DDT (4,4'-DDT), or 1,1'-(2,2,2-trichloroethylidene)bis[4-chlorobenzene], was first described 
early in the century and resynthesized during the late 1930s as part of a research program at 
Geigy (Stetler, 1983). This program was a search for a contact insecticide characterized by a 
long duration of activity. Following the discovery of the pronounced insecticidal properties of 
the new agent and the registration of the first patents in 1940, the product, formulated in 
Switzerland, was introduced to the market in the spring of 1942 for use in crop protection and 
hygiene. The epidemic-promoting circumstances of World War II and the post-war years 
brought about increased and effective use of DDT in the field of medicinal hygiene. Malaria, 
typhus, typhoid fever, and cholera were drastically reduced by the effective control of 
Anopheles mosquitoes, lice, and flies of all types or, as in the case of malaria, were virtually 
eradicated in many countries. It has been estimated that almost 1 billion people in all parts of 
the world have been saved from malaria by the use of DDT. 
4,4'-DDT is metabolized by the loss of a chlorine to yield the non-insecticidal 4,4'-DDE {(1,1'- 
(dichloroethylidene)bis(4-chlorobenzene]}, and by the substitution of a chlorine by a hydrogen 
to yield 4,4'-DDD {(1,1'-(2,2-dichloroethylidene)bis[4-chlorobenzene]}. DDT and some of its 
metabolites are toxicants, with long-term persistence in soil and water. They are widely 
dispersed by erosion, runoff, and volatilization, and accumulate in adipose tissue in wildlife and 
humans. The pronounced contact activity of DDT is due to the highly lipophilic character of the 
compound, which enables it to penetrate the insect cuticle. According to some biochemical 
models, a disturbance in the sodium balance of the nerve membranes, caused by the “fit" of the 
DDT molecule, is responsible for the poisoning of the insect. Buildup of resistance to DDT is 
connected with the enzyme catalyzed conversion into inactive DDE. DDT coatings on solid 
surfaces have a considerable duration of activity. Acute mammalian toxicity is relatively 
insignificant. 
Restrictions introduced by most Western industrialized countries on the production of DDT and 
other chlorohydrocarbons at the start of the 1970s have reduced use of chemicals to a fraction 
of the original quantities. The use of DDT was banned in the US in 1972. The special situation of 
the Third World countries, however, resulted in production peaks (on a worldwide basis) as late 
as the mid-1970s. Without sufficient quantities of DDT and dieldrin, the World Health 
Organization is unable to fulfill its vector-control programs. 
In a study published in 1974, Ogden et al. (1974) found DDT, DDE, DDD, dieldrin, and PCBs in 
concentrations well below amounts known to have either acute or chronic effects on species 
from Florida Bay. Chlorinated pesticides and PCBs in melon tissue from Atlantic bottlenose 
dolphins (Tursiops truncatus) and pygmy sperm whales (Kogia breviceps) collected in Florida 
Bay were determined by King (1987). 
10.4. PCBs ban 
Polychlorinated biphenyls (PCBs) are widely distributed in the environment, and have no known 
natural source. PCBs were manufactured by Monsanto and were available in the US from 1930 
to 1977 as a series of mixtures of congeners called Aroclors, having different average 
compositions of congeners. PCB concentrations have also been reported as Aroclors (EPA, 
1993). There are 209 congeners, having from one to ten chlorines. Twenty of these congeners 
have non-ortho chlorine substitutions and so can attain a planar structure which makes them 
similar in structure to the highly toxic polychlorinated dibenzo-p-dioxins and dibenzofurans 
(McKinney et al., 1985; Sericano et al., 1991). In the scientific literature, total PCB 
concentrations are often reported and these values are calculated based on the response factors 
of PCB congeners representative of each chlorination level. 
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