Dinoseb is banned as an herbicide in the European Union (EU) and the United States because of its toxicity.

It is used to prevent the thermally induced polymerisation of styrene and other unsaturated monomers when they are being purified by distillation.

In 1892, dinitro-ortho-cresol (2,4-dinitro-6-methylphenol), a chemical compound closely related to dinoseb, was discovered in Germany and first used as an insecticide.

[3] Dinoseb became commercially available in 1945 and was approved for use in the United States based on safety data from Industrial Bio-Test Laboratories.

[4] On January 13, 1984 the Danish ship Dana Optima lost 80 drums of Dinoseb during their trip from North Shields, England to Esbjerg, Denmark.

[5] Dinoseb was withdrawn from the market in 1986 due to an increased threat of birth defects after female field workers were exposed to the chemical.

[6] Dinoseb is an herbicide that was once widely used for weed-control when producing crops like soybeans, vegetables, fruits and nuts, or citrus.

In the present, dinoseb is banned in the EU, and the United States due to its high toxicity.

However, dinoseb is still used in China for example; evidenced by the fact that it is found in rain- and drinking water.

Dinoseb in the dissociated form is negatively charged, which causes it to move to the intermembrane space because of the electrochemical gradient that exists across the IMM.

Also, NADP can't be reduced to form NADPH, which removes the ability to create glucose from carbon dioxide.

After oral administration of dinoseb tagged with 14C to rats and mice, it turned out that 40 to 65% of the 14C was excreted in the urine and 30 to 40% ended up in the feces.

Three hours after oral or intraperitoneal administration, the 14C in the kidneys and liver of the mother was about 50% dinoseb and 50% metabolites.

Symptoms include fatigue, sweating, headaches, nausea, stomach aches and fever.

For pregnant women this substance is especially dangerous as it can cause growth defects in unborn children (it is teratogenic).

Dinoseb interferes with the oxidative phosphorylation by acting as an uncoupler, which is the production of ATP in the mitochondria.

As the membrane potential is the driving force for the production of ATP, the cell is unable to produce energy.

If the compound can pass the placental barrier, the unborn child will be exposed to dinoseb via the blood of the mother.

[7] Oral LD50 values of dinoseb range from 14 to 114 mg/kg in rats, mice, rabbits, and guinea pigs.

[18] Nowadays dinoseb is banned in a lot of places in the world due to high incidences of birth defects.