dioxin

/duy ok"sin/, n. Chem.

a general name for a family of chlorinated hydrocarbons, C₁₂H₄Cl₄O₂, typically used to refer to one isomer, TCDD, a by-product of pesticide manufacture: a toxic compound that is carcinogenic and teratogenic in certain animals. Also called TCDD Cf. Agent Orange.

[1965-70; DI-¹ + OX- + -IN²]

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Aromatic compound, any of a group of contaminants produced in making herbicides (e.g., Agent Orange), disinfectants, and other agents.

Their basic chemical structure consists of two benzene rings connected by a pair of oxygen atoms; when substituents on the rings are chlorine atoms, the molecules are particularly toxic. The best-known, usually called simply dioxin, is 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). It is extremely stable chemically; it does not dissolve in water but dissolves in oils (and thus accumulates in body fat). The extent of its human toxicity is disputed and the subject of continuing research.

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▪ chemical compound

      any of a group of chemical compounds that is an undesirable by-product in the manufacture of herbicides, disinfectants, and other agents. In popular terminology, dioxin has become a synonym for one specific dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD).

      In chemical structure, a dioxin (technically called dibenzo-p-dioxin) consists of two benzene rings connected by a pair of oxygen atoms. Each of the eight carbon atoms on the rings that are not bonded to oxygen can bind with hydrogen atoms or atoms of other elements. By convention these positions are assigned the numbers 1 through 4 and 6 through 9. The more toxic dioxins carry chlorine atoms at these positions, and the best-known one has chlorine atoms at the 2,3,7, and 8 positions. This isomer—2,3,7,8-TCDD—is extremely stable chemically. It is virtually insoluble in water and in most organic compounds but is soluble in oils. It is this combination of properties that allows this dioxin in soil to resist dilution with rainwater and causes it to seek and enter fatty tissue in the body if it is absorbed.

      Dioxin serves no useful purpose but is formed as an undesirable by-product during the synthesis of 2,4,5-trichlorophenol and some other useful compounds. The chemical 2,4,5-trichlorophenol serves as a raw material for making the herbicides Silvex and 2,4,5-T (2,4,5-trichlorophenoxyacetic acid). The latter is a major active ingredient of Agent Orange (q.v.), a defoliant formerly used in Vietnam by the U.S. military and in the United States to kill unwanted vegetation. This 2,4,5-trichlorophenol is also used in the production of hexachlorophene, an antibacterial agent formerly used in deodorants and soaps.

      The recognition in the early 1980s that residential sites at Times Beach and elsewhere in Missouri, U.S., had been contaminated by improper disposal of chemical wastes containing 2,3,7,8-TCDD led to intense public scrutiny of its possible toxic effects. Toxicologists mistakenly concluded from studies on laboratory animals that TCDD was one of the most toxic of all man-made substances and recommended that soil levels in excess of one part per billion might constitute a health risk to humans. It was known that TCDD could produce chloracne, a serious skin rash, but exposure to the chemical was also blamed for muscular dysfunctions, various bodily inflammations, impotency, birth defects, genetic mutations, and nervous system disorders. TCDD was also linked to various cancers.

      Subsequent research, however, discounted most of these inferences, which were based on the effects of very high doses of TCDD on guinea pigs and other peculiarly susceptible animals. Among humans, the only disease definitely found related to TCDD is chloracne, which develops shortly after exposure to the chemical. Epidemiological studies on industrial workers exposed to TCDD over many years show that it has a weak carcinogenic effect at high-dose exposures and no effect whatsoever at low-dose exposures. In fact, normally occurring exposure to TCDD appears to be less of a carcinogenic risk than similar exposure to asbestos, radon, or cigarette smoke. Nor has any convincing evidence been found for the association of TCDD with other bodily disorders and defects in humans, including genetic mutations.

      What toxicity TCDD does possess apparently derives from the chemical's ability to bind with a particular type of receptor protein inside some cells within the body. The resulting TCDD-receptor complex can enter the cell's nucleus and bind with its DNA, thereby disrupting the cell's machinery for producing proteins. The wide and rather puzzling array of toxic effects induced in animals by high levels of TCDD are apparently all receptor-mediated responses to that chemical. Such animals' immune systems are those most often affected, being apparently weakened or compromised by TCDD.

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