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CHAPTER 161 – Pesticides
Cynthia K. Aaron, James W. Rhee, Bram A. Dolcourt

Pesticides, a generic term used to refer to all pest-killing agents, include numerous chemicals intended for use as insecticides, herbicides, rodenticides, fungicides, and fumigants. Many of these chemicals are general protoplasmic poisons affecting a wide range of organisms, including humans. Althoughspace does not allow a comprehensive discussion of each individual chemical that may produce human toxicity, numerous chemical classes are commonly used as pesticides. These classes have associated characteristic clinical pictures that are important to recognize because patients with acute (and occasionally chronic) exposures to these agents come to the emergency department. In addition, otherpesticides with particularly unique mechanisms of toxic effects are described.
The organophosphate insecticide triethyl pyrophosphate was first synthesized in 1859 but was not used to replace nicotine as a pesticide until World War II. After World War II, these compounds were used as chemical warfare agents, as organophosphorus and carbamate insecticides,and as medicinal agents. After the negative publicity associated with the organochlorine dichlorodiphenyltrichloroethane (DDT), organophosphate insecticides soon became some of the most common pesticides for home and industrial use. Since the late 1990s, with the increased awareness of terrorism, nerve agents have gained prominence as weapons of mass destruction.[1]
Principles of DiseaseOrganophosphorus insecticides are highly lipid soluble and are readily absorbed via dermal, gastrointestinal (GI), and respiratory routes.[2] This lipid solubility results in the storage of organophosphorus compounds in body fat, making toxic systemic levels possible from gradual or rapid accumulation from repeated low-level exposures. The parent compound and its metabolites are acetylcholinesteraseinhibitors, and many parent organophosphorus compounds are less potent than their metabolites (e.g., parathion to paraoxon), which may result in delayed onset of clinical toxicity.
Organophosphorus pesticides work by persistently inhibiting the enzyme acetylcholinesterase, the enzymatic deactivator of the ubiquitous neurotransmitter acetylcholine. Because of the global penetration oforganophosphorus compounds, inhibition occurs at tissue sites (true acetylcholinesterase and represented by erythrocyte or red blood cell [RBC] cholinesterase) and in plasma (circulating pseudocholinesterase).[3,4] Inhibition of cholinesterase results in the accumulation and subsequent prolonged effect of acetylcholine at a variety of neurotransmitter receptors, including the sympathetic and parasympatheticganglionic nicotinic sites, postganglionic cholinergic sympathetic and parasympathetic muscarinic sites, skeletal muscle nicotinic sites, and central nervous system sites (Fig. 161-1).[2]

Figure 161-1. The autonomic nervous system (ANS) comprises the sympathetic and parasympathetic nervous systems. The sympathetic nervous system is also known as the thoracolumbar outflow, where the cell body liesin the spinal cord and the first synapse occurs in the sympathetic ganglia. The neurotransmitter in this first synapse is acetylcholine (ACh) (preganglionic), and the neurotransmitter in the postganglionic neuron with the target organ is norepinephrine (NE). In the parasympathetic nervous system (craniosacral outflow), nerves from the medulla and sacrum use ACh as the neurotransmitter inpreganglionic and postganglionic target organs. The ANS is divided further into the muscarinic and nicotinic receptors, where atropine can block the muscarinic receptors but not the nicotinic receptors. The neuromuscular junction uses ACh as the effector neurotransmitter. In the brain, ACh is just one of several active neurotransmitters. 

Clinical Features
Signs and Symptoms
The accumulation of...
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