Pesticides central nervous system effects

Rosenstock, L., Keifer, M., Daniell, W.E., McConnell, R., Claypoole, K. (1991). Chronic central nervous system effects of acute organophosphate pesticide intoxication. The Pesticide Health Effects Study Group. Lancet 338 223-7. 

Air-poUutant effects on neural and sensory functions in humans vary widely. Odorous pollutants cause only minor annoyance yet, if persistent, they can lead to irritation, emotional upset, anorexia, and mental depression. Carbon monoxide can cause death secondary to the depression of the respiratory centers of the central nervous system. Short of death, repeated and prolonged exposure to carbon monoxide can alter sensory protection, temporal perception, and higher mental functions. Lipid-soluble aerosols can enter the body and be absorbed in the lipids of the central nervous system. Once there, their effects may persist long after the initial contact has been removed. Examples of agents of long-term chronic effects are organic phosphate pesticides and aerosols carrying the metals lead, mercury, and cadmium. 

F. Matsumura, sponsored by the National Institute of Environmental Health Sciences (NIEHS), plans to study the toxic effects of chlorinated and pyrethroid pesticides primarily on calcium and sodium regulating processes in the nervous system. To examine the interactions of the pesticides with calcium regulating processes, researchers will use synaptosomal preparations from the brains of rats and the central nervous systems of squid. To examine the interactions of the pesticides with sodium regulating processes, they will collect antibodies directed against sodium channel proteins. 

Pesticides are used to kill household insets, rats, cockroaches, and other pests. Pesticides can be classified based on their chemical nature or use as organophosphates, carbonates, chlorinated hydrocarbons, bipyridyls, coumarins and indandiones, rodenticides, fungicides, herbicides, fumigants, and miscellaneous insecticides. The common adverse effects are irritation of the skin, eyes, and upper respiratory tract. Prolonged exposure to some chemicals may cause damage to the central nervous system and kidneys [32,33]. 

The acute toxic properties of all the organochlorine pesticides in humans are qualitatively similar. These agents interfere with inactivation of the sodium channel in excitable membranes and cause rapid repetitive firing in most neurons. Calcium ion transport is inhibited. These events affect repolarization and enhance the excitability of neurons. The major effect is central nervous system stimulation. With DDT, tremor may be the first manifestation, possibly continuing to convulsions, whereas with the other compounds convulsions often appear as the first sign of intoxication. There is no specific treatment for the acute intoxicated state, and management is symptomatic. 

Herbicides, or weed killers, may be classified as pesticide chemicals. They can kill plants on contact, or they can be translocated (i.e absorbed by one part of the plant and carried to other parts where they exert their primary toxic effect). Most commonly used herbicides have a low toxicity and have caused few adverse effects in users. Some herbicides pose more serious problems to the central nervous system (CNS) and can cause depression. The skin absorption of herbicides also may cause skin irritation, dermatitis, and photosensitization in addition to peripheral motor neuropathies. 

Carbamates also include pesticides such as Sevin, aldicarb, and carbaryl. They are more degradable than organophosphates and have lower dermal toxicides. Their toxicity is also due to inhibition of acetylcholinesterase but they do not penetrate the central nervous system, so most effects are respiratory in nature. An acetylcholinesterase, which has been carbamylated can undergo spontaneous hydrolysis in vivo, which reactivates the enzyme leading to less severe symptoms or a shorter duration of symptoms. Carbaryl has a low toxicity for mammals however, Perimicarb is highly toxic to mammals, but not readily absorbed through the skin. 

SAFETY PROFILE Poison by intravenous route. Moderately toxic by ingestion and skin contact. Human systemic effects coma, convulsions, dermatitis, mydriasis (pupiUar dilation), nausea or vomiting, stiffness. An eye and skin irritant. Experimental reproductive effects by skin contact. Mutation data reported. Can cause central nervous system disturbances. A pesticide. DEET is the active ingredient in most commercial insect repellents. When heated to decomposition it emits toxic fumes of NO,. 

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