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Extension Toxicology Network

A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and University of California at Davis. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.


Publication Date: 9/93


Trade names include Bromex, Dibrom, Fly Killer-D, Lucanal, RE 4355.


Products containing naled must bear the signal word "Danger" (3).


Naled is a fast acting, non-systemic contact and stomach poison in insects and mites (2). It is used as a short-term fumigant to control agricultural pests on ornamentals in greenhouses, animal and poultry houses, kennels and food processing plants (1, 6). Liquid formulations can be applied to greenhouse heating pipes to kill insects by vapor action. Naled is also used for municipal and other large area mosquito control programs (3). It has been used by veterinarians to kill parasitic worms (other than tapeworms) in dogs (6). Naled is available in dust, emulsion concentrate, liquid and ULV formulations (3).

Naled is one of a class of insecticides referred to as organophosphates. These chemicals act by interfering with the activities of cholinesterase, an enzyme that is essential for the proper working of the nervous systems of both humans and insects. Please refer to the Toxicology Information Brief on cholinesterase-inhibition for a more detailed description of this topic.



Naled is moderately to highly toxic by ingestion, inhalation and dermal adsorption. Vapors or fumes of naled are corrosive to the mucous membranes lining the mouth, throat and lungs, and inhalation may cause severe irritation (9). A sensation of tightness in the chest and coughing are commonly experienced after inhalation (14). As with all organophosphates, naled is readily absorbed through the skin. Skin which has come in contact with this material should be washed immediately with soap and water and all contaminated clothing should be removed. Persons with respiratory ailments, recent exposure to cholinesterase inhibitors, impaired cholinesterase production, or with liver malfunction may be at increased risk from exposure to naled. High environmental temperatures or exposure of naled to visible or UV light may enhance its toxicity (9).

The organophosphate insecticides are cholinesterase inhibitors. They are highly toxic by all routes of exposure. When inhaled, the first effects are usually respiratory and may include bloody or runny nose, coughing, chest discomfort, difficult or short breath, and wheezing due to constriction or excess fluid in the bronchial tubes. Skin contact with organophosphates may cause localized sweating and involuntary muscle contractions. Eye contact will cause pain, bleeding, tears, pupil constriction, and blurred vision. Following exposure by any route, other systemic effects may begin within a few minutes or be delayed for up to 12 hours. These may include pallor, nausea, vomiting, diarrhea, abdominal cramps, headache, dizziness, eye pain, blurred vision, constriction or dilation of the eye pupils, tears, salivation, sweating, and confusion. Severe poisoning will affect the central nervous system, producing incoordination, slurred speech, loss of reflexes, weakness, fatigue, involuntary muscle contractions, twitching, tremors of the tongue or eyelids, and eventually paralysis of the body extremities and the respiratory muscles. In severe cases there may also be involuntary defecation or urination, psychosis, irregular heart beats, unconsciousness, convulsions and coma. Death may be caused by respiratory failure or cardiac arrest (9).

Some organophosphates may cause delayed symptoms beginning 1 to 4 weeks after an acute exposure which may or may not have produced more immediate symptoms. In such cases, numbness, tingling, weakness and cramping may appear in the lower limbs and progress to incoordination and paralysis. Improvement may occur over months or years, but some residual impairment may remain in some cases (9).

Naled may cause dermatitis (skin rashes) and skin sensitization (allergies) (2, 6). It is corrosive to the skin and eyes and may cause permanent damage (3). An aerial applicator developed contact dermatitis after using Dibrom. The exposed area became red and felt burned. Later, water filled blisters formed. They became itchy and dry, then flaked off (ACGIH TLVS 4th Ed. & Supplement. 1980).

The amount of a chemical that is lethal to one-half (50%) of experimental animals fed the material is referred to as its acute oral lethal dose fifty, or LD50. The oral LD50 for naled in rats is 50 to 281 mg/kg, in mice is 330 to 375 mg/kg, and in chickens is 281 mg/kg (2, 3). Rats have tolerated a dosage of 28 mg/kg/day for 9 weeks with no visible signs of poisoning and with only moderate inhibition of cholinesterase (2). The dermal LD50 for naled in rabbits is 1,100 mg/kg, and in rats is 800 mg/kg (2, 3).

The lethal concentration fifty, or LC50, is that concentration of a chemical in air or water that kills half of the experimental animals exposed to it for a set time period. The inhalation LC50 for naled in rats is 7.7 mg/kg, and 156 mg/kg in mice (9).


Repeated or prolonged exposure to organophosphates may result in the same effects as acute exposure including the delayed symptoms. Other effects reported in workers repeatedly exposed include impaired memory and concentration, disorientation, severe depressions, irritability, confusion, headache, speech difficulties, delayed reaction times, nightmares, sleepwalking and drowsiness or insomnia. An influenza-like condition with headache, nausea, weakness, loss of appetite, and malaise has also been reported (9).

Reproductive Effects

Once in the bloodstream, naled may cross the placenta (9).

Teratogenic Effects

No information found.

Mutagenic Effects

Naled is mutagenic to bacteria (Chem. Biol. Interact. 43 (3):361-370. 1983; NIOSH RTECS Online File # 84/8309).

Carcinogenic Effects

No information found.

Organ Toxicity

Naled primarily affects the nervous system through cholinesterase inhibition, by which there is a deactivation of cholinesterase, an enzyme required for proper nerve functioning. Lab studies have shown liver damage in rats.

Fate in Humans and Animals

Naled is readily absorbed into the bloodstream through all normal routes of exposure: skin, lungs and gut. Metabolism is in the liver. Accumulation may occur in the bones (of rats). No accumulation effects have been reported in man. Excretion is through the urine (Menzie. Metab. Pesticides. 1969).


Effects on Birds

Naled is highly to moderately toxic to birds. The LD50 for naled in ducks is 52 mg/kg (NIOSH RTECS Online File # 84/8309), 65 mg/kg in grouse and 37 mg/kg in Canadian geese (4).

Effects on Aquatic Organisms

Naled is toxic to most types of aquatic life (8). Some species are especially sensitive to naled (fathead minnow, bluegill, and mosquito fish) (Hndbk Acute Tox. Chem. Fish and Aquatic Inverts. 1980). Agricultural application of 560 g/HA of naled did not kill mosquito fish or tadpoles in irrigation ditches. The 24-hour LC50 for naled in goldfish is 2 to 4 mg/l (3).

Effects on Other Animals (Nontarget species)

Naled is highly toxic to bees (3). Mule deer are more resistant than most wildlife species. The LD50 for naled in mule deer is 200 mg/kg (4).


Several environmental fate studies demonstrate that naled degrades rapidly under typical environmental conditions. Results of these studies are expressed in terms of half-life, which is the time for one half of the chemical administered to be lost through degradation. Following are results of several representative studies: The half-life of naled in water in a hydrolysis study conducted at 25 degrees C is 96 hours at pH 5, 15.4 hours at pH 7, and 1.6 hours at pH 9. The half-life of naled in water in a photolysis study is just under one day. The photolysis half-life on soil is approximately one half hour under light or dark conditions (16).

Breakdown of Chemical in Soil and Groundwater

Naled is an unlikely source of groundwater pollution. It adsorbs only weakly to soil particles, but is nearly insoluble in water (7).

Naled is not persistent in soil. It is rapidly broken down if wet, and it is moderately volatile (Spencer. Guide to Chem. in Crop Prot. 1982). Soil microorganisms break down most of the naled in the soil.

Breakdown of Chemical in Water

Naled is rapidly broken down in water. The half-life is about 2 days (even though naled is practically insoluble in water). Naled is moderately volatile.

Naled may produce a pollution hazard if dilution water is improperly disposed of, or if run-off from fire control is not properly contained (11).

Breakdown of Chemical in Vegetation

The organophosphate class of insecticides tends to be readily taken up and metabolized by plants. They tend to have short half-lives in the soil and do not carry over through successive plantings.

Plants breakdown naled and DDVP is created by the debromination of the naled molecule in a 1:1 relationship. These can be further metabolized or evaporated off (17).


Pure naled is a white solid. Technical naled is a colorless to yellow liquid with a slightly pungent odor (2, 3, 9). Naled is stable when stored away from light and under normal temperatures and pressures. It may pose a fire and explosion hazard in the presence of oxidizers. Thermal decomposition may release toxic oxides of phosphorus, and corrosive fumes of hydrogen bromide and hydrogen chloride (9). Naled is degraded by sunlight and should be stored in light-proof containers (2).

Naled is stable in anhydrous conditions, but rapidly degrades in the presence of water and by alkali. In water, it can become hydrolyzed with a half-life of 2 days at room temperature (9). Naled should be stored away from moisture. It is corrosive to metals and may attack some forms of plastic, rubber and coatings (8, 9). If it comes in contact with metals, reducing agents, or sulfhydryls, naled may release bromide and revert to dichlorvos (5). It produces highly toxic chloride fumes if it comes in contact with acids or acidic fumes (13).

Persons who work with organo-phosphate materials for long periods of time should have frequent blood tests of their cholinesterase levels. If the cholinesterase level falls below a critical point, no further exposure should be allowed until it returns to normal (10).

Protective clothing must be worn when handling naled. Before removing gloves, wash them with soap and water. Always wash hands, face and arms with soap and water before smoking, eating or drinking.

After work, remove all work clothes and shoes. Shower with soap and water. Wear only clean clothes when leaving the job. Wash contaminated clothing and equipment with soap and water after each use. Keep contaminated work clothes separate from regular laundry.

Exposure Guidelines:

Air concentrations of 1,800 mg/m3 or more are immediately threatening to life or health (9).

OSHA TWA: 3 mg/m3 (9)
ACGIH TWA (skin): 3 mg/m3 (9)
NIOSH Recommended TWA (skin): 3 mg/m3 (9)

Physical Properties:

CAS #: 300-76-5
Specific gravity: 1.96 (9)
Solubility in water: practically insoluble or insoluble (3, 9)
Solubility: Freely soluble in alcohols aromatic solvents.
Slightly soluble in aliphatic hydrocarbons, aromatic hydrocarbons, chlorinated hydro-carbons and ketones.
Sparingly soluble in mineral oils and petroleum solvents (3, 13, 15)
Boiling point: 110 degrees C (252 degrees F) at 5 mm Hg (technical) (2, 9)
Melting point: 81 degrees F (27 degrees C) (9)
Vapor pressure: 2 x 10 to the minus 3 mm Hg at 20 degrees C (2)
Oil: water partition coefficient
Koc: 180 mg/l (7)
Chemical class/use: organophosphate insecticide


Valent U.S.A. Corp.
1333 North California Bldg.
Suite 600
P.O. Box 8025
Walnut Creek, CA 94596-8025
Telephone: 510-256-2700

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received: April, 1993


  1. Meister, R.T. (ed.) 1987. Farm Chemicals Handbook. Willoughby, OH: Meister Publishing Co.
  2. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  3. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  4. Tucker, Richard. 1970. Handbook of toxicity of pesticides to wildlife. USDI Fish & Wildlife Service.
  5. Worthing, C.R. (ed.). 1987. The pesticide manual: A world compendium. 8th Ed. The British Crop Protection Council. Croydon, England.
  6. Hayes, Wayland, Jr. 1982. Pesticides studied in man. Baltimore, MD: Williams & Wilkins.
  7. U. S. Department of Agriculture, Soil Conservation Service. 1990 (Nov.). SCS/ARS/CES Pesticide Properties Database: Version 2.0 (Summary). USDA - Soil Conservation Service, Syracuse, NY.
  8. Hartley, D. and H. Kidd, (eds.) 1983. The agrochemicals handbook. Nottingham, England: Royal Society of Chemistry.
  9. Occupational Health Services, Inc. 1991 (June 9). MSDS for Naled. OHS Inc., Secaucus, NJ.
  10. Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet. Cheminova, Lemvig, Denmark.
  11. Department of Transportation. 1984. Emergency Response Guidebook: Guidebook for hazardous materials incidents. Washington, DC: U.S. DOT.
  12. TOXNET. 1985. National library of medicine's toxicology data network. Hazardous Substances Databank. Public health Service. National Institute of Health. U.S. Department of Health and Human Services. Bethesda, MD: NLM.
  13. Sax, N.I. 1975. Dangerous properties of industrial materials. 4th Ed. New York: Van Nostrand Reinhold Co.
  14. Gosselin, R.E. 1984. Clinical toxicology of commercial products. 5th Ed. Baltimore, MD: Williams & Wilkins.
  15. Windholz, M. (ed.) 1976. The Merck Index: an encyclopedia of chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
  16. Valent USA Corporation. March 1993. Dibrom concentrate - for use in mosquito control programs.
  17. Review by Valent Corporation. April, 1993.