Ethylene glycol poisoning Peter Mygind Leth a, * , Markil Gregersen b a Institute of Forensic Medicine, University of Southern Denmark, Faculty of Health Sciences, Winsløvparken 17, DK-5000 Odense C, Denmark b Institute of Forensic Medicine, University of Aarhus, Denmark Received 13 September 2004; received in revised form 10 November 2004; accepted 10 November 2004 Available online 21 January 2005 Abstract Ethylene glycol (EG) can be found in many agents, such as antifreeze. Ingestion of EG may cause serious poisoning. Adults are typically exposed when EG is ingested as a cheap substitute for ethanol or in suicide-attempts. Children may be exposed by accidental ingestion caused by decantation of EG to unlabeled bottles. EG has in itself a low toxicity, but is in vivo broken down to four organic acids: glycoaldehyde, glycolic acid, glyoxylic acid and oxalic acid. The metabolites are cell toxins that cause central nervous system depression, and cardio-pulmonary and renal failure. Glycolic acid causes severe acidosis, and oxalate is precipitated as calcium oxalate in the kidneys and other tissues. We present five case reports of fatal EG-poisoning, and review the literature concerning clinical presentation and diagnosis, pathological findings, treatment and prevention. # 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Ethylene glycol; Antifreeze; Poisoning 1. Introduction Ethylene glycol (EG) is a bitter-sweet-tasting dihydric alcohol (HO–CH 2 –CH 2 –OH) that leaves a slightly warm sensation in the mouth after ingestion. It is odor- and color- less, water-soluble and has antifreeze properties. It can be found in many agents, such as antifreeze, brake fluids, and industrial solvents. Ingestion of EG is uncommon, but may cause serious poisoning. It is readily absorbed from the GI- tract, and the maximal blood-concentration is reached within 1–4 h, and the half-life is 3–8 h [1]. Absorption through the skin or lung is minimal. The estimated lethal dose of 100% EG is approximately 1.4 ml/kg [2]. Individuals who have ingested as much as 1–2 l have survived if treated within an hour [3]. EG has an inebriating effect similar to ethanol. It has in itself a low toxicity, but is in vivo broken down by the liver enzyme alcohol dehydrogenase to four organic acids: gly- coaldehyde, glycolic acid, glyoxylic acid and oxalic acid [4]. The metabolites are cell toxins that suppress the oxidative metabolism causing central nervous system depression, and cardio-pulmonary and renal failure [5,6]. The rate-limiting step in the metabolism of ethylene glycol is the conversion of glycolic acid to glyoxylic acid. This results in an accumula- tion of glycolic acid in the blood. Glycolic acid causes severe acidosis, and oxalate is precipitated as calcium oxalate in the kidneys and other tissues [7,8]. We present five case reports of fatal EG-ingestion in order to illustrate the lethal potential of this common and widely available product, and some of the settings in which such poisonings may occur. This is followed by a literature review of the most important clinical and pathological features of EG-poisoning. 2. Case reports Patient 1, 1970: A 29-year-old man was found sitting somnolent on a chair with a 3/4 empty bottle containing 50% www.elsevier.com/locate/forsciint Forensic Science International 155 (2005) 179–184 * Corresponding author. Tel.: +45 65 50 30 00; fax: +45 65 91 62 27. E-mail address: pleth@health.sdu.dk (P.M. Leth). 0379-0738/$ – see front matter # 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.forsciint.2004.11.012