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The chemical ‘deet’ (for N,N-diethyl-meta-toluamide) is the main ingredient in nearly every commonly used mosquito repellent in the world - around eight billion doses have been applied since its introduction in 1957. The chemical was originally developed as an insect repellent by the U.S. Army in 1946, following experience with jungle warfare in World War II. But in spite of the chemical's long use, researchers are not sure exactly how deet repels mosquitoes. It has long been believed that it affects mosquito behavior without harming the insects, probably by interfering with their sense of smell and their ability to find human prey. However, a new study now suggests that deet inhibits the activity of a key central nervous system enzyme, acetylcholinesterase, in both insects and mammals. This is the same mechanism that causes the toxic effects of popular carbamate and organophosphate pesticides, as well as chemical weapons such as sarin and VX nerve gas and suggests that deet repellants are in fact insecticides and could damage the human nervous system. Organophosphates, which are among the pesticides most commonly implicated in pesticide poisoning worldwide and although carbamates are not as toxic as organophosphates, their effects can be just as severe at high enough doses. Strong evidence links both to serious health conditions caused by long-term exposure even at low doses. The researchers also found that the effects of deet were enhanced when it was used in combination with organophosphates or carbamates, as in mixed repellent-insecticide products. The researchers suggested that pregnant women and children under the age of six avoid using deet-containing mosquito . For abstract - BioMed Central Biology
Click here for more research on pesticides First Published in July 2009 |
