Introduction

Ethanol is often considered to be the most used and abused chemical substance. As a result, measurement of ethanol is one of the most frequently performed toxicological tests. Ethanol analysis is important for both clinical and forensic purposes. Alcohol is a depressant of the central nervous system (CNS), and when taken in sufficient quantities, death may result from respiratory depression. Rapid and accurate analysis in the clinical setting is extremely important for patient care. For forensic purposes, ethanol is measured for workplace drug testing, investigation of driving impairment

From: Handbook of Drug Monitoring Methods Edited by: A. Dasgupta © Humana Press Inc., Totowa, NJ

and accident investigation, and for postmortem evaluation. As the legal ramifications of impairment due to ethanol consumption can be very serious, accurate measurement of ethanol using methods and handling procedures that are defensible in a court of law is critical.

Although alcohol is often used in reference to ethanol only, the term also includes other alcohols such as methanol, isopropanol, and acetone that might also be present; the latter is a metabolite of isopropanol. Laboratories should alert users as to whether the alcohol method in use detects only ethanol or whether all alcohols are detected.

The effects of ethanol on the CNS vary according to the blood ethanol concentration. Low concentrations (<50mg/dL) are typically associated with decreased inhibitions and mild euphoria; higher concentrations (>100mg/dL) generally result in increased disorientation and loss of coordination, whereas markedly increased levels (>400mg/dL) may result in coma or death. The combination of ethanol with drugs that are CNS depressants can result in the above effects being observed at much lower ethanol concentrations. Food ingestion also influences the rate at which ethanol is absorbed. In fasting individuals, acute ingestion of ethanol results in peak blood ethanol concentrations within 0.5-2.0 h. In nonfasting individuals, peak ethanol concentrations may be achieved in anywhere from 1 to 6 h.

The metabolism of ethanol occurs primarily in the liver by hepatic alcohol dehydro-genase (ADH). Ethanol is converted to acetaldehyde by ADH and then to acetic acid by aldehyde dehydrogenase. Gastric ADH also plays a role in the metabolism of ethanol. Chronic ethanol users show lower activities of gastric ADH compared with nonusers (1). The lower levels of gastric ADH activity in chronic ethanol users result in greater bioavailability of ethanol and higher blood ethanol concentrations.

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