Comfort and Moisture Transport in Lightweight Wool and Synthetic Base Layers

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    Ken-Admin Knight


    Aaron Teasdale
    BPL Member


    Excellent review. I do wish you’d used Marmot silkwieght instead of Capilene however — it seems to resist odor better. While it’s quite durable, the latest iteration of Capilene gets very stinky very fast. The Marmot silkweight is also remarkably durable — It held up amazingly well during an extended bushwacking session through savage alders — not a single mark, and it was getting grabbed and pulled at every step. After a decade of using Capilene and wool, I was very impressed.

    Wool is a wonderful base layer, especially in winter. It offers much more range than synthetics. But, over the years, I’ve had serious durability problems with it — both socks and baselayer tops. It just hasn’t held up for me. A major bummer given its cost.

    Douglas Hus


    Locale: Ontario, Canada

    Great article, I am now not in as big a rush to buy wool. But still; I fore see a need for a new base layer.

    Most of my 3 season trips I have had the opportunity to do laundry, socks & base layers. Zip-lock bag, soap and a shake. Helps with the odour thing. Length of dry time varies.

    Weight is still "King".



    Adam Rothermich
    BPL Member


    Locale: Missouri Ozarks

    Wow Doug, I'd never thought about doing laundry in a Ziploc before. That's a great idea, I'm surprised I've never heard of it elsewhere. Its such a simple to solution to smelly clothes. I'm definitely going to keep it in mind when I do some longer trips this spring and summer.
    To stay somewhat on-topic, the only wool I own are some socks and a Smartwool beanie. The beanie is great in a wide range of temps and the socks are great too. I've been eyeing the SW Lightweight 1/4 zip too. SAC had them for $35 one day and I decided I didn't really need one. Now they haven't come back up on SAC and I can't bring myself to spend $70 on one shirt and I kick myself every time I think about how I let it slip away.


    Einstein X
    BPL Member


    Locale: The Netherlands

    I think BPL missed out on calculating a ratio, which seems to me a more objective measure in reviewing the drying characteristics of the materials:

    The weights of the samples before wetting [1]:
    Pata 12 g
    GL 10 g
    Ibex 14 g
    IB 18 g
    SW 14 g

    The weights of the samples after wetting [2]:
    Pata 47 g
    GL 54 g
    Ibex 59 g
    IB 63 g
    SW 68 g

    Absorbed mass of water [3] = [2] – [1]:
    Pata 35 g
    GL 44 g
    Ibex 45 g
    IB 45 g
    SW 54 g

    Time of drying [4]:
    Pata 65 min
    GL 75 min
    Ibex 90 min
    IB 90 min
    SW 100 min

    Now the amount of time it requires to remove 1 gram of water from the fabric is calculated by deviding [4] over [3]:
    Pata 1:52 min
    GL 1:42 min
    Ibex 2:00 min
    IB 2:00 min
    SW 1:51 min

    I think these values are very interesting. They show that each fabric takes almost the same time to loose a gram of water in the fabric. With an average time of 1:53 min and a 9,4% spread. Most interesting is that the smartwool shirt dries actually 1 second faster than the patagonia shirt. This result is also experienced in the field test.

    The only right conclusion that can be made on this experiment is that each fabric is, within significance, equal in drying performance. The only difference is that wool can hold more water per whatever unit than a synthetic shirt. Thus in absolute time it will take the wool shirt longer to dry.

    An interesting experiment would now be to let each fabric absorb exactly the same amount of water and perform a new drying test. My take on it is that they will dry in exactly the same time (with the wool shirt feeling dry earlier than the synth shirt)


    eric levine


    Locale: Northern Colorado

    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.

    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.
    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
    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
    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
    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
    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
    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
    (a permethrin-containing insecticide) during larval development increased sex-linked
    lethal mutations in fruit flies.29
    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 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
    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:
    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
    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
    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
    The LC
    (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
    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
    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
    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
    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
    is less than
    1 ppb.64 It is highly toxic to oyster larvae, with an EC
    (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
    s of several species are about 1 ppb.67
    Permethrin also caused “severe mortalities” of two kinds of zooplankton, cladocerans
    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
    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
    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, 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
    According to EPA, permethrin’s half-life (the amount of time required for half of the
    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
    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
    l Butane is in the household insecticides Raid Yard Guard Outdoor Fogger V and
    Off Yard and Deck Area Repellant 1. 101,102 It is “extremely flammable” and shortterm
    exposure causes irritation, nausea, drowsiness, convulsions, and coma.103
    P. O. B O X 1 3 9 3, E U G E N E, O R E G O N 9 7 4 4 0 / (5 4 1 )3 4 4 -5 0 4 4
    I N S E C T I C I D E F A C T S H E E T
    [ Pesticide Site Map ] * [ Main Site Map ]
    references Page 1 11:48:08 AM
    P. O. B O X 1 3 9 3, E U G E N E, O R E G O N 9 7 4 4 0 / (5 4 1 )3 4 4 -5 0 4 4
    Back to Pesticide Fact Sheet
    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
    mitochondrial complex I. J. Pharmacol. Exper. Therap. 281:855-860.
    12. International Programme on Chemical Safety. 1989. Permethrin health and safety guide. Health
    and Safety Guide No. 33. Geneva, Switzerland: World Health Organization, United Nations
    Environment Programme, and International Labor Organization.
    13. Mitchell, J.A., M.C. Wilson, and M.J. Kallman. 1988. Behavioral effects of pydrin and ambush in
    male mice. Neurotoxicol Teratol. 10:113-119.
    14. McDaniel, K.L. and V.C. Moser. 1993. Utility of a neurobehavioral screening battery for
    differentiating the effects of two pyrethroids, permethrin and cypermethrin. Neurotoxicol. Teratol.
    15. Peele, D.B. and K.M. Crofton. 1987. Pyrethroid effects on schedule-controlled behavior: Time
    and dosage relationships. Neurotoxicol. Teratol. 9:387-394.
    16. FMC Corporation. 1996. Label. Pounce 3.2 EC Insecticide. Label. Philadelphia, PA, Mar.
    17. Solaris. 1995. Material safety data sheet. Flea-B-Gon Total Flea Killer Indoor Fogger. San Ramon,
    CA, July 21.
    18. Solaris. 1995. Material safety data sheet. Ortho Total Flea Control 2. San Ramon, CA, July 21.
    19. Pfizer Animal Health. Undated. Label. Adams 14 Day Flea Dip.
    20. Blaylock, R.L. et al. 1995. Suppression of cellular immune responses in BALB/c mice following
    oral exposure to permethrin. Bull. Environ. Contam. Toxicol. 54:768-774.
    21. Stelzer, K.J. and M.A. Gordon. 1984. Effects of pyrethroids on lymphocyte mitogenic
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    24. U.S. EPA. Office of Pesticide Programs. Health Effects Division. 1997. Tox oneliners:
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    25. Spencer, F. and Z. Berhane. 1982. Uterine and fetal characteristics in rats following a postimplantational
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    31. Ref. #1, pp.76-78.
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    and adult rats. Arch. Toxicol. 67:510-513.
    39. Pall, H.S. et al. 1987. Motorneurone disease as manifestation of pesticide toxicity. The Lancet
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    40. Steventon, G.B., R.H. Waring, and A.C. Williams. 1990. Pesticide toxicity and motor neuron
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    41. Helson, B.V., K.N. Barber, and P.D. Kingsbury. 1994. Laboratory toxicology of six forestry
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    42. Cox, R.L. and W.T. Wildon. 1984. Effects of Permethrin on the behavior of individually tagged
    honey bees, Apis mellifera L. (Hymenoptera: Apidae). Environ. Entomol. 13:375-378.
    43. Taylor, K.S., G.D. Waller, and L.A. Crowder. 1987. Impairment of a classical conditioned
    response of the honey bee ( Apis mellifera L.) by sublethal doses of synthetic pyrethroid insecticides.
    Apidologie 18:243-252.
    44. Hassan, S.A. et al. 1983. Results of the second joint pesticide testing programme by the IOBC/
    WPRS-Working Group “Pesticides and Beneficial Arthropods.” Z. ang. Ent. 95:151-158.
    45. Varma, G.C. and P.P. Singh. 1987. Effect of insecticides on the emergence of Trichogramma
    brasiliensis (Hymenoptera: Trichogrammitidae) from parasitized host eggs. Entomophaga 32: 443-
    46. Jiu, G.D. and J.K. Waage. 1990. The effect of insecticides on the distribution of foraging
    parasitoids, Diaeretiella rapae (Hym.: Braconidae) on plants. Entomophaga 35:49-56.
    47. Kreutzweiser, D.P. and P.D. Kingsbury. 1987. Permethrin treatments in Canadian forests. Part 2:
    Impact on stream invertebrates. Pestic. Sci. 19:49-60.
    48. Siegfried, B.D. 1993. Comparative toxicity of pyrethroid insecticides to terrestrial and aquatic
    insects. Environ. Toxicol. Chem. 12:1683-1689.
    49. Anderson, R.L. 1982. Toxicity of fenvalerate and permethrin to several nontarget aquatic
    invertebrates. Environ. Entomol. 11:1251-1257.
    50. Ref. #1, p.59
    51. Qadri, S.S. et al. 1987. Haemotoxicity to chicken ( Gallus gallus domesticus) by technical and
    formulation grades of some phosphoric and synthetic pyrethroid esters. J. Appl. Toxicol. 7:367-371.
    52. McCorkle, F. et al. 1980. The effect of permethrin on the immune response of chickens. Poul. Sci.
    53. U.S. EPA. 1993. Data evaluation record: permethrin. Avian reproduction study. Reviewed by
    Charles G. Nace. Washington, D.C., Mar. 12.
    54. Eells, J.T. et al. 1993. Differences in the neuroexcitatory actions of pyrethroid insecticides and
    sodium channel-specific neurotoxins in rat and trout brain synaptosomes. Toxicol. Appl. Pharmacol.
    55. Haya, K. 1989. Toxicity of pyrethroid insecticides to fish. Environ. Toxicol. Chem. 8:331-391.
    56. Ref. #1, pp. 47,48,51-53.
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    57. Holdway, D.A. and D.G. Dixon. 1988. Acute toxicity of permethrin or glyphosate pulse exposure
    to larval white sucker ( Catostomus commersoni) and juvenile flagfish ( Jordanella floridae) as
    modified by age and ration level. Environ. Toxicol. Chem. 7:63-68.
    58. Rice, P.J. et al. 1997. Acute toxicity and behavioral effects of chlorpyrifos, permethrin, phenol,
    strychnine, and 2.4-dinitrophenol to 30-day-old Japanese medaka ( Oryzias latipes) Environ. Toxicol.
    Chem. 16:696-704.
    59. Kreutzweiser, D.P. and G.A. Wood. 1991. Permethrin treatment in Canadian forests. Part 3:
    Environmental fate and distribution in streams. Pestic. Sci. 33:35-46.
    60. Muir, D.C.G., B.R. Hobden, and M.R. Servos.
    1994. Bioconcentration of pyrethroid insecticides and DDT by rainbow trout: uptake, depuration, and
    effect of organic carbon. Aquat. Toxicol. 29:223-240.
    61. Kingsbury, P.D. and D.P. Kreutzweiser. 1987. Permethrin treatment in Canadian forests. Part 1:
    Impact on stream fish. Pestic. Sci. 19:35-48.
    62. Berrill, M. et al. 1993. Lethal and sublethal impacts of pyrethroid insecticides on amphibian
    embryos and tadpoles. Environ. Toxicol. Chem. 12:525-539.
    63. Yaseem, N. and Nayeemunnisa. 1992. Insecticide induced disruptions in functioning of
    developing brain of Rana cyanophlictis. Ind. J. Exper. Biol. 30:701-704.
    64. McLeese, D.W., C.D. Metcalfe, and V. Zitko. 1980. Lethality of permethrin, cypermethrin, and
    fenvalerate to salmon, lobster, and shrimp. Bull Environ. Contam. Toxicol. 25:950-955.
    65. U.S. EPA. 1993. EEB review of permethrin. Memo from A.F. Maciorowski, Ecological Effects
    Branch, to Jay Ellenberger, Special Review and Reregistration Division. Washington, D.C., July 22.
    66. Schimmel, S.C. et al. 1983. Acute toxicity, bioaccumulation, and persistence of AC 222,705,
    benthiocarb, chlorpyrifos, fenvalerate, methyl parathion, and permethrin in the estuarine
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    Daphnia magna and Ceriodaphnia dubia. Environ. Toxicol. Chem. 9:1045-1051.
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    zooplankton. Environ. Toxicol. Chem. 8:411-416.
    67. Jarboe, H.H. and R.P. Romaire. 1991. Acute toxicity of permethrin to four size classes of red
    swamp crayfish ( Procambarus clarkii) and observations of post-exposure effects. Arch. Environ.
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    72. Goolsby, D.A. and W.A. Battaglin. 1993. Occurrence, distribution and transport of agricultural
    chemicals in surface waters of the Midwestern United States. In Goolsby, D.A., L.L. Boyer, and G.E.
    Mallard. Selected papers on agricultural chemicals in water resources of the midcontinental United
    States. Open File report 93-418. Denver, CO: U.S. Geological Survey.
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    chemicalWATCH Factsheet
    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.,
    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) • [email protected]
    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.
    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 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) • [email protected]
    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.,
    (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).
    (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) • [email protected]
    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.
    (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.,
    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.
    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

    Shawn Basil


    Locale: Southeast

    In an age of West Nile virus in mosquitoes and Lyme Disease amongst ticks, I'll gladly accept the risk posed by permethrine. Any wilderness endeavor is based upon a foundation of risk management, and I find the risks involved in using permethrine acceptable versus the other options available, such as being comsumed by insects or annointing my body in the more abrasive DEET option.

    Now can we please get back to the topic of comfort and moisture control in merino wool products?

    Is that cavalier enough for you?

    Thomas Knighton


    Locale: Southwest GA

    >Now can we please get back to the topic of comfort and >moisture control in merino wool products?
    >Is that cavalier enough for you?

    Here here!

    I know how to deal with bugs in multiple ways…moisture control is still an area I have a lot more to learn about ;)


    Phil Barton
    BPL Member


    Locale: Oklahoma

    Shawn expresses my thoughts very well. In light of the risk of insect borne disease, permethrin is a reasonable choice. There is no such thing as a free lunch.

    eric levine


    Locale: Northern Colorado

    Now now,

    The off topic was started by folks asking which material was most compatible laced with Permethrin, a class C carcinogen. It was not started by me, who believes in giving people at least a clue, then cheerfully letting them choose their own poison. Since 80% of west nile virus has no effect save longterm future immunity, things could be worse.

    Adulticides harm our environment and damage our planet's ecosystems (remember Rachel Carson?), so I usually assume outdoors people would be humble enough to show it some respect.

    For the past 5 months I've been using Picaridin, a non-deet presumably much safer repellent said to be just as effective. Only Cutter Advanced outdoorsman has enough concentration (15%) to be truly useful. The standard in Europe is ~19.2%

    Friends of mine have acid tested it with VERY good results in the Colorado's Rawah's this year.

    My results have about equaled Sawyer controlled release deet, which is 20%. Equal to 20% deet was not enough for several really infested trails I hiked, but it did save my rear.

    donald buckner


    Locale: Southeast U.S.

    As a hunter first, and a backpacker second, I am a fan of both synthetic and wool, but only recently used the really thin wool base layers. I prefer the wool to the synthetic for most applications. This is after a week of hunting in the Northwest Territories, Canada. I live in the Southeast, and redbugs (chiggers) and ticks and really bad in early hunting season. The permethrin works well for ticks, but I have found deet works best for chiggers and mosquitos. The device called thermacell is a lifesaver where mosquitos are a serious problem. (Walmart,$25). I don't know the weight, but it is not very heavy, and might be con sidered even for backpacking. I don't know how the native americans made it in some of the rotten insect conditions in the southeast. In the Northwest T. Canada, I underestimated the temps, so I layered icebreaker wool then Patagonia zip T, then Golite hooded windshirt, then a soft shell camo zip T, wool fleece blend vest, and finally a packable gortex rain jacket to withstand temps around 40F with 15-20mph winds,(and a good bit of 35mph boat ride around a big lake). I was very pleased with this setup and by layering the wool under the Patagonia, I did not have the stink issues. Of course, when running around the tundra, multiple layers were shucked to keep from overheating.

    Forrest G McCarthy
    BPL Member


    Locale: Planet Earth

    Great article. The objective and scientific testing procedure produced credible and highly informative data. I would love to have one of the clown shirts! Maybe an all wool replica?

    The resonance of wool in outdoor apparel should be credited to New Zealand. In the late 90’s New Zealand companies, such as Icebreaker (, refined the processing of merino wool and produced an attractive line of highly functional outdoor garments. A regular visitor to New Zealand during that time I was an early convert. My wardrobe of Icebreaker products includes briefs, t-shirts, long sleeve shirts, leggings, and a hoodie. Marino base and insulating layers are my first chose on any outing with the exception of the hottest summer or desert adventures. On those hottest days I prefer a light nylon (Exoficio) shirt and pants. But that is another story.

    I would like to comment on wool verses synthetics in extremely wet environments. The articles research did a wonderful job examining drying times. However, experiments that investigated insulating values while fabrics were wet maybe equally revealing. I prefer wool for both base and insulating layers when subjected to indomitable moisture. White water packrafting or “tramping” in New Zealand are prime examples of these moist and cold activities. It has been my observation that wool is a far greater insulter when saturated then any synthetic.

    The challenging maritime weather of New Zealand Zealand’s South is legendary. My Kiwi accomplices have long advocated merino wools superior performance in cold, wet, and variable weather. Merino wools superior performance, odiferous appeal, and environmental benefits make it my first chose when packing for any outing.

    John Haley


    Locale: New York/Vermont Border

    For this winter season I have now accumulated an Icebreaker Exp 320 Conquest Hoodie, Icebreaker Bodyfit Oasis 200 Crewe top and Icebreaker Bodyfit 200 leggings, an Icebreaker 320 weight cap, and also Icebreaker glove liners. So far I've been able to layer under shell outerwear and be as warm as I've ever been without the usual buildup of moisture happening. I've been using Smartwool socks again this year since that's the one item that Icebreaker doesn't seem to make.

    Michael Davis


    Locale: South Florida


    Let us know how you like the Icebreaker Exp 320 Conquest Hoodie. I am a "dyed in the wool" merino fan and have been looking (read, drooling) at this piece for a while. I have every other weight of merino garments from the "big 3", Smartwool, Icebreaker and Ibex.

    Of all of them, I think that Icebreaker makes the most comfortable clothes; "snuggly" is how I describe them. Ibex makes extra durable material but it's somewhat "hard" and their stupid little logos that are embroidered are down-right scratchy. I have no complaints with Smartwool.

    Because at this thickness, 320 gm/m2, wool gets pretty heavy, I'm also considering a PowerStretch hoodie instead (with thin wool baselayer) to save weight. I'm not sure if this approach would actually save the weight and I'm also worried that the PowerStretch hoodie will take up more room in my pack when not wearing it, compared to the Conquest Hoodie.

    John Haley


    Locale: New York/Vermont Border

    Hi Michael…

    I got the Conquest first and was so pleased with it that I went for all the rest. I couldn't believe that a hoodie of that weight would be so comfortable against bare skin. The Conquest hoodie is heavy at 22 ounces (large), but being the EXP weave it is extremely warm and wind resistant. I have worn it alone with no base layer on 35F days, albeit with no strong wind.

    I wrote to Icebreaker about weight recommendations on the base layer and was told that the 200 would probably fit my needs better than the very warm 260, particularly for the bottoms. One weight would be just as comfortable as the other against the skin.

    Forrest G McCarthy
    BPL Member


    Locale: Planet Earth

    My wife has the Conquest Hoodie and is very happy with it. She wears it mainly as a wintertime insulating layer. I have a Nomad Hoodie and wear it year round.

    Kavin Davidson raised the question of the durability of wool, especially when wet. I have developed holes in several of my Icebreaker garments. They all occurred while wearing merino as an outer layer when bushwhacking. To my memory the wool was not particularly wet. I doubt other base/insulating fabrics would have faired better. The holes did not continue to grow as they often do with Polypro or Capiline. I was able to easily stitch the holes closed.

    Michael Davis


    Locale: South Florida

    John or Forrest,

    Can you post the weight (and size) of your Conquest Hoodie?


    John Haley


    Locale: New York/Vermont Border


    I answered that question in my original post. The Conquest hoodie, in size Large, weighs 22oz. BTW, the hoodie is quite a bit larger than the Bodyfit 200 base layer. The Bodyfit 200 in a large fits both my top and legs like skin (I'm 6'1" and 186#), the hoodie in 320 EXP is more like a normal sweater fit. It does fit easily over the base layer.

    Michael Davis


    Locale: South Florida

    Thanks John,

    Sorry about asking to repeat the weight.

    It's getting bad when I can't remember back just 2 posts! I'm glad they display my name when logged into this website so I don't forget who I am. :-(

    BTW: I'm exactly the same height & weight as you so fit should be the same.

    Thanks again,

    john griffith
    BPL Member


    Locale: Southeast U.S.

    I can usually expect a plethora of keen insights from the forum comments after the articles. For once I'm disappointed at the lack of depth. All you guys are talking about is weight, warmth, drying time. I'm a total capilene guy. There is a certain amount of joy to be had when being out in the dead of winter with a hiking partner, and after a few days of putting in hard miles with windshirt/raingear on top of your baselayer, being the one that clearly smells the worst inside the tiny little tent that you don't dare ventillate because it's ten degrees outside. Does nobody else get this? Capilene rules!

    LeRoy Schmeling


    I camp in the dampness of the Boundary Waters area of Northern Minnesota. Wool has become my BL of choice. I've gotten good deals on Terramar products.

    Re water: I started treating my garments with the wash in water based DWR products and really like the result. There is less water absorption, they shed light showers and dry quicker.


    James Moughan


    I think these values are very interesting. They show that each fabric takes almost the same time to loose a gram of water in the fabric. With an average time of 1:53 min and a 9,4% spread. Most interesting is that the smartwool shirt dries actually 1 second faster than the patagonia shirt.

    2 years late ッ but this is a really good catch. When hiking, drenching your base layer should be rare if you control venting and such, so merino seems clearly superior.

    BPL Member


    Yes, great catch. This is a key variable IMO.

    I like the feel and performance of wool baselayers and the sustainbility but my concerns are cost and durability. I have polyester baslayers that are 15 years old and still going strong whereas I just had to retire a Smartwoll microlight base layer after 4 years of average use (too ma ny rips and tears). My wife suggested that it might last longer if it was not dried in a dryer so I am trying that for my icebreaker replacement. I also have another durability question. I find that most of my wool sweaters end up with moth holes in them long before they wear out, is the same true for merino baselayers? I assume it is…

    Mitchell Keil


    Locale: Deep in the OC

    Has anyone, including the testers and staff anything to say about the SPF of Wool vs Synthetics. I have worn both during many hikes. I prefer the wool and have used an Icebreaker LS 200 crew as my go to shirt/baselayer in everything from 30degrees to 90degrees in the Sierras and the San Gs near LA. I am very sun sensitive and from my observations whether I am wearing a high SPF rated synthetic or my wool I seem to get the same result: no over exposure to harmful solar radiation. But I can't really find anything online or from the manufacturers of wool apparel that indicates wool's sun protective qualities.

    Any comments or citations?

    Einstein X
    BPL Member


    Locale: The Netherlands

    Now this is an odd article! I read it already three years ago, as you can also see in the post date of the "Companion forum thread to" post. Even though being an old (but good) article it popped up in my iGoogle's BPL RSS reader as a fresh and new article. Or it least I was of the opinion that the 5 newest articles that BPL publishes will appear in my iGoogle page. So how come this one popped up??


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