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|Example of Acute Exposure data from MEDITEXT.|
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Example Content from MEDITEXT for 111-46-6:
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ACUTE EXPOSURE INFORMATION
- USES: Diethylene glycol is an industrial solvent and intermediate in the polymers and higher glycols. It can also be found in radiator fluid, antifreeze, brake fluid, Sterno, wall stripper, and in cleaning solutions.
- TOXICOLOGY: Diethylene glycol is metabolized to 2-hydroxyethoxyacetaldehyde by alcohol dehydrogenase oxidation, then to 2-hydroxyacetic acid (HEAA) by aldehyde dehydrogenase. HEAA causes acidosis, renal failure, and neurologic dysfunction. It is thought that the parent compound is toxic as well. Therefore, despite alcohol dehydrogenase blockade, patients may go on to develop signs of end organ toxicity.
- EPIDEMIOLOGY: Inadvertent exposures to low concentration products are relatively common but generally do not result in significant toxicity. Large, deliberate acute ingestions may cause life-threatening toxicity. Most fatalities have involved epidemics where people (primarily children) were repeatedly exposed due to contaminated medication in developing countries with weak manufacturing controls and limited access to intensive medical care.
- WITH POISONING/EXPOSURE
- MILD TO MODERATE TOXICITY: Common initial symptoms are heartburn, followed by nausea and abdominal cramps, vomiting and occasionally diarrhea. Headaches are also reported.
- SEVERE TOXICITY: Inebriation and metabolic acidosis may develop early. Later symptoms include back pain and severe abdominal pain; pancreatitis has also been reported after poisoning. Polyuria develops, followed by oliguria, anuria, and renal failure. Hepatotoxicity may develop. CNS depression, obtundation, or coma are common late in the course of toxicity, generally 3 to 5 days after exposure. Metabolism produces an acidosis caused by a toxic metabolite of the parent compound. CNS and respiratory depression, coma, respiratory arrest, and pulmonary edema have preceded death in reported cases. Tremors and rare seizures may accompany uremia. Peripheral and/or cranial neuropathies with bulbar palsy may develop weeks after severe poisoning.
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