Salivation, lacrimation, urination, and

Organophosphates. The acute toxicity of organophosphate pesticides is basically derived from the anticholinesterase property of these chemicals. This property, which results in accumulation of acetylcholine at synapses and myoneural junctions, is responsible for both the insecticidal activity and mammalian toxicity. Early symptoms of organophosphate poisoning in humans include, among others, miosis (pinpoint pupils) and blurred vision, and a response known as the SLUD (salivation, lacrimation, urination, and diarrhea) syndrome all of these are the result of muscarinic effects (12-15). Clinical manifestations of more severe poisoning involve predominantly nicotinic and central effects which include convulsions, paralysis, depressed respiration and cardiovascular functions, and coma (12-15). Death is usually due to respiratory failure, accompanied by cardio-vascular failure (13). 

The effects of ACh on bodily secretions and excretion are generally stimulatory. They may be remembered with the mnemonic SLUD —increased salivation, lacrimation, urination and defecation. 

Acetylcholine is broken down by the acetylcholinesterase enzyme to choline and acetate. The time required for hydrolysis of acetylcholine is less than a millisecond. If the enzyme is depleted or inhibited, then excessive acetylcholine accumulation in the body can cause toxicity. Symptoms are salivation, lacrimation, urination, diarrhea, muscle tremor, and fasciculation. 

The acute effects of aldicarb exposure are due to cholinergic overstimulation and may include the SLUDGE syndrome (salivation, lacrimation, urination, diarrhea, gastrointestinal cramping, and emesis), respiratory depression, bronchospasms, increased bronchial secretions, pulmonary edema, blurred vision, miosis, headache, tremors, muscle fasciculations, convulsions, mental confusion, coma, and death due to respiratory failure. Recovery from nonlethal exposures occurs very rapidly, usually within a few hours. 

The acute effects of exposure are due to cholinergic overstimulation and may include the SLUDGE (salivation, lacrimation, urination, diarrhea. 

Acute toxicity includes pupillary constriction, stimulation of GI tract (cramps, nausea, vomiting, and diarrhea [NVD]) and urinary tract (incontinence, urination), bronchoconstriction (wheezing, dyspnea), increased glandular secretions (sweating, salivation, lacrimation), bradycardia and hypotension, skeletal muscle fasciculations and then paralysis (e.g., respiratory muscles), and CNS effects (behavioral excitation, depression of cardiovascular [CV] and respiratory centers). 

Regardless of their subclassification, all of these compounds have the identical mechanism of action, which is inhibition of acetylcholinesterase at nerve junctions where the molecule acetylcholine is the neuotransmitter. Most acute signs of toxicity are expressed as uncontrollable activity of the nervous system, which clinically is presented as salivation, lacrimation, urination, defecation, and dyspnea. After lethal doses, death results from failure of the respiratory system. Variations in the specific nerves affected, in how the body metabolizes the individual chemical, in where the chemical enters the body, and in the route of administration employed will change the specific clinical presentation seen for an individual exposure scenario. 

The general symptoms of exposure to a nerve agent in gas form can be remembered by the acronym DUMBELS diarrhea, urination, miosis, bronchoconstric-tion (dyspnea, wheezing), emesis (vomiting), lacrimation, and salivation. Some prefer the acronym SLUDGEM salivation, lacrimation, urination, diarrhea, gastric upset, emesis, and miosis (Table S3.1). 

Acute toxicity studies in laboratory animals have shown that tetrachlorvinphos is one of the least toxic organophosphorus insecticides with an oral LD50 of > 2000 mg kg in laboratory animals. General signs of acute poisoning include salivation, diarrhea, urination, lacrimation, sweating, blurred vision, miosis, bradycardia, increased bronchial secretions, emesis, headache, dizziness, anxiety, lethargy, seizures, and depression of respiratory and cardiovascular centers. 

Extremely toxic by oral route moderately toxic by inhalation exhibits acute, delayed, and chronic effects cholinesterase inhibitor symptoms are those of phosphate — or carbamate esters—the major signs of which are increased salivation, lacrimation, spontaneous urination, blurred vision, pinpoint pupils, tremor, twitching of muscle and loss of coordination confusion, convulsions, and coma may occur as well other signs of poisoning include nausea, vomiting, cramps, diarrhea, slow heart rate, shortness of breath, and pulmonary edema (U.S. ERA 1988) death may result from respiratory arrest (Gosselin et al. 1984) the probable lethal dose from ingestion in adult human could be... 

Neurotoxins can be inhaled, ingested or absorbed. Once in the body it binds with critical neurotransmitters (acetylcholinesterase) initially causing excitation of the nervous system, conduction, then paralysis. Common signs are Diarrhea, Urination, Miosis, Broncho-spasm, Emesis, Lacrimation, and Salivation. 

Neurological effects, such as muscle twitching, ataxia, and increased salivation, urination, defecation, and lacrimation were observed in male Sprague-Dawley rats exposed to >65.1 mg/m... 

Perhaps the most prominent and well-studied class of synthetic poisons are so-called cholinesterase inhibitors. Cholinesterases are important enzymes that act on compounds involved in nerve impulse transmission - the neurotransmitters (see the later section on neurotoxicity for more details). A compound called acetylcholine is one such neurotransmitter, and its concentration at certain junctions in the nervous system, and between the nervous system and the muscles, is controlled by the enzyme acetylcholinesterase the enzyme causes its conversion, by hydrolysis, to inactive products. Any chemical that can interact with acetylcholinesterase and inhibit its enzymatic activity can cause the level of acetylcholine at these critical junctions to increase, and lead to excessive neurological stimulation at these cholinergic junctions. Typical early symptoms of cholinergic poisoning are bradycardia (slowing of heart rate), diarrhea, excessive urination, lacrimation, and salivation (all symptoms of an effect on the parasympathetic nervous system). When overstimulation occurs at the so-called neuromuscular junctions the results are tremors and, at sufficiently high doses, paralysis and death. 

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