This information is from:



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Caroline Cox is NCAP’s staff scientist.


Naled (see Figure 1) is an insecticide

in the organophosphate pesticide

family that is commonly used to

kill adult (flying) mosquitoes. Naled

has been registered for use in the U.S.

since 1959 and is sold under the brand

name Dibrom. AMVAC Chemical Corporation

has been the major manufacturer

of naled since 1998.1


About one million pounds of

naled are used every year in the U.S.

Approximately 70 percent of this is

used for mosquito control; almost

all of this is applied aerially. The remaining

30 percent is used in agriculture.

Major agricultural uses are on

cotton in California and Louisiana, on

alfalfa in Idaho and Oregon, and on

grapes in California.2

Mode of Action

Like all organophosphate insecticides,


Naled is an insecticide in the organophosphate pesticide family used primarily for mosquito control. Dibrom is a

common brand name for naled products. About one million pounds are used annually in the U.S.

Like all organophosphates, naled is toxic to the nervous system. Symptoms of exposure include headaches, nausea,

and diarrhea. Naled is more toxic when exposure occurs by breathing contaminated air than through other kinds of

exposure. In laboratory tests, naled exposure caused increased aggressiveness and a deterioration of memory and


Naled’s breakdown product dichlorvos (another organophosphate insecticide) interferes with prenatal brain

development. In laboratory animals, exposure for just 3 days during pregnancy when the brain is growing quickly

reduced brain size 15 percent.

Dichlorvos also causes cancer, according to the International Agency for Research on Carcinogens. In laboratory

tests, it caused leukemia and pancreatic cancer. Two independent studies have shown that children exposed to

household “no-pest” strips containing dichlorvos have a higher incidence of brain cancer than unexposed children.

Aerial applications of naled can drift up to one-half mile.

According to the U.S. Environmental Protection Agency, naled is moderately to highly toxic to birds and fish. It also

reduced egg production and hatching success in tests with birds and reduced growth in tests with juvenile fish.

convulsions, paralysis, and death.3

Breakdown Products

Naled breaks down into dichlorvos,

another organophosphate insecticide,

in animals and soil.4,5 (See Figure 2.)

Inert Ingredients

Like most pesticides, commercial

naled-containing insecticides contain

ingredients other than naled. Many of

these ingredients, according to U.S.

pesticide law, are called “inert.” Except

for tests of acute effects, toxicology

tests required for the registration

of a pesticide are not conducted with

the combination of ingredients found

in commercial products.6

Most inert ingredients are not identified

on product labels, and little information

about them is publicly available.

For information about the inert ingredients

in Dibrom products, see

“Inerts in Dibrom Products,” p. 17.

Symptoms of Exposure

Symptoms of exposure to naled and

all organophosphate insecticides

include headaches, muscle twitching,

nausea, diarrhea, difficult breathing,

naled kills insects by inhibiting acetylcholinesterase

(AChE), an enzyme involved

in the transmission of nerve impulses

from one nerve cell to another.

This causes a “jam” in the transmission

system, resulting in restlessness,

Figure 1


1,2-dibromo-2,2-dichloroethyl dimethyl










Figure 2





P Cl



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Dibrom Concentrate (EPA Registration

No. 5481-480) contains the

inert ingredient aromatic hydrocarbon

solvent (Chemical Abstract Services

number 64742-94-5), also

called solvent naphtha.1 This solvent

contains two aromatic hydrocarbons,

naphthalene and 1,2,4-


Dibrom 8 Emulsive (EPA Registration

No. 5481-479) contains


Dibrom 8 Miscible (EPA Registration

No. 34704-351) contains solvents4

whose ingredients can include

naphthalene and trimethylbenzene.


Naphthalene has been classified

by EPA as a possible human carcinogen

because it caused lung tumors

in mice following inhalation.

Naphthalene exposure also causes

headaches, restlessness, lethargy,

nausea, diarrhea, and anemia.

Anemia in newborns can be caused

by exposure during pregnancy.6

1,2,4-trimethylbenzene is

irritating to eyes and skin. It can

depress the central nervous system

and cause headache, fatigue, nausea,

and anxiety. It has also caused

asthmatic bronchitis.7

1. U.S. EPA. Office of Prevention, Pesticides

and Toxic Substances. Office of Pesticide

Programs. 2002. Letter from L.V. Moos, Information

Resources and Services Division

acting director, to NCAP, July 25.

2. Shell Chemical Company. 2002. Material

safety data sheet: Shellsol® A150.

3. Amvac Chemical Corp. 2002. Material safety

data sheet: Dibrom® 8 Emulsive.

4. Platte Chemical Co. 2001. Material safety

data sheet: Dibrom 8 Miscible.

5. Shell Chemical Company. 2002. Material

safety data sheet: Shellsol A100.

6. Hazardous Substance Data Bank. 2002.


7. Hazardous Substance Data Bank. 2002.



depression, seizures, and loss of consciousness.


Toxicity to the Nervous


A symptom of exposure to naled

that occurs at low doses (whether by

breathing, through the skin, or orally)

is inhibition of acetylcholinesterase

(AChE). In studies conducted by naled

manufacturers, exposure of rats to

naled in air at a dose of 0.3 milligrams

per kilogram of body weight

(mg/kg) per day for three weeks, skin

exposures of 20 mg/kg per day for 4

weeks, and oral exposure of 10 mg/

kg per day for 4 weeks caused inhibition

of AChE.

Long-term exposure also caused

AChE inhibition; reduced AChE activity

occurred in dogs exposed orally to

2 mg/kg per day for 1 year and in rats

exposed orally to the same dose for 2


In addition, the long-term study with

dogs found that doses of 2 mg/kg per

day also caused mineralization of the

spinal cord.8

Naled’s breakdown product dichlorvos

inhibits the activity in rats of a

nervous system enzyme called neuropathy

target esterase. In experiments

conducted by biochemists at the Postgraduate

Institute of Medical Education

and Research (India), doses of 6

mg/kg per day reduced the enzyme’s

activity by about 40 percent. Inhibition

of this enzyme causes partial paralysis

of the hind legs followed by


Toxicity Caused by Breathing


Naled is more potent when exposure

occurs through breathing than

when exposure occurs through eating

contaminated food or drinking contaminated

water. Toxicologists at the

University of California found that inhalation

was 20 times more toxic to

rats than oral dosing (dosing through

the mouth) of naled.10 (See Figure 3.)

The U.S. Environmental Protection

Agency (EPA) came to a similar conclusion

based on tests submitted to

the agency by naled’s manufacturer:

the dose required to cause cholinesterase

inhibition through inhalation

exposure was less than 1/6 of the lowest

oral dose causing the same effect.11

An additional study by the University

of California researchers mentioned

above found that small droplets

of naled (the size produced by

ultra low volume sprayers often used

in mosquito spraying) were about

four times more acutely toxic than

larger droplets.12

Effects on Behavior

Exposure to naled has multiple

effects on behavior. In a study conducted

by naled’s manufacturer, naled

caused reduced muscle strength, slow

responses to stimulation, and reduced

activity in rats. These behavioral

changes occurred at all but the lowest

dose level tested in males and all dose

levels tested in females,13 suggesting

that females are more sensitive than

males to naled poisoning.

Exposure to naled’s breakdown

product dichlorvos causes increased

aggression and impaired memory. The

Indian biochemists mentioned above

found that fighting was about 5 times

Figure 3

Acute Toxicity of Naled

Source: Berteau, P.A. and W.A. Dean. 1978.

A comparison of oral and inhalation toxicities

of four insecticides to mice and rats. Bull.

Environ. Contam. Toxicol. 19: 113-120.

Breathing Oral






Median lethal dose to rats in milligrams per kilogramwith

95% confidence intervals(Smaller lethal dose = higher toxicity)

Naled is more acutely toxic from exposure via

breathing than from oral exposure.

Type of exposure


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entists found that injections of

dichlorvos at weekly intervals in

mice caused a 3-fold increase in the

number of mutations in liver cells.26 A

team of geneticists from the National

Research Centre (Egypt) found that

oral doses of dichlorvos given to mice,

or feeding mice diclorvos-treated

beans, increased the incidence of chromosome

abnormalities in both spleen

and sperm cells.27

Ability to Cause Cancer


EPA classifies naled as a “Group E”

chemical. Group E chemicals have

demonstrated “evidence of noncarcinogenicity”

in laboratory tests.28

Naled’s breakdown product dichlorvos,

however, is classified as “possibly

carcinogenic to humans,” with “sufficient

evidence in experimental animals”

for its carcinogenicity by the

International Agency for Research on

Carcinogens. The agency gave

dichlorvos this classification because

it caused forestomach tumors, leukemia,

and pancreatic tumors in laboratory

tests with rats and mice.29

In children, exposure to dichlorvos

has been linked with increased cancer

risks. Researchers at the University

of North Carolina found an association

between exposure to dichlorvos

“no-pest” strips during pregnancy

or during childhood and the incidence

of three types of childhood cancer:

leukemias, brain tumors, and lymphoma.

30 Missouri Department of

Health researchers found similar results

for childhood brain cancer.31

Effects on the Immune System

Both naled and its breakdown product

dichlorvos inhibited an enzyme in

white blood cells called monocyte esterase,

according to a study conducted

by researchers at the Technicon Science

Center.32 (See Figure 5, p. 19.)

Monocyte esterases are an “integral

component”33 of the process by which

white blood cells eliminate virus-infected

cells from our bodies and monitor

for precancerous cells.33


A study submitted to EPA by Shell

Chemical Co. showed that “the toxic

Figure 4

Exposure to Naled’s Breakdown Product Increases

Aggressiveness and Disrupts Learning

Source: Sarin, S. and K.D. Gill. 1998. Biochemical and behavioral deficits in adult rat following

chronic dichlorvos exposure. Pharmacol. Biochem. Behavior 59: 1081-1086.

In laboratory animals, exposure to naled’s breakdown product dichlorvos causes more frequent

fighting and hinders learning.






Number of fighting episodes(per minute, with standard deviations)

more common among exposed rats

than among unexposed ones.9 Exposed

animals also required more trials than

unexposed ones to learn an avoidance

behavior, indicating a “severe

deterioration in their memory and

learning functions.”14 (See Figure 4.)

Eye and Skin Irritation

Naled is a “severe” eye irritant and

is “corrosive” to skin.15 All three frequently

used commercial Dibrom products

pose similar hazards. Labels of

two of the products warn “causes irreversible

eye and skin damage”16,17 and

the third states that it is “corrosive”

and “causes eye damage and skin damage.”

18 Skin irritation was documented

by physicians soon after naled’s use

in the U.S. began.19

Effects on the Circulatory


In a long-term feeding study conducted

by naled’s manufacturer, naled

caused anemia in dogs at all but the

lowest dose level tested. Exposures of

2 mg/kg per day reduced the number

of red blood cells and the amount of

hemoglobin (the oxygen-carrying pigment)

in the blood.20

Effects on Reproduction

Dichlorvos, naled’s breakdown

product, interferes with prenatal brain

development. Biologists at the

University of Oslo found that dosing

guinea pigs with 15 mg/kg of

dichlorvos twice daily for three days

during pregnancy caused a significant

(15 percent) decrease in the offspring’s

brain size. The guinea pigs

were dosed with dichlorvos between

the 40th and 50th day of their pregnancy,

a time when the fetal brain is

undergoing a growth spurt.21

In addition, University of Michigan

researchers showed that naled exposure

causes delays in the development

of rat embryos. For example, exposure

of pregnant rats on the ninth day

of their pregnancy caused a significant

delay in the closing of the

embryo’s neural tube.22

Naled and dichlorvos can be passed

from mothers to their offspring through

nursing. German researchers found

both insecticides in milk from cows

that had been treated with naled.23

Ability to Cause Genetic

Damage (Mutagenicity)

Naled damaged bacteria’s genetic

material in laboratory tests conducted

by geneticists at Monash University

(Australia)24 as well as biologists at

Texas Tech University.25

Naled’s breakdown product

dichlorvos also causes genetic damage.

A team of Greek and Dutch sci-

Unexposed Exposed

Fighting Learning an



Unexposed Exposed






Number of trials required tolearn an avoidance behavior(with standard deviations)


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effects of naled were potentiated by

co-administration of Ciodrin, malathion,

and methyl parathion.”34 All three are

insecticides in the organophosphate


Special Susceptibility

Malnourished individuals may be

particularly susceptible to naled poisoning.

Researchers from the Institute

of Hygiene and Occupational Health

(Bulgaria) studied naled’s effects on

rats that were fed a low-protein diet

and found that naled was almost twice

as toxic to them as it was to rats fed a

normal diet. (See Figure 6.) In addition,

the rats fed a low-protein diet

developed liver damage from their

naled exposure.35

Contamination of Food

The U.S. Department of Agriculture

documented contamination of strawberries,

peppers, and beans with naled’s

breakdown product dichlorvos.36

Water Contamination

Insecticides in naled’s chemical family,

the organophosphates, are com-

Figure 6

Malnutrition Increases Naled’s Toxicity


Kaloyanova, F. and M. Tasheva. 1983. Effect of protein malnutrition

on the toxicity of pesticides. In Pesticide chemistry: Human welfare and

the environment. Vol. 3. Mode of action, metabolism, and toxicology,

ed. Miyamoto, J and P.C. Kearney. Oxford: Pergamon Press. Pp.








Naled inhibits the activity of an immune system enzyme. It is also more toxic to malnourished animals than animals fed a normal diet.

Median lethal dose(milligrams per kilogram of body weight in rats)

mon contaminants of urban streams

and rivers.37 However, neither naled

or its breakdown product dichlorvos

were included in the national water

quality monitoring program currently

being conducted by the U.S. Geological

Survey.38 This means that no systematic

information is available about

naled contamination of U.S. streams,

rivers, or wells. EPA also does not

have monitoring data for naled or its

breakdown products in ground or surface


Air Contamination

Naled can persist in air up to several

days after treatment. University of

California, Davis toxicologists measured

both naled and its breakdown product

dichlorvos in the air around a naledtreated

orange grove for three days

after application.40


Aerial applications of naled drift

(move from the target site during application)

for significant distances. Entomologists

from the University of

Florida measured naled contamination

750 meters (2400 feet) downwind from

sprayed areas. They suggest that nospray

buffer zones greater than 750

meters in width “be placed around ecologically

sensitive areas.”41

Effects on Beneficial Insects

Because it is a broad spectrum insecticide,

it is not surprising that naled

impacts beneficial insects, those that

provide important economic benefits

to farmers. In a study submitted as

part of naled’s registration process,

naled was “highly toxic”42 to honey

bees. Follow-up studies found that this

toxicity decreased rapidly during the

first day after treatment.42 Naled’s

toxicity to other species of bees

(alfalfa leafcutting bees and alkali

bees) is more persistent than for honey

bees.43 It can “mimic long residual

[persistent] materials,” reducing

leafcutting bee numbers 48 hours after


Parasitoid wasps (wasps that lay

their eggs in juvenile stages of other

insects, which then are killed as the

wasps hatch and develop) can also be

poisoned by low-level exposure to

Figure 5

Naled (and Dichlorvos)

Inhibit the Immune System


Lee, M.J. and H.C. Waters. 1977. Inhibition of monocyte esterase

activity by organophosphate insecticides. Blood 50:947-951.






Concentration inhibiting a white blood cell enzyme(monocyte esterase) by 50 %(parts per billion in blood sample)

Naled Dichlorvos

Low protein diet Normal diet

Note: Smaller lethal dose

indicates higher toxicity


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Sprayed sites

naled. According to U.S. Department

of Agriculture researchers, a wasp that

parasitizes fruit flies was killed by a

naled and protein bait mixture designed

to kill fruit flies.45

Naled is also highly toxic to a

predatory mite.46

A University of Florida zoologist

studied areas in Florida where regular

mosquito spraying occurred with

Dibrom and another insecticide. He

found a “major loss” in insect diversity

in sprayed sites. Wasps showed

“some of the most dramatic drops in

species diversity.”47 Scale insects,

whose populations are normally controlled

by parasitic wasps, increased.47

Effects on Birds

According to EPA, naled is moderately

to highly toxic to birds. The most sensitive

species tested by naled’s manufacturer

during the registration process

was the Canada goose, killed by 37

mg/kg of naled.48

According to tests conducted by

naled’s manufacturer, this insecticide

also affects bird reproduction. Mallard

ducks eating food treated with naled

laid fewer eggs, produced fewer viable

eggs, and hatched fewer ducklings

than unexposed mallards.48

Effects on Fish

According to EPA, naled is very

highly toxic to lake trout; highly toxic

to rainbow trout, cutthroat trout, and

catfish; and moderately toxic to sunfish,

minnow, and bass. The most

sensitive species in tests submitted

to EPA by naled’s manufacturer was

lake trout, with an LC50 (median lethal

concentration; the dose required

to kill 50 percent of test animals) of

87 parts per billion (ppb).49

Naled also causes effects on fish

other than death. In a test conducted

by naled’s manufacturer, a concentration

of 15 ppb impaired the growth of

fathead minnows.49

Effects on Other Aquatic


Ecologically important insects are

killed by naled. According to a naled

manufacturer, a concentration of 8 ppb

kills stoneflies.50 Research conducted

by the Arctic Health Research Center

(Alaska) showed that water striders

were killed 300 feet from a naled

fogger.51 Stoneflies are important nutrient

cyclers in streams and water striders

are scavengers and predators.52,53

Aquatic arthropods are also impacted

by naled. Waterfleas are killed

by less than 0.5 ppb of naled in tests

conducted by naled’s manufacturer,

and less than 0.2 ppb disrupts

waterflea growth. Shrimp are killed

by less than 10 ppb.54

According to EPA, naled is “very

highly toxic” to oysters.55

Sea urchins are also sensitive to

naled exposure. University of Miami

researchers showed that concentrations

of less than 4 ppb disrupt normal

development of embryos.56

Effects on Endangered


Evaluations by both EPA and the

U.S. Fish and Wildlife Service have

concluded that use of naled puts endangered

mammals, fish, mussels, and

other species at risk.57

In addition, there is field evidence

of naled’s hazards for endangered

species. Dibrom spraying (along with

spraying of another insecticide) was

“directly correlated with the precipitous

decline in the Schaus Swallowtail

populations on Key Largo [FL],”47 according

to a University of Florida zoologist.

This swallowtail is listed as an

endangered species under both Florida

and federal law.47

A University of Florida entomologist

studying a different rare butterfly,

the Florida lacewing, found higher

populations in unsprayed areas than

in sprayed areas. (See Figure 7.) He

concluded that “it is likely that chemical

applications play an important role

in affecting the population size and

behavior of these species.”58

Effects on Plants

Insecticides are typically not expected

to damage plants. However,

University of California researchers

showed that naled treatment caused

brown lesions in celery and bronzing

Figure 7

Naled Mosquito Spraying Reduces Populations of Rare Butterflies

Source: Salvato, M. 2001. Influence of mosquito control chemicals on butterflies (Nymphalidae,

Lycaenidae, Hesperiidae) of the lower Florida Keys. J. Lepidop. Soc. 55:8-14.

Number of Florida lacewing butterflies per hectare(average of 63 sampling dates in 1997 and 1998)






Naled spraying reduced populations of a rare butterfly, the Florida lacewing, in the Florida


Unsprayed sites


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of strawberries.59,60 The strawberry

damage was accompanied by reduced

photosynthesis (using sunlight to produce

sugars) and closing of leaf openings

(stomata).60 Brazilian researchers

found that naled also “drastically reduced”

tomato pollen germination.61

In aquatic plants, naled reduces

photosynthesis. In laboratory tests, a

naled concentration of 1 ppm reduced

photosynthesis by estuary algae by

over 50 percent.62

Efficacy of Mosquito


The U.S. Centers for Disease Control

and Prevention has written that

“adulticiding, application of chemicals

to kill adult mosquitoes by ground or

aerial applications, is usually the least

efficient mosquito control technique.”63

Naled is no exception. For example,

researchers from the New York Department

of Health showed that 11

years of naled spraying was “successful

in achieving short-term reductions

in mosquito abundance,”64 but populations

of the disease-carrying mosquito

of concern “increased 15-fold”64 over

the 11 years of spraying.


1. U.S. EPA. 2002. Interim reregistration eligibility

decision for naled. Case number 0092. (Unpublished

document.) p. 3.

2. Ref. # 1, pp. 4-6.

3. Ware, G.W. 2000. The pesticide book. Fresno

CA: Thomson Publications. Pp. 181-183.

4. U.S. EPA. Office of Pesticide Programs. Health

Effects Division. 1999. Human health risk assessment:


status.htm. Pp. 22-23.

5. U.S. EPA. 1997. EFED’s Reregistration Chapter

C for naled. Memo from J. Peckenpaugh, S.

Temes, and C. Laird, Environmental Fate and

Effects DIv., to K. Monk, Special Review and

Reregistration Div.

status.htm. p. 17.

6. 40 Code of Federal Regulations § 158.340.

7. Reigart, J.R. and J.R. Roberts. 1999. Recognition

and management of pesticide poisonings.

Fifth edition. U.S. EPA. Office of Pesticide Programs.

p. 34.


8. Ref. #4, p. 15-17, 28.

9. Sarin, S. and K.D. Gill. 1998. Biochemical and

behavioral deficits in adult rat following chronic

dichlorvos exposure. Pharmacol. Biochem.

Behavior 59: 1081-1086.

10. Berteau, P.A. and W.A. Dean. 1978. A comparison

of oral and inhalation toxicities of four insecticides

to mice and rats. Bull. Environ.

Contam. Toxicol. 19: 113-120.

11. Ref. #4, pp. 26-28.

12. Berteau, P.E., W.A. Deen, and R.L. Dimmick.

1977. Effect of particle size on the inhalation

toxicity of naled aerosols. (Abstract.) Toxicol.

Appl. Pharmacol. 41: 183.

13. Ref. #4, pp. 23-24.

14. Sarin, S. and K.D. Gill. 1999. Dichlorvos induced

alterations in glucose homeostasis: Possible implications

on the state of neuronal function in

rats. Mol. Cell. Biochem. 199:97-92.

15. Ref. #4, p. 15.

16. Amvac. Undated. Dibrom Concentrate insecticide.


17. Amvac. Undated. Dibrom 8 Emulsive. Naled insecticide.


18. Platte Chemical Co. 1995. Dibrom 8 Miscible.


19. Edmundson, W.F. and J.E. Davies. 1967. Occupational

dermatitis from naled. Arch. Environ.

Health 15: 89-91.

20. Ref. #4, p. 17.

21. Mehl, A. et al. 1994. The effect of trichlorfon

and other organophosphates on prenatal brain

development in the guinea pig. Neurochem. Res.


22. Beaudoin, A.R. and D.L. Fisher. 1981. An in

vivo/in vitro evaluation of teratogenic action.

Teratol. 23:57-61.

23. Dedek, W. et al. 1980. Abbau und ausscheidung

von 32P-naled in der milch. Die Nahrung 24:767-

772. (Abstract in English.)

24. Hanna, P.J. and K.F. Dyer. 1975. Mutagenicity

of organophosphorus compounds in bacteria and

Drosophila. Mut. Res. 28: 405-420.

25. Shiau, S.Y., R.A. Huff, and I.C. Felkner. 1981.

Pesticide mutagenicity on Bacillus subtilis and

Salmonella typhimurium detectors. J. Agric. Food

Chem. 29:268-271.

26. Pletsa, V. et al. 1999. Induction of somatic mutations

but not methylated DNA adducts in ëlacZ

transgenic mice by dichlorvos. Cancer Let.


27. Amer, S.M., F.A.E. Aly, and S.M. Donya. 2000.

Cytogenetic effect of the organophosphorous insecticide

DDVP and its residues in stored faba

beans in somatic and germ cells of the mouse.

Cytologia 65:295-303.

28. Ref. #4, p. 18.

29. International Agency for Research on Carcinogens.

1991. Occupational exposures in insecticide

applications, and some pesticides. IARC

Monographs 53: 267.

30. Leiss, J.K. and D.A. Savitz. 1995. Home pesticide

use and childhood cancer: A case-control

study. Amer. J. Publ. Health 85: 249-252.

31. Davis, J.R. et al. 1993. Family pesticide use

and childhood brain cancer. Arch. Environ.

Contam. Toxicol. 24: 87-92.

32. Lee, M.J. and H.C. Waters. 1977. Inhibition of

monocyte esterase activity by organophosphate

insecticides. Blood 50:947-951.

33. Newcombe, D.S. 1992. Immune surveillance,

organophosphorous exposure, and lymphomagenesis.

Lancet 339: 539-541.

34. U.S. EPA. Office of Pesticides and Toxic Substances.

1982. Naled registration standard: Toxicology

chapter. Memo from I. Mauer, Hazard

Evaluation Div., to B. Kapner, Special Pesticides

Review Div., Dec. 22. p. 13.

35. Kaloyanova, F. and M. Tasheva. 1983. Effect of

protein malnutrition on the toxicity of pesticides.

In Pesticide chemistry: Human welfare and the

environment. Vol. 3. Mode of action, metabolism,

and toxicology, ed. Miyamoto, J and P.C.

Kearney. Oxford: Pergamon Press. Pp. 527-529.

36. U.S. Dept. of Agriculture. 2002. Pesticide data

program: Annual summary calendar year 2000.

Appendix E. p. 13.


37. U.S. Geological Survey. 1999. The quality of

our nation’s waters—nutrients and pesticides.

USGS Circular 1225. p. 62.


38. U.S. Geological Survey. 1999. Pesticides analyzed

in NAWQA samples: Use, chemical analyses,

and water-quality criteria. http://

39. Ref. # 5, pp. 20, 22.

40. Hall, G.L. et al. 1997. Development and validation

of an analytical method for naled and dichlorvos

in air. J. Agric. Food Chem. 45:145-148.

41. Hennessey, M.K., H.N. Nigg, and D.H. Habek.

1992. Mosquito (Diptera: Culicidae) adulticide

drift into wildlife refuges of the Florida Keys.

Environ. Entomol. 21: 714-721.

42. Ref. # 5, pp. 5-6.

43. Johansen, C.A. et al. 1983. Pesticides and bees.

Environ. Entomol. 12: 1513-1518.

44. Torchio, P.F. 1983. The effects of field applications

of naled and trichlorfon on the alfalfa

leafcutting bee, Megachile rotundata (Fabricus).

J . Kansas Entomol. Soc. 56:62-68.

45. Purcell, M.F., J.D. Stark, and R.H. Messing.

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