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Home , Methanol, Toxication

TheJoufnalofEmergencyMedicine, Vol. 1, pp. 51-58,1983 Printed in the USA*Copyright 0 1983 Pergamon Press Ltd

METHANOL

Charles E. Becker, MD

Northern California Occupational Health Center, San Francisco General Hospital and Medical Center; and the Department of Medicine, University of California-San Francisco Reprint address: San Francisco General Hospital, Building 30, 5th Floor, 1001 Potrero Avenue, San Francisco, CA 94110

??Abstract - poisoning is an uncom- significantly higher in cases of severe methanol mon but an extremely hazardous intoxication. poisoning than in mild cases. Once the diagno- Since methanol is a versatile and is having sis is suspected, a blood level from methanol increasing usage in an energy-conscious society, should be returned rapidly. Treatment of meth- a high index of suspicion and swift laboratory anol after good supportive care is to di- confirmation is essential in managing this poi- minish the metabolic degradation of methanol soning. Methanol poisoning may occur in spor- with simultaneous and then to perform adic or epidemic circumstances. Chronic expos- hemodialysis and alkalinization to counteract ure may occur in the occupational setting. Man metabolic . Folate should also be ad- is uniquely susceptible to , ministered to enhance metabolic breakdown of perhaps dependent upon folate . formate. Alcoholic patients may be especially Classic symptoms of methanol toxicity can only susceptible to methanol poisoning due to rela- occur in laboratory animals who are rendered tive folate deficiency. folate deficient. Folate may be useful in humans enhancing removal of the toxic products of 0 Keywords-methanol; formate; 4-methyl methanol poisoning. The responsible pyrazole; anion and osmolar gaps for metabolism of methanol is dehydro- genase. Ethanol has a higher affinity for this en- zyme and is preferentially metabolized. Simul- Methanol (methyl alcohol) can be derived taneous ethanol and methanol administration from a large number of unused and dis- may confuse the onset of the intoxication. Pyra- carded potential energy sources, and has zoles may also be used to inhibit alcohol dehy- excellent mixing properties. drogenase thus preventing the intoxication. The For this reason it has been proposed as a most important initial symptom of methanol additive, as a home heating mate- poisoning is visual disturbance. The symptoms rial, and as feedstock in bacterial synthesis may be delayed up to 24 hours after ingestion for protein. The home application of meth- due to simultaneous alcohol administration and metabolic processes. Laboratory evidence of se- anol includes the use of “canned heat,” such vere with increased anion as Sterno@, and the use of windshield wash- and osmolar gaps strongly suggest the clinical ing materials. In addition, it is a common diagnosis. There may be an important associa- component of paints, varnishes, , tion between mean corpuscular volume which is solutions, and is utilized both in

Selected Topics- devoted to a broad range of articles from prehospital care and new ======technologies to toxicologic emergencies and disaster management -is coordinated by Kenneth Kulig, MD, of the Rocky Mountain Center. RECEIVED: I8 November 1982; ACCEPTED: 19 January 1983 0736-4679/83$3.00 f .OO

51 Charles E. Becker denaturing ethanol and as an alternative Swartz and his colleagues4 reported an fuel source. epidemic in the State Prison of Southern Methanol is generally obtained from the Michigan in May 1979. In this instance sev- destructive of ; the greater eral inmates obtained a quantity of diluent, the extent of distillation the more palatable ordinarily used in photocopying machines, the of the methanol. Methanol may which was nearly pure methanol. The in- contain impurities which impart to it a dis- mates distributed this fluid in smail quanti- agreeable odor and taste. Without impuri- ties as “homemade” spirits. Forty-six defi- ties methanol more easily contributes to nite cases of intoxication were identified; dangerous accidental and deliberate poison- they were either treated initially in the pris- ings which can reach epidemic proportions. on infirmary, or referred to a local hospital The of methanol was not un- center for further evaluation and treat- derstood for many years. , brandies, ment. Three deaths occurred; one speci- and whiskeys containing a substantial per- men of the beverage retrieved from an in- centage of methanol were sold in the late mate revealed a pink fruity liquid which 1800s. Results of early experiments with was 4% methanol by weight. animals were inconsistent in describing Children have also become intoxicated methanol’s toxicity. It was not until the by methanol. A lo-week-old infant was late 1920s when a group of workers in Ger- admitted to a hospital with a methanol level many were poisoned with chemically pure of 213 mg/dL nine hours after methanol methanol that the true toxicity of methanol was mistaken for distilled and mixed was generally accepted. Bennett and his as- with formula.5 An 8-month-old child died sociates’ reported their observations on when methanol-soaked pads were placed 323 patients who ingested bootleg whiskey on the chest to treat a common cold.6 Fur- in Atlanta, Georgia during 5 days in Octo- ther emphasizing the dermal and respira- ber 195 1. Forty-one deaths occurred when tory absorption of methanol, the Polish 90 gallons of the methanol-contaminated literature reports a painter who accidental- whiskey were distributed throughout the ly spilled methanol on his clothes and shoes city. Later analysis of the confiscated ma- but continued to wear the soaked gar- terial showed it contained 35% to 40% ments; blindness developed within several methanol. As word of the poisoning spread days.7 by rumor, newspaper, and radio, a minor panic developed and numerous asympto- matic individuals presented themselves to Methanol Toxicology be evaluated. Kane and coworkers* report- ed an epidemic of poisoning in 18 individ- Pure methanol is a colorless liquid, has a uals (of whom 8 died) when a diluted paint specific gravity of 0.8 1, a of thinner was used as an alcoholic beverage 65”C, and a slight odor distinctly different in Lexington, Kentucky. The liquor was from that of ethanol. Methanol can be ab- served as a party refreshment. Naraqui sorbed through the skin, and through the and associates3 reported a severe outbreak respiratory and gastrointestinal tracts. The of methanol poisoning in Port Moresby, current threshold limit value for methanol New Guinea, in March 1977 when 28 men in industry is 200 ppm (260 mg/m3). Nor- attended a party and consumed the con- mal methanol blood concentrations derived tents of a drum of methanol that had been from endogenous production and dietary found in another village. Some of these in- sources are approximately 1.5 mg/L. There dividuals may have consumed as much as is great variability in the mean 600 mL of pure methanol. Four died, six among animal species. had bilateral , and two The special susceptibility of man to had persistent difficulty with speech. methanol toxicity is thought to be due not Methanol Poisoning 53 to methanol itself, but to its metabolite, ing the flow of the axoplasm and thus caus- formate. Review of clinical findings in epi- ing the pathological condition of the eye.13 demic situations and in isolated cases shows Current evidence does not suggest that for- great variation in the dose of methanol maldehyde causes these effects on the eye. required to produce acidosis, blindness, Due to their high rate of metabolism of and death. Some of this clinical confusion formate, rats do not accumulate it; hence, may be explained by individual metabolic rats do not manifest methanol toxicity. A differences, associated ethanol consump- folate-dependent system is likely to be re- tion, or availability of essential cofactors sponsible for the oxidation of needed for methanol or formate metabo- to dioxide in the of rats, mon- lism. The smallest amount of methanol re- keys, and probably in humans. The level of ported to cause death is 15 mL of 40% folate appears to be critical for formate methanol; the highest dose recorded for a metabolism in animals. The classic symp- survivor is in the range of 500 to 600 mL.3 toms of methanol toxicity in rats can only Most cases of severe human poisoning oc- be produced by rendering these animals fo- cur by the oral route. Occasional cases oc- late deficient.14 Experiments in monkeys cur by skin contact and inhalation. strongly suggest that folate decreases for- Methanol is rapidly absorbed from the mate accumulation after methanol over- gastrointestinal iract, with peak absorp- dose by stimulating formate oxidation; tion occurring in 30 to 60 min depending this suggests that folate may be useful in on the presence or absence of food in the reducing the toxicity of methanol.r4 stomach. Methanol distributes in total The enzyme primarily responsible for body water, although its passage through methanol oxidation in the liver is alcohol cellular membranes may be different from dehydrogenase (ADH). Ethanol has a that of water. The primary method of higher enzyme affinity for ADH and is elimination of methanol in humans is by its preferentially metabolized; as a result, oxidation to , formic acid, methanol is eliminated primarily by extra- and . Methanol may also hepatic routes when ethanol is present. exit the body with induced vomiting, and a Ethanol concentrations in the range of 100 small amount is excreted in the breath, to 200 mg/dL are clinically regarded as be- sweat and urine. Increasing urine flow ing optimal for saturating alcohol dehy- would be expected to increase methanol drogenase to prevent methanol metabo- excretion to some extent, but forced diure- lism. Although zero-order kinetics have sis would not be expected to significantly been utilized to describe ethanol elimina- increase clearance of methanol.* Several tion, several investigators have shown dose- reviews9J0 have described the metabolism dependent characteristics of ethanol.15 of methanol and its metabolites in humans. Pyrazoles are also known to be potent It is difficult to study methanol poisoning inhibitors of , but in experimental animals because in non- pyrazole compounds in general are too primates doses of methanol that predicta- toxic for human use. One pyrazole com- bly cause toxic reactions in humans cause pound, 4-methyl-pyrazole (4-MP), alone only intoxication similar to that of etha- or in combination with other therapy, may nol. Recent studies, I1 however, using rhe- be of value in methanol or glycol sus and pig tail monkeys have been able . r6,17 to provide a model for human methanol Recent studies in isolated cases of meth- intoxication. In monkeys treated with for- anol poisoning suggest that the associated mate alone, toxic effects developed in the metabolic acidosis is a result of formic acid similar to those observed in hu- accumulation.ls The key role of formate in mans.‘* Formate probably inhibits cyto- causing pathological damage to the eye as chrome oxidase in the optic nerve, disturb- well as causing acidosis has only recently 54 Charles E. Becker been appreciated due to new assay tech- The most important initial symptom of niques for formic acid.18 Thus some of the methanol poisoning is visual disturbance. variability in the toxicology of methanol is Complaints of blurred vision with a rela- based upon presence of folate deficiency, tively clear sensorium strongly suggests the simultaneous alcohol consumption, and diagnosis of methanol poisoning. Head- total dose of methanol ingested. ache, dizziness, nausea, vomiting and ab- Pathological findings of methanol poi- dominal pain may accompany visual dis- soning have been described in detail.rggThe turbances. Frequently there is a complaint primary site of the ocular injury produced of breathlessness, even if acidosis is not by methanol is in the optic nerve head and pronounced. In severe cases an odor of the intraorbital portion of the optic nerve, formalin has been noted on the breath or in rather than in the retinal ganglia. Hemor- the urine. The development of bradycardia, rhages into portions of the brain are also prolonged coma, seizures, and resistant an important aspect of methanol poison- acidosis indicate a poor prognosis. ing. Cerebral computed tomography in Physical findings in methanol poison- methanol intoxication has shown necrotic ing are generally nonspecific. The acidotic, areas in the putamen.’ The putamen may tachypnic patient may appear acutely ill. be a specific target for methanol toxicity. Fixed, dilated pupils have been described Pathological damage to the liver, pancreas in severe cases. Opthalmological examina- and kidneys have also been described but tions may be normal but may also show se- are not specific. vere hyperemia of the optic disc and retinal edema. Optic atrophy is a late finding, On occasions, nuchal rigidity suggests menin- Clinical Symptoms of gitis. Two-thirds of patients with methanol Methanol Poisoning poisoning complain of headache associat- ed with dizziness. The most common cause The appearance of clinical symptoms in of death in methanol poisoning is a peculi- methanol poisoning is affected by the ar, sudden cessation of respiration.‘,8 amount of ethanol simultaneously ingest- ed and by associated medical conditions. Particularly important is the time it takes Laboratory Diagnosis symptoms to develop and the identifica- tion of abnormal laboratory test results Laboratory evidence of metabolic acidosis specifically referable to methanol. In epi- with increased anion and osmolar gaps demic circumstances the diagnosis of strongly suggests the clinical diagnosis of methanol poisoning may be easily estab- methanol poisoning. The decreased serum lished; however, in isolated cases the diag- bicarbonate concentration is a uniform nosis may be confusing. Methanol may be feature of severe methanol poisoning. ingested by alcoholic patients as an alcohol There is often a pronounced substitute, and the sporadic case in a which is not explained on the basis of dia- chronic alcoholic presents special prob- betic acidosis, lactic acidosis, uremic acido- lems for clinical diagnosis. It may be dif- sis, starvation, or alcoholic . ficult to elicit symptoms of visual dis- , , and sali- turbances, and there may be a long delay cylate are that may cause an anion in the onset of symptoms. Associated head gap. Ethylene glycol will usually not cause trauma may provide confusing neurolog- visual symptoms and may be associated ical findings, and early evidence of acido- with oxylate crystals in the urine. Ethylene sis may be misinterpreted as alcoholic glycol may also be associated with central ketoacidosis. nervous system excitation, and increase in Methanol Poisoning 55

muscle with hypocalcemia. The Table 1. Several Toxic Substances and their toxicology laboratory can quickly assess Effect on Serum Osmolality at Representative High Blood Levels blood salicylate levels. Osmolality is a reflection of the number Sample Expected of dissolved in a liquid. In the Blood Osmolalities clinical laboratory, osmolality is usually Molecular Level (mosmlkg Substance Weight (ppm) of water) determined by measuring the freezing point of the solution. Sodium, urea, and Ethanol 46 350 80 lsopropanol 60 350 60 are substances that primarily contribute to Ethylene normal serum osmolality. The difference Glycol 62 200 40 Methanol 32 80 30 between the measured osmolality and the 144 15 calculated osmolality from known concen- trations of major osmolar constituents in the serum is known as the osmolar gap. Us- ing the formula shown in Figure 1, the cal- normal serum glucose. Occasional cases of culated mean serum osmolality of normal isoniazid poisoning, , persons is approximately 285 mosm/kg lead, or intoxication may confuse H,O with a standard deviation of +4.2 the differential diagnosis in an alcoholic mosm/kg H,O. Theoretically, a substance patient. will significantly contribute to the osmo- Swartz and his colleagues4 noted an lality of the serum only when it exhibits a unexpected hematological findings in the high blood level and has a low molecular epidemic of methanol poisoning at the State weight. In an emergency room the serum Prison of Southern Michigan. They found osmolality determined by freezing point an association between red blood cell in- lowering is a rapid measure of detecting in- dices and the clinical severity of methanol with ethanol, , poisoning. The mean corpuscular volume ethylene glycol and methanol. Thus, visual (MCV) was significantly higher in cases symptoms, acidosis, anion gap, and unex- with moderate or severe complications of plained osmolar gap will lead to the clinical methanol poisoning. They also found that diagnosis of methanol poisoning. the mean corpuscular hemoglobin concen- Table 1 shows molecular weights, and tration (MCHC) was significantly lower in expected osmolalities of ethanol, isopropyl those methanol poisoned patients with the alchohol, ethylene glycol, methanol and highest MCV. These results suggested to ethchlorvynol. Isopropyl alcohol may also them that hemoconcentration alone could cause depressed not explain the tendency toward a higher function and an unexplained osmolar gap. hematocrit and hemoglobin concentration However, it does not cause severe acidosis, in the more severely poisoned patients. and will cause acetonemia with a relatively They concluded that in severe methanol poisoning there is a primary increase in red blood cell size which correlates well with the severity of methanol poisoning. These investigators also performed in vitro ex- 2 Na + z + FE = 285 f 4.2 mosmlkg H,O periments incubating normal red blood cells in toxic concentrations of methanol. There were no changes in red blood cell in- Figure 1. Formula to calculate serum osmolali- dices after 48 hours of incubation. Similar ty. Na = serum sodium concentration mEq/L; results were found in experiments using BS= blood glucose concentration mg/dL; BUN = blood urea concentration formic acid rather than methanol itself. mgldl. They concluded that the red blood cell 56 Charles E. Becker

Table 2.The Approximate Loading Dose and Infusion Rates of Ethanol in Treating Methanol Poisoning in a 70.kg Adult

Loading Dose During After Dialysis

Ethanol (sp gr 0.79) 42 g 12-18 glh 5-11 g/h Intravenously, 10% (7.9 g/dL) 530 mL SO-230 mL/h 80-140 mUh Orally, 43% (86 proof, 34 g/dL) 125 mL 35-55 mL/h 15-35 mUh

indices in vitro are not affected by simple Because ethanol competes for alcohol de- addition of the toxins to whole blood. The hydrogenase, the enzyme responsible for mechanism responsible for their clinical metabolizing methanol to formic acid, it is findings in these methanol poisoned pa- essential to block ADH by administering tients remains unexplained. the less toxic ethanol. Ethanol has a higher affinity for, and is preferentially metabo- lized by, alcohol dehydrogenase. The dose dependent characteristic of ethanol metab- Treatment olism which occurs at increased levels, and its variability induced by chronic ethanol It is essential that a blood methanol level intake require the frequent monitoring of be determined as soon as possible if meth- blood ethanol levels to ensure appropriate anol poisoning is suspected. If clinical alcohol concentrations. suspicion of methanol poisoning is high, With the initiation of dialysis, ethanol treatment with ethanol should not be de- will also be eliminated in the dialysate; this layed pending the reporting of blood meth- requires further alterations in the dose of anol levels. Methanol levels in excess of 50 ethanol. Table 2 lists the approximate mg/dL are probably a clinical indication loading dose and infusion rates during and for hemodialysis and ethanol treatment. after dialysis in a 70-kg adult. Ethanol dis- With levels below 50 mg/dL ethanol treat- tributes in body water, so that a loading ment should be begun or continued and the dose of 42 g will achieve a blood concentra- test repeated. tion of approximately 100 mg/dL in a 70-kg The first treatment for methanol poi- patient. During dialysis approximately 12 soning, as in all poisoning circumstances, to 18 g/h should be given, and after dialy- is to establish respiration and create an ar- sis between 5 to 11 g/h. If the patient is tificial airway if necessary. Emesis can be awake or a nasogastric tube is in place, induced if the patient is neither comatose then the oral route can be utilized for etha- nor seizing and has not lost the gag reflex. nol by using a 43% (86 proof) alcohol. If these contraindications exist, the patient Ethanol may also be given intravenously should be endotracheally intubated and although high concentrations of ethanol gastric lavage carried out with a large bore may damage veins and be painful for the tube. patient. A 10% intravenous solution is In addition to attempts to limit absorp- usually optimal. The estimates of ethanol tion, there are three major modalities of levels given here should be verified by fre- treatment for severe methanol poisoning: quent ethanol determinations, especially

??diminishing the metabolic degradation during dialysis. It is desirable to maintain to toxic products the ethanol infusion until methanol levels ??dialysis to enhance removal of methanol are undetectable. and its toxic products and to improve Since folate dependent systems are acid-base balance likely responsible for the oxidation of ??alkalinization to counteract the metabol- formic acid to carbon dioxide in humans, ic acidosis it is probably useful to administer folic Methanol Poisoning 57

Table 3. indications for Ethanol Therapy and/or dosis in methanol poisoning, treatment Dialysis after Suspected Methanol with bicarbonate therapy may also be nec- Ingestion essary. The quantity of bicarbonate to be indications for Ethanol Therapy administered should be adjusted according 1. History of methanol ingestion, if level to estimates of sodium intake, concern for not immediately available. potassium balance, and careful monitor- 2. Peak methanol level greater than 20 mg/dL in an asymptomatic patient. ing of cardiovascular status. A special 3. Metabolic acidosis unexplained with in- problem occurs in patients with a relatively creased anion and osmolar gaps. low methanol level who have visual symp- Indications for Ethanol Therapy toms. In this situation the laboratory test and Hemodialysis: for methanol should be repeated and con- 1. Methanol levels greater than 50 mg/dL, firmed with osmolality estimates. If visual even in an asymptomatic patient. 2. Methanol poisoning with severe acidosis impairment is present hemodialysis should not correctable with sodium bicarbonate. be begun independent of the methanol level. 3. Visual symptoms and suspected metha- In a recent epidemic of methanol poi- nol poisoning when confirming labora- tory studies not available. soning, Swartz and his colleagues4 felt that once initial acidosis had been corrected with bicarbonate, neither sustained alkali nor dialysis was required if ethanol treat- acid to patients poisoned with methanol, ment was maintained. These observations although this has never been tested in hu- have yet to be repeated by others. man clinical studies. Since the effective Alcoholic patients are likely to be folate dose of folic acid has not been tested one deficient, and thus are more susceptible to should probably administer at least 50 mg methanol toxicity. Even if the relative in- folic acid intravenously every four hours. crease in MCV in methanol poisoning is This large dose is nontoxic. Also, 4-methyl- not the result of folic acid deficiency, ther- pyrazole (4-MP) may be a useful adjunct apy with folate cannot be expected to be to methanol poisoning if it becomes avail- toxic and therefore would hardly be dan- able for human use. gerous to administer in this setting. Al- Table 3 lists indications for ethanol though conservative treatment may suffice therapy and dialysis in suspected methanol in moderately severe methanol poisoning, poisonings. With confirmation of the di- hemodialysis procedures are still considered agnosis of methanol poisoning and identi- the preferred treatment in severe cases. fication of a high blood level (greater than Methanol poisonings, whether they oc- 50 mg/dL), hemodialysis is indicated.z0v21 cur epidemically or sporadically, are un- Peritoneal dialysis has been shown to be common but extremely hazardous poison- less efficacious than hemodialysis.22 Sor- ings. It is likely that methanol, which is a bent-based regeneration hemodialysis sys- versatile fuel, will have increasing usage in tems have become readily available for an energy conscious society. It will be im- routine use in patients with acute and portant that methanol-containing products chronic renal failure. However, the sor- have appropriate labeling and packaging bent-based hemodialysis systems have that will discourage accidental intoxication. been shown to be ineffective in the treat- A high index of suspicion and quick labo- ment of methanol poisoning.23 ratory confirmation are essential factors in Because of the PI ofound metabolic aci- managing methanol poisoning. 58 Charles E. Becker

REFERENCES

1. Bennett L Jr, Cary FH, Mitchell GL, et al.: Acute al.: Methanol poisoning: Ocular toxicity produced methyl alcohol poisoning: A review based on ex- by formate. Toxicol Appl Pharmacol 1978; 45: periences in an outbreak of 323 cases. Medicine 201-208. 1953; 32:431-463. 14. Noker PE, Eells JT, Tephly TR: Methanol toxici- 2. Kane RL, Talbert W, Harlan J, et al.: A metha- ty: Treatment with folic acid and 5-formyl tetra- nol poisoning outbreak in Kentucky. Arch Envi- hydrofolic acid. Alcoholism: Clin Exp Res 1980; ron Health 1968; 17:119-129. 4:378-383. 3. Naraqi S, Dethlefs RF, Slobodniuk RA, et al.: 15. McCoy HG, Cipolle RJ, Ehlers SM, et al.: Severe An outbreak of acute methyl methanol poisoning: Application of a pharmaco- in New Guinea. Aust NZ J Med 1979; 965-68. kinetic model for ethanol therapy and hemodialy- 4. Swartz RD, Millman RP, Billi JE, Bondar NP, sis. Am J Med 1979; 67:805-8b?. Migdal SD, Simonian SK, Monforte JR, McDon- 16. Blomstrand R. Ellin A. Lof A. et al.: Bioloeical ald FD, Harness JK, Cole KL: Epidemic metha- effects and metabolic interactions after chr&ic nol poisoning; clinical and biochemical analysis and acute administration of 4-methylpyrazole of a recent episode. Medicine 1981; 60:373-382. and ethanol to rats. Arch Biochem Siophys 1980; 5. Wenzl JE, Mills SD, McCall JT: Methanol poi- 199:591-605. soning in an infant-successful treatment with 17. McMartin KE, Hedstrom KG, et al.: Studies on peritoneal dialysis. Am J Dis Child 1965; 116: the metabolic interactions between 4-methylpyra- 445-447. zole and methanol using the monkey as an animal 6. Kahn A, Blum D: Methyl alcohol poisoning in an model. Arch Biochem Biophyr 1980; 199:606- 8-month old boy: An unusual route of inxotica- 614. tion. J Pediatr 1979; 94:841-843. 18. McMartin KE, Ambre JJ, Tephly TR: Methanol 7. Dutkiewicz B, Konczalik J, Karwacki W: Skin poisoning in human subjects: Role for formic absorption of administration of methanol in acid accumulation in the metabolic acidosis. Am men. Int Arch Occup Environ Health 1980; 48: JMed 1980; 68:414-418. 81-88. 19. Aquilonius SM, Bergstrom K, Enoksson P, et al.: 8. Chinard FP, Frisell WR: Methanol intoxication: Cerebral computed tomography in methanol in- Biochemical and clinical aspects. J Med Sot NJ toxication J Comput As&t Tomogr 1980; 4:425- 1976; 73:712-719. 428. 9. Roe E: The metabolism and toxicity of methanol. 20. Gonda A, Gualt H, Churchill D, et al.: Hemodi- Pharmacol Rev 1955; 7:399-412. alysis for methanol intoxication. Am JMed 1978; 10. Tephly TR, Watkins WD, Goodman JI: The bio- 64:749-758. chemical toxicoloav of methanol. in Wavland JH 21. Tobin M, Lianos E: Hemodialysis for methanol Jr (ed): Essays i;Toxicology. i974, vbl 5, pp. intoxication. Dialysis 1979; 3:97-106. 149-177. 22. Keyvan-Larijarni H, Tannenberg AM: Methanol 11. Use of folate analogue in treatment of methyl al- intoxication. Comparison of peritoneal dialysis cohol toxic reactions is studied (A Report from and hemodialysis treatment. Arch Intern Med the NII-I). JAMA 1979; 242:1951-1962. 1974; 134:293-296. 12. Baumbach GL, Cancilla PA, Martin-Amag G, et 23. Whalen JE, RichardCJ, Ambre J: Inadequatere- al.: Methyl alcohol poisoning: IV. Alterations of moval of methanol and formate using the sorbent the morphological findings of the retina and optic based regeneration hemodialysis delivery system. nerve. Arch Ophthalmol 1977; 95:1859-1965. C/in NephrolI979; 11:318. 13. Martin-Amat G, McMartin KE, Hayreh SS, et