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Lawsuits filed on behalf of both US and Vietnamese veterans sought compensation for damages.
Agent Orange was to a lesser extent used outside Vietnam.
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When TCDD binds to Ah R, the protein moves to the nucleus, where it influences gene expression. began a full-scale production of 2,4-D and 2,4,5-T and would have used it against Japan in 1946 during Operation Downfall if the war had continued. tested 1,100 compounds, and field trials of the more promising ones were done at British stations in India and Australia, in order to establish their effects in tropical conditions, as well as at the U. Between 19, trials were conducted in Tanganyika, at Kikore and Stunyansa, to test arboricides and defoliants under tropical conditions. considered the British precedent in deciding that the use of defoliants was a legal tactic of warfare.
Several herbicides were discovered as part of efforts by the USA and the British to develop herbicidal weapons for use during World War II. Department of the Army contracted the botanist and bioethicist Arthur Galston, who discovered the defoliants later used in Agent Orange, and his employer University of Illinois at Champaign-Urbana to study the effects of 2,4-D and 2,4,5-T on cereal grains (including rice) and broadleaf crops. Army ran tests of various 2,4-D and 2,4,5-T mixtures at the Bushnell Army Airfield in Florida. By the end of the war, the relationship between the two countries was well established. The chemicals involved were 2,4-D, 2,4,5-T, and endothall (3,6-endoxohexahydrophthalic acid). Secretary of State Dean Rusk advised President John F.
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The main ingredients of Agent Orange comprise an equal mixture of two phenoxyl herbicides – 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) – in iso-octyl ester form, which contained traces of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
Agent Orange dries quickly after spraying and breaks down within hours to days when exposed to sunlight (if not bound chemically to a biological surface such as soil, leaves and grass) and is no longer harmful. Dioxin enters the body by attaching to a protein called the aryl hydrocarbon receptor (Ah R), a transcription factor.
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