China
Africa
Explore chapters and articles related to this topic
Basic Chemical Hazards to Human Health and Safety — I
Published in Jack Daugherty, Assessment of Chemical Exposures, 2020
The cholinesterase test measures the amounts of two enzymes that hydrolyze acetylcholinesterase. Pseudocholinesterase, which is also called PCHE or serum cholinesterase, is produced primarily in the liver, but small amounts are found in the pancreas, intestine, heart, and white matter of the brain. Even though physicians and scientists do not fully understand the function of pseudocholinesterase, when a chemical inhibits cholinesterase it also affects pseudocholinesterase, which can be observed. Acetylcholinesterase, the second choline enzyme, is present in nerve tissues, red cells of the spleen, and the gray matter of the brain and transmits impulses across nerve endings to muscle fiber. Hence, paralysis occurs when the enzyme is inhibited. Organophosphates inactivate acetylcholinesterase directly. When organophosphate poisoning is suspected, either cholinesterase enzyme may be measured, but pseudocholinesterase is usually chosen. Pseudocholinesterase levels range from 8 to 18 units/ml as determined by a kinetic colorimetric technique.
Toxic Responses of the Nervous System
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
The neurotransmitter system of the neuron represents yet another target for certain neurotoxic substances. A classic example of neurotoxicity due to disruption of the neurotransmitter system involves inhibition of acetylcholinesterase by various organophosphorus insecticides. During normal impulse conduction, the neurotransmitter, acetylcholine, is released from synaptic end bulbs of an axon into the synapse. The neurotransmitter molecules then interact with receptors on the dendrite of an opposing neuron to continue impulse conduction. An endogenous enzyme, acetylcholinesterase, then inactivates the acetylcholine molecules. However, when present in the synaptic region, organophosphorus compounds bind with the endogenous acetylcholinesterase molecules rendering the enzyme ineffective. Consequently, the acetylcholine transmitter accumulates in the synapse and inappropriately continues impulse conduction. The signs and symptoms of organophosphate poisoning are predictable based on this mechanism of action and include increased salivation, lacrimation, and sweating; ataxia, tremors, muscle fasciculations, and convulsions; constriction of the pupils; bronchial constriction; and increased peristalsis with consequent development of nausea, vomiting, abdominal cramps, and diarrhea. In fatal organophosphorus poisoning, death is due to asphyxiation resulting from respiratory failure. However, in most acute exposures, full recovery occurs following cessation of the exposure.
List of Chemical Substances
Published in T.S.S. Dikshith, and Safety, 2016
Acephate is a colorless to white, solid organophosphate insecticide. Exposures to acephate cause poisoning to animals and humans. Acephate inhibits acetylcholine esterase (AchE), the essential nervous system enzyme, and causes characteristic organophosphate poisoning. The symptoms of toxicity include, but are not limited to, headache, nervousness, blurred vision, weakness, nausea, fatigue, stomach cramps, diarrhea, difficulty breathing, chest pain, sweating, pin-point pupils, tearing, salivation, clear nasal discharge and sputum, vomiting, muscle twitching, muscle weakness, and in severe poisonings, convulsions, respiratory depression, coma, and death. Acephate causes cholinesterase inhibition leading to overstimulation, respiratory paralysis, and death.
Evaluating risk, exposure, and detection capabilities for chemical threats in water
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Marisa Pfohl, Erin Silvestri, John C. Lipscomb, Emily Snyder, Stuart Willison
Both acephate and methamidophos are known to produce toxicity via inhibition of the acetylcholinesterase enzyme, leading to a toxic and at times fatal accumulation of acetylcholine. However, methamidophos is known to be more potent in humans than its precursor acephate. Symptoms of organophosphate poisoning include excessive sweating, nausea, vomiting, weakness, seizures, and paralysis. The human health risk of the organophosphates at low doses is not well characterized (CDC 2013). The risk of oral exposure to methamidophos was evaluated and a chronic HHBP drinking water value of 0.6 µg/L was derived. The drinking water value is based upon a PAD which takes the RfD and applies an additional Food Quality Protection Act of 1996 (FQPA) safety factor to account for both potential prenatal and/or postnatal toxicity and the completeness of the database with respect to exposure and toxicity for women of child-bearing age, infants, and children (U.S. EPA 2017c). The study used as the basis of the chronic PAD was an 8-week subchronic oral toxicity study in rats which measured brain ChE inhibition. The no-observed-adverse-effect level (NOAEL) dose was 0.03 mg/kg/day to which a total UF of 100 was applied, followed by a FQPA safety factor of 3 to derive an ultimate PAD of 0.0001 mg/kg/day (U.S. EPA 2006).