The main action mechanism by which p,p-DDT causes the death of insects is the destabilization of the sodium channel, the main vehicle that propagates excitation signals on the surface of neurons, so that affected neurons become easily excitable. Insects poisoned by DDT show typical hyperexci-tation symptoms that lead to exhaustion and death. This phenomenon may be better understood as an electrophysio-logical manifestation in which neurons affected by DDT show a typical excitation pattern called "repetitive discharges." Such a neuron that has been excited by a stimulus remains in an excited state and continues to discharge for several minutes.
The most well-known use of insecticidal DDT is probably for mosquito control in malaria eradication programs. The most frequently used technique was that of "wall painting" of the interior of buildings with DDT in areas where malaria was prevalent. Because mosquitoes transmit malaria directly from human to human (i.e., without going through other hosts), this method effectively cuts off the link to continued transmission. The two key properties of DDT responsible for its effectiveness are the extreme susceptibility of mosquitoes to DDT and the long-lasting nature of DDT, particularly in indoors and dry environments.
DDT was also well known for its role in the control of cotton insect pests that posed a serious problem to cotton growers in the southern United States. The most commonly used formulation was a mixture of DDT and toxaphene. DDT was also used to control many other pests including the bark beetle vectoring Dutch elm disease, locusts, and forest pests (e.g., spruce budworm); these wider uses resulted in environmental loading of DDT-R.
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