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● INSECTICIDE FACTSHEET

Caroline Cox is NCAP’s staff scientist.

BY CAROLINE COX

Sumithrin (see Figure 1) is an

insecticide in the synthetic pyrethroid

pesticide family. It is also called dphenothrin. Marketed as an insecticide

since 1977,1 it is sold by many pesticide companies using a variety of

brand names, including Raid, Enforcer,

Ortho, and Anvil.2 There are about

250 sumithrin-containing pesticide

products registered for sale in the U.S.2

Pyrethroid insecticides are related

chemically to the insecticidally active

compounds called pyrethrins extracted

from chrysanthemum flowers. Chemists have designed the structure of synthetic pyrethroids to make them both

potent and stable in sunlight.3

Like most synthetic pyrethroid insecticides, sumithrin exists as a mixture of stereoisomers,1 molecules that

have the same atoms linked in the

same order, but differ in their spatial

arrangement.4 Sumithrin is a mixture

of 2 stereoisomers which are both insecticidally active.1 (See Figure 1.)

Synthetic pyrethroid insecticides,

SUMITHRIN (D-PHENOTHRIN)

The synthetic pyrethroid insecticide sumithrin is commonly used to kill household insects and mosquitoes. The U.S.

Environmental Protection Agency (EPA) estimates that about 100 million applications of sumithrin are made

annually in U.S. homes, yards, and gardens.

Sumithrin is a neuropoison. Symptoms of exposure include dizziness, headache, fatigue and diarrhea.

In laboratory tests, sumithrin has damaged the liver and the kidneys. It has also caused anemia and increased the

incidence of liver cancer.

In breast cancer cells, sumithrin increases the expression of a gene that is involved with proliferation of cells in the

mammary gland. Sumithrin can also mimic certain activities of the sex hormone estrogen and keep another sex

hormone from binding to its normal receptors.

Thousands of cat poisonings and some dog poisonings have been reported following the use of some sumithrincontaining flea control products.

Low concentrations of sumithrin (as low as one part per billion) kill fish and other aquatic animals. Sumithrin is also

highly toxic to bees.

Environmental Protection Agency

(EPA) survey estimated in 1992 that

almost 100 million applications of

sumithrin were made annually in U.S.

homes, yards, and gardens. About 2/3

of these applications occurred indoors.6

How Does Sumithrin

Kill Insects?

Sumithrin kills insects by disrupting

the transmission of nerve impulses

along axons, the elongated parts of

nerve cells. Synthetic pyrethroids allow excessive amounts of sodium atoms to enter nerve cells, stimulating

the nerve cells and eventually causing

paralysis. This mode of action is similar to that of the organochlorine insecticide DDT.3

Pyrethroids’ effects on human nerves

are similar to their effects on insect

nerves.5 However, human nerves are

generally less susceptible to pyrethroid

poisoning. This is because human

nerves are intrinsically less sensitive,

pyrethroids are less potent at the

higher body temperatures in humans,

and human nerves recover more

quickly from poisoning.7

Synergists

About a dozen sumithrin products,

including sumithrin, “are widely perceived as being safe”5 according to

one neurotoxicologist. However, sumithrin poses a variety of hazards for

human and environmental health, and

those are the focus of this article.

Use

Sumithrin is primarily used to kill

household insects, insects which pose

public health problems (mosquitoes,

for example), insects in stored grains,

and lice.1 The International Programme

on Chemical Safety estimated in 1989

that worldwide use was about 70 to

80 tons per year;1 more recent estimates are not publicly available. A U.S.

Figure 1

Sumithrin

3-phenoxybenzyl (1R)- trans-chrysanthemate

O

3-phenoxybenzyl (1R)- cis-chrysanthemate

COO—CH2

O COO—CH2
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including the Anvil products used to

kill mosquitoes, contain piperonyl butoxide.8 This chemical is used to

synergize (to make more toxic) sumithrin and other insecticides. Piperonyl butoxide is classified as a carcinogen by EPA, causes atrophied testes,

and reduces the activity of important

immune system components. For detailed information about the hazards

of piperonyl butoxide see JPR 22(2):12-

20 or www.pesticide.org.

Inert Ingredients

Like most pesticides, sumithrin insecticides contain ingredients in addition to sumithrin. Many of these ingredients, according to U.S. pesticide

law, are called “inert.”9 In general, they

have not been publicly identified, and

are not included in most of the testing

required in order to register these pesticides.10 “Inert Ingredients” (right)

summarizes the hazards of some inert

ingredients used in sumithrin products.

Symptoms of Exposure

Sumithrin and other synthetic pyrethroids are “neuropoisons” and symptoms of exposure are related to their

effects on the nervous system.11 According to Medical University of South

Carolina physicians, acute (short-term)

symptoms of exposure to sumithrin

and other synthetic pyrethroids include “dizziness, salivation, headache,

fatigue, diarrhea, and irritability to

sound and touch.”12

Effects on the Liver

According to a laboratory study submitted to EPA by a manufacturer as

part of the registration process,

sumithrin damages the liver. In a longterm (two-year) study in which rats

were fed sumithrin, the livers of exposed animals weighed more than

those of unexposed animals. In addition, concentrations of enzymes that

are indicators of liver damage increased

in exposed animals. These effects occurred at the middle and high dose

levels tested in this experiment.13

Similar increases in liver weight

were found in studies of dogs fed

sumithrin and rats breathing sumithrincontaminated air. Both studies were

conducted as part of the registration

process.14,15

Effects on the Kidneys

Two laboratory studies submitted as

part of the registration process suggest that male kidneys may be particularly susceptible to sumithrin.16,17

(See Figure 2.) At all dose levels tested,

“INERT” INGREDIENTS

Almost 100 sumithrin products contain petroleum distillates as inert

ingredients.1 One of these distillates is hydrotreated kerosene (Chemical

Abstracts Services (CAS) number 64742-47-8).2 According to the International Agency for Research on Cancer (IARC), exposure to hydrotreated

kerosene caused skin tumors in a laboratory study.3,4 Three other petroleum distillates (with CAS numbers 64742-55-8, 64742-56-9, and 64742-94-

5) are used in Anvil mosquito control products.5,6 One of these petroleum

distillates causes tremors and difficulty breathing,7 the second caused skin

tumors, according to IARC,8,9 and the third contains two hazardous

chemicals, naphthalene and trimethyl benzene.10 Naphthalene exposure

has caused lung tumors, cataracts, and anemia11 while trimethyl benzene

can depress the central nervous system and cause asthmatic bronchitis.12

Many household sumithrin products are sold in aerosol spray cans,

and these products often contain “inert” propellants that pose a variety

of hazards. These propellants include propane and isobutane.2 Both of

these propellants can cause dizziness when inhaled and are “extremely

flammable.”13,14

1. Based on a survey of labels of sumithrin insecticide products conducted during May, 2003.

Labels were retrieved from: U.S. EPA and Calif. Dept. of Pesticide Regulation. 2003. USEPA/

OPP chemical ingredients database. www.cdpr.ca.gov/docs/epa/epachem.htm.

2. U.S. EPA. 2002. Response to Freedom of Information Act request 01245-03.

3. National Institute for Occupational Safety and Health (NIOSH). 1997. Registry of Toxic Effects of

Chemical Substances: Kerosene (petroleum), hydrotreated. ww.cdc.gov/niosh/rtecs/oa53fc00.html.

4. International Agency for Research on Cancer (IARC). 1989. Occupational exposures in petroleum refining. IARC Monographs 45:39. www-cie.iarc.fr/htdocs/monographs/vol45/45-01.htm.

5. Clarke Mosquito Control Products, Inc. 1999. Material safety data sheet: Anvil 2+2 ULV. Rosedale, IL.

6. Clarke Mosquito Control Products, Inc. 1999. Material safety data sheet: Anvil 10+10 ULV. Rosedale, IL.

7. NIOSH. 2000. Registry of Toxic Effects of Chemical Substances: Mineral oil, petroleum distillates, solvent - dewaxed light paraffinic (mild or no solvent - refining or hydrotreatment).

ww.cdc.gov/niosh/rtecs/py7aa095.html.

8. NIOSH. 2000. Registry of Toxic Effects of Chemical Substances: Mineral oil, petroleum distillates, hydrotreated (severe) light paraffinic. ww.cdc.gov/niosh/rtecs/py7aac4c.html.

9. IARC. 1987. Mineral oils: Untreated and mildly-treated oils; Highly treated oils. IARC Monographs (Suppl. 7):252. www-cie.iarc.fr/htdocs/monographs/suppl7/mineraloils.html.

10. Shell Chemical Co. 2003. Material safety data sheet: Shellsol® A150. ww.euapps.shell.com/

MSDS/GotoMsds.

11. IARC. 2002. Naphthalene. IARC Monographs 82:367. www-cie.iarc.fr/htdocs/monographs/vol82/82-06.html.

12. Hazardous Substance Data Bank (HSDB). 2002. 1,2,4-trimethylbenzene. http://toxnet.nlm.nih.gov.

13. HSDB. 2002. Propane. http://toxnet.nlm.nih.gov.

In male mice, sumithrin reduced kidney weight 14. HSDB. 2002. Isobutane. http://toxnet.nlm.nih.gov.

at all dose levels tested.

Figure 2

Sumithrin Damages Kidneys

Source: U.S. EPA. Office of Pesticides and

Toxic Substances. 1989. Memo from E.R.

Budd, Health Effects Div. to J.M. Tavano,

Registration Div. Washington, D.C., Mar.

16. See attached Data Evaluation Report

for MRID No. 402764-02. Kidney weight (grams)

1.0

0.8

0.6

Sumithrin dose

(100 mg per kg of body weight per day)

012 3 4 5
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on reproduction in laboratory studies.

In the two-generation study of rats

mentioned in the “Effects on Kidneys”

section, the uterus was smaller in female rats exposed to the middle and

high doses of sumithrin than in unexposed rats.17

In a second study of sumithrin’s effects on reproduction submitted during the registration process, pregnant

rabbits exposed to sumithrin (at a dose

of 500 mg/kg) had more miscarriages

than unexposed rabbits. In addition,

the sex ratio of the offspring of exposed mothers was different from that

of unexposed mothers; more males

were born to exposed animals. Also,

a brain-related defect occurred in the

offspring of rabbits exposed at the dose

level of 500 mg/kg. This defect, hydrocephaly, results in an abnormally

large amount of fluid around the brain,

leading to an enlarged skull and atrophy of the brain.22

Carcinogenicity

(Ability to Cause Cancer)

Sumithrin’s ability to cause cancer

has not yet been evaluated by EPA

(as of May 2002).23

However, in two of the laboratory

(45-450 milligrams per kilogram of

body weight (mg/kg) per day), male

mice exposed to sumithrin in a twoyear study developed smaller kidneys

than unexposed males.16 A study in

which rats were fed sumithrin for two

generations also found small kidneys

in the first generation males.17

Effects on Blood

In the study of dogs mentioned on

p. 11, sumithrin exposure also caused

anemia. In dogs fed sumithrin for one

year, both the number of red blood

cells and the amount of hemoglobin

(the oxygen-carrying molecule in the

blood4) were decreased.14 Anemia occurred at dose levels of 80 mg/kg per

day. This was the highest dose tested

in this study.14

Effects on Hormones

The impact of environmental contaminants on the functions of human

and animal hormone systems has been

a significant concern in the last decade.18 Hormones are biologically active molecules that control all responses and functions of the body.

Dramatic changes in the activity of cells

in humans and other animals “are

In laboratory tests, sumithrin disrupts the normal functioning of hormone systems.

Figure 3

Sumithrin Mimics the Activity of a Sex

Hormone

Source: Go, V. et al. 1999. Estrogenic potential of certain pyrethroid

compounds in the MCF-7 human breast carcinoma cell line. Environ.

Health Persp. 107:173-177. Relative ability to express the pS2 gene

6

5

4

3

2

1

0

Unexposed Exposed to

sumithrin (30 μM)

Figure 4

Sumithrin Displaces a Sex Hormone from its

Receptors

Source: Eil, C. and B.C. Nisula. 1990. The binding properties of

pyrethroids to human skin fibroblast androgen receptors and to sex

hormone binding globulin. J. Steroid Biochem. 35:409-414.

caused by extremely small amounts”

of hormones or other chemicals that

disrupt this system.19

Sumithrin has these kinds of effects

on hormones. Researchers at the Mt.

Sinai School of Medicine showed that

sumithrin can mimic estrogens, sex

hormones, in one of their biological

activities. The researchers looked at

the activity of a gene called pS2 because the expression of pS2 is activated by estrogens. They found that

in human cells sumithrin (as well as

another synthetic pyrethroid insecticide, fenvalerate) activates the expression in cells of pS2 like estrogens do.20

(See Figure 3.)

Sumithrin also keeps androgens,

other sex hormones, from binding to

their normal receptors in human tissue. Scientists from Brown University

and the National Institutes of Health

showed that in genital skin cells

sumithrin could displace an androgen

from its normal receptors. When compared to other synthetic pyrethroids,

sumithrin is intermediate in its displacement potency.21 (See Figure 4.)

Effects on Reproduction

Sumithrin has a variety of effects

Exposed to an

estrogen (10 nM)

Note: Lines

above bars

are standard

deviations

0 0.2 0.4 0.6 0.8 1.0

Bioallethrin

Fenvalerate

Sumithrin

Permethrin

Resmethrin

Relative ability to displace an androgen

(Bioallethrin = 1)
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carcinogenicity studies submitted in

support of sumithrin’s registration,

long-term (two-year) exposure to

sumithrin increased the incidence of

liver cancer. The studies include one

done on mice and another done on

rats. In the study with mice, liver cancer was relatively common (it occurred

in 18 percent of the unexposed animals tested) and sumithrin exposure

caused cancer incidence to increase

to almost 25 percent.16 In the study

with rats, liver cancer was relatively

rare (no liver cancer was found in

unexposed animals) but increased to

an incidence of almost 15 percent in

exposed animals.13 (See Figure 5.)

In addition, a study from the Mt.

Sinai School of Medicine links

sumithrin with breast cancer. In this

study, physicians used a culture of

breast cancer cells. They looked at the

expression of a gene that is involved

in the proliferation of mammary tissue, and therefore in the development

of breast cancer. Exposure to sumithrin

increased the expression of this gene.24

Synergy

Enzymes called plasma esterases

Programme on Chemical Safety,

sumithrin is “very toxic to aquatic organisms.”29 In tests submitted as part

of sumithrin’s registration, the most

sensitive fish species was the rainbow

trout. The LC50 (median lethal concentration; the dose that kills half of a

test population) for rainbow trout was

1.4 parts per billion (ppb). All LC50s

for fish were less than 100 ppb.30

The labels of about 80 sumithrincontaining insecticides contain warning statements about toxicity to fish.8

Sumithrin also bioconcentrates in

fish. This means that the concentration of sumithrin in fish tissues is

greater than the concentration in the

water in which the fish lives. According to a study conducted by Sumitomo

Chemical Company, bioconcentration

factors in carp range from 210 to 730.31

(The bioconcentration factor is the ratio between the concentration of a

chemical in fish tissues and the concentration in water.32) When fish were

simultaneously exposed to sumithrin

and the synergist piperonyl butoxide

(as in Anvil insecticide products), the

bioconcentration factor of one form of

sumithrin increased dramatically.

Bioconcentration factors in this experiment varied from 2400 to 3800.31

Effects on Other Aquatic

Animals

Sumithrin is highly toxic to water

fleas, a species that is used in pesticide testing to represent aquatic animals. In a test submitted to EPA for

sumithrin’s registration, concentrations

of less than 1 ppb reduced successful

egg hatch in water fleas. A slightly

higher concentration (2 ppb) reduced

the survival of larval water fleas.

Sumithrin is even more toxic to shrimp;

concentrations of 0.03 ppb killed mysid

shrimp.30

Effects on Bees

Since sumithrin is a broad spectrum

insecticide, it is perhaps not surprising that tiny amounts of sumithrin kill

bees. In a test submitted to EPA as

part of sumithrin’s registration, 0.07

micrograms killed honey bees.30 This

puts sumithrin into EPA’s highest toxicity group for bee toxicity. This toxicity group includes any pesticides that

detoxify pyrethroids in mammals. The

activity of these enzymes is inhibited

by a common family of insecticides,

the organophosphates; this means that

“simultaneous exposure to these insecticides will increase the toxicity of

pyrethrins and pyrethroids.”25

Effects on Pets

Cats, especially young cats, are particularly susceptible to pyrethroid insecticides, possibly because cats’ livers are relatively slow in detoxifying

pyrethroids.26 Two sumithrin flea control products manufactured by Hartz

Mountain Corporation have recently

caused a large number of cat poisonings. EPA estimates that there were

thousands of incidents, including some

deaths, between May 2000 and November 2002. At that time Hartz agreed

to relabel the two products to reduce

cat exposure.27

Seizures and death have also occurred after use of sumithrin on dogs,

but not in as large numbers as the cat

incidents.28

Effects on Fish

According to the International

15

12

9

6

3

0

Figure 5

Ability of Sumithrin to Cause Cancer

Source: Calif. Environmental Protection Agency. Dept. of Pesticide Regulation. Medical

Toxicology Branch. 1996. Summary of toxicology data: Phenothrin, June 20. www.cdpr.ca.gov/

docs/toxsums/toxsumlist.htm Percentage of animals with liver cancer

In a laboratory study of rats, sumithrin increased the incidence of liver cancer.

0 200 400 600 800 1000

Dose of sumithrin

(milligrams per kilogram of body weight per day)
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kill bees in amounts of 2 micrograms

per bee or less.33

Resistance

Insecticide resistance occurs when

repeated exposure over generations

kills the most susceptible individuals

in an insect population. The survivors

have genetically determined characteristics that allow them to survive exposures to the insecticide that would usually be lethal.34

Sumithrin resistance has been reported in cockroaches, aphids, mosquitoes and lice.35-38 The resistance

ratio, the ratio between the amount of

sumithrin needed to kill a resistant insect and the amount needed to kill a

susceptible one, can be over 50 in

both cockroaches and lice.36,39,40

The synergist piperonyl butoxide is

sometimes used to “negate” resistance,

to kill resistant individuals, but is not

always successful.34

Sumithrin resistance can be quite

common. French physicians found that

60 percent of the lice populations in

the Paris elementary school students

they studied were resistant to sumithrin.38 Widespread resistance has

also been found in lice in the United

Kingdom.41

Insects resistant to one pyrethroid

insecticide are often resistant to many

pyrethroids. This means that insects

can develop resistance to sumithrin

without actually having been exposed

to the insecticide.42 

References

1. United Nations Environment Programme, International Labour Organization, and World Health

Organization. 1989. d-Phenothrin health and

safety guide. IPCS International Programme on

Chemical Safety. Health and Safety Guide No.

32. www.inchem.org.

2. U.S. EPA and Calif. Dept. of Pesticide Regulation. 2003. USEPA/OPP chemical ingredients

database. www.cdpr.ca.gov/docs/epa/

epachem.htm.

3. Ware, G.W. 2000. The pesticide book. 5th edition. Fresno CA: Thomson Publications. Pp. 65-

67,177-178.

4. National Library of Medicine. Undated. Medline

Plus health information; Medical dictionary.

www.nlm.nih.gov/medlineplus/mplusdictionary.html.

5. Soderlund, D.M. 2002. Agents affecting sodium

channels. In Handbook of neurotoxicology, vol.

1, ed. E.J. Massaro. Totowa NJ: Humana Press

Inc. Pp. 47-68.

6. Whitmore, R.W., J.E. Kelly, and P.L. Reading.

1992. National home and garden pesticide use

survey. Final report, vol. 1: Executive summary,

results, and recommendations. Table G.1. Research Triangle Park NC: Research Triangle Institute.

7. Narahashi, T. et al. 1998. ion channels as targets for insecticides. NeuroToxicology 19:581-

590.

8. Based on a survey of labels of sumithrin insecticide products conducted during May, 2003. Labels were retrieved from: U.S. EPA and Calif.

Dept. of Pesticide Regulation. 2003. USEPA/

OPP chemical ingredients database.

www.cdpr.ca.gov/docs/epa/epachem.htm.

9. Federal Insecticide, Fungicide and Rodenticide

Act § 2(a) and 2(m).

10. 40 Code of Federal Regulations § 158.340.

11. United Nations Environment Programme, International Labour Organization, and World Health

Organization (WHO). 1990. d-Phenothrin. Environmental Health Criteria 96. Geneva, Switzerland: WHO. Pp. 9-10.

12. Reigart, J.R. and J.R. Roberts. 1999. Recognition and management of pesticide poisonings.

Fifth edition. Washington, D.C.: U.S. EPA. Pp.

87-88. www.epa.gov/pesticides/safety/

healthcare.

13. Calif. Environmental Protection Agency. Dept.

of Pesticide Regulation. Medical Toxicology

Branch. 1996. Summary of toxicology data:

Phenothrin, June 20. www.cdpr.ca.gov/docs/

toxsums/toxsumlist.htm

14. U.S. EPA. Office of Pesticides and Toxic Substances. 1989. Sumithrin (d-phenothrin) - review

of toxicity studies submitted by Sumitomo Chemical Company in support of EAP#1H45283 and

EPA Registration No. 10308-6. Memo from E.R.

Budd, Health Effects Div. to J.M. Tavano, Registration Div. Washington, D.C., Mar. 16. See

attached Data Evaluation Report for MRID No.

402764-01.

15. U.S. EPA. Office of Prevention, Pesticides, and

Toxic Substances. 1995. D-phenothirin

(sumithrin) -submission of a 90-day inhalation

toxicity study in rats. (EPA ID 06905). Washington, DC, June 13.

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of toxicity studies submitted by Sumitomo Chemical Company in support of EAP#1H45283 and

EPA Registration No. 10308-6. Memo from E.R.

Budd, Health Effects Div. to J.M. Tavano, Registration Div. Washington, D.C., Mar. 16. See

attached Data Evaluation Report for MRID No.

402764-02.

17. U.S. EPA. Office of Pesticides and Toxic Substances. 1989. Sumithirin (d-phenothrin - review

of rat reproduction study. Memo from W. Dykstra,

Health Effects Div. to J. Tavano, Registration

Div. Washington, D.C., Jul. 27.

18. National Research Council. Commission on the

Life Sciences. Board on Environmental Studies

and Toxicology. Committee on Hormonally Active Agents in the Environment. 1999. Hormonally active agents in the environment. Washington, D.C.: National Academy Press, p. 10.

19. Eubanks, M.W. 1997. Hormones and health.

Environ. Health. Persp. 105:482-487.

20. Go, V. et al. 1999. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human

breast carcinoma cell line. Environ. Health Persp.

107:173-177.

21. Eil, C. and B.C. Nisula. 1990. The binding properties of pyrethroids to human skin fibroblast

androgen receptors and to sex hormone binding

globulin. J. Steroid Biochem. 35:409-414.

22. U.S. EPA. Office of Pesticides and Toxic Substances. 1991. Sumithrin. Review of developmental toxicity in rabbits. Memo from P.M.

Hurley, Health Effects Div., to R. King,

Reregistration Div. Washington, D.C., Nov. 7.

23. U.S. EPA. Office of Pesticide Programs. Science Information Management Branch. Health

Effects Division. 2002. List of chemicals evaluated for carcinogenic potential. Unpublished

document dated May 22.

24. Kasat, K., V. Go, V., and B.G. Pogo. 2002. Effects of pyrethroid insecticides and estrogen on

WNT10B proto-oncogene expression. Environ.

Int. 28:429-432.

25. Campbell, A. and M. Chapman. 2000. Handbook of poisoning in dogs and cats. Malden MA:

Blackwell Science. Pp. 44.

26. Ref. # 25, pp. 42-45.

27. U.S. EPA. Undated. Questions and answers:

Label instructions tightened on flea & tick control products for pets. www.epa.gov/pesticides/

factsheets/hartzq_a.htm.

28. U.S. EPA. Office of Prevention, Pesticides and

Toxic Substances. Undated. Review of incident

data for four Hartz Mountain flea and tick control products (2596-146, -147, -148, -150). Memo

from V.A. Dobozy, Health Effects Div. to A.

Layne, Registration Div. and others.

29. International Programme on Chemical Safety and

the Commission of European Communities.

2001. d-Phenothrin. ICSC:0313.

www.inchem.org/documents/icsc/icsc/

eics0313.htm.

30. U.S. EPA. Office of Pesticide Programs. 2003.

Pesticide ecotoxicity database. Unpublished.

Received from EPA on May 13.

31. Miyamoto, M. et al. 1992. Effect of metabolism

on bioconcentration of geometric isomers of dphenothrin in fish. Chemosphere 24:2001-2007.

32. BioTech Resources and Indiana Univ. 1995-98.

BioTech life science dictionary. http://

biotech.icmb.utexas.edu/search/dict-search.html.

33. U.S. EPA. Office of Pesticide Programs. Undated. Label review manual. Chap. 9. Environmental hazards. www.epa.gov/oppfead1/labeling/

lrm/chap-09.htm.

34. Cochran, D.G. 1995. Insect resistance to pyrethrins and pyrethroids. In J.E. Casida and G.B.

Quistad, eds. Pyrethrum flowers: Production,

chemistry, toxicology, and uses. New York NY:

Oxford Univ. Press. p. 234-248.

35. Michigan State Univ. Center for Integrated Plant

Systems. Undated. The database of arthropods

resistant to pesticides. www.cips.msu.edu/resistance. (See entries for both sumithrin and

phenothrin.)

36. Picollo, M.I. et al. 1998. Laboratory studies of

susceptibility and resistance to insecticides in

Pediculus capitis (Anoplura; Pediculidae). J.

Med. Entomol. 35:814-817.

37. Picollo, M.I. et al. 2000. Resistance to insecticides and effect of synergists on permethrin toxicity in Pediculus capitis (Anoplura: Pediculidae)

from Buenos Aires. J. Med. Entomol. 37:721-

725.

38. Chosidow, O. et al. 1994. Controlled study of

malathion and d-phenothrin lotions for Pediculus humanus var capitis-infested schoolchildren.

The Lancet 344:1724-1727.

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