Insecticide poisoning specific insecticides

Baculovimses, especially nuclear polyhedrosis viruses (NPV) and granulosis viruses (GV), appear to be exceptionally well suited for IPM because of their extreme insect specificity. They are stomach poisons and are slow-acting. In vitro production is difficult and the products are more expensive than the bacterial insecticides. Their high host specificity is viewed as a commercial disadvantage, and improvements in formulations and appHcation techniques are needed. 

Diagnosis of organophosphate poisoning (including methyl parathion) can be confirmed by evaluation of serum (plasma) cholinesterase and erythrocyte cholinesterase. However, cholinesterase inhibition is not specific for organophosphates. For example, carbamate insecticides also result in cholinesterase inhibition, which is usually transitory. Erythrocyte cholinesterase measurement is a specific test for... 

The wide publicity given DDT and the many new pesticides that have been developed during the past few years has made the public aware of the widespread use of spray chemicals. Many misstatements about the poisonous properties of these new products have caused abnormal concern and fear over the possible presence of excessive amounts of spray residues on food crops. This concern is a natural one, because the public does not realize the very small amount of the insecticidal residue that may remain on a single service of food, which usually does not exceed 0.25 pound in weight. Nor does the public realize that only a relatively small percentage of the food we eat has ever been treated with a spray or dust of a specific pesticide. 

Irreversible anticholinesterases include the organophosphorus inhibitors and ambenonium, which irreversibly phosphorylate the esteratic site. Such drugs have few clinical uses but have been developed as insecticides and nerve gases. Besides blocking the muscarinic receptors with atropine sulphate in an attempt to reduce the toxic effects that result from an accumulation of acetylcholine, the only specific treatment for organopho-sphate poisoning would appear to be the administration of 2-pyridine aldoxime methiodide, which increases the rate of dissociation of the organophosphate from the esteratic site on the enzyme surface. 

Most of the signs and symptoms resulting from diazinon poisoning are due to the inhibition of an enzyme called acetylcholinesterase in the nervous system. This enzyme is also found in your red blood cells and a similar enzyme (serum cholinesterase) is found in blood plasma. The most common test for exposure to many organophosphorus insecticides, including diazinon, is to determine the level of cholinesterase activity in the red blood cells or plasma. This test requires only a small amount of blood and is routinely available in your doctor s office. It takes time for this enzyme to completely recover to normal levels following exposure. Therefore, a valid test may be conducted a number of days following the suspected exposure. This test indicates only exposure to an insecticide of this type. It does not specifically show exposure to diazinon. 

Some bromine compounds are covered specifically under Hazardous Materials Regulations. Other compounds may usually be shipped under the classification of chemicals, not otherwise indexed by name, without special requirements unless from their nature they would fall under a category such as combustible liquid, compressed gas, corrosive liquid (or solid), disinfectant liquid (or solid), dmg, dye intermediate (liquid), fire extinguisher, flammable gas (liquid or solid), insecticide, medicine, oxidizer or oxidizing material, poisonous liquid (gas or solid), solvent, or tear gas. Specific provisions apply to each of these categories and appropriate packaging and labeling are required. 

Insects poisoned with rotenone exhibit a steady decline in oxygen consumption and the insecticide has been shown to have a specific action in interfering with the electron transport involved in the oxidation of reduced nicotinamide adenine dinudeotide (NADH) to nicotinamide adenine dinucleotide (NAD) by cytochrome h. Poisoning, therefore, inhibits the mitochondrial oxidation of Krebs-cycle intermediates which is catalyzed by NAD. 

Research on anesthetic gases during the nineteenth century facilitated the development and use of poisonous war gases in the twentieth. This led to attempts to counteract the effects of chemical warfare agents and other toxic compounds, particularly arsenicals, introduced by Paul Ehrlich (1854-1915) for the treatment of syphilis. This resulted in the synthesis of the first specific chemical antidote, British anti-Lewisite (BAL), in 1945 by R.A. Peters, L.A. Stocken, and R.H.S. Thompson in Oxford. Studies on the mechanistic bases for toxicity were applied to the synthesis of effective insecticides. For example, during the 1940s, the Swiss chemist Paul Muller discovered a compound, now known as DDT, that poisons insects on contact. 

Of direct relevance for pesticide science is the antagonist atropine. This toxicant also binds specifically to the muscarinic receptors where it blocks the effect of ACh. The symptoms are therefore the opposite of those caused by muscarine or acetylcholine (pupil dilation, dry mouth, inhibition of sweating, tachycardia, palpitations, hallucinations, delirium, etc.). Atropine is an important antidote when one is poisoned with a cholinesterase-inhibiting insecticide. 

Phenylmethylsulfonyl fluoride prevents delayed neurotoxicity from OPs if administered before exposure but potentiates neurotoxicity if administered after exposure (Pope and Padilla 1990). Alcohol and drug abuse also potentiate insecticide toxicity, but symptoms are not specific (Calabrese 1978). Protein-deficient diets increase susceptibility to OP poisoning (Boyd and Chen 1968 Krijnen and Boyd 1971). Special diets increase risks for infants, food faddists, and individuals with protein deficiency, including persons in developing countries with protein-deficient diets. Individuals with vitamin A, vitamin C, or methionine deficiencies may be susceptible to CH insecticides (Calabrese 1978). The environmental temperature and fat solubility of OPs have marked effects on their toxicities (J. E. Davies et al. 1975 Wheeler 1987). 

Another area that would be of direct benefit to the medical personnel responsible for treating pesticide exposure in humans is the development of antidotal and symptomatic treatment for the various classes of pesticides. Although we have more specific antidotes available to treat pesticide poisoning than for any other single class of acute poisons, the number of antidotes is small for non-insecticidal pesticides and these cases must be treated symptomatically. The current acute toxicity protocols do not currently provide the kind of clinical information that is needed in such cases. 

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