PMEP Home Page --> Pesticide Active Ingredient Information --> EXTOXNET: The Extension Toxicology Network --> Dienochlor to Glyphosate --> Dinoseb

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


Product names for pesticides containing dinoseb included Basanite, Caldon, Chemox, Chemsect DNBP, Dinitro, Dynamyte, Elgetol, Gebutox, Hel- Fire, Kiloseb, Nitropone, Premerge, Sinox General, Subitex, and Vertac Weed Killer. Approximately 180 different compounds contained some level of dinoseb as an active ingredient before its cancellation by the EPA.


Dinoseb is a phenolic herbicide used in soybeans, vegetables, fruits and nuts, citrus, and other field crops for the selective control of grass and broadleaf weeds in corn. It is also used as an insecticide in grapes; and as a seed crop drying agent.

In October 1986, the EPA issued an emergency suspension order which immediately prohibited further sale, distribution, and use of pesticide products containing dinoseb in the United States (2). This action was based on the significant risk of birth defects and other adverse health effects for applicators and other persons with substantial dinoseb exposure (3). Since that time, the use of dinoseb has been cancelled in the United States. The product is now not commercially available in the U.S. (10).



Dinoseb is a highly to extremely toxic compound, and is labeled with a DANGER signal word.

Exposure to dinoseb can occur by direct contact, ingestion, and inhalation. Inhalation of dusts and sprays may be irritating to the lungs and eyes, and may cause serious illness. Symptoms occurring in humans include fatigue, thirst, sweating, insomnia, weight loss, headache, flushing of the face, nausea, abdominal pain, and occasional diarrhea.

Dinoseb is absorbed through animal and human skin, and direct skin contact will cause irritation, yellow stains, burns, and dermatitis. Spray operators have died upon dermal exposure to dinoseb. In one fatality, a farm worker was using a backpack hand-held sprayer that leaked dinoseb onto his body and penetrated his skin (11).

The oral LD50 of dinoseb for rats is 25-46 mg/kg, and dermal LD50 for rabbits is 75-80 mg/kg (8).


At chronic and acute exposure levels, dinoseb interferes with a cell's ability to convert food (such as glucose) into useable energy for the body. More specifically, it disturbs the production of ATP, a chemical in the cell that provides energy for all cellular activities (9). This interference is the basis for most all toxic effects related to the compound (9).

Reproductive Effects

Dinoseb is reported to adversely affect reproduction in rats and mice at levels that are commonly found among occupational workers. Decreased sperm count and abnormal sperm shape were observed in male rats and mice after three weeks at low exposure levels (about 10 mg/kg/day) for 30 days (11, 12). In a separate study, rats were exposed to relatively small quantities of dinoseb through their diet for a total of 22 weeks. Effects such as decreased fertility, slow weight gain and poor survival of newborns appeared to be related this pesticide (5).

Because of the adverse effects observed in laboratory animals at low chronic exposure levels, it is believed that dinoseb may cause decreased fertility or sterility in humans (9).

Teratogenic Effects

Dinoseb is a potential teratogen (9). Low levels of dinoseb fed to rats and rabbits caused birth defects in the fetuses of exposed females. When dinoseb was administered to pregnant mice, its breakdown products were found in the embryos. However, no teratogenic effects were noted.

Various tests of mice and rats fed or injected with small amounts of dinoseb (around 10 mg/kg) have shown maternal toxicity, decreased fetal body weights and changes in fetal development (12). In some studies of mice, oral doses to pregnant mothers caused an increased death rate in the exposed animals but caused no fetal damage (8). Other studies indicate that dinoseb is a stronger teratogen when injected than when ingested. At low feeding levels the compound was responsible for skeletal deformities and neurological problems in the newborn rats (9).

It is primarily due to the risks of birth defects in humans that this pesticide was banned for use in the United States by the EPA.

Mutagenic Effects

Dinoseb was not mutagenic in laboratory studies performed to date.

Carcinogenic Effects

Dinoseb is classified as a possible human carcinogen. While not carcinogenic to male mice, it was found to be carcinogenic to female mice. The compound caused liver cancer in the animals at moderate to high doses (9).

Organ Toxicity

Dinoseb has the potential to damage human eyes; cataracts can develop with exposure to low levels of the compound. It may also affect the immune system, liver, kidneys, and spleen (5).

Fate in Humans and Animals

Dinoseb is absorbed through the skin. The chemical is excreted in the urine and feces and is metabolized in the liver. Breakdown products are found in the liver, kidneys, spleen, blood and urine (5). Dinoseb can also pass through the placenta into the fetus of experimental animals.


Dinoseb is highly toxic to fish (8). It is more toxic to fish in acidic water than in neutral or alkaline water. The species that have been tested include the cutthroat and lake trout, fathead minnow, and catfish (1).

The compound is also very toxic to birds, mammals, and invertebrates and may pose a threat to nontarget aquatic organisms including endangered species (9). During normal (field) applications, dinoseb could affect the survival of aquatic life if water from treated irrigation ditches is released into a stream or river without sufficient holding or detoxifying time. Dinoseb has caused fish-kills in small Scottish streams when washed from fields by rain. It also has the potential to cause field kills of pheasants and songbirds.

Dinoseb is rapidly taken up by fish. However, when the exposed fish are placed in clean water, the chemical is rapidly eliminated. Thus, the accumulation of the chemical in aquatic life is not a significant environmental risk (1).


Dinoseb affects plants by direct contact. No true translocation occurs within the plant. Twenty-eight days after topical application of dinoseb to apple fruits, about a third of the chemical remained. Breakdown products were found in apple skin and flesh. Dinoseb residues have not been detected in food samples. Dinoseb persists on treated crop soils for 2-4 weeks, under average conditions of use.

Water soluble salts of dinoseb leach readily in soil. However, oil soluble or water soluble formulations of true (non-salt) dinoseb leach much less. There is some evidence that the herbicide binds to certain organic and clay soils. Dinoseb does not accumulate in soil because of microbial breakdown.

Over a ten year period, dinoseb was found to be one of three particularly persistent contaminants in Ontario wells. Entry to the wells was due to spills of concentrated and dilute herbicide, drift during spraying, and from storm runoff. Well water concentrations ranged from 0.05-5,000 ppb in these wells, and removal of dinoseb proved to be very difficult (4). Dinoseb is stable in surface water and has been found in streams at about 5 ppb.


Dinoseb is a dark reddish-brown solid or dark orange viscous liquid, depending on the temperature. It has a pungent odor. Dinoseb is corrosive to mild steel in the presence of water.

Toxic fumes are emitted upon decomposition of dinoseb. The chemical name for dinoseb is 2-(Sec-butyl)-4,6-dinitrophenol, and synonyms include 2,4-dinitro-6-(1-methylpropyl)phenol and 2,4-dinitro-6- sec-butylphenol.

The triethanolamine salt of dinoseb contains over 200 mg/kg N- nitrosodie-thanolamine, a highly toxic contaminant.

Exposure Guidelines:

NOEL: 3 mg/kg/day (Dinitrophenol)
ADI: 1.11 ug/kg (for females at least 13 years old)
Drinking water health advisory: Drinking Water Equivalent Level (DWEL): 0.035 mg/L

Physical Properties

CAS #: 88-85-7
Solubility in water: 0.0052 g/100 g (25 degrees C)
Solubility in solvents: Soluble in alcohol, ethanol, heptane, spray oil, and most organic solvents and oils.
Melting point: 32-42 degrees C
Vapor pressure: 1 torr (151.1 degrees C), 760 torr (332 degrees C)
Log P: 0.0 (151.1 degrees C)
Kow: 2138(6)
Kd: 2.4 x 10 to the minus 5 power
BCF: 135.1(7)


P.O. Box 681428
Indianapolis, IN 46268-1189
Telephone: 317-871-8422

Review by Basic Manufacturer:

Comments solicited: December, 1992
Comments received:


  1. Call, D.J., et al. 1984. J. Environ. Qual. 13(3):493-498.
  2. Federal Register, October 14, 1986. 51 FR 36634.
  3. Federal Register, October 14, 1986. 51 FR 36650.
  4. Frank, R., Sirons, G.J., and Ripley, B.D. 1979. Pesticides Monitoring Journal 13(1):120-127.
  5. Hall, L., et al. 1978. Toxicol. Appl. Pharm. 45(1):235-236.
  6. Saarikoski, J., Lindstrom, R., Tyynela, M., and Viluksela, M. 1986. Ecotoxicol. Environ. Safety 11:158-173.
  7. Spacie, A. and Hamelink, J.L. 1982. Environ. Toxicol. Chem. 1: 309-320.
  8. National Library of Medicine. 1992. Hazardous Substances Databank. Dinoseb.
  9. Walker, Mary M. and Lawrence H. Keith. 1991. EPA's Pesticide Fact Sheet Database. Lewis Publishers. Chelsea, MI.
  10. Farm Chemicals Handbook. 1992. Meister Publishing Company. Willoughby, OH.
  11. Gasiewicz, Thomas A. 1991. Nitro Compounds and Related Phenolic Pesticides. in Handbook of Pesticide Toxicology, Volume 3, Classes of Pesticides. Wayland J. Hayes and Edward R. Laws editors. Academic Press, NY.
  12. Health Advisories for 50 Pesticides. 1988. United States Environmental Protection Agency.