Endosulfan is an organochlorine insecticide and acaricide, which acts by blocking the GABA-gated chloride channel of the insect (IRAC group 2A). It became highly controversial due to its acute toxicity, potential for bioaccumulation, and role as an endocrine disruptor. Because of its threats to human health and the environment, a global ban on the manufacture and use of endosulfan was negotiated under the Stockholm Convention in April 2011. The ban took effect in mid-2012, with certain uses exempted for five additional years. More than 80 countries, including the European Union, Australia, New Zealand, several West African nations, the United States, Brazil, and Canada had already banned it or announced phase-outs by the time the Stockholm Convention ban was agreed upon. It is still used extensively in India and China despite laws against its use. It is also used in a few other countries. It is produced by the Israeli firm Makhteshim Agan and several manufacturers in India and China. On May 13, 2011, the India Supreme Court ordered a ban on the production and sale of endosulfan in India, pending further notice.

Endosulfan has been used in agriculture around the world to control insect pests including whiteflies, aphids, leafhoppers, Colorado potato beetles and cabbage worms. Due to its unique mode of action, it is useful in resistance management; however, as it is not specific, it can negatively impact populations of beneficial insects. It is, however, considered to be moderately toxic to honey bees, and it is less toxic to bees than organophosphate insecticides.

The World Health Organization estimated worldwide annual production to be about 9,000 tonnes (t) in the early 1980s. From 1980 to 1989, worldwide consumption averaged 10,500 tonnes per year, and for the 1990s use increased to 12,800 tonnes per year.^{[citation needed]}

Endosulfan is a derivative of hexachlorocyclopentadiene, and is chemically similar to aldrin, chlordane, and heptachlor. Specifically, it is produced by the Diels-Alder reaction of hexachlorocyclopentadiene with cis-butene-1,4-diol and subsequent reaction of the adduct with thionyl chloride. Technical endosulfan is a 7:3 mixture of stereoisomers, designated α and β. α- and β-Endosulfan are configurational isomers arising from the pyramidal stereochemistry of the tetravalent sulfur. α-Endosulfan is the more thermodynamically stable of the two, thus β-endosulfan irreversibly converts to the α form, although the conversion is slow.

Endosulfan is alleged to be responsible for many fatal pesticide poisoning incidents around the world by NGOs opposing pesticide usage. Endosulfan is also a xenoestrogen—a synthetic substance that imitates or enhances the effect of estrogens—and it can act as an endocrine disruptor, causing reproductive and developmental damage in both animals and humans. It has also been found to act as an aromatase inhibitor. Whether endosulfan can cause cancer is debated. With regard to consumers' intake of endosulfan from residues on food, the Food and Agriculture Organization of United Nations has concluded that long-term exposure from food is unlikely to present a public health concern, but short-term exposure can exceed acute reference doses.

Endosulfan is acutely neurotoxic to both insects and mammals, including humans. The US EPA classifies it as Category I: "Highly Acutely Toxic" based on a LD₅₀ value of 30 mg/kg for female rats, while the World Health Organization classifies it as Class II "Moderately Hazardous" based on a rat LD₅₀ of 80 mg/kg. It is a GABA-gated chloride channel antagonist, and a Ca²⁺, Mg²⁺ ATPase inhibitor. Both of these enzymes are involved in the transfer of nerve impulses. Symptoms of acute poisoning include hyperactivity, tremors, convulsions, lack of coordination, staggering, difficulty breathing, nausea and vomiting, diarrhea, and in severe cases, unconsciousness. Doses as low as 35 mg/kg have been documented to cause death in humans, and many cases of sublethal poisoning have resulted in permanent brain damage. Farm workers with chronic endosulfan exposure are at risk of rashes and skin irritation.

EPA's acute reference dose for dietary exposure to endosulfan is 0.015 mg/kg for adults and 0.0015 mg/kg for children. For chronic dietary expsoure, the EPA references doses are 0.006 mg/(kg·day) and 0.0006 mg/(kg·day) for adults and children, respectively.

Theo Colborn, an expert on endocrine disruption, lists endosulfan as a known endocrine disruptor, and both the EPA and the Agency for Toxic Substances and Disease Registry consider endosulfan to be a potential endocrine disruptor. Numerous in vitro studies have documented its potential to disrupt hormones and animal studies have demonstrated its reproductive and developmental toxicity, especially among males. A number of studies have documented that it acts as an antiandrogen in animals. Endosulfan has shown to affect crustacean molt cycles, which are important biological and endocrine-controlled physiological processes essential for the crustacean growth and reproduction. Environmentally relevant doses of endosulfan equal to the EPA's safe dose of 0.006 mg/kg/day have been found to affect gene expression in female rats similarly to the effects of estrogen. It is not known whether endosulfan is a human teratogen (an agent that causes birth defects), though it has significant teratogenic effects in laboratory rats. A 2009 assessment concluded the endocrine disruption in rats occurs only at endosulfan doses that cause neurotoxicity.