PMEP Home Page --> Pesticide Active Ingredient Information --> EXTOXNET: The Extension Toxicology Network --> Carbaryl to Dicrotophos --> Diazinon

E  X  T  O  X  N  E  T
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 of this product include Knox Out, Spectracide and Basudin. Diazinon may be found in formulations with a variety of other pesticides such as pyrethrins, lindane and disulfoton.


Diazinon is a non-systemic organo-phosphate insecticide used on home gardens and farms to control a wide variety of sucking and leaf eating insects. It is used on rice, fruit trees, sugarcane, corn, tobacco, potatoes and on horticultural plants. It is also an ingredient in pest strips. Diazinon has veterinary uses against fleas and ticks. Nearly 2.6 million pounds of diazinon were used each year prior to 1983 (6).

Some of the older formulations of diazinon were unstable and contained a number of potent impurities such as sulfotepp and monothiono-TEEP (6). Newer products do not contain impurities which increase the risk associated with diazinon use. In 1988 EPA cancelled the registration of diazinon for use on golf courses and sod farms. They cited die-offs of birds which often congregate in these areas.



Diazinon is classified as slightly toxic to moderately toxic, depending on the formulation. It carries the signal words CAUTION or WARNING. Toxic effects of diazinon are due to the inhibition of acetylcholinesterase. The range of doses that results in toxic effects varies widely with formulation and with the individual species being exposed. The toxicity of encapsulated formulations is relatively low because diazinon is not released readily while in the digestive tract. Some formulations of the compound can be degraded to more toxic forms. This transformation may occur in air, particularly in the presence of moisture, and by ultraviolet radiation. Most modern diazinon formulations in the United States are now stable.

Several independently documented cases of diazinon poisoning have occurred among agricultural applicators and among household residents. In the latter case, poisoning followed indoor spraying of a relatively concentrated (25%) solution of diazinon.

The symptoms associated with diazinon poisoning in humans include weakness, headaches, tightness in the chest, blurred vision, non- reactive pinpoint pupils, salivation, sweating, nausea, vomiting, diarrhea, abdominal cramps, and slurred speech. Death has occurred in some instances from both dermal and oral exposures at very high levels.

Repeated single dose LD50s range from 2.75 mg/kg/day to nearly 450 mg/kg/day for rats (8). Still others have reported LD50s as high as 720 mg/kg/day (4).


Chronic effects have been observed at doses ranging from 10 mg/kg/day for swine to 1,000 mg/kg/day for rats. These effects included only visibly recognizable symptoms of toxicity (gross toxicities). Certain effects such as the inhibition of red blood cell cholinesterase, and enzyme response occurred at much lower doses in the rats. No-effect doses have ranged from 0.02 mg/kg/day in humans to 0.1 mg/kg/day in rats. These values are based on inhibition of the enzyme acetylcholinesterase. Enzyme inhibition has been documented in red blood cells, in blood plasma, and in brain cells at varying doses and with different species.

Reproductive and Teratogenic Effects

The data on reproductive and developmental effects due to chronic exposure is limited. One study has shown that injection of diazinon into chicken eggs resulted in skeletal and spinal deformities in the chicks. Bobwhite quail born from eggs treated in a similar manner showed skeletal deformities but no spinal abnormalities. Acetylcholine was significantly affected in this latter study (3). Tests with hamsters and rabbits at low doses (0.125-0.25 mg kg) showed no developmental effects while tests with dogs and pigs at higher levels (1.0-10.0 mg/kg) revealed gross abnormalities (2).

Mutagenic Effects

Tests have revealed the potential for diazinon to be mutagenic, but no fully conclusive evidence exists to support this notion (7). The mutagenicity in humans remains unevaluated.

Carcinogenic Effects

Diazinon is not considered carcinogenic. Test on rats over a two year period at moderate doses (about 45 mg/kg) did not cause tumor development in the test animals.

Organ Toxicity

Diazinon itself is not a potent cholinesterase inhibitor. However, in animals it is converted to diazoxon (a substitution of oxygen for the sulfur molecule), a compound that is a strong enzyme inhibitor.

Fate in Humans and Animals

Metabolism and excretion rates for diazinon are rapid. The half life of the pesticide in animals is about 12 hours. The product is passed out of the body through urine and in the feces. The metabolites account for around 70% of the total amount excreted. Cattle exposed to diazinon may store the compound in their fat over the short term. One study showed that the compound cleared the cows within two weeks after spraying stopped. Application of diazinon to the skin of cows resulted in trace amounts in milk 24 hours after the application.


Birds are quite susceptible to diazinon poisoning and therefore regulations are in place to protect them from hazards posed by turf and golf course treatments. The EPA in 1988 concluded that the use of diazinon in these areas poses a "widespread and continuous hazard" to birds. Bird kills associated with diazinon use have been reported in every area of the country and at all times of the year. The EPA further concluded that Canadian geese and mallard ducks would be exposed to LC50 concentrations in very short periods of time after application (from 15 to 80 minutes depending on the application rate of the pesticide). Birds are significantly more susceptible to diazinon than other wildlife. LD50s for birds range from 2.75 mg/kg to 40.8 mg/kg/day (5).

Most fish are very sensitive to diazinon. Rainbow trout have a LC50 of 90-140 ppb. In hard water, lake trout and cutthroat trout are somewhat more resistant. Warm water fish such as fathead minnows and goldfish are even more resistant (LC50s ranging from 0.5 ppm to 15 ppm). There is some evidence that saltwater fish are more susceptible than are freshwater fish. Bioconcentration ratios range from 200 in minnows to 17.5 for guppies. Howard (8) states that based on these experimental figures, "diazinon will not be expected to significantly bioconcentrate in aquatic systems." Other studies show that diazinon has been found to concentrate in fish 300-600 times the ambient water concentration. This is a relatively low bioaccumulation level as compared to a very persistent compound like DDT which may accumulate to about 60,000 times background levels.


Diazinon seldom migrates below the top 1.3 centimeters (1/2 inch) in soil but can stay biologically available for six months under conditions of low temperature and low moisture. The average time for 50% degradation in soil is two to four weeks. Bacterial enzymes can speed the breakdown of diazinon and have been used in treating emergency situations such as spills (3). The breakdown rate is also highly dependent on the acidity of water. At highly acidic levels, one half of the compound disappeared within 12 hours while in a neutral solution, the pesticide took six months to degrade to one half of the original concentration. Diazoxon is unstable in soil. Howard (8) notes that the pesticide was detected in 54 wells in California and in tap water in Ottawa, Canada and in Japan. Diazinon has also been detected (but not quantified) in Lake Erie and Lake Ontario.

In plants, a lower temperature and a high oil content tend to increase the persistence of diazinon (5). Generally the half-life is rapid in leafy vegetables, forage crops and grass. The range is from two days to 14 days. In treated rice plants only 10% of the residue was present after nine days. Diazinon is absorbed by plant roots when applied to the soil and translocated to other parts of the plant.

Exposure Guidelines:

0.01mg/kg/day rat
0.02mg/kg/day monkey
0.02mg/kg/day humans
Drinking Water: 0.014 mg/l (ppm)
DWEL: 0.003 mg/l
ADI: 0.002 mg/kg/day
TLV-TWA: 0.1 mg/m3
RfD: 0.00009 mg/kg/day (OPP)
HA: 0.0006 mg/l lifetime

Physical Properties:

CAS #: 333-41-5
Solubility in water: 60 mg/l
Solubility in solvent: Petroleum ether, alcohol, benzene
Melting Point: decomposes >120 degrees C
Vapor Pressure: 6 x 10 to the minus 5 power mm Hg
Partition Coefficient: 1.9-4.2 (log)
Adsorption Coefficient: 1,000 ml/g


Ciba-Geigy Corp
PO BOX 18300
Greensboro, NC 27419

Review by Basic Manufacturer:

Comments solicited: January, 1992
Comments received: April, 1992


  1. The Agrochemicals Handbook. 1991. The Royal Society of Chemistry. Cambridge, England
  2. National Research Council (1977). Drinking Water and Health, Advisory Center on Toxicology, Assembly of Life Sciences, Safe Drinking Water Committee, National Academy of Sciences, Washington, DC.
  3. Eisler, Ronald (1986). Diazinon Hazards to Fish, Wildlife and Invertebrates: A Synoptic Review. U.S. Department of the Interior, Fish and Wildlife Service, Contaminant Hazards Reviews, Report number 9, Biological Report 85(1.9).
  4. National Library of Medicine. (1992). Hazardous Substance Databank. TOXNET, Medlars management Section, Bethesda, MD.
  5. Bartsch, Elisabeth (1974). Diazinon II. Residue in Plants, Soil and Water, Residue Reviews, 51:37-68.
  6. Vettorazzi, G. (1976). II Carbamate and Organophosphorous Pesticides Used in Agriculture and Public Health, Residue Reviews 63:1- 44.
  7. Gallo, Michael A. and Nicholas J. Lawryk. (1991). Organic Phosphorus Pesticides. in Handbook of Pesticide Toxicology, Volume 2, Classes of Pesticides. Wayland J. Hayes and Edward R. Laws editors.Academic Press, Inc., NY.
  8. Howard, Philip H. (1991). Fate and Exposure Data for Organic Chemicals, Volume III, Pesticides. Lewis Publishers, Chelsea, MI.