Chemical structure:
It was first synthesized in 1873, and its insecticidal properties were discovered by the Swiss scientist [Paul Hermann Müller]? in 1942 who was awarded the 1948 Nobel Prize in Physiology and Medicine for his efforts. DDT is the best known of a number of chlorine-containing pesticide?s used in the 1940s and 1950s. It was extensively used during World War II among Allied troops and certain civilian populations to control insect typhus? and malaria vectors, and was then extensively used as an agricultural insecticide after 1945. In the 1950s doses of DDT and other insecticides had to be doubled or trebled as resistant insect strains developed, and evidence began to grow that the chemical was concentrated in the food chain. The compound is stable and concentrates in fatty tissue, reaching dangerous levels in carnivores high in the food chain. It is also excreted in milk.
In 1962 [Rachel Carson]?'s book [Silent Spring]? was released. The book argued that pesticide?s, and especially DDT, were poisoning both wildlife and the environment and also endangering human health. The public reaction to Silent Spring launched the modern environmental movement, and DDT became a prime target of the growing anti-chemical and anti-pesticide movements during the 1960s.
DDT was banned from use in Norway and Sweden in 1970, the United Kingdom in 1984, and the United States in 1972 where it is classified in EPA? Toxicity Class II. It is still used in other (primarily tropical) countries where mosquito?-borne malaria is a larger health problem than DDT's potential toxicity.
DDT is highly persistent in the environment, with a reported [half life]? of between 2-15 years and is immobile in most soils. Routes of loss and degradation include runoff, volatilization, photolysis and biodegradation? (aerobic and anaerobic). These processes generally occur only very slowly. Breakdown products in the soil environment are DDE (1,1-dichloro-2,2-bis(p-dichlorodiphenyl)ethylene) and DDD (1,1-dichloro-2,2-bis(p-chlorophenyl)ethane), which are also highly persistent and have similar chemical and physical properties.
Controversy remains in some scientific circles over DDT's actual toxicity, however. Some scientists have protested that the laboratory animal studies done in 1969 (and which led to the banning of DDT in much of the developed world) which showed that DDT caused an increase in liver cancer was inconsistent with observations in the wild, given that DDT had been used widely during the preceding three decades with no increase in liver cancer in any of the human populations among whom it had been sprayed. When the World Health Organization investigated the 1969 mouse study, they found that both experimental and control groups had developed a surprising number of tumors. Further investigation revealed that the food fed to both groups were moldy and contained aflatoxin, a carcinogen. When the tests were repeated using uncontaminated foods, neither group developed abnormal numbers of tumors. The studies showing that DDT is responsible for the thinning of predatory bird eggshells have also been called into question. Since DDT remains one of the most effective pesticides available to combat the spread of malaria in tropical countries, and is also one of the great spectres of the environmentalist movement, this debate is likely to remain vigorously argued for the forseeable future.
DDT is created by the reaction of trichloromethanal with chlorobenzene (C6H5Cl). Trade or other names for DDT include Anofex, Cesarex, Chlorophenothane, Dedelo, p,p'-DDT, Dichlorodiphenyltrichloroethane, Dinocide, Didimac, Digmar, ENT 1506, Genitox, Guesapon, Guesarol, Gexarex, Gyron, Hildit, Ixodex, Kopsol, Neocid, OMS 16, Micro DDT 75, Pentachlorin, Rukseam, R50 and Zerdane.
DDT is an organochlorine. Some organochlorines have been shown to have weak estrogenic activity, that is, they are chemically similar enough to estrogen to trigger hormonal responses in contaminated animals. This sort of activity has been observed in DDT in laboratory studies involving mouse and rat test subjects, but available epidemiological evidence does not indicate that these effects have occurred in humans as a result of DDT exposure.
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