Chapter 11: Clinical Toxicology of Insecticides
Published:19 Jan 2012
Some insects compete for our food, some damage construction materials and some are important disease vectors in humans and animals. Hence, it is not surprising that chemicals (insecticides) have been developed that kill insects and other arthropods. More recently introduced insecticides, such as the neonicotinoids, have been produced with the intent that humans and animals will not be harmed by their appropriate use. This chapter reviews the clinical features and management of exposure to organophosphorus (OP) and carbamate insecticides, neonicotinoids, phosphides and pyrethroids. In the developing world where the ambient temperature is often high and personal protection equipment often not worn, poisoning particularly from OP and carbamate insecticides is common in an occupational setting, though more severe cases are due to deliberate ingestion of these pesticides. Both of these insecticides produce the cholinergic syndrome. The neonicotinoids, a major new class of insecticide, were introduced on the basis that they were highly specific for subtypes of nicotinic receptors that occur only in insect tissues. However, deliberate ingestion of substantial amounts of a neonicotinoid has resulted in features similar to those found in nicotine (and OP and carbamate) poisoning, though the solvent in some formulations may have contributed to their toxicity. Phosphides interact with moisture in air (or with water or acid) to liberate phosphine, which is the active pesticide. Inhalation of phosphine, however, is a much less frequent cause of human poisoning than ingestion of a metal phosphide, though the toxicity by the oral route is also due to phosphine liberated by contact of the phosphide with gut fluids. It is then absorbed through the alimentary mucosa and distributed to tissues where it depresses mitochondrial respiration by inhibiting cytochrome c oxidase and other enzymes. Dermal exposure to pyrethroids may result in paraesthesiae, but systemic toxicity usually only occurs after ingestion, when irritation of the gastrointestinal tract and CNS toxicity, predominantly coma and convulsions, result.