permethrin causes deformities and
other developmental problems in tadpoles, and reduces the number of
oxygen-carrying cells in the blood of birds.
Permethrin has been found in streams and rivers throughout the United
States. It is also routinely found on produce, particularly spinach,
tomatoes, celery, lettuce, and peaches.
A wide variety of insects have developed resistance to permethrin. High
levels of resistance have been documented in cockroaches, head lice, and
tobacco budworm.
BY CAROLINE COX
Caroline Cox is JPR’s editor.
Permethrin is used to kill pest in-sects in agriculture, home pest control, forestry, and
in public health programs, including head lice control. It was first marketed in 1973.
Worldwide, the dominant use of permethrin is on cotton, accounting for about 60 percent
(by weight) of the permethrin used.1 In the U.S., al-most 70 percent of the permethrin
used in agriculture is used on corn, wheat, and alfalfa.2 Over 100 million applications of
permethrin are made each year in U.S. homes, and over 18 million applications are made
1
in yards and gardens.3
Permethrin is a synthetic pyrethroid. Like most members of this family of insecticides,
it has four isomers, molecules made up of the same atoms with different threedimensional
structures. (See Figure 1)
Mode of Action
Permethrin, like all synthetic pyrethroids, kills insects by strongly exciting their
nervous systems. Permethrin makes the nervous system hypersensitive to stimuli from
sense organs. Rather than sending a single impulse in response to a stimulus, permethrinexposed
nerves send a train of impulses. This excitation occurs because permethrin
blocks the movement of sodium ions from outside to inside of the nerve cells.
Permethrin’s mode of action is similar to that of the organochlorine insecticide DDT.5
Acute Lethal Dose
Permethrin’s LD50 (the amount of permethrin that kills 50 percent of a population of
test animals) is variable. In a summary of nine oral LD50 tests using rats, the LD50 varied
from 430 milligrams per kilogram of body weight (mg/kg) to over 4,000 mg/kg. Some of
this variability occurs because the proportions of isomers in the test materials vary. The
cis isomers are about ten times more toxic than the transisomers.6
Neurotoxicity
In mammals, permethrin has complex effects on the nervous system. As in insects, it
causes repetitive nerve impulses. It also inhibits a variety of nervous system enzymes:
ATPase, whose inhibition results in increased release of the neurotransmitter
acetylcholine 7; monoamine oxidase-A, the enzyme which maintains normal levels of
three other neurotransmitters 8; and acetylcholinesterase, the enzyme that breaks down
acetylcholine.9 (Two large families of insecticides, the organophosphates and the
carbamates, are acetylcholinesterase inhibitors.) In addition, permethrin inhibits a
nervous system receptor, the GABAA receptor, producing excitability and
convulsions.10 Finally, permethrin inhibits respiration (the process by which cells use
sugars as an energy source) in a manner similar to other neurotoxic drugs.11 It is
therefore not surprising that permethrin causes a wide variety of neurotoxic symptoms.
At relatively high doses, these neuro-toxic symptoms of permethrin include tremors,
incoordination, hyperactivity, paralysis, and an increase in body temperature. These
symptoms can persist up to three days.12 Other behavioral effects have been observed at
lower doses. For example, sublethal exposure of mice to the permethrin-containing
insecticide Ambush increased activities like chewing 13 ; sublethal exposure of rats to
permethrin increased aggressive behavior, agitation, and resistance to being captured 14 ;
and permethrin disrupted a learned feeding behavior in rats at doses of about 20 percent
2
of the LD50. 15
Eye and Skin Irritation
Permethrin-containing products can be irritating to both eyes and skin. For example,
the agricultural insecticide Pounce 3.2 EC “causes moderate eye irritation.”16 Ortho Total
Flea Control 2 and Solaris Flea-B-Gon Total Flea Killer Indoor Fogger both cause
“tearing, swelling, and blurred vision.”17,18 They also cause “redness, swelling, and
possibly blistering” of the skin.17,18 Adams 14 Day Flea Dip “causes eye injury”19 and
“may cause al-allergic reactions”19 on skin.
Effects on the Immune System
Experiments with laboratory animals indicate that the immune system (used by living
things to defend themselves from disease) “appears to be a sensitive target for permethrin
activity.” Ingestion of permethrin reduces the ability of immune system cells called Tlymphocytes
to recognize and respond to foreign proteins. Doses equivalent to 1/100 of
the LD50 , inhibited T-lymphocytes over 40 percent. Permethrin ingestion also reduced
the activity of a second type of immune system cell, natural killer cells, by about 40
percent.20(See Figure 2.) In tests using mouse cell cultures, permethrin had similar effects
on the immune system, inhibition of two kinds of lymphocytes.21 Researchers concluded
that “the immune system is exquisitely sensitive … at exposure levels that cause no overt
toxicity.”20
Effects on Reproduction
Permethrin affects both male and female reproductive systems. It binds to receptors
for androgen, a male sex hormone, in skin cells from human males, causing researchers
to “advise protection from any form of contact or ingestion of the pyrethroids.” 22
Permethrin also binds to a different receptor, called the peripheral benzodiazepine
receptor, that stimulates production of the male sex hormone testosterone.23 In addition,
permethrin caused reduced testes weights in a long-term feeding study of mice.24 In
females, permethrin exposure has caused embryo loss in pregnant rabbits24 and in
pregnant rats.25
Mutagenicity
Permethrin was mutagenic (damaging to genetic material) in three tests with human
cell cultures, one with hamster cells, and one with fruit fly larvae. In cultures of human
lymphocytes (white blood cells), permethrin exposure caused an increase in chromosome
aberrations, chromosome fragments,26 and DNA lesions.27 In hamster ovary cell
cultures, permethrin exposure caused chromosome aberrations.28 Exposure to Ambush
3
(a permethrin-containing insecticide) during larval development increased sex-linked
lethal mutations in fruit flies.29
Carcinogenicity
According to the U.S. Environmental Protection Agency (EPA), permethrin is a
possible human carcinogen (chemical that causes cancer).30 EPA found that permethrin
increased the frequency of lung tumors in female mice, and increased the frequency of
liver tumors in male and female mice.24 The World Health Organization reports that
permethrin increased the frequency of lung tumors in females in two out of the three
mouse studies it reviewed. (See Figure 3.) Lung tumors increased with increasing
permethrin exposure in the third study, but the increase was not statistically significant.31
There are no publicly available studies of the carcinogenicity of permethrin-containing
insecticide products.
There are two molecular mechanisms which could explain permethrin’s
carcinogenicity. First, permethrin reduces the activity of an enzyme involved in the
breakdown of the amino acid tryptophan. This can lead to the buildup of carcinogenic
tryptophan breakdown products.32 Second, permethrin inhibits what is called “gap
junctional intercellular communication” (GJIC), chemical communication between cells.
GJIC plays an important role in the growth of cells, and some cancer promoting
chemicals inhibit GJIC.33
Other Chronic Effects
The liver is a sensitive target for permethrin effects. When EPA summarized 17 mediumand
long-term laboratory studies that exposed rats, mice, and dogs to permethrin, effects
on the liver were noted at the “lowest effect level” in all of them.24 Other chronic effects
in laboratory tests include enlarged adrenal glands at all doses tested in a rabbit feeding
study, and increased kidney weights at all doses tested in a rat feeding study.24
Synergy
Synergy occurs between two or more chemicals when their combined exposure causes
more adverse effects than the sum of their individual effects. A possible cause of the
health problems reported by 30,000 veterans who served in the Persian Gulf War is
exposure to a combination of chemicals, including permethrin. The combination of
permethrin, the anti-nerve gas drug pyridostigmine bromide, and the insect repellent
DEET has been tested in laboratory animals. Neurotoxic symptoms, including decreased
activity, diarrhea, shortness of breath, tremors, inability to walk, and damage to nerves,
were observed in hens exposed to all three chemicals, but not in hens exposed to
permethrin alone. Permethrin with just pyridostigmine bromide or just DEET also caused
tremors and inability to walk, but symptoms were not as severe.35
4
Other pesticides interact synergistically with permethrin with in other species.
Permethrin and the herbicide atrazine synergistically induce growth of the soil fungus
Pythium ultimum, 36 and permethrin and the insecticide amitraz are synergistically toxic
to the bollworm.37
Individual Susceptibility
Individuals vary in their susceptibility to permethrin, as has been illustrated by the
following research:
l Based on tests with laboratory animals, it appears children may be more sensitive to
permethrin than adults. Permethrin is almost 5 times more acutely toxic to 8-day-old
rats than it is to adult rats.38(See Figure 4.)
l Since sulfates are involved in one of the major pathways by which permethrin is
broken down in humans, individuals with defects in sulfate-related enzymes may be
unable to easily break down permethrin, leading to increased susceptibility to motor
neuron disease.39,40
l Individuals with genetic variants of the enzyme pseudocholinesterase that have
reduced activity are at higher risk of adverse effects from exposure to certain
chemicals, including the permethrin combination implicated in symptoms seen in
Gulf War veterans.35
“ It appears children may be more
sensitive to permethrin than adults.
Permethrin is almost 5 times more
acutely toxic to 8-day-old rats than it is to
adult rats.”
Effects on Nontarget Animals
Beneficial Arthropods: As a broad spectrum insecticide, it is not surprising that
permethrin impacts beneficial arthropods, those that are useful in agriculture. Examples
include the following:
5
l Permethrin is acutely toxic to honey bees; the median lethal dose is 0.008
micrograms per bee.41 Sublethal exposures cause increased abnormal behavior
(trembling, etc.), decreased foraging,42 and impairment of bees’ learning.43
l The International Organization for Biological Control tested the acute toxicity of
permethrin to 13 species of beneficial arthropods and found that permethrin caused
99 percent mortality of 12 of the species, and over 80 percent mortality of the other.
Effects were persistent, lasting over 30 days.44 Sublethal doses also impact
beneficial arthropods: permethrin inhibited the emergence of a parasitoid wasp from
eggs of the rice moth Corcyra cephalonica 45 and disrupted the foraging pattern of
another parasitoid wasp as it searched for its aphid prey.46 (Parasitoids are insects
that lay their eggs in, on, or near their prey. The eggs hatch and the larvae consume
the prey as they develop. They often keep populations of agricultural pests at low
levels.)
Aquatic Insects: Because it is a broad spectrum insecticide, permethrin has severe
impacts on aquatic insects. Permethrin applications to forest streams caused “a major
increase in the density of drifting invertebrates” described as “catastrophic.” (Drifting
animals are those that are sufficiently poisoned by the insecticide that they are washed
down-stream.) Most applications were also followed by “rapid depletion of bottom
fauna,” insects that live in the stream bed. Recovery required between 1 and 18
months.47 Mayflies and damselflies are the most sensitive species.49 Permethrin also
bioconcentrates in aquatic insects; bioconcentration factors in stoneflies ranged from 43
to 570. 49
Birds: While permethrin’s acute toxicity to birds is low,50 it causes other ad-verse
effects. Three-week dietary exposure of chickens reduced hemoglobin (oxygen carrying
protein) levels, and red blood cell counts, while increasing the number of white blood
cells.51 The reduction in hemoglobin occurred at the lowest dose tested, 33 mg/kg.51
Permethrin also caused decreased immune responses in chicks,52 and damaged mallard
ovaries.53
Fish: Permethrin is highly toxic to fish. This toxicity is due, in part, to the sensitivity of
their nervous system.54 Fish also lack the enzymes that break down permethrin in other
animals.55
The LC
50
(the concentration that kills 50 percent of a population of test animals) is less
than 1 part per million (ppm) for almost all fish species tested, and for some fish is less
than 1 part per billion (ppb). Agricultural permethrin products called emulsifiable
concentrates are about twice as toxic to fish as permethrin alone. Small fish are less
6
tolerant of permethrin than large fish, and it is more toxic in cold water than in warm
water.56 Fish also have a particular developmental stage when they are most susceptible.57
Sublethal effects on fish include abnormal swimming, a reduced startle response, and
loss of equilibrium.58
Permethrin bioconcentrates in fish, so that concentrations in fish are higher than the
concentration in the water in which the fish live. Bioconcentration factors (the ratio
between the concentration in the fish and the concentration in the water) up to 113 have
been measured in brook trout,59 up to 613 in Atlantic salmon,59 and up to 631 in rainbow
trout.60
Complex effects of permethrin on fish have been documented by the Canadian Forest
Service in field studies. They found that diets of trout and salmon were altered when
permethrin killed the insects these fish use as food. In some cases, diets were altered for
a year following treatment. Reductions in fish growth rates, and migration to untreated
areas followed; recovery required four months. The researchers concluded that
permethrin is “not an acceptable treatment for large-scale use in forest areas containing
fish-producing
water.”61
Amphibians: Permethrin disrupts the growth and development of tadpoles. Exposure
slowed growth for two to three weeks, and increased the frequency of a tail abnormality.
(See Figure 5.) The increase in this deformity occurred at the lowest concentration of
permethrin tested, 0.1 ppm. At this concentration tadpoles also responded to prodding in
a jerky and disorganized way, making them vulnerable to predation. Tadpoles exposed to
an even lower concentration (0.05 ppm) reduced their feeding for several weeks after
exposure.62
Permethrin also effects brain function in tadpoles. Concentrations of 0.25 ppm
decreased the amounts of two specific proteins in the brain, while increasing the total
amount of protein. One of the proteins is associated with learning. Activity of several
nervous system enzymes, including acetylcholinesterase, decreased.63
Other Aquatic Animals: Permethrin is very highly toxic to lobster; the LC
50
is less than
1 ppb.64 It is highly toxic to oyster larvae, with an EC
50
(the concentration causing
abnormal development in half of the larvae) of less than 1 ppm.65 Permethrin
bioconcentrates in oysters, with a bioconcentration factor of 1900. 66 Water fleas are also
very sensitive to permethrin exposure; LC
50
s of several species are about 1 ppb.67
Permethrin also caused “severe mortalities” of two kinds of zooplankton, cladocerans
7
and copepods with recovery taking about 3 months.68
Mysid shrimp are killed by permethrin at concentrations so low that they cannot be
detected in water (the LC 50 is 0.02 ppb). This means that “any detection of these
insecticides in estuarine waters would likely be associated with adverse effects.”66
Another animal that is very sensitive to permethrin is crayfish; LC
50
s for the red swamp
crayfish vary from 0.4 to 1.2 ppb. Researchers concluded that “even the lowest
operational treatment level used for insect management would seriously impact crayfish
populations.”67
Residues on Food
The Food and Drug Administration’s (FDA’s) monitoring program routinely finds
permethrin on food. In 1996, it was the 13th most commonly detected pesticide.68 Similar
results were found in monitoring of 14 fruits and vegetables by the U.S. Department of
Agriculture; permethrin was the 10th most frequently detected pesticide and was often
found on spinach (60 percent of the samples tested) and tomatoes (11 percent of the
samples tested).69 Permethrin was also frequently found on celery and lettuce.70
Permethrin has also been found in baby food: FDA’s 1996 monitoring found it in 12
percent of the samples tested. The Environmental Working Group found permethrin was
the most commonly detected pesticide in peach baby food (44 percent of the samples
tested) and was also found in plums (11 percent of the samples tested).71
Contamination of Water
Permethrin has been found in ground and surface water. The U.S. Geological Survey
has found permethrin in streams and rivers in the Mississippi River Basin, 72 the Central
Columbia Plateau (Washington and Idaho),73 the Georgia-Florida Coastal Plain,74 the
San Joaquin-Tulare Basin (California),75 and the Ozark Plateau (Arkansas and nearby
states).76 Permethrin has also been found in groundwater in Virginia.76
Drift
Drift, pesticide movement during application away from the target area, has been
measured for two types of permethrin applications: aerial and back pack mistblower.
Aerially applied permethrin drifted 180-240 meters (590- 790 feet) under conditions
“highly conducive” to drift.78 These researchers sug-gested using buffers of 150 meters
(490 feet). Back pack mistblower applications of permethrin drifted 150 meters.79
Persistence
According to EPA, permethrin’s half-life (the amount of time required for half of the
8
original amount of a chemical to break down or move away from the study site) was 17
days in a North Carolina agricultural soil and 43 days in Illinois.80 When used as a
termiticide, permethrin persists longer; soil concentrations did not decline during the first
year.81 Permethrin also persists longer in tree needles, foliage, and bark, up to 363 days.82
The ability of permethrin to persist in the environment was graphically illustrated by a
study of an application of permethrin ear tags to cattle. Permethrin was found on all
surfaces analyzed, not only on the cattle, but also on the bark of trees in their pasture, on
a fence pole, and in grass. Some residues were found three months after the ear tags were
applied.83
Resistance
Resistance (the evolution of a strain of insect that is able to tolerate a particular
insecticide) to permethrin has been documented in a wide variety of insects. These
species include pear psylla,84fall army-worm, 85 German cockroach,86 spotted tentiform
leafminer,87 diamondback moth,88 house fly,89 stable fly,90 head lice,91-93 and tobacco
budworm.94 Many of these species are resistant to other synthetic pyrethroids as well as
permethrin. The level of resistance is less than tenfold in some of the species but high
levels of resistance have been observed in cockroaches (45-fold),86lice (up to 385-fold)91
and budworm (1400-fold).94
Inert Ingredients
Like most pesticide products, permethrin insecticides contain ingredients that are
typically claimed as trade secrets by pesticide manufacturers. Limited information about
“inerts” in permethrin products is available. Examples include:
l Xylenes are in the agricultural insecticides Pounce 3.2 EC,16 Ambush 2E,95 and
Ambush 50. 96 Xylenes cause eye and skin irritation, headaches, nausea, confusion,
tremors, and anxiety in exposed humans. In laboratory tests, xylenes have caused
kidney damage, fetal loss, and skeletal anomalies in offspring.97
l Methyl paraben is in the head lice cream rinse Nix,98 regulated as a drug not as a
pesticide. Methyl paraben is a skin sensitizer, and causes eye, skin, digestive, and
respiratory irritation.99
l Dimethyl ether is in the household insecticides Flea-B-Gon Total Flea Killer
Indoor Fogger 17 and Ortho Total Flea Control 2. 18 It causes respiratory, skin, and
eye irritation and depresses the cen-tral nervous system. It is also a severe fire
hazard.100
l Butane is in the household insecticides Raid Yard Guard Outdoor Fogger V and
9
Off Yard and Deck Area Repellant 1. 101,102 It is “extremely flammable” and shortterm
exposure causes irritation, nausea, drowsiness, convulsions, and coma.103
References
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PERMETHRIN
BY CAROLINE COX
Back to Pesticide Fact Sheet
References
1. World Health Organization. 1990. Permethrin. Environmental Health Criteria 94. Geneva,
Switzerland: World Health Organization, United Nations Environment Programme, and International
Labor Organization. Pp.25-26.
2. Gianessi, L.P. and J.E. Anderson. 1995. Pesticide use in U.S. crop production. National summary
report. Washington, D.C.: National Center for Food and Agricultural Policy.
3. Whitmore, R.W., J.E. Kelly, and P.L. Reading. 1992. National home and garden pesticide use
survey. Final report, Volume 1: Executive summary, results, and recommendations. Research Triangle
Park, NC: Research Triangle Institute.
4. Ref. # 1, p.18.
5. Vijverberg, H.P.M. and J. van den Bercken. 1990. Neurotoxicological effects and the mode of
action of synthetic pyrethroids. Crit. Rev. Toxicol. 21:105-126.
6. Ref. #1, p.64.
7. Al-Rahji, D.H. 1990. Properties of Ca2+ + Mg2+-ATPase from rat brain and its inhibition by pyrethroids.
Pest. Biochem. Physiol. 37:116-120.
8. Rao, G.V. and K.S.J. Rao. 1993. Inhibition of monoamine oxidase-A of rat brain by pyrethroids -
an in vitro kinetic study. Mol. Cell. Biochem. 124:107-114.
9. Rao, G.V. and K.S.J. Rao. 1995. Modulation of acetylcholinesterase of rat brain by pyrethroids in
vivo and an in vitro kinetic study. J. Neurochem. 65:2259-2266.
10. Ramadan, A,A, et al. 1988. Action of pyrethroids on GABA A receptor function. Pest. Biochem.
Physiol. 32:97-105.
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11. Gassner, B. et al. 1997. The pyrethroids permethrin and cyhalothrin are potent inhibitors of the
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chemicalWATCH Factsheet
SYNTHETIC PYRETHROIDS
Pesticide products containing 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,
they were chemically designed 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.
What are Synthetic Pyrethroids?
Synthetic pyrethroids are synthesized derivatives
of naturally occurring pyrethrins,
which are taken from pyrethrum, the oleoresin
extract of dried chrysanthemum flowers.
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.
While chemically and toxicologically similar,
pyrethrins are extremely sensitive to light,
heat and moisture. In direct sunlight, halflives
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.,
1984).
Pyrethroids and Health Effects
Pyrethroids 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 by LD50’s, 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).
Pyrethroids 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).
Signs 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.
Endocrine Disruption and Breast Cancer
Many 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 possible human carcinogens.
Pyrethroids and the Environment
While 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
Beyond Pesticides
National Coalition Against the Misuse of Pesticides
701 E Street, S.E., Suite 200 • Washington DC 20003 • 202-543-5450 (v) • 202-543-4791 (f) • ncamp@ncamp.org • www.beyondpesticides.org
susceptible non-target aquatic organisms
(Mueller-Beilschmidt, 1990). The nonlethal
effects of pyrethroids on fish include damage
to the gills and behavioral changes.
Pyrethroids 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.
Pyrethroids Residues / Persistence
As 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. As a general
rule, 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 resmethrin, permethrin and sumithrin.
Synergists
Both 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
permethrin, resmethrin and sumithrin, including
ScourgeTM and AnvilTM, used along the
East Coast for mosquito control to combat
the West Nile Virus, contain the synergist
PBO.
PBO inhibits important liver enzymes responsible
for breakdown of some toxins, in-
Beyond Pesticides
National Coalition Against the Misuse of Pesticides
701 E Street, S.E., Suite 200 • Washington DC 20003 • 202-543-5450 (v) • 202-543-4791 (f) • ncamp@ncamp.org • www.beyondpesticides.org
cluding 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 al.,
1994).
Permethrin
(PounceTM, TorpedoTM, DragnetTM)
Prior 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.) 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 years.
Permethrin 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. 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).
Resmethrin
(ScourgeTM, Raid Flying Insect KillerTM)
Resmethrin 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,
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.
Resmethrin 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. Resmethrin is extremely
toxic to fish, other aquatic life and
bees. The domestic manufacturer of
Synthetic Pyrethroids chemicalWATCH Factsheet References
Beyond Pesticides
National Coalition Against the Misuse of Pesticides
701 E Street, S.E., Suite 200 • Washington DC 20003 • 202-543-5450 (v) • 202-543-4791 (f) • ncamp@ncamp.org • www.beyondpesticides.org
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.
Sumithrin
(AnvilTM, d-Phenothrin)
Sumithrin 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 nonfood
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 bearing the word CAUTION
on its label. The oral rat LD50 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).
Symptoms 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 demonstrates
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).
Cassagrande, R.A. 1989. “Considerations
for state label for PermanoneTM.” RI
Pesticide Relief Advisory Board.
Providence, RI.
“EPA’s Recent Bets.” Science, vol. 218,
December 3, 1981.
Extension Toxicology Network (ETN).
1996. Permethrin.” Pesticide
Information Profiles. .
Extension Toxicology Network (ETN).
1994. Pyrethroids.” Pesticide
Information Profiles. .
Extension Toxicology Network (ETN).
1996. Resmethrin.” Pesticide
Information Profiles. .
Garey, J. and M. Wolff. 1998. “Estrogenic
and Antiprogestagenic Activities
of Pyrethroid Insecticides.” Biochem
Biophys Res Commun. 251 (3): 855-9
Go, V. et al. 1999. “Estrogenic Potential of
Certain Pyrethroid Comounds in the
MCF-7 Human Breast Carcinoma
Cell Line.” Environmental Health
Perspectives. 107:3
Gosselin, R.E. 1984. Clinical Toxicology of
Commercial Products. Williams
and Wilkins. Baltimore, MD.
Hallenbeck, W.H. and K.M. Cunningham-
Burns. Pesticides and Human Health.
Springer-Verlag, New York, NY.
Hayes, W.H., Pesticides Studied in Man,
Williams & Wilkins. Baltimore,
MD. 1982.
“Hormonal and Environmental Factors
Affecting Cell proliferation and
Neoplasia in the Mammary Gland.”
Progress in Clinical and Biological
Research (PCBR). 394:211-53, 1996.
Kaloyanova, F. and S. Tarkowski, eds,
Toxicology of Pesticides - Interm
Document 9, World Health
Organization, Copenhagen, 1982.
Klaassen, C.D. et al., eds, Casarett and
Doull’s Toxicology, Macmillan
Publishing Co., New York, NY.
Kolmodin-Hedman, B., et al. 1982.
“Occupational exposure to some
synthetic pyrethroids (permethrin
and fenvalerate).” Arch. Toxicol.
50:27-33.
Mueller-Beilschmidt, Doria. 1990.
“Toxicology and Environmental Fate
of Sythetic Pyrethrois.” Journal of
Pesticide Reform. 10 (3):32-37.
National Research Council. 1987.
Regulating Pesticides in Food: The
Delaney Paradox. National Academy
Press, Washington, DC.
Olkowski, W. 1989. “Natural and synthetic
pyrethrum insecticides: Finding your
way through the maze.” Common
Sense Pest Quarterly. 5(1):8-12.
Reigart, J., M.D. et al., Recognition and
Management of Pesticide Poisonings,
EPA, 1999.
Scourge Insecticide Product Label with
SBP-1382/Piperonyl Butoxide 18% +
54% MF. U.S. EPA Reg. No. 432-667.
AgrEvo, montvale, NJ.
Takahashi, O., et al., 1994. “Chronic toxicity
studies of piperonyl butoxide in F344
rats: induction of hepatocellular
carcinoma.” Fund. Appl. Toxicol. 22:
293-303.
Thomson, W.T. 1984. Agricultural
Chemicals: Insecticides. Thompson
Publications, Fresno, CA.
U.S. EPA. 1979. Environmental Fate Review
of Permethrin (activated sludge
metabolism study). November 29.
Office of Pesticide Programs.
Washington, DC.
U.S. EPA. 2000. For Your Information,
Synthetic Pyrethroids for Mosquito
Control. Washington, DC. May.
U.S. EPA. 1997. Office of Pesticide
Programs list of chemicals evaluated
for carcinogenic potential. Memo from
W.L. Burnman, HED, to HED branch
chiefs. Washington, DC. February 19.
World Health Organization (WHO). 1990.
d-Phenothrin. Environmental Health
Criteria. Geneva.
Wright, C., et al. 1981. “Insecticides in the
ambient air of rooms following their
application of control of pests.” Bull.
Environ. Contam. Toxicol. 26:548-553.
The 18th century Venetian adventurer, romancer, and alchemist Giovanni Casanova
reportedly said, "In the hands of the wise, poison is medicine. In the hands of a fool,
medicine is poison."
And in the hands of a pet owner who isn’t careful, the wrong kind of medicine can have
disastrous consequences.
Advancements in medicine over the last several decades have given us a cornucopia of
drugs that can help cure or alleviate many ills, both in humans and in animals. But
what’s good for the goose is definitely not always good for the German shepherd. A
medication that works for you may not work for your dog, and what works for your dog
may not work for your cat, rabbit, or ferret.
"People think that cats are like little dogs, and they’re all like little people. They don’t
think about it, and they don’t read the [medication’s] label," said Dr. Petra Volmer,
assistant professor of toxicology at the University of Illinois College of Veterinary
Medicine. "Someone thinks, ‘I use naproxen and it works great for my back. My dog has
a sore leg, so let’s give him some naproxen.’"
Animals of different species process drugs in widely varying ways. Dogs, for example,
are very sensitive to non-steroidal anti-inflammatory drugs (NSAIDs) that are common
in their humans’ medicine cabinets. This class of drugs includes pain medications like
acetylsalicylic acid (aspirin), ibuprofen (Advil and Nuprin), acetaminophen (Tylenol),
phenylbutazone ("bute," a common painkiller for horses) and naproxen.
According to pet poisoning guidelines issued by the American Veterinary Medical
Association, as little as two tablets of regular strength aspirin or Tylenol can cause
significant tissue damage in dogs, and repeated doses significantly increase the risk of
death.
Cats are even more sensitive to NSAIDs because they have less of the enzyme that is
required to detoxify and utilize the drugs: just two extra-strength Tylenol can be deadly.
This page is a special feature of Working Dogs
Cyberzine
Bad Medicine
Written by: Erin Harty, Staff Writer - VetCentric.com
1
NSAID metabolites can impair the function of a cat’s red blood cells, which carry
oxygen from the lungs to all the cells of the body. If the red blood cells aren’t performing
their job properly, a cat can suffocate from lack of oxygen.
Well-meaning owners often assume that these common, over-the-counter drugs are safe
for their pets in smaller doses. "It has nothing to do with size; it’s the way they
metabolize it. With everything, we assume that cats are twice as sensitive," said Jill
Richardson, DVM, veterinary poison information specialist at the American Society for
the Prevention of Cruelty to Animals’ National Animal Poison Control Center.
The problems aren’t limited to human medications—a drug that may be safe and useful
for one animal can be deadly for another. Many of the calls to the National Animal
Poison Control Center are regarding accidental poisonings from topical flea medications.
Products that are designed for dogs often contain a drug called permethrin, which has a
wide safety range when used on Fido. But just a few drops of the product may cause
Fluffy the cat to suffer potentially fatal seizures.
Rabbits are also extraordinarily sensitive to flea medications intended for both dogs and
cats. The Frontline brand in particular has been blamed for several rabbit deaths,
although the manufacturer has never suggested that the product be used on rabbits.
"Drugs in rabbits are very different from dogs and cats. Extremely different, in some
cases," said George Flentke, a biochemist in the toxicology department at the University
of Wisconsin. "I always recommend that people contact a bunny-savvy vet [before using
any medication.] They keep up on this stuff."
Although the packaging for any such products will explicitly say that they’re only for use
on the species for which they’re intended, owners sometimes mix up medications that are
meant for other pets. Or they simply won’t read the label, and will (erroneously) assume
that a product can be used on any animal.
"Think about what you’re doing. Animals are different from people, and different from
each other. All different species metabolize things differently," said Dr. Volmer. "If
you’re not sure [if a medication is safe], call your vet or ask an animal poison control
center."
In some cases, pets get themselves into poisoning trouble. Dogs may dig discarded
medication out of the trash, or chew up an entire box of cold medicine, contents and all.
Cats may lick the sugar coating off tablets of Advil that are left on the side of the sink. A
ferret with run of the house might get into a kitchen cabinet and help itself to some
Prozac.
Large breeds of dogs are the most frequent mass-consumers of medications. "They’re
less finicky. They don’t think, they just eat," said Dr. Volmer. "And they don’t stop at
2
one [tablet]. They have to eat the whole package."
Ferrets also seem prone to overdose accidents because they’re extremely curious and
have the appetites of dogs, according to Dr. Richardson. Cats, on the other hand, won’t
usually eat something unless it tastes good; their overdoses are most often humancaused.
According to guidelines issued by the National Animal Poison Control Center, all
prescription and over-the-counter drugs should be kept safely out of pets’ reach,
preferably in closed cabinets. Pain killers, cold medicines, anti-cancer drugs,
antidepressants, vitamins and diet pills can all be lethal to animals.
Also beware of herbal medications, Dr. Richardson warns. Just because something is
billed as "natural" doesn’t mean it won’t have adverse affects on a pet. One particular
herbal diet aid has caused numerous accidental poisonings.
"It contains mahuang, which is like herbal ephedrine, and guarana, which is like caffeine.
We’ve had so many horrible cases on that," said Dr. Richardson. She recently treated a
miniature pincher who’d eaten 30 to 50 of the pills. A lethal dose of this drug is 6
milligrams per kilogram of body weight; the pinscher consumed 7 times that, and
eventually died.
In most cases, animals have a good chance of survival if their owners seek medical
attention immediately. A veterinarian can pump the animal’s stomach, administer
activated charcoal and perform diuresis, all of which will help minimize the dangerous
effects of the drug. The sooner a veterinarian sees a pet, the more likely the case will
have a happy ending.
"We do have some ‘miracle cases.’ But not very many of them would have made it if
someone hesitated or waited a day or two," said Dr. Richardson. "I think in most cases
we get here, if we get the information early, the animals are treated promptly and
appropriately."
Article republished here with permission from VetCentric.com
Copyright(c) 2000 by VetCentric.com
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ABCNEWS.com : Is Spraying For West Nile Pointless? Page 1
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August 15, 2003
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A truck sprays pesticides into the air in an area
threatened by West Nile. (ABCNEWS.com)
Useless Spraying?
West Nile Deterrent May Not Be Best
Solution
By Erin Hayes
Aug. 8 —If you live in one of the 34 states
where West Nile virus has been discovered,
should you draw comfort from the clouds of
pesticides being sprayed into the air to kill off
mosquitoes?
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Maybe not.
"The chemicals have not been adequately tested for their
human health effects," cautioned Dr. Sheldon Krimsky, a
pesticide-risk expert at Tufts University. "There is a lot of
circumstantial evidence that they cause cancer in animal
studies, that they are hormone disruptors. Remember, these
are neurotoxins," Krimsy said, adding that most studies done
on the effects of spraying focused on agricultural spraying —
not spraying in populated areas.
"We simply don't know what effects it's going to have, the
indiscriminate spraying on human populations," he added.
So far this year, officials have reported 112 human cases of
West Nile, more than half in the past week, according to the
Centers for Disease Control and Prevention (CDC). Most of
these infections are in Louisiana. Mississippi and Illinois also
have reported human infections of the virus, which began
showing up in the United States in New York three years
ago.
Residents Protest Dangerous Pesticides
In Hays County, Texas, residents effectively stopped
spraying in many of their neighborhoods. They protested,
carrying posters decrying the "chemical warfare" on their
families. County commissioners agreed to severely limit
mosquito spraying near those homes.
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ABCNEWS.com : Is Spraying For West Nile Pointless? Page 2
http://abcnews.go.com/sections/wnt/DailyNews/westnile_spraying020808.html 08/16/03 12:33:07 AM
• Study: DEET Is Best
Bug Repellent
In Jefferson County, Ala., health officials are trying to decide
what to do. Many cities, including Birmingham, have been
spraying for weeks. County officials, though, haven't started
their own spraying efforts because they aren't convinced
spraying is all that effective against mosquitoes.
But after a case of West Nile infection was recently discovered in Alabama, some
residents began demanding that the county spray.
Brian Debrow, the environmental health program manager at the Jefferson County Health
Department, says the county may start spraying in order to ease anxiety. "The public likes
seeing the trucks going down the road and spraying for mosquitoes," he said. "It gives
them a sense of security they feel like something is being done."
CDC: Least Effective Deterrent
Scientists at the CDC, which is leading the surveillance effort on West Nile virus, do not
take a position on whether local health departments should spray for mosquitoes. But they
do point out that spraying is the least effective method of slowing the spread of the insects.
Since adult mosquitoes only live for about two weeks at the most— whether they're
sprayed or not— the most effective way to limit mosquitoes is to keep them from
breeding. And that means emptying out pools of water where they lay their eggs.
"These would include things like old tires, cans, flower pots and so forth, just do an
inspection and see what's out there that might serve as a breeding ground for the
mosquitoes," points out Dr. Julie Gerberding, the director of the CDC.
And that's exactly what Washington, D.C. health officials are doing. They've decided that
spraying pesticides into the air is too risky, especially since the incidence of asthma in the
city is already high.
Instead, they are targeting small amounts of pesticides directly into pools of standing water
and ditches where mosquitoes are breeding. And they're going door-to-door with
pamphlets that explain to residents how best to avoid mosquitoes altogether.
Even so, in the states where West Nile virus has been discovered, there is pressure on
health officials to appear to be fighting the virus on every front and many feel the most
convincing approach is the most visible one—spraying chemicals out where everyone can
see.
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Duke Pharmacologist Says Animal
Studies on DEET's Brain Effects
Warrant Further Testing and Caution
in Human Use
DURHAM, N.C. -- A Duke University Medical
Center pharmacologist is recommending caution
when using the insecticide DEET, after his
animal studies last year found the chemical
causes diffuse brain cell death and behavioral
changes in rats after frequent and prolonged use.
Mohamed Abou-Donia, Ph.D. has also called
for further government testing of the chemical's
safety in short-term and occasional use,
especially in view of Health Canada's recent
decision to ban products with more than 30
percent of the chemical. Every year,
approximately one-third of the U.S. population
uses insect repellents containing DEET,
available in more than 230 products with
concentrations up to 100 percent.
While the chemical's risks to humans are still
being intensely debated, Abou-Donia says his
30 years of research on pesticides' brain effects
subject keywords : toxicology, chemical
exposure, insecticide
date : 5/1/2002
contact : Becky Levine , (919)
660-1308 or (919) 684-
4148
levin005@mc.duke.edu
Mohamed B. Abou-Donia, Ph.D.
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1
clearly indicate the need for caution among the
general public.
His numerous studies in rats, two of them
published last year, clearly demonstrate that
frequent and prolonged applications of DEET
cause neurons to die in regions of the brain that
control muscle movement, learning, memory
and concentration. Moreover, rats treated with
an average human dose of DEET (40 mg/kg
body weight) performed far worse than control
rats when challenged with physical tasks
requiring muscle control, strength and
coordination. Such effects are consistent with
physical symptoms in humans reported in the
medical literature, especially by Persian Gulf
War veterans, said Abou-Donia.
"If used sparingly, infrequently and by itself,
DEET may not have negative effects – the
literature here isn't clear," he said. "But frequent
and heavy use of DEET, especially in
combination with other chemicals or
medications, could cause brain deficits in
vulnerable populations."
Children in particular are at risk for subtle brain
changes caused by chemicals in the
environment, because their skin more readily
absorbs them, and chemicals more potently
affect their developing nervous systems, said
Abou-Donia. Commonly used preparations like
insecticide-based lice-killing shampoos and
insect repellents are assumed to be safe because
severe consequences are rare in the medical
literature. Yet subtle symptoms -- such as
muscle weakness, fatigue or memory lapses --
might be attributed erroneously to other causes,
he said.
With heavy exposure to DEET and other
insecticides, humans may experience memory
loss, headache, weakness, fatigue, muscle and
joint pain, tremors and shortness of breath, said
Abou-Donia. His earlier research, examining the
brain effects of three chemicals used during the
Persian Gulf War, clearly demonstrated that
chickens exhibited similar signs that the Gulf
Cancer
Duke Study: High Mutation
Rates in Cancer Cells Can Be
Caused By Non-DNADamaging
Stresses
01/14/01
The Dangers of DEET 06/21/02
If you're headed for the beach
this summer, you might want to
forget the sunscreen, and pack
the sunblock instead.
05/18/01
2
War veterans complained of upon returning
from service. (Journal of Toxicology and
Experimental Health, May, 1996, Volume 48, p.
35 - 56).
Such overt symptoms are not seen immediately
after use but may manifest themselves months
or years after exposure, making a cause-andeffect
relationship difficult to establish , said
Abou-Donia. By studying animals such as
chickens and rats, however, researchers are able
to compress the time between exposure and the
onset of symptoms: 10 months of a rat's life is
several years in a human's life. Moreover,
researchers can study layers of the rats' brains at
various stages after exposure to measure the
chemical's effects on the brain.
Indeed, Abou-Donia's two most recent studies
demonstrate the severe brain and behavioral
deficits that rats experience after two months of
daily skin applications with DEET and
permethrin, another common insecticide,
(Experimental Neurology, 2001, volume 172 ,
p.153- 171); and following 60 days of exposure
to DEET and permethrin, and 15 days of
pyridostigmine bromide, an anti-nerve gas agent
(Journal of Toxicology and Environmental
Health, 2001, volume 64, p. 373-384). Both
studies examined the effects of each drug alone
and in combination.
In each study, the treated animals initially
appeared to be normal, just like the control
group, said Abou-Donia. But when challenged
with neurobehavioral tasks that required muscle
control, strength and coordination, the rats
demonstrated serious impairments. Moreover, a
detailed analysis of their brains clearly showed
that large numbers of brain cells were dying
within three critical brain structures: the cerebral
cortex, which controls muscles and movement;
the hippocampal formation, which controls
memory, learning and concentration; and the
cerebellum, which synchronizes body
movements.
In addition, many of the surviving brain cells
3
showed signs of degeneration and damage
consistent with the presence of harmful
byproducts called oxygen free radicals (also
known as reactive oxygen species), which can
damage DNA and cell membranes in the brain
and the nervous system.
The most severe brain cell changes and
sensorimotor deficits were seen among rats
exposed to combinations of DEET, permethrin
and the anti-nerve gas agent pyridostigmine
bromide, which reduces the body's normal
ability to inactivate pesticides. Such findings
confirmed Abou-Donia's 1996 and 2001 animal
studies demonstrating that harmless doses of
these three chemicals proved highly toxic to the
brain and nervous system when used in
combination.
"The take home message is to be safe and
cautious when using insecticides," said Abou-
Donia. "Never use insect repellents on infants,
and be wary of using them on children in
general. Never combine insecticides with each
other or use them with other medications. Even
so simple a drug as an antihistamine could
interact with DEET to cause toxic side effects.
Don't spray your yard for bugs and then take
medications. Until we have more data on
potential interactions in humans, safe is better
than sorry."
contact
sources :
Mohamed Abou-Donia Ph.D. ,
(919) 684-2221
donia@acpub.duke.edu
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