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CORK Bibliography: Nonbeverage Alcohol

32 citations. January 1997 to present

Prepared: March 2009

Abramson S; Singh AK. Treatment of the alcohol intoxications: Ethylene glycol, methanol and isopropanol. (review). Current Opinion in Nephrology and Hypertension 9(6): 695-701, 2000. (32 refs.)

Intoxications with ethylene glycol, methanol, and isopropanol are among the most common ingestions, in the treatment of which a nephrologist plays an important role. These three substances have the ideal characteristics for intervention by hemodialysis, and the three parent compounds and their metabolites are readily dialyzable. Two of the three substances, ethylene glycol and methanol, are metabolized to more toxic substances, so that an early treatment strategy that removes the parent compound or blocks its metabolism can prevent the development of many of the adverse events that are often seen in these ingestions. Fomepizole, an inhibitor of alcohol dehydrogenase, slows the metabolism of these substances and is now approved by the US Food and Drug Administration for use in ethylene glycol intoxication. The present review addresses recent advances in the diagnosis and treatment of intoxication with ethylene glycol, methanol and isopropanol.

Albertson TE. Plenty to fear from toxic alcohols. Critical Care Medicine 27(12): 2834-2836, 1999. (19 refs.)

This brief review discusses toxicity associated with methanol and ethylene glycol ingestion. The author reviews metabolism, mortality, clinical presentation, diagnosis, and clinical management. Despite aggressive management following methanol ingestion, with dialysis and ethanol infusion -- the recommended treatment, visual damage is not uncommon.

Anderson CA; Rubinstein D; Filley CM; Stears JC. MR enhancing brain lesions in methanol intoxication. Journal of Computer Assisted Tomography 21(5): 834-836, 1997. (23 refs.)

Methanol intoxication can cause necrosis of the putamen and subcortical white matter that is evident on neuroimaging. We report a 47-year-old man with significant methanol intoxication who had enhancing lesions in the caudate nuclei, putamina, hypothalamus, and subcortical white matter by MRI. This case demonstrates that contrast enhancement of brain lesions can be observed after methanol poisoning.

Bendtsen P; Jones AW; Helander A. Urinary excretion of methanol and 5-hydroxytryptophol as biochemical markers of recent drinking in the hangover state. Alcohol and Alcoholism 33(4): 431-438, 1998. (35 refs.)

Twenty healthy social drinkers (9 women and 11 men) drank either 50 g of ethanol (mean intake 0.75 g/kg) or 80 g (mean 1.07 g/kg) according to choice as white wine or export beer in the evening over 2 h with a meal. After the end of drinking, at bedtime, in the following morning after waking-up, and on two further occasions during the morning and early afternoon, breath-alcohol tests were performed and samples of urine were collected for analysis of ethanol and methanol and the 5- hydroxytryptophol (5-HTOL) to 5-hydroxyindol-3-ylacetic acid (5-HIAA) ratio. The participants were also asked to quantify the intensity of hangover symptoms (headache, nausea, anxiety, drowsiness, fatigue, muscle aches, vertigo) on a scale from 0 (no symptoms) to 5 (severe symptoms). The first morning urine void collected 6-11 h after bedtime as a rule contained measurable amounts of ethanol, being 0.09 +/- 0.03 g/l (mean +/- SD) after 50 g and 0.38 +/- 0.1 g/l after 80 g ethanol. The corresponding breath-alcohol concentrations were zero, except for three individuals who registered 0.01-0.09 g/l. Ethanol was not measurable in urine samples collected later in the morning and early afternoon. The peak urinary methanol occurred in the first morning void, when the: mean concentration after 80 g ethanol was similar to 6-fold higher than pre-drinking values. This compares with a similar to 50-fold increase for the 5-HTOL/5-HIAA ratio in the first morning void. Both methanol and the 5-HTOL/5-HIAA ratio remained elevated above pre-drinking baseline values in the second and sometimes even the third morning voids. Most subjects experienced only mild hangover symptoms after drinking 50 g ethanol (mean score 2.4 +/- 2.6), but the scores were significantly higher after drinking 80 g (7.8 +/- 7.1). The most common symptoms were headache, drowsiness, and fatigue. A highly significant correlation (r = 0.62- 0.75, P < 0.01) was found between the presence of headache, nausea, and vertigo and the urinary methanol concentration in the first and second morning voids, whereas 5-HTOL/5-HIAA correlated with headache and nausea. These results show that analysing urinary methanol and 5-HTOL furnishes a way to disclose recent drinking after alcohol has no longer been measurable by conventional breath-alcohol tests for at least 5-10 h. The results also support the notion that methanol may be an important factor in the aetiology of hangover.

Brent J. Current management of ethylene glycol poisoning. Drugs 61(7): 979-988, 2001. (40 refs.)

Ethylene glycol, a common antifreeze, coolant and industrial solvent, is responsible For many instances of accidental and intentional poisoning annually, Following ingestion, ethylene glycol is first hepatically metabolised to glycoaldehyde by alcohol dehydrogenase. Glycoaldehyde is then oxidised to glycolic acid, glyoxylic acid and finally oxalic acid. While ethylene glycol itself causes intoxication, the accumulation of toxic metabolites is responsible for the potentially fatal acidosis and renal failure, which characterises ethylene glycol poisoning. Treatment of ethylene glycol poisoning consists of emergent stabilisation, correction of metabolic acidosis, inhibition of further metabolism and enhancing elimination of both unmetabolised parent compound and its metabolites. The prevention of ethylene glycol metabolism is accomplished by the use of antidotes that inhibit alcohol dehydrogenase. Historically, this has been done with intoxicating doses of ethanol. At a sufficiently high concentration, ethanol saturates alcohol dehydrogenase, preventing it from acting on ethylene glycol, thus allowing the latter to be excreted unchanged by the kidneys. However, ethanol therapy is complicated by its own inherent toxicity, and the need to carefully monitor serum ethanol concentrations and adjust the rate of administration. A recent alternative to ethanol therapy is fomepizole, or 4- methylpyrazole. Like ethanol, fomepizole inhibits alcohol dehydrogenase; however it does so without producing serious adverse effects. Unlike ethanol, fomepizole is metabolised in a predictable manner, allowing for the use of a standard, validated administration regimen. Fomepizole therapy eliminates the need for the haemodialysis that is required in selected patients who are non-acidotic and have adequate renal function.

Brooks DE; Wallace KL. Acute propylene glycol ingestion. Journal of Toxicology. Clinical Toxicology 40(4): 513-516, 2002. (15 refs.)

Background: We describe a case of acute propylene glycol toxicity following ingestion of ethanol and propylene glycol-containing antifreeze in which blood lactate, scrum propylene glycol, ethanol, and CO2 concentrations were serially measured. Case Report: A 61-year- old man was hospitalized after acute ingestion of ethanol and automotive antifreeze. His clinical presentation and course were essentially unremarkable. Initial lab tests revealed serum ethanol concentration, 167 mg/dL, normal scrum electrolytes and osmol gap, 120 mOsm/kg. Intravenous 10% ethanol infusion was begun for suspected ethylene glycol toxicity and discontinued at approximately 17 hours post-ingestion. Toxicological analysis of urine was positive for ethanol and propylene glycol, and negative for ethylene glycol, methanol, and isopropanol. Blood lactate was mildly elevated and serum CO2 concentration was normal. Gas chromatographic analysis of serial serum specimens for propylene glycol concentration revealed a maximum value of 470 mg/dL at 7 hours and a nonlinear decline to below detection limit (3 mg/dL) at 57 hours after antifreeze ingestion. The patient was discharged on hospital day 2. Conclusion: The propylene glycol elimination pattern, absence of significant acid-base disturbance, and minimal lactate elevation in this case are consistent with ethanol-related inhibition of propylene glycol metabolism. The effect of ethanol on clinical outcome after acute propylene glycol intoxication remains uncertain.

Carnahan RM; Kutscher EC; Obritsch MD; Rasmussen LD. Acute ethanol intoxication after consumption of hairspray. Pharmacotherapy 25(11): 1646-1650, 2005. (13 refs.)

A 61-year-old woman with a history of alcohol dependence came to the emergency department with ethanol intoxication. Her serum ethanol concentration was 322 mg/dl. When questioned, she admitted to consuming a 14-oz bottle of hairspray mixed with water because of its denatured alcohol content. The woman had used nonbeverage sources of alcohol on a regular basis for a number of years after learning of the practice from fellow attendees of Alcoholics Anonymous meetings. Her primary reason for this behavior was to hide her continued alcohol abuse from her family She consumed hairspray that contained 50% denatured alcohol by volume; the amount she ingested was equal to 7 fluid oz of ethanol, the equivalent of 14 1.25-oz shots of 80-proof liquor. Her serum ethanol concentration was consistent with that predicted by pharmacokinetic equations based on the consumption of one bottle of hairspray. The hairspray product contained specially denatured alcohol 40-B, which consists of ethanol and small quantities of t-butyl alcohol and denatonium benzoate. Ethanol is the substance of primary toxicologic concern. Clinicians need to be aware that numerous nonbeverage sources of alcohol exist and should be considered when a patient presents with acute intoxication. The source and its components should be identified as soon as possible in order to assess other potential toxicities.

Chong CF. Methanol is a highly toxic alcohol. (letter). Resuscitation 61(3): 368-369, 2004. (3 refs.)

DeMerlis CC; Schoneker DR. Review of the oral toxicity of polyvinyl alcohol (PVA). (review). Food and Chemical Toxicology 41(3): 319-326, 2003. (33 refs.)

Polyvinyl alcohols (PVA) (CAS no. 9002-89-5) are synthetic polymers used in a wide range of industrial, commercial, medical and food applications. The purpose of this review, this critical evaluation of the available information on PVA, is to support the safety of PVA as a coating agent for pharmaceutical and dietary supplement products. All the available information on PVA gleaned from a comprehensive search of the scientific literature were critically evaluated. Orally administered PVA is relatively harmless. The safety of PVA is based on the following: (1) the acute oral toxicity of PVA is very low, with LD(50)s in the range of 15-20 g/kg; (2) orally administered PVA is very poorly absorbed from the gastrointestinal tract; (3) PVA does not accumulate in the body when administered orally; (4) PVA is not mutagenic or clastogenic; and (5) NOAELs of orally administered PVA in male and female rats were 5000 mg/kg body weight/day in the 90-day dietary study and 5000 mg/kg body weight/day in the two-generation reproduction study, which was the highest dose tested. A critical evaluation of the existing information on PVA supports its safety for use as a coating agent for pharmaceutical and dietary supplement products.

deRoux SJ; Marker E; Stajic M. Fatalities by ingestion of propylene glycol. Journal of Forensic Sciences 50(4): 939-941, 2005. (19 refs.)

Propylene glycol (PG), a widely used solvent and lubricant, is thought to have low toxicity when ingested. Three cases were identified where PG, either alone or in combination with other chemical agents contributed to death. The decedent in whom PG was the sole agent was a 32-year-old schizophrenic man with cardiomegaly and renal impairment. The blood PG concentration was 4410 mg/L at least 9.5 h following ingestion.

Dorval M; Pichette V; Cardinal J; Geadah D; Ouimet D; Leblanc M. The use of an ethanol- and phosphate-enriched dialysate to maintain stable serum ethanol levels during haemodialysis for methanol intoxication. Nephrology, Dialysis, Transplantation 14(7): 1774-1777, 1999. (10 refs.)

Methanol toxicity requires prompt and effective treatment based on ethanol administration and haemodialyis. This is a case report of 37 year old women brought to an emergency room for visual disturbances after having ingested some unknown solvents 24 hr earlier. The patient was uncooperative which complicated the physical exam. Laboratory values are provide, which included a profound metabolic acidosis. The emergency management undertaken is outlined in detail, including solute concentrations in dialysis.

Emadi A; Coberly L. Intoxication of a hospitalized patient with an isopropanol-based hand sanitizer. New England Journal of Medicine 356(5): 530-531, 2007. (4 refs.)

This is a case report of a hospitalized patient admitted for chest pain, for which the workup was unremarkable. Prior to discharge the following day, the patient, an active alcoholic became acutely hypotensive and delirious. Laboratory tests proved normal, as were the results of arterial blood gas and serum ethanol measurements, toxicology screening, blood and urine cultures, and computed tomography of the head. Urinalysis showed a trace of acetone. in response to the odor of acetone in the patient's room, tests of serum isopropyl alcohol (isopropanol) and acetone levels were ordered. The results showed an isopropanol level of 13.6 mg per deciliter, and an acetone level was 269.4 mg per deciliter (normal range, 0 to 1.9 for both). The patient was also observed drinking the the alcohol-based hand wash from its dispenser. When queried the patient noted the hand cleaner label read, "Active ingredient 63% v/v isopropyl alcohol." It is suggested that hospitals may wish to re-label these dispensers, substituting isopropanol or propane-2-ol for the word "alcohol".

Gilg T. Methanol and congeners as markers of alcohol use and abuse. IN: Wurst RM, ed. New and Upcoming Markers of Alcohol Consumption. Berlin: DR Dietrich Steinkopff Verlag, 2001. pp. 35-52

Congener analysis and especially methanol contribute to evaluate and differentiate a declared consumption of various alcoholic beverages, e.g. to judge post offence drinking claims. Methanol with serum (or urinary) levels exceeding 10 mg/l cannot be achieved by short time drinking, except with fruit brandy (which can be identified by concomitantly elevated levels of butanol - 2 and MEK (methyl ethyl ketone, as its metabolic product). Numerous results and experiences indicate that methanol, as well as acetone > 7 mg/l and isopropanol > 2 mg/l resp. acetone + isopropanol > 9 mg/l, are markers for recent heavy drinking resp. long periods of alcoholization. At least they indicate alcohol abuse in blood or urine samples taken in alcoholized states or in earlier phases (hours) after drinking. The biological turnover (half time Apr. 2, 4 hours in methanol) has to be considered, which -- as generally in marker studies -- may affect the outcome of studies with respect to sensitivity. Its main use is more the detection of heavy prolonged drinking as in traffic and social medicine and in intensive care units to recognize possible withdrawals than as a relapse marker. It fits in the time screen of other markers as a short time marker. Methanol metabolism presents interesting aspects in view of the development of addiction and dependency (influence on the Cl metabolism) as well as on hangover and withdrawal.

Hack JB; Chiang WK; Howland MA; Patel H; Goldfrank LR. The utility of an alcohol oxidase reaction test to expedite the detection of toxic alcohol exposures. Academic Emergency Medicine 7(3): 294-297, 2000. (25 refs.)

The purpose of the exploratory study conducted was to extend the utility of a rapidly performed and readily available test (Alcohol Screen dipstick) to detect the presence of toxic alcohols. Identification of the presence of these is important so that interventions can be instituted before the parent alcohols metabolize into their toxic metabolites. Quantitative determinations are not readily available even in academic medical settings. Diagnosis is chiefly by history, and nonspecific signs and symptoms. The study demonstrated that the currently available test, the Alcohol Screen dipstick, used in a novel way, can help in the differential diagnosis. It is also sensitive to methanol in serum as low as 3.125 mg/dL. It dipstick reacted poorly with ethylene glycol and isopropanol/

Haffner HT; Banger M; Graw M; Besserer K; Brink T. The kinetics of methanol elimination in alcoholics and the influence of ethanol. Forensic Science International 89(1/2): 129-136, 1997. (37 refs.)

Methanol concentrations were studied during the end phase of ethanol elimination and for about five hours afterwards in 12 alcoholics admitted with alcohol intoxication for acute care. The rate of ethanol elimination (beta(60)) ranged from 0.114 g/kg/h to 0.270 g/kg/h (mean 0.178+/-0.045 g/kg/h). The methanol concentration was found to remain almost steady as long as ethanol levels were relatively high, and changed only to an extent that could be explained by the combined opposing influences of methanol excretion and endogenous synthesis. There was no significant relationship between the rate of ethanol elimination and the methanol level. The methanol concentration began to decrease when the ethanol concentration had fallen to under 0.2 g/kg. When the ethanol concentration had fallen to base levels, methanol was eliminated at a rate characterized by an elimination constant (k(el)) of 0.212-0.481 h(-1), and a half life of 1.44-3.27 h. There was a positive correlation between the rate of ethanol elimination and the rate of methanol elimination (r=0.642; p<0.05).

Haviv YS; Safadi R; Osin P. Accidental isopropyl alcohol enema leading to coma and death. (letter). American Journal of Gastroenterology 93(5): 850-851, 1998

Jacobsen D. New treatment for ethylene glycol poisoning. (editorial). New England Journal of Medicine 340(11): 879-881, 1999. (9 refs.)

Jones AE; Summers RL. Detection of isopropyl alcohol in a patient with diabetic ketoacidosis. Journal of Emergency Medicine 19(2): 165-168, 2000. (12 refs.)

A 29-year-old man presented to the Emergency Department with acute mental status changes. He was unable to give a history. He was found to be in diabetic ketoacidosis, although his family reported no prior history of diabetes. A toxic exposure work-up revealed the presence of isopropyl alcohol in the patient's blood. His condition improved with treatment of the ketoacidosis, and he subsequently denied any exposure to isopropyl alcohol prior to presentation to the hospital. This case provides further support to a growing body of evidence that the detection of isopropyl alcohol may not represent an acute ingestion but, rather, a byproduct of acetone metabolism in certain disease states.

Jones AW; Helander A. Time course and reproducibility of urinary excretion profiles of ethanol, methanol, and the ratio of serotonin metabolites after intravenous infusion of ethanol. Alcoholism: Clinical and Experimental Research 23(12): 1921-1926, 1999. (37 refs.)

Background: The aim of this study was to determine the time course and reproducibility of urinary excretion profiles of ethanol, methanol, and ratio of serotonin metabolites, 5-hydroxytryptophol (5HTOL) to 5-hydroxyindoleacetic acid (5HIAA), under strictly controlled conditions. Methods: Nine healthy volunteers (6 women and 3 men) received 0.40 g of ethanol/kg of body weight on two occasions by constant rate intravenous infusion 30 min. Urine was voided before administration of ethanol and thereafter every 60 min for a total of 8 hr. Concentrations of ethanol and methanol in urine were determined by headspace gas chromatography, and the serotonin metabolites 5HTOL and 5HIAA were measured by gas chromatography-mass spectrometry and high- performance liquid chromatography, respectively. Results: The peak concentration of ethanol in urine occurred at 30 or 60 min after the infusion ended. The peak concentration of methanol and the 5HTOL/5HIAA ratio developed more gradually, reaching a plateau at 213 to 220 min and 200 to 220 min postinfusion, respectively. The concentration-time profiles of ethanol and the 5HTOL/5HIAA ratio varied more between subjects than within subjects (p < 0.001), whereas the inter- and intraindividual variation in the pharmacokinetics of methanol were not significantly different (p > 0.05). The concentration of methanol and the 5HTOL/5HIAA ratio remained above the endogenous levels at 8-hr postinfusion despite the fact that urinary ethanol was no longer measurable (<0.01 g/liter) after 5 to 6 hr. Conclusions: Measuring the concentrations of methanol and the ratio of serotonin metabolites (5HTOL/5HIAA) in urine is a more sensitive way to monitor recent drinking, compared with analysis of ethanol in body fluids. Moreover, the concentration-time profiles of methanol and the 5HTOL/5HIAA ratio showed a good test-retest stability. The present intravenous infusion experiment confirms previous work on these markers when ethanol was given perorally. The urinary methanol and the 5HTOL/5HIAA ratio have applications in forensic and clinical medicine as indicators of acute alcohol consumption.

Khan F; Alagappan K; Cardell K. Overlooked sources of ethanol. Journal of Emergency Medicine 17(6): 985-988, 1999. (8 refs.)

The case of a 55-year-old female who presented to the emergency department with acute ethanol intoxication and suicidal ideation is reported. After initiating routine management, we discovered that her serum ethanol levels remained persistently elevated as a result of the patient's secretly ingesting mouthwash. This occurred after she was searched and allowed to retain personal hygiene products. Alcohol-dependent patients may consume ethanol products that are not manufactured for ingestion. These products include cosmetics, cough and cold remedies, and personal hygiene products. The ethanol content of these nonbeverage ethanol (NBE) products exceeds that of many conventional alcoholic beverages. Financial constraints and ease of availability are factors leading to their consumption. This report serves as a reminder to be aware of the existence and popularity of NBE in order to avoid potential morbidity and even mortality associated with its use.

Krautt JA; Kurtztt I. Toxic alcohol ingestions: Clinical features, diagnosis, and management. (review). Clinical Journal of the American Society of Nephrology 3(1): 208-225, 2008. (129 refs.)

Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early.

Laakso O; Haapala M; Jaakkola P; Laaksonen R; Luomanmaki K; Nieminen J et al. FT-IR breath test in the diagnosis and control of treatment of methanol intoxications. Journal of Analytical Toxicology 25(1): 26-30, 2001. (22 refs.)

A portable Fourier transform infrared (FT-IR) multicomponent point-of-care analyzer was tested for the diagnosis of methanol intoxications. Breath analysis with FT-IR was fast and easy, and no sample preparation was needed. The analyzer was adequately sensitive and accurate in detecting and quantifying clinically relevant amounts of ethanol and methanol in the breath of seriously ill patients. FT-IR spectometry was also suitable for nearly on-line monitoring of the exhaled ethanol and methanol during hemodialysis. The breath analysis results correlated well with blood samples. The FT-IR method used also has a traceable calibration to physical properties of the analyte, and the measured spectra can be saved for later analysis.

Leon DA; Saburova L; Tomkins S; Andreev E; Kiryanov N; Mckee M et al. Hazardous alcohol drinking and premature mortality in Russia: A population based case-control study. Lancet 369(9578): 2001-2009, 2007. (35 refs.)

Background: The reason for the low life expectancy in Russian men and large fluctuations in mortality are unknown. We investigated the contribution of alcohol, and hazardous drinking in particular, to male mortality in a typical Russian city. Methods: Cases were all deaths in men aged 25-54 years living in Izhevsk occurring between Oct 20, 2003, to Oct 3, 2005. Controls were selected at random from the city population and were frequency matched to deaths by age. Interviews with proxy informants living in the same household as cases were done between Dec 11, 2003, and Nov, 16 2005, and were obtained for 62% (1750/2835) of cases and 57% (1750/3078) of controls. We ascertained frequency and usual amount of beer, wine, and spirits consumed and frequency of consumption of manufactured ethanol-based liquids not intended to be drunk (non-beverage alcohol), and markers of problem drinking. Complete information on markers of problem drinking, frequency of alcohol consumption, education, and smoking was available for 1468 cases and 1496 controls. Findings: 751 (51%) cases were classed as problem drinkers or drank non-beverage alcohol, compared with 192 (13%) controls. The mortality odds ratio (OR) for these men, compared with those who either abstained or were non-problematic beverage drinkers, was 6.0 (95% CI 5.0-7-3) after adjustment for smoking and education. The mortality ORs for drinking non-beverage alcohol in the past year (yes vs no) was 9.2 (7.2-11.7) after adjustment for age. Adjustment for volume of ethanol consumed from beverages lowered the OR to 8.3 (6.5-10.7), and further adjustment for education and smoking reduced it to 7.0 (5.5-9.0). A strong direct gradient with mortality was seen for frequency of non-beverage alcohol drinking independent of volume of beverage ethanol consumed. 43% of mortality was attributable to hazardous drinking (problem drinking or non-beverage alcohol consumption, or both) adjusted for smoking and education. Interpretation Almost half of all deaths in working age men in a typical Russian city may be accounted for by hazardous drinking. Our analyses provide indirect support for the contention that the sharp fluctuations seen in Russian mortality in the early 1990s could be related to hazardous drinking as indicated by consumption of non-beverage alcohol.

Lindinger W; Taucher J; Jordan A; Hansel A; Vogel W. Endogenous production of methanol after the consumption of fruit. Alcoholism: Clinical and Experimental Research 21(5): 939-943, 1997. (24 refs.)

After the consumption of fruit, the concentration of methanol in the human body increases by as much as an order of magnitude. This is due to the degradation of natural pectin (which is esterified with methyl alcohol) in the human colon. In vivo tests performed by means of proton-transfer-reaction mass spectrometry show that consumed pectin in either a pure form (10 to 15 g) or a natural form (in 1 kg of apples) induces a significant increase of methanol in the breath (and by inference in the blood) of humans. The amount generated from pectin (0.4 to 1.4 g) is approximately equivalent to the total daily endogenous production (measured to be 0.3 to 0.6 g/day) or that obtained from 0.3 liters of 80-proof brandy (calculated to be 0.5 g). This dietary pectin may contribute to the development of nonalcoholic cirrhosis of the liver.

Liu JJ; Daya MR; Mann NC. Methanol-related deaths in Ontario. Journal of Toxicology. Clinical Toxicology 37(1): 69-73, 1999. (13 refs.)

Objective: Methanol poisoning accounts for several deaths annually in the province of Ontario. Our study was aimed at identifying the associated epidemiological factors for fatal outcomes following methanol poisoning in order to develop preventative strategies. Methods: The records of the Ontario Provincial Coroner's Office were: reviewed retrospectively for all poison-related, alcohol-related, anal chronic alcohol use-related deaths for the period of January 1, 1986 to December 31, 1991. Age, gender, reason for ingestion (accidental or intentional), and source of methanol for each victim were recorded. Results: There were 43 fatalities during this period, 39 males and 4 females with a mean age of 45 years (range 18-80). Suicide attempts accounted for 21 (49%) cases while the remaining 22 (51%) deaths were classified as accidental. Fourteen (64%) of these 22 patients consumed products labeled as methyl alcohol or wood alcohol as a substitute for ethanol. In 3 cases, the accidental ingestion was the direct result of methanol being improperly stored in containers normally associated with ethanol. The remaining 5 patients were poisoned through the consumption of liquor from illicit sources. Conclusions: Over half of the methanol-related deaths in Ontario are accidental and potentially preventable. Possible preventative strategies include mandatory product relabeling to eliminate the word alcohol, enhanced public education, and the addition of aversive agents to methanol-containing commercial products.

McKee M; Suzcs S; Sarvary A; Adany R; Kiryanov N; Saburova L et al. The composition of surrogate alcohols consumed in Russia. Alcoholism: Clinical and Experimental Research 29(10): 1884-1888, 2005. (7 refs.)

Background: In the course of a case-control study examining determinants of premature death among working age men, it became clear that a significant percentage of the population (7.3%) were drinking a variety of surrogate alcohol products (products not legally sold for consumption). In this population, where there is a high death rate from alcohol-related causes, including acute alcohol poisoning, it was important to know what these products contained. Methods: The identity of products being consumed was identified from the survey of controls. Representative samples were obtained and subjected to analysis using gas chromatography and mass spectrometry to determine their composition. Results: Three broad groups of product were identified: samogon (home-produced spirits); medicinal compounds; and other spirits (mainly sold as aftershaves). Commercially produced vodkas were used for comparison. Samogon contained lower quantities of ethanol than vodka [mean, 39 vs. 44 volumetric percentage (v/v%), respectively] but in addition contained certain toxic long-chain alcohols. Medicinal compounds contained only ethanol, at a higher concentration that vodka (mean, 66 v/v%), while the other spirits, which were also essentially pure ethanol, contained a mean of 94 v/v%. Conclusions: A significant number of Russian men are drinking products that have either very high concentrations of ethanol or contaminants known to be toxic. These products are untaxed and thus much less expensive than vodka. There is an urgent need for policy responses that target their production and consumption.

Merritt BA; Okyere CP; Jasinski DM. Isopropyl alcohol inhalation: Alternative treatment of postoperative nausea and vomiting. Nursing Research 51(2): 125-128, 2002. (15 refs.)

Background. The mechanisms for postoperative nausea and vomiting are numerous and pathways not well elucidated. Although many medications have been developed to help prevent postoperative nausea and vomiting, the search for better approaches to recovery treatment continues. Objective: The purpose of this study was to evaluate the effectiveness of isopropyl alcohol (IPA) inhalation for treatment of postoperative nausea and vomiting for patients who have general anesthesia for a surgical procedure. Method. Participants were recruited from an urban hospital on the East Coast of the United States. Participants were assigned to an experimental or control group and IPA inhalation was compared to the standard anti-emetic treatment for rescue treatment in the immediate postoperative period. Postoperative nausea and vomiting was rated using a descriptive ordinal scale. Results: The results of this study show IPA to be effective and that there was no significant difference between the standard treatment protocol and treatment with IPA. Treatment with IPA was significantly more cost effective than standard drug treatment. Discussion: Further research is recommended to evaluate the length of effectiveness, standard dose needed, most effective mode of inhalation, and factors blocking IPA effectiveness.

Morgan BW; Todd KH; Moore B. Elevated blood lead levels in urban moonshine drinkers. Annals of Emergency Medicine 37(1): 51-54, 2001. (6 refs.)

Study objective: During a study of problem drinking, we found that surprisingly large numbers of emergency department patients reported moonshine consumption. Because of sporadic reports of moonshine- associated lead toxicity in rural areas, we suspected that urban ED patients might have previously unidentified elevated blood lead levels caused by moonshine consumption. We initiated an active screening program to identify patients with moonshine-associated elevated blood lead levels. Methods: We performed a prospective case-finding effort at a large urban ED in Atlanta, GA, screening ail patients admitted to the ED for a B-month period during times when study personnel were available. Patients reporting moonshine consumption within the preceding 5 years were asked to participate. After written informed consent, subjects completed a structured interview administered by one of the investigators, and blood was obtained for determination of a whole blood lead level. We recorded the numbers of patients reporting moonshine consumption, time of most recent consumption, other potential sources of lead exposures, and whole blood lead levels. Results: Of 49 patients reporting consumption of moonshine within the past 5 years, 25 (51%) of 49 had elevated blood lead levels( >15 mug/dL), with 15 (31%) of 49 having extremely elevated blood lead levels (>50 mug/dL). Recent moonshine consumption (within the past month) was reported by 38 (78%) of 49 patients. Of these 38 recent consumers, 23 (61%) had elevated lead levels compared with only 2 (18%) of 11 of those reporting more remote consumption (risk difference 42%; 95% confidence interval 15% to 70%). Conclusion: A high percentage of patients who reported moonshine consumption had elevated blood lead levels. Emergency physicians should consider screening to determine the prevalence of moonshine consumption in their practice settings, as well as the possibility of lead intoxication among patients with suggestive symptoms. All patients reporting moonshine consumption within the past 5 years should be tested for lead exposure.

Nzerue CM; Harvey P; Volcy J; Berdzenshvili M. Survival after massive ethylene glycol poisoning: Role of an ethanol enriched, bicarbonate-based dialysate. International Journal of Artificial Organs 22(11): 744-746, 1999. (12 refs.)

A 38-year old man presented with drowsiness 14 hours after ingesting about 1200 mls (40 ounces) of antifreeze in a suicide attempt. He was successfully treated with an ethanol enriched, bicarbonate based-dialysate. With a concomitant peripheral intravenous infusion of ethanol, this enrichment of the dialysate helped maintain the intradialytic ethanol concentration between 97-135 mg/dl over an 8 hour dialysis session. The patient developed acute tubular necrosis and required further dialysis. He made a complete recovery after three weeks and was discharged with a serum creatinine of 1.4 mg/dl.

Parna K; Lang K; Raju K; Vaeli M; McKee M. A rapid situation assessment of the market for surrogate and illegal alcohols in Tallinn, Estonia. International Journal of Public Health 52(6): 402-410, 2007. (25 refs.)

Objectives: To understand the phenomenon of consumption of surrogate and illegal alcohols in Tallinn, capital of Estonia. Methods: This study, conducted in Tallinn in May 2006, used rapid situation assessment. Interviews with key informants in relevant settings such as emergency departments of hospitals, accommodation for the homeless, police etc. (n = 22), with alcohol abusers (n = 33), natural observations of surrogate sale and consumption venues (n = 46), and tracking of trade data were carried out. Results: Key informants confirmed that consumption of illegal and surrogate alcohols are widely used by alcohol abusers, a finding confirmed by the alcohol abusers. Availability of surrogates varied by area of the city, mainly sold from street kiosks. Illegally produced spirits were also easily available. Sales of surrogates appear to have increased in recent years. Conclusion: A range of alcohol-containing substances that appear to be easily available at low cost, and that have high concentration of ethanol or contaminants known to be toxic, were identified in Tallinn. Alcohol policies in Estonia should address the consumption and availability of these substances.

Peces R; Alvarez R. Effectiveness of hemodialysis with high-flux polysulfone membrane in the treatment of life-threatening methanol intoxication. Nephron 90(2): 216-218, 2002. (8 refs.)

Methanol poisoning may result in metabolic acidosis, blindness and death. In this report, we describe a case of life-threatening methanol intoxication in a 44-year-old man who was treated successfully with supportive care, ethanol infusion, folic acid and early hemodialysis with a high-flux polysulfone dialyzer. We conclude that hemodialysis as implemented in this case is a safe and effective approach to the management of methanol poisoning.

Phillips BJ; Jenkinson P. Is ethanol genotoxic? A review of the published data. Mutagenesis 16(2): 91-101, 2001. (112 refs.)

The genotoxic effects of ethanol, as an industrial chemical rather than as a component of beverages, are discussed. Section headings in this review of the literature include: (1) results of "standard" genotoxicity tests -- bacterial mutations assays, chromosome aberration tests in vitro, cell mutation assays, micronucleus assays in vivo, chromosome aberration tests in vivo, dominant lethal assay; (2) supplementary information on genetic effects -- deoxyribonucleic acid (DNA) adduct formation, mutation in Drosophila, fungi, yeast and plant cells, sister chromatid exchange (SCE), chromosomal effects in alcoholics, non-disjunction and aneuploidy; and (3) discussion -- acetaldehyde as a mutagenic metabolite, general metabolic disturbances, and physico-chemical effects. It is concluded that there is no evidence that ethanol is a genotoxic hazard as an industrial chemical. Some degree of genotoxicity may result from excessive alcohol consumption but this is not considered relevant to workplace exposures.

Piagnerelli M; Lejeune P; Vanhaeverbeek M. Diagnosis and treatment of an unusual cause of metabolic acidiosis: Ethylene glycol poisoning. Acta Clinica Belgica 54(6): 351-356, 1999. (34 refs.)

Ethylene glycol intoxication is a rare but dangerous type of poisoning. It causes a severe acidosis with high anion and osmolal gaps. Clinical manifestations of the ethylene glycol intoxication can be divided in three phases: a neurologic stage, with hallucinations, stupor and coma; the second stage is cardiovascular with cardiac failure. Renal failure characterizes the third stage, due to acute tubular necrosis. After aggressive gastric emptying, the main treatment is ethanol or 4- methypyrazole, which can be given either orally or intravenous, with supportive measures for all symptoms or diseased organ.

Sutton TL; Foster RL; Liner SR. Acute methanol ingestion. Pediatric Emergency Care 18(5): 360-363, 2002. (47 refs.)

Methanol poisoning is an insidious event that can culminate in severe metabolic disturbances, permanent neurologic dysfunction, blindness, and death. Although numerous adult cases have been extensively reviewed, there is a paucity of reports about pediatric ingestions. We present a case of acute methanol intoxication in a 6-year-old male patient who presented with headache, nausea, altered mental status, and drowsiness. His blood methanol level was 350 mg/dL (109.4 mmol/L), despite the absence of any history or identifiable source of methanol. Treatment with ethanol, alkalinization, and hemodialysis resulted in full recovery without residua. Unusual facets of this case are the child's relatively older age, the extremely high methanol blood level, and, most remarkably, the complete lack of visual disturbances on routine ophthalmologic evaluation.

Tayfun C; Kurtaran HK; Bulakbasi N; Pabuscu Y; Tasar M; Somuncu I. Cerebral and orbital magnetic resonance imaging findings in methyl alcohol intoxication. International Journal of Neuroradiology 5(3): 145-150, 1999. (40 refs.)

Purpose: To assess the cerebral and orbital magnetic resonance imaging (MRI) findings in patients with methyl alcohol intoxication and variable degrees of visual impairment. Methods: Cerebral and orbital MRI examinations were performed in nine patients. All of the patients were men ranging from 20 to 26 years of age (mean age 22 years). Standard cerebral MRI protocols and short- time invasion recovery (STIR) sequences were performed for the orbital MRI examinations. Results: No relevant MRT findings were encountered in four of the nine patients, Three of the remaining five patients had putaminal necrosis, which appeared hypointense on T-1-weighted spin echo MRI and hyperintense on T-2-weighted spin echo MRI. In two of these five patients, putaminal necrosis (damage) was hyper intense in both T-1- weighted and T-2-weighted spin echo sequences, a finding interpreted as hemorrhage. In addition to putaminal necrosis, one patient had cortical necrosis at both frontoparietal lobes adjacent to the midline and mild optic atrophy, but the intrinsic signal intensity of the optic nerves was normal. Another had left frontal lobe paramedian cortical necrosis, characterized by hyperintense appearance on T-2- weighted spin echo sequences. Except for one, no patient had pathologic changes in the orbital structures. Conclusion: Methyl alcohol intoxication may cause putaminal necrosis detectable on MRI, with or without cerebral and cerebellar gray or white matter lesions, in accordance with patient history and clinical findings.

Tuohy KA; Nicholson WJ; Schiffman F. Agitation by sedation. Lancet 361(9354): 308, 2003. (5 refs.)

A case report of a 56-year-old female withdrawing from alcohol after a 40-year-history of heavy alcohol consumption is presented. She complained of symptoms suggestive of alcohol withdrawal and was treated with intravenous lorazepam, receiving 432 mg over 10 hours. However, she developed worsening tachycardia, hypertension, and agitation requiring sedation with morphine and endotracheal intubation. Blood chemistries revealed an apparent concentration of ethylene glycol of 23.6 mmol/L. After treating the patient for ethylene glycol, the laboratory revealed that the interpreted ethylene glycol was actually propyl glycol, the solvent in which the intravenous lorazepam is prepared. After subsequent appropriate treatment, the patient's symptoms subsided and she was discharged to a temporary rehabilitation center. The authors note that propylene glycol is used as a solvent for many intravenous medications used to treat alcohol withdrawal, including diazepam, lorazepam, and chlordiazepoxide. It is also used as a food additive. Intoxication with the glycol begin to develop at a serum concentration of 2.4 mmol/L, can mimic alcohol withdrawal, and include a decline in mental status, seizures, and arrhythmias. Notifying laboratory personnel of the use of a medication containing propylene glycol allows the use of a standard containing both ethylene and propylene glycol.

Williams RH; Erickson T. Evaluating toxic alcohol poisoning in the emergency setting. Laboratory Medicine 29(2): 102-108, 1998. (33 refs.)

Ingestion of a toxic alcohol often occurs when an alcoholic patient cannot obtain ethanol and thus, seeks an ethanol substitute. Methanol produces visual disturbances, while ethylene glycol produces pulmonary and renal disturbances. Ingestion of isopropanol results in acetone production that can lead to central nervous system depression. Unlike methanol and ethylene glycol poisoning, however isopropanol poisoning generally does not produce major disturbances in acid-base balance. Most clinical laboratories do not perform toxic alcohol analyses. Thus the clinician relies on interpretation of other clinical laboratory data to ascertain the presence or absence of a toxic alcohol.

Yayci N; Agritmis H; Turla A; Koc S. Fatalities due to methyl alcohol intoxication in Turkey: An 8- year study. Forensic Science International 131(1): 36-41, 2003. (35 refs.)

The aim of this study is to examine methyl alcohol poisoning cases from the medico-legal point of view. The records of the Morgue Department of Council of the Forensic Medicine were reviewed retrospectively for all methyl alcohol poisonings for the period of 27.10.1992 and 30.05.2001. The victim's age, sex, death year, death place, methyl alcohol blood levels, the source of methyl alcohol, accompanying laboratory results and histopathologic tissue changes were recorded. The number of deaths due to the methyl alcohol poisoning was 271 during that period of time. Two hundred and forty-two of the (89.3%) total 271 methyl alcohol fatalities were men and 29 (10.7%) of were women. The largest age group was 36-40 years old, followed by 41-45. The methyl alcohol blood concentrations ranged widely from 50 to 755 mg for per 100 ml. There were 222 cases (81.9%) with the methyl alcohol blood concentrations over 100 mg/dl. Twenty-nine (10.7%) victims were poisoned through the consumption of cologne and three of them with alcoholic beverage named "Raki". Consumed products were not known in all other cases because of insufficient patient history and data. As a conclusion, regarding the distribution according to years, mortality due to methyl alcohol intoxication in our country have been proceeding on a certain level. In order to decrease the mortality due to methyl alcohol intoxication, some precautions should be developed that could prevent the production and consumption of alcoholic beverages illegally produced

Yieh FS; Chou PI. Bilateral methanol optic neuropathy after intravenous administration. Journal of Toxicology. Cutaneous and Ocular Toxicology 21(3): 169-174, 2002. (9 refs.)

A 21-year-old man was evaluated for bilateral vision loss following intravenous methanol administration. The sudden bilateral visual loss was associated with retinal splinter hemorrhage and cotton wool spots following self-intravenous administration of 250 mL denatured alcohol (95% alcohol + 100 ppm methanol). Glaucomatous-like cupping of the optic discs developed with partial recovery of visual function, especially in the left eye. Methanol is a highly toxic substance to the optic nerves. A single low dose of methanol (25 mg for this patient) was sufficient to produce optic nerve damage.

Zaman F; Pervez A; Abreo K. Isopropyl alcohol intoxication: A diagnostic challenge. art. no. E12. American Journal of Kidney Diseases 40(3): NIL_38-NIL_41, 2002. (14 refs.)

Isopropyl alcohol (IPA) Is an ingredient of commonly used household solutions. Accidental and suicidal ingestion of IPA sometimes can be fatal if it goes unrecognized and untreated. There are few published reports on IPA Intoxication. We describe a case of repeated IPA Ingestion In a single Individual, followed by a review of the literature on the subject. The differential diagnosis, diagnostic pitfalls, and therapeutic Interventions In patients with IPA Intoxications are discussed.

Zuba D; Piekoszewski W; Pach J; Winnik L; Parczewski A. Concentration of ethanol and other volatile compounds in the blood of acutely poisoned alcoholics. Alcohol 26(1): 17-22, 2002. (26 refs.)

The presence of volatile compounds, such as acetone, acetaldehyde, methanol, ethanol, isopropanol, and n-propanol, in the blood of 169 acutely poisoned alcoholics was determined. The clinical diagnosis of addiction was made on the basis of a patient interview as well as physical, psychological, and psychiatric examination. At the time of the patients' admission to the clinic, the mean concentration of ethanol in blood was 3.14 +/- 1.10 g/l and its elimination rate in the studied group was 0.27 +/- 0.08 g/kg/h, an elimination rate significantly higher (P < .001) than that of social drinkers, which averages to 0.014 +/- 0.04 g/kg/h. The presence of other volatile compounds in the blood of alcohol-addicted patients is common. The calculated elimination rate constant of methanol was about 0.2 h(-1). This rate seems to indicate that, in heavy drinkers, the elimination of methanol may be relatively fast even if the ethanol concentration is above I g/l. The elimination of other volatile compounds can be accelerated by large doses of ethanol, although it is not correlated with actual blood ethanol level. Moreover, in most of the blood samples with a methanol concentration below 10 mg/l, the measured concentration of acetone was below 7 mg/l and that of isopropanol was below 2 mg/l.