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Most chemical insecticides act by poisoning the nervous system. The central and peripheral nervous system of insects is fundamentally similar to that of mammals. A small amount of pesticide can be fatal to an insect, primarily because of the insect's small size and high rate of metabolism. While that same amount will not be fatal to a person, it may still cause harm.

The similarities of nervous system structure make it nearly impossible to design insecticides that affect only target insect pests; consequently, insecticides may affect non-pest insects, people, wildlife, and pets. Some insecticides harm water quality or affect organisms in other ways; for example, the insecticide carbaryl (a carbamate insecticide, further discussed below) is listed as a carcinogen by the state of California and as a possible hormone disruptor by the state of Illinois' EPA. The newer insecticides are designed to be more specific and less persistent in the environment.

The most prominent classes of insecticides are organochlorines, organophosphates, carbamates, and pyrethroids.


The chemical structure of organochlorines is diverse, but they all contain chlorine, which places them in a larger class of compounds called chlorinated hydrocarbons. Organochlorines, which include DDT, demonstrate many of the potential risks and benefits of insecticide use.

While organochlorines have the advantage of being cheap to manufacture and are effective against target species, they have serious unintended consequences. Organochlorines disrupt the movement of ions such as calcium, chloride, sodium, and potassium into and out of nerve cells. Depending on the specific structure of the organochlorine chemical, it may also affect the nervous system in other ways. At one time organochlorines were thought to be ideal because they are very stable, slow to degrade in the environment, dissolve in fats (and are therefore readily taken up by insects), and seemingly harmless to mammals. Unfortunately it eventually became clear that the attributes of persistence and fat solubility were actually very undesirable: the organochlorines passed up the food chain, where they bioaccumulated in the fat of large animals and humans and were passed on to nursing young. The global use and transport of organochlorines resulted in the contamination of wildlife around the globe, including in Arctic and Antarctic regions where these insecticides are rarely if ever used. A decline in the number of birds that prey on animals exposed to DDT was one of the first signs of the unintended consequences. Unexpectedly, DDT caused a thinning of the birds' eggshells and resulted in the death of their developing young.

Organochlorines like DDT are now largely banned in industrialized countries but they are still manufactured and used in developing countries. (Banned pesticides are still manufactured in some industrialized countries and exported.) Organochlorine insecticides provide many important lessons about the desirable and undesirable properties of pesticides.

Organophosphates and Carbamates

Organophosphates and carbamates have very different chemical structures, but share a similar mechanism of action and will be examined here as one class of insecticides.

Organophosphates were initially developed in the 1940s as highly toxic biological warfare agents (nerve gases). Modern derivatives, including sarin, soman, and VX, were stockpiled by various countries and now present some difficult disposal problems. Researchers created many different organophosphates in their search for insecticides that would
target selected species and would be less toxic to mammals. When the organophosphate parathion was first used as a replacement for DDT, it was believed to be better as it was more specific. Unfortunately there were a number of human deaths because workers failed to appreciate the fact that parathion's short-term (acute) toxicity is greater than DDT's.

The problem with organophosphates and carbamates is that they affect an important neurotransmitter common to both insects and mammals. This neurotransmitter, acetylcholine, is essential for nerve cells to be able to communicate with each other. Acetylcholine released by one nerve cell initiates communication with another nerve cell, but that stimulation must eventually be stopped. To stop the communication, acetylcholine is removed from the area around the nerve cells, and an enzyme, acetylcholinesterase, breaks down the acetylcholine. Organophosphates and carbamates block the enzyme and disrupt the proper functioning of the nerve cells. Hence, these insecticides are called acetylcholinesterase inhibitors.

Structural differences between the various organophosphates and carbamates affect the efficiency and degree to which the acetylcholinesterase is blocked. Nerve gases are highly efficient and permanently block acetylcholinesterase, while the commonly used pesticides block acetylcholinesterase only temporarily. The toxicity of these pesticides presents significant health hazards, and researchers continue to work to develop new insecticides that have fewer unintended consequences.


One of the newer classes of insecticide, synthetic pyrethroids are loosely based upon the naturally occurring pyrethrum found in chrysanthemum flowers. Synthetic pyrethroids were first developed in the 1980s, but the naturally occurring pyrethrum was first commercially used in the 1800s. Their use has increased significantly over the last 20 years. The chemical structure of pyrethroids is quite different from that of organochlorines, organophosphates, and carbamates but the primary site of action is also the nervous system. Pyrethroids affect the movement of sodium ions (Na+) into and out of nerve cells, causing the nerve cells to become hypersensitive to neurotransmitters. Structural differences between various pyrethroids can change their toxic effects on specific insects and even mammals.

Synthetic pyrethroids are more persistent in the environment than natural pyrethrum, which is unstable in light and breaks down very quickly in sunlight.

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