The following information was generated from the 

Hazardous Substances Data Bank (HSDB), 

a database of the National Library of Medicine's TOXNET system 

(http://toxnet.nlm.nih.gov) on February 24, 2011. 

Query: Records containing the term METHANOL 

1 

NAME: METHANOL 

HSN: 93 

RN: 67-56-1 

HUMAN HEALTH EFFECTS: 

TOXICITY SUMMARY: 

 Methanol occurs naturally in humans, animals and plants. It is a natural 

 constituent in blood, urine, saliva and expired air. ... The two most 

 important sources of background body burdens for methanol and formate are 

 diet and metabolic processes. Methanol is available in the diet 

 principally from fresh fruits and vegetables, fruit juices ... fermented 

 beverages ... and diet foods (principally soft drinks). The artificial 

 sweetner aspartame is widely used and, on hydrolysis, 10% (by weight) of 

 the molecule is converted to free methanol, which is available for 

 absorption. ... Exposures to methanol can occur in occupational settings 

 through inhalation or dermal contact. ... Methanol is readily absorbed by 

 inhalation, ingestion and dermal exposure, and it is rapidly distributed 

 to tissues according to the distribution of body water. A small amount of 

 methanol is excreted unchanged by the lungs and kidneys. ... Methanol is 

 metabolized primarily in the liver by sequential oxidative steps to 

 formaldehyde, formic acid and carbon dioxide. The initial step involves 

 oxidation to formaldehyde by hepatic alcohol dehydrogenase ... In step 2, 

 formaldehyde is oxidized by formaldehyde dehydrogenase to formic acid/or 

 formate depending on the pH. In step 3, formic acid is detoxified to 

 carbon dioxide by folate-dependent reactions. Elimination of methanol from 

 the blood via the urine and exhaled air and by metabolism appears to be 

 slow in all species, especially when compared to ethanol. ... It is the 

 rate of metabolic detoxification, or removal of formate that is vastly 

 different between rodents and primates and is the basis for the dramatic 

 differences in methanol toxicity observed between rodents and primates. 

 The acute and short term toxicity of methanol varies greatly between 

 different species, toxicity being highest in species with a relatively 

 poor ability to metabolize formate. In such cases of poor metabolism of 

 formate, fatal methanol poisoning occurs as a result of metabolic acidosis 

 and neuronal toxicity, whereas, in animals that readily metabolize 

 formate, consequences of CNS depression (coma, respiratory failure, etc.) 

 are usually the cause of death. Sensitive primate species (humans and 

 monkeys) develop increased blood formate concentrations following methanol 

 exposure, while resistant rodents, rabbits and dogs do not. Humans and 

 non-human primates are uniquely sensitive to the toxic effects of 

 methanol. Overall methanol has a low acute toxicity to non-primate 

 animals. ... In the rabbit, methanol is a moderate irritant to the eye. It 

 was not skin sensitizing ... There is no evidence from animal studies to 

 suggest that methanol is a carcinogen ... The inhalation of methanol by 

 pregnant rodents throughout the period of embryogenesis induces a wide 

 range of concentration-dependent teratogenic and embryolethal effects. 

 Treatment-related malformations, primarily extra or rudimentary cervical 

 ribs and urinary or cardiovascular defects, were found in fetuses of rats 

 ... Increased incidences of exencephaly and cleft palate were found in the 

 offspring of ... mice ... There was increased embryo/fetal death ... and 

 an increasing incidence of full litter resorptions. Reduced fetal weight 

 was observed ... Fetal malformations ... included neural and ocular 

 defects, cleft palate, hydronephrosis and limb anomalies. Humans (and 

 non-human primates) are uniquely sensitive to methanol poisoning and the 

 toxic effects in these species are characterized by formic acidemia, 

 metabolic acidosis, ocular toxicity, nervous system depression, blindness, 

 coma and death. Nearly all of the available information on methanol 

 toxicity in humans relates to the consequences of acute rather than 

 chronic exposures. A vast majority of poisonings involving methanol have 

 occurred from drinking adulterated beverages and from methanol-containing 

 products. Although ingestion dominates as the most frequent route of 

 poisoning, inhalation of high concentrations of methanol vapor and 

 percutaneous absorption of methanolic liquids are as effective as the oral 

 route in producing acute toxic effects. The most noted health consequences 

 of longer term exposure to lower levels of methanol is a broad range of 

 ocular effects. ... The toxicity is manifest if formate generation 

 continues at a rate that exceeds its rate of metabolism. ... The minimum 

 lethal dose of methanol in the absence of medical treatment is between 0.3 

 and 1 g/kg. The minimum dose causing permanent visual defects is unknown. 

 ... Wide interindividual variability of the toxic dose is a prominent 

 feature in acute methanol poisoning. Two important determinants of human 

 susceptibility to methanol toxicity appear to be (1) concurrent ingestion 

 of ethanol, which slows the entrance of methanol into the metabolic 

 pathway, and (2) hepatic folate status, which governs the rate of formate 

 detoxification. The symptoms and signs of methanol poisoning, which may 

 not appear until after an asymptomatic period ... include visual 

 disturbances, nausea, abdominal and muscle pain, dizziness, weakness and 

 disturbances of consciousness ranging from coma to clonic seizures. Visual 

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 disturbances ... range from mild photophobia and misty or blurred vision 

 to markedly reduced visual acuity and complete blindness. In extreme cases 

 death results. The principal clinical feature is severe metabolic acidosis 

 of the anion-gap type. The acidosis is largely attributed to the formic 

 acid produced when methanol is metabolized. ... Visual disturbances of 

 several types (blurring, constriction of the visible field, changes in 

 color perception, and temporary or permanent blindness) have been reported 

 in workers ... No other adverse effects of methanol have been reported in 

 humans except minor skin and eye irritation. ... Methanol is of low 

 toxicity to aquatic organisms, and effects due to environmental exposure 

 to methanol are unlikely to be observed, except in the case of a spill. 

 [Environmental Health Criteria 196: Methanol pp. 1-9 (1997) by the 

 International Programme on Chemical Safety (IPCS) under the joint 

 sponsorship of the United Nations Environment Programme, the International 

 Labour Organisation and the World Health Organization.] **PEER REVIEWED** 

HUMAN TOXICITY EXCERPTS: 

 /HUMAN EXPOSURE STUDIES/ ...Teacher aides who worked at or near spirit 

 duplicators that used a 99% methanol duplicator fluid /were studied/. The 

 exposures ranged from 1 hr/day for 1 day/wk to 8 hr/day for 5 days/wk and 

 had occurred for 3 years. Since the introduction of the equipment, the 

 aides began to experience headaches, dizziness and eye irritation, blurred 

 vision and nausea/upset stomach while working near the machines. 

 Fifteen-minute breathing zone samples near 21 operating machines contained 

 between 475 and 4000 mg/cu m of methanol vapor. Fifteen of these samples 

 exceeded the NIOSH recommended 15-min standard of 1050 mg/cu m (800 ppm). 

 The aides were also exposed while collating and stapling papers 

 impregnated with the fluid up to 3 hr earlier and these exposures ranged 

 from 235-1140 mg/cu m . The results suggested that chronic effects may 

 occur when methanol concentrations exceed the threshold limit value (TLV) 

 of 260 mg/cu m (200 ppm). The effects reported in the study... were 

 similar in nature but appeared less severe than those reported from acute 

 poisoning by methanol [WHO; Environ Health Criteria 196: Methanol p.111 

 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /HUMAN EXPOSURE STUDIES/ The minimal lethal dose of methanol in humans 

 has not been determined. It has been suggested that ingestion of about 1 

 g/kg can cause death if the patient is untreated and has not consumed 

 ethanol. In 10 adults acutely intoxicated with methanol, a latency period 

 before treatment exceeding 10 hr and a blood formate level above 0.5 g/L 

 was reported to be predictive of severe methanol poisoning. [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V6 p.379] **PEER REVIEWED** 

 /HUMAN EXPOSURE STUDIES/ A study of the wooden heel industry in 

 Massachusetts showed average methanol vapor concentrations ranging from 

 160 to 780 ppm, with no definite evidence of injury to the exposed 

 workers. There was no mention of symptoms or complaints in spirit 

 duplicating processes in which exposures ranged from 400 to 1000 ppm. In 

 small, poorly ventilated rooms, headaches occurred among employees using 

 methanol in duplicating machines. The air concentrations were calculated 

 for two unventilated sizes of compartment and two types of Ditto fluid 

 (one containing 5% and the other 45% methanol, though some fluids 

 contained up to 100% methanol). Air concentrations from evaporation of 1 

 pint of fluid were as follows: 510 and 1000 ppm with 5% solutions for 

 1000- and 512- cu ft rooms, respectively; 4500 and 8870 ppm with 45% 

 methanol solution, respectively. The human tolerance values for exposure 

 for methanol were then determined. For single exposures, the estimated 

 tolerance value was 1000 ppm for 1 hr, 500 ppm for 8 hr, 200 ppm for 24 

 hour, and 200 ppm for 40 hr, based on five 8 hr working days. [Bingham, 

 E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. 

 John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.380] **PEER 

 REVIEWED** 

 /HUMAN EXPOSURE STUDIES/ In 23 workers who, partly due to unfavorable 

 working conditions (blackout precautions during wartime), had been exposed 

 to methanol concentrations up to about 8300 ppm, no symptoms were seen 

 apart from one case of "temporary blindness. " [Bingham, E.; Cohrssen, 

 B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V6 p.380] **PEER REVIEWED** 

 /HUMAN EXPOSURE STUDIES/ From ophthalmoscopic and histological evidence, 

 both the retina and the optic nerve have been postulated as the primary 

 sites of the toxic lesion produced by formate in methanol poisoning. 

 Permanent visual damage in methanol-poisoned humans is associated with 

 exposures usually greater than 20 hr to blood formate concentrations in 

 excess of 7 mM or 322 mg/dL. The initiating effect in the ocular toxicity 

 of formic acid is believed to involve the inhibition of cytochrome 

 oxidase, which is located in the mitochondria and is involved in oxidative 

 phosphorylation. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.380] **PEER REVIEWED** 

 /HUMAN EXPOSURE STUDIES/ The effects of methanol vapor (249 mg/cu m; SD + 

 7 mg/cu m) for 75 min on neurobehavioral measures were studied in 12 

 healthy young men. The exposure produced significant increases 

 (approximately 3 fold) in blood and urine methanol levels but no changes 

 in plasma formate level. Although most of the neurobehavioral end-points 

 were unaffected by exposure to methanol, statistically significant effects 

 and trends were found for a cluster of variables, including the latency of 

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 the p-200 component of event-related potentials, performance on the 

 Sternberg memory task and subjective measures of fatigue and 

 concentration. However, the effects were small and did not exceed the 

 normal range. [WHO; Environ Health Criteria 196: Methanol p.113 (1997). 

 Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /HUMAN EXPOSURE STUDIES/ ...The charts of the patients/treated in the same 

 intensive care unit for severe methanol poisoning/ admitted between 1987 

 and 2001 were reviewed. Inclusion criteria were: a history of deliberate 

 methanol ingestion, with a blood methanol concentration > 20 mg/dL (6.2 

 mmol/L) or a high anion gap metabolic acidosis. Indications for 

 hemodialysis were: blood methanol concentration > 50 mg/dL (15.8 

 mmol/L), metabolic acidosis (bicarbonate < 15 mmol/L, arterial pH 

 < 7.30), visual toxicity. Antidotal therapy included ethanol 

 administration in 22 cases, and fomepizole in 3 cases. Serial blood 

 measurements were obtained for pH, bicarbonate, methanol and formate. 

 Endogenous and hemodialysis elimination half-lives were calculated as t1/2 

 =0.693/Ke. Fick principle was applied for hemodialysis clearance 

 calculation. The records of 25 methanol poisoned patients were analysed. 

 Among them, 18 patients had sufficient data to allow accurate 

 determinations of formate kinetics. Formate half-life elimination during 

 hemodialysis was 1.80+/-0.78 hr, which was statistically different from 

 the values observed before or in the absence of dialysis (6.04+/-3.26 hr, 

 P=0.004). The mean hemodialysis formate clearance rate calculated in eight 

 cases was 176+/-43 mL/min. A rebound in plasma formate concentration was 

 observed in three patients after the discontinuation of hemodialysis. 

 [Hantson P et al; Hum Exp Toxicol 24 (2): 55-9 (2005)] **PEER REVIEWED** 

 <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15850279&query_hl=50" 

 target=new>PubMed Abstract 

 /HUMAN EXPOSURE STUDIES/ ...This is a retrospective analysis of the 

 medical records of 25 consecutive patients admitted to the intensive care 

 unit after severe intentional methanol poisoning. Acute renal impairment 

 was defined as a serum creatinine concentration higher than 177 micro 

 mol/L and/or a urinary output on admission and for the first 24 hr below 

 0.5 mL/kg/hr. Clinical pathological signs of acute renal injury were found 

 in 15 patients. In comparison with the 10 other patients taken as control 

 group, the patients who developed renal injury had a lower blood pH value 

 on admission, a higher serum osmolality, and a higher peak formate 

 concentration. Two factors contributing to renal injury could be 

 identified: hemolysis and myoglobinuria. The role of osmotic changes 

 (osmotic nephrosis) or of a direct cytotoxic effect of formic acid remains 

 speculative. Analysis of proteinuria suggests that proximal tubular cells 

 may be preferentially affected. Results of histopathological evaluation of 

 the kidney on a limited sample size (n=5) were inconclusive but suggestive 

 of possible hydropic changes in the proximal tubule secondary to methanol 

 toxicity. Acute renal injury may be associated with other signs of 

 severity in methanol poisoning, but it is almost always reversible in 

 survivors. Indicators of acute renal injury were identified. The 

 pathophysiology of this acute renal injury is multifactorial and far more 

 complex than shock-related tubular necrosis. [Verhelst D et al; Int J 

 Toxicol 23 (4): 267-73 (2004)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15371171&query_hl=4" 

 target=new>PubMed Abstract 

 /HUMAN EXPOSURE STUDIES/ ...Twenty-one-year retrospective chart review 

 (1980-2000) from suspected methanol poisoning patients treated with 

 ethanol in two large pediatric tertiary care centers. A total of 60 

 children (median age of 24 months) received ethanol for suspected methanol 

 poisoning: 39 orally and 21 intravenously. Median initial methanol level 

 was 4.16 mmol/L (13.3 mg/dL) (range 0 to 87.5 mmol/L or 0 to 280 mg/dL). 

 Median duration of ethanol treatment was 16 hours (range 1.5 to 72 hours). 

 None [0% (95% CI 0-5%)] of the 60 patients developed symptomatic 

 hypoglycemia. Of the 50 patients that had a glucose level measured, none 

 [(0% [95% CI 0-6%)] had a serum glucose concentration < 2.78 mmol/L 

 ( < 50 mg/dL). Eight patients [16% (95% CI 8-30%)] had at least one 

 serum glucose concentration between 2.78-3.61 mmol/L (50-65 mg/dL), but 

 none of those had symptoms compatible with hypoglycemia. A total of 42 

 patients [84% (95% CI 70-92%)] had all their serum glucose concentrations 

 > 3.61mmol/L ( > 65 mg/dL). There was no identifiable difference in 

 the glucose intake between the serum glucose concentration groups. Six out 

 of the 60 patients [10% (95% CI 4-21%)] were described as more drowsy 

 after ethanol but none was comatose or needed intubation. No child showed 

 signs of hypothermia [0/40 (95% CI 0-8%)] (rectal temperature < 35 

 degrees C), hepatotoxicity (0/12) (AST or ALT > 100 U/L) or even 

 thrombophlebitis (0/21). None of the 22 patients with toxic levels of 

 methanol ( > or = 26.2 mmol/L- > or = 20 mg/dL) died or had 

 ethanol-induced morbidity despite wide variation in ethanol levels. The 

 rate of clinically important adverse effects related to ethanol used as an 

 antidote to treat methanol poisoning in children was either absent or low 

 in a tertiary care pediatric hospital setting. There was no morbidity or 

 mortality associated with ethanol when it was used despite wide variation 

 in ethanol levels. [Roy M et al; J Toxicol Clin Toxicol 41 (2): 155-61 

 (2003)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12733853&query_hl=24" 

 target=new>PubMed Abstract 

 /SIGNS AND SYMPTOMS/ SYMPTOMATOLOGY: A latency usually of 12-18 hours, 

 during which time the only clinical signs are those of a generally mild 

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 and transient state of inebriation as after ethanol. Headache, anorexia, 

 weakness, fatigue, leg cramps, vertigo, restlessness. Nausea, occasionally 

 vomiting and diarrhea. Violent abdominal pain, back pain, leg pain. Apathy 

 or delirium progressing sometimes rapidly to coma. Rarely excitement, 

 mania, and convulsions. Dimness of vision with dilated pupils, reacting 

 poorly, if at all, to light, followed often by bilateral blindness 

 (transient or permanent). Eyes are often sensitive to pressure, and eye 

 movements are painful. Breathing is rapid and shallow, not usually deep 

 and labored as seen in other types of metabolic acidosis. Mild tachycardia 

 is common, but the blood pressure is usually well maintained. Death in 

 coma is due to respiratory failure or rarely to circulatory collapse. 

 Protracted convalescence with asthenia. Blindness is usually permanent. 

 [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial 

 Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-277] 

 **PEER REVIEWED** 

 /SIGNS AND SYMPTOMS/ Effects seen from either of the 2 most common routes 

 of occupational exposure (inhalation and percutaneous absorption) include: 

 headache, dizziness, nausea, vomiting, weakness, vertigo, chills, shooting 

 pains in the lower extremities, unsteady gait, dermatitis, multiple 

 neuritis characterized by paresthesia, numbness, prickling, and shooting 

 pain in the back of the hands and forearms, as well as edema of the arms, 

 nervousness, gastric pain, insomnia, acidosis, and formic acid in the 

 urine. Eye effects, such as blurred vision, constricted visual fields, 

 blindness, changes in color perception, double vision, and general visual 

 disturbances have been reported. Eye examination have shown sluggish 

 pupils, pallid optic discs, retinal edema, papilledema, hyperemia of the 

 optic discs with blurred edges and dialated veins. [NIOSH; Criteria 

 Document: Methyl Alcohol p.68-9 (1976) DHEW Pub. NIOSH 76-148] **PEER 

 REVIEWED** 

 /SIGNS AND SYMPTOMS/ Acute methanol toxicity in humans is characterized 

 in a well-defined pattern. Depending on the amount consumed, a narcotic 

 effect varying from mild to severe results from central nervous system 

 depression. This is followed by an asymptomatic interval lasting 10 to 48 

 hr, although 12 to 24 hr is most common. The latent period is then 

 followed by headaches, nausea, dizziness, and vomiting, followed by severe 

 abdominal pain and difficult, periodic breathing (Kussmaul breathing). The 

 individual also experiences blurred vision, photophobia, and pains in the 

 eyes. Depending on the amount of methanol consumed, the individual 

 susceptibility and the time at which treatment began, these visual 

 disturbances may either recede or develop within a few days into visual 

 impairments or total blindness. The appearance of these symptoms coincides 

 with increasing acidosis caused by accumulation of formic acid. In severe 

 cases, this leads to coma and eventually death from respiratory failure. 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.380] **PEER 

 REVIEWED** 

 /SIGNS AND SYMPTOMS/ The neurotoxic effects of methanol on the visual 

 system can involve transient abnormalities such as peripapillary edema, 

 optic disc hyperemia, diminished pupillary reactions to light, and central 

 scotomata. Permanent ocular abnormalities include optic disc pallor, 

 attenuation of arterioles, sheathing of arterioles, diminished pupillary 

 reactions to light, diminished visual acuity, central scotomata, and other 

 nerve fiber bundle defects. Pallor of the optic disc is an end-stage sign 

 of irreversible effects of the visual system and may appear 1 to 2 months 

 after an acute methanol dosage (or possibly following chronic occupational 

 exposure to methanol vapor). [WHO; Environ Health Criteria 196: Methanol 

 p.103 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /SIGNS AND SYMPTOMS/ ...A high frequency rate of DIC-syndrome is shown for 

 the condition /of intoxication of alcohol surrogates/. A majority of 

 thrombi accumulates at places with the highest concentrations of toxic 

 substances as well as at those places, through which poisoning substances 

 are brought out of the body, i.e. in the liver (since toxic substances are 

 introduced perorally) and kidneys. Thrombi were detected in all internals, 

 including the brain, in lethal intoxication. The immediate toxic effect 

 from methanol and from higher spirits can matter in the genesis of 

 changes, including acute swelling and chromatolysis with subsequent cell 

 death. Exclusively cerebral or coagulopathic-cerebral types of 

 thanatogenesis were registered in studied case of intoxication. 

 [Bogomolova IN et al; Sud Med Ekspert 47 (5): 22-5 (2004)] **PEER 

 REVIEWED** 

 /SIGNS AND SYMPTOMS/ There have been reports of diminished vision or 

 blindness from skin application of methanol or preparations that contain 

 methanol for the relief of pain, for the removal of varnish from skin, as 

 well as following accidental exposure. The concentration of airborne 

 methanol ranged from 365 to 3080 ppm; 15 of 21 measurements exceeded 800 

 ppm. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 

 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.381] 

 **PEER REVIEWED** 

 /SIGNS AND SYMPTOMS/ Chronic poisoning from repeated exposure to methanol 

 vapor were manifested by conjunctivitis, headache, giddiness, insomnia, 

 gastric disturbances, and bilateral blindness. [American Conference of 

 Governmental Industrial Hygienists. Documentation of Threshold Limit 

 Values for Chemical Substances and Physical Agents and Biological 

 Exposure Indices for 2001. Cincinnati, OH. 2001., p. 2] **PEER REVIEWED** 

Iris Camacho, 6308MM Page 4 of 69

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 /SIGNS AND SYMPTOMS/ Symptoms... of methanol poisoning consist of 

 headache, vertigo, vomiting, severe upper abdominal pain, back pain, 

 dyspnea, motor restlessness, cold clammy extremities, blurring of vision, 

 hyperemia of optic disc, ...diarrhea. ...Pulse is slow in severely ill 

 patients, and bradycardia constitutes grave prognostic sign. [Hardman, 

 J.G., L.E. Limbird, P.B., A.G. Gilman. Goodman and Gilman's The 

 Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw-Hill, 

 2001., p. 1886] **PEER REVIEWED** 

 /SIGNS AND SYMPTOMS/ Visual disturbance, the most distinctive aspect of 

 methanol poisoning in human beings, become evident soon after the onset of 

 acidosis. Dialated, unreactive pupils and dim vision are characteristic. 

 The ocular lesion, which involves chiefly the ganglion cells of the 

 retina, is a destructive inflammation followed by atrophy. In the short 

 term, the retina is congested and edematous, and the edges of the optic 

 disc may be blurred. The final result is bilateral blindness, which is 

 usually permanent. [Hardman, J.G., L.E. Limbird, P.B., A.G. Gilman. 

 Goodman and Gilman's The Pharmacological Basis of Therapeutics. 10th ed. 

 New York, NY: McGraw-Hill, 2001., p. 1886] **PEER REVIEWED** 

 /CASE REPORTS/ ...All methanol-poisoned patients admitted to /three 

 intensive care units in university-affiliated teaching hospitals/ and 

 treated with fomepizole from 1987-1999 (n=14) /were included in the 

 retrospective clinical study/. The median plasma methanol concentration 

 was 50 mg/dL (range 4-146), anion gap 22.1 mmol/L (11.8-42.2), arterial pH 

 7.34 (7.11-7.51), and bicarbonate 17.5 mmol/L (3.0-25.0). Patients 

 received oral or intravenous fomepizole until blood methanol was 

 undetectable. The median cumulative dose was 1250 mg (500-6000); the 

 median number of twice daily doses was 2 (1-16). Four patients underwent 

 hemodialysis for visual impairment present on admission. Four patients 

 with plasma methanol concentrations of 50 mg/dL or higher and treated 

 without hemodialysis recovered fully. Patients without pretreatment visual 

 disturbances recovered, with no sequelae in any case. There were no 

 deaths. Fomepizole was safe and well tolerated, even in the case of 

 prolonged treatment. Analysis of methanol toxicokinetics in 5 patients 

 demonstrated that fomepizole was effective in blocking methanol's toxic 

 metabolism. Fomepizole appears safe and effective in the treatment of 

 methanol-poisoned patients. [Megarbane B et al; Intensive Care Med 27 (8): 

 1370-8 (2001)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11511951&query_hl=34" 

 target=new>PubMed Abstract 

 /CASE REPORTS/ ...Two autopsy cases showing the classic neuropathologic 

 injuries in acute methanol poisoning: putamen and white matter necrosis 

 and hemorrhage /are presented/. In Case 1, putamen hemorrhages were 

 striking; white matter pathology predominated in Case 2. The precise 

 mechanism of methanol toxicity is unclear. Direct toxicity of metabolites, 

 particularly formic acid, as well as ischemic injury and acidosis likely 

 play a role. [Feany MB et al; Brain Pathol 11 (1): 121-2 (2001)] **PEER 

 REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11145199&query_hl=36" 

 target=new>PubMed Abstract 

 /CASE REPORTS/ ...A 27-yr-old man who was admitted 22 hours after 

 poisoning and presented a peak blood methanol concentration of 12.9 g/L. 

 Treatment included correction of metabolic acidosis, ethanol infusion, 

 hemodialysis and peritoneal dialysis. The patient survived with moderate 

 visual sequelae and esophageal stenosis. [Hantson P et al; Eur J Emerg Med 

 7 (3): 237-40 (2000)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11142277&query_hl=38" 

 target=new>PubMed Abstract 

 /CASE REPORTS/ ...Two cases of acute ocular damage following methanol 

 ingestion are presented. One patient underwent extensive 

 electrophysiological and psychophysical testing. Both patients reported 

 transient visual disturbances. In each patient vision was 6/6 in both eyes 

 at presentation but subsequently improved to 6/4. Color vision (Ishihara 

 plates) and pupillary reactions were normal. The optic discs were 

 hyperemic and swollen and retinal edema extended along the major vascular 

 arcades. There was cystoid macular edema and 'pseudo cherry red spots' 

 were observed. Automated field analysis revealed a generalized depression 

 of retinal sensitivity, an enlargement of one blind spot and paracentral 

 scotomas. The scotopic ERG was subnormal with diminished a- and 

 b-waveforms and the cone response to flicker was reduced. The pattern VER 

 P2 waveform was normal in latency but decreased in amplitude. ... 

 [McKellar MJ et al: Aust N Z J Ophthalmol 25 (3): 225-30 (1997)] **PEER 

 REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9296298&query_hl=44" 

 target=new>PubMed Abstract 

 /CASE REPORTS/ A case is described of an experimental physicist who 

 developed parkinsonism, apparently as delayed toxic effect of long 

 exposure to vapors of methanol in the laboratory. Clinical and magnetic 

 resonance imaging (MRI) supported the diagnosis, after exclusion of 

 hereditary diseases and primary degenerative diseases. Screening for heavy 

 metals in urine and plasma ceruloplasmin was negative. This case 

 illustrates the neurotoxic delayed effect of long-term exposure to 

 methanol with no episodes of acute intoxication. [Finkelstein Y, Vardi J; 

 Neurotoxicology 23 (4-5): 521-25 (2002)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12428724" 

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 target=new>PubMed Abstract 

 /CASE REPORTS/ ...A case of a 26-year-old woman who ingested 250-500 mL of 

 methanol in the 38th week of pregnancy /was reported/. Five hours after 

 methanol ingestion, the woman was slightly acidotic and had a serum 

 methanol level of 2,300 mg/L and a formic acid concentration of 336 mg/L. 

 Treatment consisted of ethanol and bicarbonate administration together 

 with hemodialysis. Six days later, the woman gave birth to an infant with 

 no signs of distress; Apgar scores were 9/10 and 10/10 at 1 and 5 minutes, 

 respectively. At the time of birth, the blood formic acid level was 2.4 

 mg/L in the mother and was below the detection level in the infant. A 10 

 year follow-up of the child revealed no visual disturbances. [DHHS/NTP; 

 NTP-CERHR Expert Panel Report on the Reproductive and Developmental 

 Toxicity of Methanol p.52 (April 2002) NTP-CERHR-MeOH-02. Available from, 

 as of July 20, 2005: 

 http://cerhr.niehs.nih.gov/news/methanol/methanol_final.pdf] **PEER 

 REVIEWED** 

 /CASE REPORTS/ Acute methanol intoxication in 24 men: 9 had no ocular 

 effects; 7 had transient effects: Peripapillary edema, optic disc 

 hyperemia, diminished pupillary light reaction, central scotoma. Eight had 

 permanent optic disc pallor, arteriole attenuation and sheathing, 

 diminished pupillary light reaction, diminished visual acuity, central 

 scotoma, and other nerve fiber bundle effects. /There was/ complete 

 blindness in 2, severe visual deficit in 4 /others/. [Dethlefs R, Naraqi 

 S; Med J Aust 2 (10): 483-5 (1978)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=739940" 

 target=new>PubMed Abstract 

 /CASE REPORTS/ Two cases which were described as multiple neuritis in men 

 engaged in shellacking furniture with shellac dissolved in methyl alcohol 

 /were reported/. Symptoms reported were paresthesia, numbing, prickling, 

 and shooting pain in the back of the hands and forearms, in addition to 

 edema of the arms. Both men sought medical aid promptly, and the resultant 

 cessation of exposure probably prevented the development of serious 

 sequelae of methyl alcohol intoxication. It was considered that these 2 

 cases were due to the inhalation of the vapor of the wood alcohol 

 employed. [Jelliffe SE; Med News 86: 387-90 (1905) as cited in NIOSH; 

 Criteria Document: Methyl Alcohol p.27-8 (1976) DHEW Pub. NIOSH 76-148] 

 **PEER REVIEWED** 

 /CASE REPORTS/ The case of a businessman who had been in the habit of 

 drinking quite regularly, in small quantities, for a period of at least 3 

 months an illicit whiskey which apparently contained 35% Columbian spirits 

 (methyl alcohol). When observed, the subject was suffering from severe 

 gastric irritability, marked hyperesthesia in both arms and hands, 

 incomplete paralysis of the extensors, and waist drop. He also had a mild 

 degree of ptosis of the eyelids and a restricted partial amblyopia. He 

 recovered after 4 months of treatment but still had some residual blurring 

 of vision. [Jelliffe SE; Med News 86: 387-90 (1905) as cited in NIOSH; 

 Criteria Document: Methyl Alcohol p.28 (1976) DHEW Pub. NIOSH 76-148] 

 **PEER REVIEWED** 

 /CASE REPORTS/ A case of methyl alcohol poisoning in a worker who was 

 involved in varnishing the inside of beer vats /is described/. Work 

 commenced on December 3, 1911, and continued on the following day with no 

 medical complaints. On December 5, the worker experienced headache, 

 vertigo, unsteady gait, nausea, vomiting, and acted as if intoxicated; 

 consequently he did not work on this day. On December 7, the worker began 

 having visual disturbances. At this time, he consulted a physician who 

 diagnosed methyl alcohol poisoning. On December 12, an ophthalmologist 

 made the following observations: the pupils were practically nonreactive 

 to light, there was retinal edema, and initial vision (eccentric) was 

 right 1/200 and left 2/200. In three weeks, his vision had improved to 

 20/30 in each eye. Six to 7 months later, with no additional methyl 

 alcohol exposure, visual acuity remained stable, while pupillary response 

 to light remained sluggish. In addition, researchers described a 

 progressive contraction of the visual fields during the entire period of 

 observation. ...The progressive constriction of visual fields corresponded 

 to degenerated bundles of fibers and groups of ganglion cells becoming 

 confluent as the degenerative process spread. It was concluded that this 

 case was produced solely by inhalation of methyl alcohol vapor. The 

 airborne concentration of methyl alcohol to which the worker was exposed 

 was not determined. [Tyson HH; Arch Ophthalmol 16: 459-71 (1912) as cited 

 in NIOSH; Criteria Document: Methyl Alcohol p.29 (1976) DHEW Pub. NIOSH 

 76-148] **PEER REVIEWED** 

 /CASE REPORTS/ ...Five patients that presented to the /emergency 

 department/ (ED) following deliberate solvent inhalation were evaluated 

 for elevated methanol levels. All were abusing the solvent for 6-12 hours 

 prior to arrival and were chronic abusers of this product. The initial 

 mean /methanol/ (MeOH) level was 19.3 mg/dL (range 10-26). The initial 

 serum bicarbonate ranged from 13 to 20 mmol/L and the initial anion gap 

 ranged from 13 to 31. The mean serum formate level was 31.7 ug/mL (range 

 3.6-64) with a reference range of 0-12. All had an undetectable ethanol 

 level. No patient had visual complaints and all had normal visual acuity. 

 No patients were treated with an alcohol dehydrogenase inhibitor or 

 dialysis, though all received intravenous folate. All had improved 

 acidosis within 4 hours of arrival to the ED. [Bebarta V et al; J Toxicol 

 Clin Toxicol 41 (5): 674-675 (2003)] **PEER REVIEWED** 

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 /CASE REPORTS/ Reports of cases of poisoning due to methanol inhalation 

 are relatively rare, although in one report there had been about 100 known 

 cases of failing sight or death due to inhalation of "wood alcohol. " 

 Usually exposure was in more confined spaces with poor ventilation. There 

 was one case reported of a woman who died after inhaling 4000 to 13,000 

 ppm methanol over 12 hr. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.380] **PEER REVIEWED** 

 /CASE REPORTS/ /A/ case involved a painter who spent three days painting 

 the engine room of a submarine with a methanol containing varnish. No 

 details were given of the varnish composition or the methanol 

 concentration in the air. On the first day, the painter experienced 

 dizziness; on the second day, he showed exuberance; and on the third day, 

 increased irritability. He also complained of abdominal pain, insomnia, 

 double vision, and ptosis (drooping eyelids). The patient's sight became 

 severely restricted in the left eye, pupils dilated, the optic disks 

 pallid, and the retinal vein engorged. His gait became uncoordinated, and 

 he suffered acidosis. Under treatment, the patient's condition improved 

 gradually over three weeks, and his sight eventually returned to normal. 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.380] **PEER 

 REVIEWED** 

 /CASE REPORTS/ An outbreak of acute methanol intoxication involving 28 

 young men in Papua New Guinea in 1977, each of whom consumed an equivalent 

 of 60-600 mL pure methanol, resulted in all becoming hospitalized within 

 8-36 hr due to acute metabolic acidosis, severe visual impairment and 

 acute pancreatitis. Four died within 72 hr after hospitalization. Of 24 

 who recovered, 16 showed no residual complications, 6 had bilateral visual 

 impairment and 2 had difficulty in speech as well as visual impairment. 

 [WHO; Environ Health Criteria 196: Methanol p.101 (1997). Available from, 

 as of July 18, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] 

 **PEER REVIEWED** 

 /CASE REPORTS/ ...In Atlanta, Georgia, USA, in 1951, when within a 5-day 

 period, 323 people consumed bootlegged whiskey contaminated with 35-40% 

 methanol and 41 of them died. ...The poisoning of 18 individuals /was 

 reported/, of whom 8 died, when a diluted paint thinner containing 

 approximately 37% (by volume) methanol was used as an alcoholic beverage 

 in Lexington, Kentucky, USA. An epidemic in the State Prison of Southern 

 Michigan in 1979 in which methanol diluent used in photocopying machines 

 was used as "home-made" spirits (containing approximately 3% methanol) 

 resulted in 46 definite cases of methanol intoxication and 3 deaths. 

 Methanol poisoning among 23 servicemen in an Army hospital in Korea who 

 had ingested bootleg sake contaminated with methanol was reported. 

 ...Acute methanol poisoning in 49 naval personnel who consumed drinks made 

 from duplicating fluid containing a high concentration of methanol /was 

 also reported/. [WHO; Environ Health Criteria 196: Methanol p.101 (1997). 

 Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /CASE REPORTS/ A case was reported of a 46-yr-old man who, after consuming 

 a beverage containing methanol, exhibited one of the highest reported 

 serum methanol levels (4930 mg/L), well above those at which ethanol 

 treatment and hemodialysis are recommended (200 mg/L and 500 mg/L, 

 respectively). The lowest serum pH was 7.0 with a hydrogen carbonate level 

 of 8.8 and an anion gap of 42.8. Additionally, his visual acuity decreased 

 to a complete loss of vision. The patient was aggressively treated with 

 hemodialysis and ethanol infusion, regained his vision with a visual 

 acuity of 20/30 bilaterally and suffered no neurological sequelae. [WHO; 

 Environ Health Criteria 196: Methanol p.104 (1997). Available from, as of 

 July 18, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

 /CASE REPORTS/ Extensive white and grey matter brain damage was seen in an 

 alcoholic 37-year-old man who consumed 1900 mL of windshield washer fluid 

 containing methanol. Both CT scan and MR imaging revealed diffuse white 

 matter edema and damage throughout frontal and parietal lobes. Bilateral 

 changes in the basal ganglia and necrosis and hemorrhage of putamen were 

 also noted. Autopsies from victims of lethal methanol poisonings revealed 

 gross pathology in the visceral organs, the brain, lung, liver, kidney and 

 the CNS, all of which involved a variety of edematous, hemorrhagic and 

 degenerative changes. [WHO; Environ Health Criteria 196: Methanol p.105 

 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /CASE REPORTS/ A 39-yr-old woman intentionally ingested Amberes shoe dye 

 containing both methanol and aniline. She subsequently developed 

 life-threatening methanol poisoning, methemoglobinemia, hemolytic anemia, 

 and sulfhemoglobinemia. Treatment involved methylene blue infusion, 

 emergent hemodialysis, fomepizole therapy, and blood products. [Katz KD et 

 al; J Emerg Med 27 (4): 367-9 (2004)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15498617&query_hl=56" 

 target=new>PubMed Abstract 

 /CASE REPORTS/ ...A 28-yr-old pregnant woman EGA 30 weeks with HIV 

 infection and asthma presented to the emergency department in respiratory 

 distress. She was acidotic (pH 7.17) with an anion gap of 26, and fetal 

 bradycardia was noted. Her son was delivered by emergency C-section 

 (birthweight 950 g, Apgars 1 and 3) and required aggressive resuscitation. 

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 During his hospital course, acidosis (initial pH 6.9) persisted despite 

 fluid, blood, and bicarbonate administration. His mother also had 

 persistent metabolic acidosis despite fluids, bicarbonate, and dopamine. 

 Results of other laboratory tests on the mother included undetectable 

 ethanol and salicylates and an osmolar gap of 41. An ethanol drip was 

 initiated for the mother 36 hr after admission when a methanol level of 54 

 mg/dL was reported. When consulted on hospital day 3, our regional poison 

 center recommended hemodialysis for the mother and administering 

 fomepizole and testing the methanol level of the newborn (61.6 mg/dL). 

 Because the infant developed a grade 4 intraventricular bleed, no further 

 therapy was offered, and he died on day 4. His mother died on day 10. 

 [Belson M, Morgan BW; J Toxicol Clin Toxicol 42 (5): 673-7 (2004)] **PEER 

 REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15462163&query_hl=1" 

 target=new>PubMed Abstract 

 /CASE REPORTS/ Treatment thresholds for methanol poisoning are based on 

 case reports and published opinion. Most guidelines recommend treatment 

 for a methanol level > or = 20 mg/dL in a nonacidotic patient. No 

 supportive data have been offered nor has the time of the exposure been 

 addressed. For instance, no distinction has been drawn between a methanol 

 level drawn 1 hr vs. 24 hr from ingestion. ...All published cases of 

 methanol poisoning /were analyzed/ to determine the applicability of the 

 20 mg/dL threshold in a nonacidotic patient, specifically those arriving 

 early for care (within 6 hr) with a peak or near-peak blood methanol 

 concentration. ...Dating to 1879, 372 articles in 18 languages were 

 abstracted using a standard format; 329 articles (2433 patients) involved 

 methanol poisoning, and 70 articles (173 patients) met inclusion criteria. 

 Only 22 of these patients presented for care within 6 hr of ingestion with 

 an early methanol level. All but 1 patient was treated with an inhibitor 

 of alcohol dehydrogenase (ADH). A clear acidosis developed only with a 

 methanol level > or = 126 mg/dL. The patient that did not receive an 

 ADH inhibitor was an infant with an elevated early methanol level (46 

 mg/dL) that was given folate alone and never became acidotic. Intra and 

 inter-rater reliability were 0.95. Nearly all reports of methanol 

 poisoning involve acidotic patients far removed from ingestion. The small 

 amount of data regarding patients arriving early show that 126 mg/dL is 

 the lowest early blood methanol level ever clearly associated with 

 acidosis. Contrary to conventional teaching, there are case reports of 

 acidosis after only a few hours of ingestion. The data are insufficient to 

 apply 20 mg/dL as a treatment threshold in a nonacidotic patient arriving 

 early for care. [Kostic MA, Dart RC; J Toxicol Clin Toxicol 41 (6): 

 793-800 (2003)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14677789&query_hl=20" 

 target=new>PubMed Abstract 

 /CASE REPORTS/ ...An adult male presented with central blindness after 

 ingesting methanol. Initial visual acuity was < 20/800 (finger counting 

 at 1-2 feet) with retinal edema on fundoscopy, arterial pH 7.19, methanol 

 97 mg/dL (30 mmol/L), formate 14.3 mmol/L, and ethanol undetectable. The 

 patient was treated with ethanol, then fomepizole intravenously (15, 10, 

 then 5 mg/kg), and hemodialysis. Methanol metabolism was effectively 

 blocked by fomepizole even after ethanol had been eliminated, and the 

 patient recovered 20/20 vision by day 14 with normal fundoscopy. This case 

 report confirms highly efficient inhibition of alcohol dehydrogenase by 

 fomepizole, as well as demonstrate the safety of fomepizole in a patient 

 already exhibiting end-organ retinal toxicity. The potential for 

 fomepizole to inhibit retinol dehydrogenase, an isoenzyme of alcohol 

 dehydrogenase essential to vision, did not appear to be clinically 

 significant in this symptomatic methanol-poisoned patient. [Sivilotti ML 

 et al; J Toxicol Clin Toxicol 39 (6): 627-31 (2001)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11762672&query_hl=32" 

 target=new>PubMed Abstract 

 /BIOMONITORING/ Volunteers in the dermal exposure portion of the 

 experiment ... consisted of the four subjects who participated in the 

 inhalation study and four additional male subjects (age 26-33 years). Mean 

 pre-exposure blood and breath methanol levels were measured at 1.2 mg/L 

 and 0.2 ppm, respectively. One hand from each volunteer was placed in a 

 beaker containing neat methanol (99.8% purity) for time periods of 0, 2, 

 4, 8, and 16 minutes. Blood and breath methanol samples were taken 

 immediately after exposure and at 12 additional time points for 8 hours 

 following exposure. ... Blood and breath methanol concentrations peaked at 

 about 45 and 15 minutes following exposure and were measured at 11.3 mg/L 

 and 9.3 ppm, respectively. Authors noted that exposure to one hand ( < 3% 

 of body surface area) for 16 minutes resulted in a blood methanol 

 concentration that is about equal to that achieved by breathing 400 ppm 

 methanol vapors for 8 hours. It was speculated by study authors that the 

 rapid rise in breath, compared to blood methanol levels, occurs because 

 methanol is first transported to the central circulation and lungs prior 

 to becoming equally distributed throughout all body water. The study 

 authors estimated that following a dermal exposure, 2 hours would need to 

 pass before methanol blood concentrations could be estimated from breath 

 levels. [DHHS/NTP; NTP-CERHR Expert Panel Report on the Reproductive and 

 Developmental Toxicity of Methanol p.14 (April 2002) NTP-CERHR-MeOH-02. 

 Available from, as of July 20, 2005: 

 http://cerhr.niehs.nih.gov/news/methanol/methanol_final.pdf] **PEER 

 REVIEWED** 

 /BIOMONITORING/ ...A study /was conducted/ to determine if methanol in 

 breath is a useful indicator of blood levels following oral or dermal 

Iris Camacho, 6308MM Page 8 of 69

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 exposure. ... In the inhalation portion of the experiment, mean 

 pre-exposure blood and breath methanol concentrations were measured at 

 2.65 mg/L and 1.3 ppm, respectively, in 4 subjects (3 males and 1 female, 

 age 31-55 years). Each subject was exposed to 0, 100, 200, 400, and 800 

 ppm methanol vapors [purity not specified] for 8 hours. ... Following 6 

 and 8 hours of exposure, 4 blood and breath samples were taken at 5-minute 

 intervals. ... Blood and breath levels of methanol were significantly 

 increased at 6 and 8 hours. Peak blood levels were 11.1 and 13.4 mg/L at 

 each respective time period. Breath concentrations were highest 

 immediately after the 6- and 8-hour exposure (71.7 and 76.9 ppm, 

 respectively), but rapidly declined within 15 minutes of breathing clean 

 air (3.5 and 3.3 ppm). The authors suggested that the initial high 

 concentration of breath methanol reflected absorption and desorption of 

 methanol from airways. Therefore, the authors concluded that methanol 

 breath levels would be useful for estimating blood concentrations only 

 after 10-15 minutes of breathing clean air because that is the time needed 

 for desorption of methanol from airways. [DHHS/NTP; NTP-CERHR Expert Panel 

 Report on the Reproductive and Developmental Toxicity of Methanol p.14 

 (April 2002) NTP-CERHR-MeOH-02. Available from, as of July 20, 2005: 

 http://cerhr.niehs.nih.gov/news/methanol/methanol_final.pdf] **PEER 

 REVIEWED** 

 /OTHER TOXICITY INFORMATION/ Methanol toxicity in humans ... is 

 characterized by a latent period of many hours followed by a metabolic 

 acidosis and ocular toxicity. This is not observed in most lower animals. 

 The metabolic acidosis and blindness is apparently due to formic acid 

 accumulation in humans ... a feature not seen in lower animals. The 

 accumulation of formate is due to a deficiency in formate metabolism, 

 which is, in turn, related, in part, to low hepatic tetrahydrofolate (H4 

 folate). An excellent correlation between hepatic H4 folate and formate 

 oxidation rates has been shown within and across species. Thus, humans ... 

 possess low hepatic H4 folate levels, low rates of formate oxidation and 

 accumulation of formate after methanol. Formate, itself, produces 

 blindness ... humans also have low hepatic 10-formyl H4 folate 

 dehydrogenase levels, the enzyme which is the ultimate catalyst for 

 conversion of formate to carbon dioxide. [Tephly TR; Life Scl 48 (11): 

 1031-41 (1991)] **PEER REVIEWED** 

 /OTHER TOXICITY INFORMATION/ ...Experience with 16 organ donors who died 

 as a result of acute methanol intoxication in 10 Spanish hospitals over 

 the last 14 yr /is presented/. Between October 1985 and July 1999, 16 

 organ donors with brain death caused by acute methanol intoxication, 13 

 females and three males with a mean age of 38.4 +/- 7.6 yr (interval: 

 26-55 yr), allowed 37 elective transplants to be performed: 29 kidneys, 

 four hearts and four livers for 37 recipients, and one urgent liver 

 transplantation to a recipient with fulminant hepatitis. The immediate 

 postoperative period was favorable for the 38 graft recipients. None of 

 the graft recipients presented gap anion metabolic acidosis in the 

 immediate postoperative period, nor symptomatology or lesions of the CNS 

 characteristic of methanol intoxication. Two patients died during the 

 first month post-transplantation, a liver recipient and a heart recipient, 

 at 16 and 24 days, respectively, because of acute rejection of the graft. 

 At 1 month after transplantation 35 of the 36 recipients had been 

 discharged from hospital with normal-functioning grafts. The last of the 

 recipients, a kidney recipient, was discharged at 6 wk with 

 normal-functioning graft. Actuarial survival of the graft and patient of 

 kidney recipients at 1, 3 and 5 yr was 92.6, 77.8, and 75%, and 100, 88.9 

 and 83.3%, respectively; with average serum creatinines of 139.9 +/- 42.9, 

 150.4 +/- 42.8, and 164.4 +/- 82.5 micromol/L, respectively. At 1 yr after 

 transplantation the three heart recipients and two of the three liver 

 recipients had normal-functioning graft. Methanol intoxication is not 

 transferred from the donor to the recipient. The survival of the graft and 

 kidney, heart and liver recipients using organs from donors who die 

 because of methanol does not differ in the short- and long-term from the 

 transplants performed with organs from donors who die from other causes. 

 [Lopez-Navidad A et al; Clin Transplant 16 (3): 151-62 (2002)] **PEER 

 REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12010136&query_hl=28" 

 target=new>PubMed Abstract 

 /OTHER TOXICITY INFORMATION/ ...Published information about 

 methanol-intoxicated patients is reviewed and combined with findings in 

 studies in volunteers given small doses of methanol, as well as 

 occupational exposure limits (OELs), to indicate a tolerable ("safe") 

 daily dose of methanol in an adult as 2 g and a toxic dose as 8 g. The 

 simultaneous ingestion of ethanol has no appreciable effect on the 

 proposed "safe" and "toxic" doses when considering exposure over several 

 hours. Thus, assuming that an adult consumes 4 x 25-mL standard measures 

 of a drink containing 40% alcohol by volume over a period of 2 hr, the 

 maximum tolerable concentration (MTC) of methanol in such a drink would be 

 2% (v/v) by volume. However, this value only allows a safety factor of 4 

 to cover variation in the volume consumed and for the effects of 

 malnutrition (i.e., folate deficiency), ill health and other personal 

 factors (i.e., ethnicity). In contrast, the current EU general limit for 

 naturally occurring methanol of 10 g methanol/l ethanol [which equates to 

 0.4% (v/v) methanol at 40% alcohol] provides a greater margin of safety. 

 [Paine A, Davan AD; Hum Exp Toxicol 20 (11): 563-8 (2001)] **PEER 

 REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11926610&query_hl=30" 

 target=new>PubMed Abstract 

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SKIN, EYE AND RESPIRATORY IRRITATIONS: 

 /Methanol/ is an eye and skin irritant. [Lewis, R.J. Sax's Dangerous 

 Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van 

 Nostrand Reinhold, 1996., p. 2174] **PEER REVIEWED** 

MEDICAL SURVEILLANCE: 

 The following medical procedures should be made available to each employee 

 who is exposed to methyl alcohol at potentially hazardous levels: 1. A 

 complete history and physical examination should be given to detect 

 existing conditions that might place the employee at increased risk, and 

 to establish a baseline for future health monitoring. Examination of the 

 skin, liver, kidneys, and eyes should be stressed. Skin disease: Methyl 

 alcohol is a defatting agent and can cause dermatitis on prolonged 

 exposure. Persons with ... existing skin disorders may be susceptible to 

 the effects of this agent. Liver function tests: Methyl alcohol may cause 

 liver damage. A profile of liver function should be obtained by utilizing 

 a medically acceptable array of biochemical tests. Kidney disease: 

 Although methyl alcohol has not been proven to be kidney toxin in humans, 

 the importance of this organ in the elimination of toxic substances 

 justifies special consideration in those with impaired renal function. Eye 

 disease: Because methyl alcohol may cause optic atrophy and blindness, 

 those with existing eye diseases may be at increased risk from exposure. 

 The aforementioned medical examinations should be repeated on an annual 

 basis. In addition, anyone developing the above-listed conditions or who 

 has been splashed in the eyes with, has ingested, or otherwise has been 

 exposed to methyl alcohol should be placed under medical surveillance. 

 [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). 

 NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. 

 DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. 

 Government Printing Office, Jan. 1981., p. 1] **PEER REVIEWED** 

 Special tests which may be used include: Determination of methyl alcohol 

 in blood and methyl alcohol and formic acid in urine; estimation of alkali 

 reserve which may be impaired because of acidosis following accidental 

 ingestion. [Sittig, M. Handbook of Toxic and Hazardous Chemicals and 

 Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 

 1985., p. 583] **PEER REVIEWED** 

 A study was performed among 20 workers employed in a printing office at 3 

 different work places (methanol concentration of 85, 101 and 134 ppm) to 

 determine whether the concentration of formic acid in blood or urine and 

 the methanol content of alveolar air permit the estimation of methanol 

 exposure. Blood, urine and end expiratory air were collected at the 

 beginning and the end of the shift. For comparison formic acid 

 concentrations were determined in the morning and in the afternoon in 

 blood and urine of 36 and 15 control persons, respectively. The 

 concentration of formic acid in blood increased significantly from 3.2:2.4 

 mg/L before to 7.9:3.2 mg/L after the shift in the exposed workers (mean 

 increase 4.7:3.8 mg/L). The corresponding concentrations in urine were 

 13.1:5.3 mg/l. This difference is also significant. In the control groups 

 there was a small but significant decrease of formic acid concentration in 

 blood from 5.6:4.5 mg/L in the morning to 4.9:4.2 mg/L in the afternoon. 

 In urine, the formic acid concentrations in the morning (11.9:6.4 mg/L) 

 and in the afternoon (11.7:5.6 mg/L) were not significantly different. The 

 increase of formic acid concentration in blood during the shift is the 

 most useful parameter for monitoring methanol-exposed persons. [Baumann K, 

 Angerer J; Int Arch Occup Environ Health 42 (3-4): 241-9 (1979)] **PEER 

 REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=422265" 

 target=new>PubMed Abstract 

 A sampling strategy was developed to detect personal exposure to methanol 

 and formic acid vapors. Formic acid is the metabolic end product of 

 methanol, and part of inhaled formic acid is excreted directly in urine, 

 so that urinary formic acid would reveal exposure to both agents. A linear 

 relationship to inhaled vapors, however, could be shown only if urinary 

 sampling were delayed until 16 hr (next morning) after exposure. Exposure 

 to methanol vapor at the current Finnish hygienic limit level (200 ppm) 

 produced 80 mg formic acid/g creatinine; exposure to formic acid at the 

 hygienic limit (5 ppm) caused 90 mg/g creatinine. The similarity of these 

 figures may indicate a common toxicological foundation of these 

 empirically set values. [Liesivuori J, Savolainen H; Am Ind Hyg Assoc J 48 

 (1): 32-34 (1987)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3565260" 

 target=new>PubMed Abstract 

 Headspace gas chromatography was used to determine the concentration of 

 ethanol and methanol in blood samples from 519 individuals suspected of 

 drinking and driving in Sweden where the legal alcohol limit is 0.50 mg/g 

 in whole blood (11 mmol/L). The concentration of ethanol in blood ranged 

 from 0.01 to 3.52 mg/g with a mean of 1.83 + or - 0.82 mg/g (+ or - 

 standard deviation). The frequency distribution was symmetrical about the 

 mean but deviated from normality. A plot of the same data on normal 

 probability paper indicated that it might be composed of two 

 subpopulations (bimodal). The concentration of methanol in the same blood 

 specimens ranged from 1 to 23 mg/L with a mean of 7.3 + or - 3.6 mg/L (+ 

 or - standard deviation) and this distribution was markedly skew (+). The 

 concentration of ethanol (x) and methanol (y) were positively correlated 

 (r= 0.47, P < 0.001) and implies that 22% (r2) of the variance in 

 blood-methanol can be attributed to its linear regression on 

 blood-ethanol. The regression equation was y= 3.6 + 2.1 x and the standard 

Iris Camacho, 6308MM Page 10 of 69

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 error estimate was 0.32 mg/L. This large scatter precludes making reliable 

 estimates of blood-methanol concentration from measurements of 

 blood-ethanol concentration and the regression equation. But higher 

 blood-methanol concentrations are definitely associated with higher 

 blood-ethanol in this sample of Swedish drinking drivers. Frequent 

 exposure to methanol and its toxic products of metabolism, formaldehyde 

 and formic acid, might constitute an additional health risk associated 

 with heavy drinking in predisposed individuals. The determination of 

 methanol in blood of drinking drivers in addition to ethanol could 

 indicate long-standing ethanol intoxication and therfore potential problem 

 drinkers or alcoholics. [Jones AW, Lowinger H; Forensic Sci Int 37 (4): 

 277-85 (1988)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3410397" 

 target=new>PubMed Abstract 

POPULATIONS AT SPECIAL RISK: 

 Persons with existing skin, kidney, liver, or eye disorders may be at an 

 increased risk when exposed to methanol. [Mackison, F. W., R. S. Stricoff, 

 and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health 

 Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 

 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. 1] 

 **PEER REVIEWED** 

 Folate-deficient individuals might be at greater risk from inhalation of 

 low concentrations of methanol, compared to normal individuals. Human 

 populations that are potentially at high risk of folate deficiency include 

 pregnant women, the elderly, individuals with poor-quality diets, 

 alcoholics and individuals on certain medications or with certain 

 diseases. [WHO; Environ Health Criteria 196: Methanol p.113 (1997). 

 Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 It has been suggested that the metabolic acidosis due to methanol might be 

 exacerbated in individuals with diabetes since it is well known that these 

 patients suffer from diabetic ketoacidosis. However, there are no clinical 

 or experimental data on any interaction between methanol acidosis and 

 diabetic ketoacidosis. [WHO; Environ Health Criteria 196: Methanol p.113 

 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

PROBABLE ROUTES OF HUMAN EXPOSURE: 

 STUDY OF WOOD HEEL INDUSTRY IN MA SHOWED AVG METHANOL VAPOR CONCN RANGING 

 FROM 160-170 PPM, WITH NO DEFINITE EVIDENCE OF INJURY TO EXPOSED WORKERS 

 ... CONCN BETWEEN 400 & 1000 PPM IN SPIRIT DUPLICATING PROCESSES /WERE 

 REPORTED/. NO MENTION WAS MADE OF SYMPTOMS OR COMPLAINTS, BUT THESE CONCN 

 WERE CONSIDERED EXCESSIVE. ... [American Conference of Governmental 

 Industrial Hygienists. Documentation of the Threshold Limit Values and 

 Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference 

 of Governmental Industrial Hygienists, 1986., p. 372] **PEER REVIEWED** 

 ALTHOUGH INDIVIDUAL RESPONSES OF MAN TO METHYL ALCOHOL MAY VARY 

 CONSIDERABLY, INDUSTRIAL EXPOSURES ARE NOT VERY HAZARDOUS IF CONCN ARE 

 MAINTAINED WITHIN UPPER LIMIT OF 200 PPM BY PROPER VENTILATION. [Clayton, 

 G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: 

 Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 

 1981-1982., p. 4541] **PEER REVIEWED** 

 NIOSH (NOES Survey 1981-1983) has statistically estimated that 1,219,371 

 workers (295,849 of these are female) are potentially exposed to methanol 

 in the US(1). Occupational exposure to methanol may occur through 

 inhalation and dermal contact with this compound at workplaces where 

 methanol is produced or used(SRC). Monitoring data indicate that the 

 general population may be exposed to methanol via inhalation of ambient 

 air, ingestion of food and drinking water(SRC). [(1) NIOSH; International 

 Safety Cards. Methanol. 67-56-1. Available at 

 http://www.cdc.gov/niosh/ipcs/nicstart.html as of Jul 1, 2005.] **PEER 

 REVIEWED** 

BODY BURDEN: 

 Methanol was detected in 1 of 12 samples of human milk collected from 

 volunteers in 4 USA cities(1). Methanol has been detected in expired human 

 air(2,3,4); in one study, it was detected in 3.6% of 387 expired air 

 samples collected from 54 volunteers at a geometric mean concn of 0.549 

 ng/l(4). [(1) Pellizzari ED et al; Bull Environ Contam Toxicol 28: 322-8 

 (1982) (2) Krotosynski B; J Chromat Sci 15: 239-44 (1977) (3) Krotosynski 

 BK, O'Neill HJ; J Environ Sci Health Part A-Environ Sci Eng 17: 855-83 

 (1982) (4) Krotosynski BK et al; J Anal Toxicol 3: 255-43 (1979)] **PEER 

 REVIEWED** 

MINIMUM FATAL DOSE LEVEL: 

 The minimum lethal dose of methanol in the absence of medical treatment is 

 between 0.3 and 1 g/kg. [Environmental Health Criteria 196: Methanol pp. 8 

 (1997) by the International Programme on Chemical Safety (IPCS) under the 

 joint sponsorship of the United Nations Environment Programme, the 

 International Labour Organisation and the World Health Organization.] 

 **PEER REVIEWED** 

EMERGENCY MEDICAL TREATMENT: 

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EMERGENCY MEDICAL TREATMENT: 

 

EMT COPYRIGHT DISCLAIMER: 

Portions of the POISINDEX(R) and MEDITEXT(R) database have been provided here 

for general reference. THE COMPLETE POISINDEX(R) DATABASE OR MEDITEXT(R) 

DATABASE SHOULD BE CONSULTED FOR ASSISTANCE IN THE DIAGNOSIS OR TREATMENT OF 

SPECIFIC CASES. The use of the POISINDEX(R) and MEDITEXT(R) databases is at your 

sole risk. The POISINDEX(R) and MEDITEXT(R) databases are provided "AS IS" and 

"as available" for use, without warranties of any kind, either expressed or 

implied. Micromedex makes no representation or warranty as to the accuracy, 

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OF MERCHANTABILITY AND FITNESS FOR A PARTICULAR PURPOSE OR USE ARE HEREBY 

EXCLUDED. Micromedex does not assume any responsibility or risk for your use of 

the POISINDEX(R) or MEDITEXT(R) databases. Copyright 1974-2011 Thomson 

MICROMEDEX. All Rights Reserved. Any duplication, replication, "downloading," 

sale, redistribution or other use for commercial purposes is a violation of 

Micromedex' rights and is strictly prohibited.<p>The following Overview, *** 

METHANOL ***, is relevant for this HSDB record chemical. 

LIFE SUPPORT: 

 o This overview assumes that basic life support measures 

 have been instituted. 

CLINICAL EFFECTS: 

 0.2.1 SUMMARY OF EXPOSURE 

 0.2.1.1 ACUTE EXPOSURE 

 A) USES: One of the toxic alcohols that is found in 

 windshield wiper fluid, gas line antifreeze, fuels, 

 photocopy fluid, solvents, carburetor cleaner, and as 

 an adulterant in homemade ethanol distillates. 

 B) TOXICOLOGY: An alcohol that causes intoxication similar 

 to ethanol and is metabolized to formaldehyde and 

 formic acid via alcohol dehydrogenase and aldehyde 

 dehydrogenase, respectively. Formic acid causes a 

 metabolic acidosis and causes blindness through direct 

 retinal toxicity. Toxicity is most common after 

 ingestion but has been reported with inhalation and 

 dermal exposures. 

 C) EPIDEMIOLOGY: Uncommon exposure that can result in 

 significant morbidity and mortality. 

 D) WITH POISONING/EXPOSURE 

 1) MILD TO MODERATE TOXICITY: Patients will initially 

 have signs of acute intoxication, such as ataxia, 

 sedation, and disinhibition. Patients may also 

 complain of abdominal pain, nausea, vomiting, and 

 headache. Acidosis or signs of visual impairment 

 suggest a more severe poisoning. 

 2) SEVERE TOXICITY: Severe metabolic acidosis develops 

 hours after exposure (if ethanol is not coingested) 

 and may lead to multiorgan dysfunction including 

 hypotension, tachycardia, dysrhythmias, seizures, 

 coma, and pancreatitis. In addition, ocular toxicity 

 may develop; manifestations include mydriasis, 

 hyperemic optic discs, and papilledema. Visual 

 impairment may develop, which may range from 

 blurry/hazy vision to color vision defects to 

 "snowfield" vision to total blindness. Permanent 

 sequelae after severe intoxication may include basal 

 ganglia necrosis with parkinsonian features (ie, 

 tremor, rigidity, bradykinesia) and blindness. 

 0.2.3 VITAL SIGNS 

 0.2.4 HEENT 

 0.2.4.1 ACUTE EXPOSURE 

 A) WITH POISONING/EXPOSURE 

 1) Blurred or double vision, constricted visual fields, 

 spots before the eyes, sharply reduced visual acuity, 

 optic atrophy, blindness, nystagmus, and whiteness in 

 the visual field have been described. Fixed, dilated 

 pupils suggest severe poisoning. 

 a) Onset of effects may be delayed for 12 to 24 hours. 

 Fundoscopic findings may be normal or may show 

 peripapillary edema, hyperemia of the optic disc, or 

 retinal edema. 

 0.2.5 CARDIOVASCULAR 

 0.2.5.1 ACUTE EXPOSURE 

 A) WITH POISONING/EXPOSURE 

 1) Tachycardia is fairly common; bradycardia may develop 

 in fatal poisonings. Cardiac failure and severe 

 hypotension may occur. 

 0.2.6 RESPIRATORY 

 0.2.6.1 ACUTE EXPOSURE 

 A) WITH POISONING/EXPOSURE 

 1) Tachypnea from metabolic acidosis is common. Sudden 

 respiratory failure may occur in the terminal stages. 

 0.2.7 NEUROLOGIC 

 0.2.7.1 ACUTE EXPOSURE 

 A) WITH POISONING/EXPOSURE 

 1) Seizures, coma, and symptoms similar to ethanol 

 "hangover" may occur. 

 2) Permanent sequelae may include basal ganglia infarcts, 

 parkinsonism, toxic encephalopathy, polyneuropathy, 

 optic atrophy, and blindness. 

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 0.2.8 GASTROINTESTINAL 

 0.2.8.1 ACUTE EXPOSURE 

 A) WITH POISONING/EXPOSURE 

 1) Abdominal pain, anorexia, nausea, and vomiting may 

 occur. In severe poisonings, acute necrotizing 

 pancreatitis has been reported. 

 0.2.10 GENITOURINARY 

 0.2.10.1 ACUTE EXPOSURE 

 A) WITH POISONING/EXPOSURE 

 1) Acute renal failure and hematuria have been reported. 

 0.2.11 ACID-BASE 

 0.2.11.1 ACUTE EXPOSURE 

 A) Metabolic acidosis is classic. Concurrent ethanol 

 ingestion may delay acidosis for 18 to 24 hours or 

 longer. 

 0.2.12 FLUID-ELECTROLYTE 

 0.2.12.1 ACUTE EXPOSURE 

 A) WITH POISONING/EXPOSURE 

 1) Hypomagnesemia, hypokalemia, and hypophosphatemia have 

 been reported. 

 0.2.15 MUSCULOSKELETAL 

 0.2.15.1 ACUTE EXPOSURE 

 A) WITH POISONING/EXPOSURE 

 1) Rhabdomyolysis may occur in severe poisonings. 

 0.2.20 REPRODUCTIVE HAZARDS 

 A) Methanol, together with other solvents, has been linked 

 with birth defects of the central nervous system in 

 humans (Holmberg, 1979), but methanol cannot be 

 considered a human reproductive hazard, because of mixed 

 or poorly documented exposures. 

 0.2.21 CARCINOGENICITY 

 0.2.21.1 IARC CATEGORY 

 A) IARC Carcinogenicity Ratings for CAS67-56-1 (IARC 

 Working Group on the Evaluation of Carcinogenic Risks 

 to Humans, 2006; IARC Working Group on the Evaluation 

 of Carcinogenic Risks to Humans, 2007; IARC Working 

 Group on the Evaluation of Carcinogenic Risks to 

 Humans, 2010; IARC Working Group on the Evaluation of 

 Carcinogenic Risks to Humans, 2010a; IARC Working Group 

 on the Evaluation of Carcinogenic Risks to Humans, 

 2008; IARC, 2004): 

 1) Not Listed 

LABORATORY: 

 A) Monitor mental status, vital signs, and ECG. 

 B) In patients with significant CNS depression or metabolic 

 acidosis, obtain arterial or venous blood gases. 

 C) Obtain a serum methanol and ethanol concentration and 

 serial serum electrolytes; calculate anion gap. 

 D) If serum methanol cannot be obtained in a timely fashion, 

 measure serum osmolality and calculate osmolal gap. The 

 osmolal gap is equal to the measured serum osmolality 

 minus (2 x serum sodium + BUN/2.8) + glucose/18 + 

 ethanol/4.6). An elevated osmolal gap (greater than 10) 

 suggests the presence of toxic alcohols, but a normal 

 osmolal gap does NOT rule this out. 

TREATMENT OVERVIEW: 

 0.4.2 ORAL EXPOSURE 

 A) MANAGEMENT OF MILD TO MODERATE TOXICITY 

 1) Obtain a methanol level, serum chemistry, and a serum 

 pH. A thorough visual exam should be performed, 

 including visual acuity. An elevated osmolar gap 

 suggests the presence of methanol or another alcohol 

 but cannot be used to rule out a significant exposure. 

 If a methanol concentration is readily available 

 (results known within 2 hours) and the patient is 

 asymptomatic, then alcohol dehydrogenase (ADH) 

 inhibition can be delayed until the methanol 

 concentration is available. Patients with a methanol 

 concentration of more than 25 mg/dL or metabolic 

 acidosis should be treated with ADH inhibition. If 

 methanol concentrations cannot readily be measured, 

 patients with a history of a potentially toxic 

 ingestion, symptomatic patients, and those with 

 suspected methanol intoxication with an anion gap 

 metabolic acidosis or an osmolal gap greater than 10 

 mOsm should be treated with ADH inhibition. Folate 

 should also be intravenously administered to patients 

 requiring ADH inhibition. In patients who receive ADH 

 inhibition who have a significant methanol 

 concentration, consider hemodialysis since the apparent 

 half-life of methanol under these circumstances is 

 quite prolonged. 

 B) MANAGEMENT OF SEVERE TOXICITY 

 1) Patients presenting with severe acidosis, signs or 

 symptoms of visual changes, or depressed level of 

 consciousness should be started immediately on an ADH 

 inhibitor and intravenous folate. Hemodialysis should 

 be initiated and should be continued until the methanol 

 concentration is undetectable and the serum pH is 

 normal. Treat seizures with benzodiazepines. 

 C) DECONTAMINATION 

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 1) PREHOSPITAL: There is no role for prehospital 

 decontamination. 

 2) HOSPITAL: In general, gastrointestinal decontamination 

 is not very useful because methanol is rapidly absorbed 

 and binds poorly to activated charcoal. Insertion of a 

 nasogastric tube to aspirate gastric contents may be 

 useful in rare patients who present shortly after large 

 ingestions. 

 D) AIRWAY MANAGEMENT 

 1) Endotracheal intubation may be necessary in patients 

 with significant CNS or respiratory depression. Extreme 

 care must be taken to increase minute ventilation 

 sufficiently to prevent severe acidemia in intubated 

 patients. 

 E) ANTIDOTE 

 1) Treat patients with either ethanol or fomepizole 

 (4-methylpyrazole) to prevent the production of 

 formate. Indications include documented plasma methanol 

 concentration greater than 20 mg/dL (greater than 200 

 mg/L) OR documented recent history of ingesting toxic 

 amounts of methanol and osmolal gap greater than 10 

 mOsm/L OR history or strong clinical suspicion of 

 methanol poisoning with at least 2 of the following 

 criterion: arterial pH less than 7.3; serum bicarbonate 

 less than 20 mEq/L; osmolol gap greater than 10 mOsm/L. 

 a) ETHANOL VS FOMEPIZOLE: Fomepizole is easier to use 

 clinically, requires less monitoring, does not cause 

 CNS depression or hypoglycemia, and may obviate the 

 need for dialysis in some patients. Ethanol requires 

 continuous administration and frequent monitoring of 

 serum ethanol and glucose levels and may cause CNS 

 depression and hypoglycemia (especially in children). 

 The drug cost associated with ethanol use is generally 

 much lower than with fomepizole; however, other costs 

 associated with ethanol use (eg, continuous 

 intravenous infusion, hourly blood draws, nursing 

 costs, and ethanol levels, possibly greater use of 

 hemodialysis) may make the costs more comparable. 

 b) ETHANOL: Ethanol is given to maintain a serum ethanol 

 concentration of 100 to 150 mg/dL. This can be 

 accomplished by using a 5% or 10% ethanol solution 

 administered intravenously through a central line. 

 Intravenous therapy dosing, which is preferred, is 0.8 

 g/kg as a loading dose (8 mL/kg of 10% ethanol) 

 administered over 20 to 60 minutes as tolerated, 

 followed by an infusion rate of 80 to 150 mg/kg/hr 

 (for 10% ethanol, 0.8 to 1.3 mL/kg/hr for a 

 nondrinker; 1.5 mL/kg/hr for a chronic alcoholic). 

 During hemodialysis, either add ethanol to the 

 dialysate to achieve 100 mg/dL concentration or 

 increase the rate of infusion during dialysis (10% 

 ethanol, 2.5 to 3.5 mL/kg/hr). Oral ethanol may be 

 used as a temporizing measure until intravenous 

 ethanol or fomepizole can be obtained, but it is more 

 difficult to achieve the desired stable ethanol 

 concentration. The loading dose is 0.8 g/kg (4 mL/kg) 

 of 20% {40 proof}) ethanol diluted in juice 

 administered orally or via nasogastric tube. 

 Maintenance dose is 80 to 150 mg/kg/hr (20% {40 

 proof}) ethanol; 0.4 to 0.7 mL/kg/hr for a nondrinker; 

 0.8 mL/kg/hr for a chronic alcoholic). Concentrations 

 greater than 30% (60 proof) ethanol should be diluted. 

 For both modalities, blood ethanol levels must be 

 monitored hourly and adjusted accordingly, and both 

 require patient monitoring in an ICU setting. 

 c) FOMEPIZOLE: Fomepizole is administered as a 15 mg/kg 

 loading dose, followed by 4 bolus doses of 10 mg/kg 

 every 12 hours. If therapy is needed beyond this 

 48-hour period, the dose is then increased to 15 mg/kg 

 every 12 hours for as long as necessary. Fomepizole is 

 also effectively removed by hemodialysis; therefore, 

 doses should be repeated following each round of 

 hemodialysis. 

 d) FOLATE: Folate increases clearance of formate. 

 Administer 50 mg every 4 hours to any patient 

 requiring ADH inhibition. 

 F) ENHANCED ELIMINATION 

 1) Methanol and its metabolites (formaldehyde and formic 

 acid) are readily removed by hemodialysis. Emergent 

 hemodialysis is indicated in any methanol-intoxicated 

 patient with an anion gap metabolic acidosis (pH less 

 than 7.3), visual disturbances, or CNS depression. 

 Because methanol is cleared very slowly once ADH 

 inhibitors are administered, hemodialysis should also 

 be considered in patients with methanol concentrations 

 greater than 50 mEq/L, even in the absence of acidosis 

 or severe symptoms. 

 G) PATIENT DISPOSITION 

 1) OBSERVATION CRITERIA: Intentional ingestions should be 

 evaluated in a health care facility. Potential serum 

 levels can be calculated using methanol percentage, 

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 amount ingested, and patient weight and all levels 

 potentially greater than 25 mg/dL should be evaluated 

 in a health care facility. 

 2) ADMISSION CRITERIA: Patients who are acidotic, have 

 visual symptoms, or have serum methanol concentrations 

 above 25 mg/dL should be admitted. 

 3) CONSULT CRITERIA: Consult a poison center or medical 

 toxicologist in cases of severe poisonings, in cases 

 where a methanol level is not readily available, or in 

 cases where the ingestion is uncertain. Consult a 

 nephrologist for any patient who may require 

 hemodialysis. 

 H) PITFALLS 

 1) Depending on the timing of the presentation, an 

 increased osmolar gap or an increased anion gap may not 

 always be present. An increased anion gap will not be 

 present in patients presenting early, and an increased 

 osmol gap may not be present in patients presenting 

 late. When calculating osmolarity, the ethanol level 

 needs to be taken into account in the calculation. A 

 normal osmolal gap does not rule out the possibility of 

 methanol intoxication. Patients who are ethanol 

 intoxicated will have a later presentation of their 

 acidosis, as the ethanol is effectively blocking the 

 metabolism of the methanol. 

 I) PHARMACOKINETICS 

 1) Methanol is rapidly and readily absorbed. The apparent 

 half-life of methanol is approximately 8 to 28 hours. 

 The volume of distribution is approximately 0.6 L/kg. 

 It is not protein bound. 

 J) TOXICOKINETICS 

 1) When alcohol dehydrogenase inhibitors are being used, 

 the apparent half-life is increased to approximately 50 

 hours. 

 K) DIFFERENTIAL DIAGNOSIS 

 1) Exposure to other alcohols, such as ethanol, ethylene 

 glycol, isopropyl alcohol, and other glycol ethers. A 

 broad variety of other toxins and medical causes can 

 also result in a metabolic acidosis. 

 0.4.3 INHALATION EXPOSURE 

 A) Intentional inhalational exposures can result in 

 significant methanol levels and should be treated 

 similarly to oral ingestions. 

 B) INHALATION: Move patient to fresh air. Monitor for 

 respiratory distress. If cough or difficulty breathing 

 develops, evaluate for respiratory tract irritation, 

 bronchitis, or pneumonitis. Administer oxygen and assist 

 ventilation as required. Treat bronchospasm with inhaled 

 beta2 agonist and oral or parenteral corticosteroids. 

 0.4.4 EYE EXPOSURE 

 A) DECONTAMINATION: Irrigate exposed eyes with copious 

 amounts of room temperature water for at least 15 

 minutes. If irritation, pain, swelling, lacrimation, or 

 photophobia persist, the patient should be seen in a 

 health care facility. 

 0.4.5 DERMAL EXPOSURE 

 A) OVERVIEW 

 1) Rarely has repeated dermal exposure resulted in severe 

 methanol toxicity. It should be treated similarly to an 

 ingestion exposure. 

 2) DECONTAMINATION: Remove contaminated clothing and wash 

 exposed area thoroughly with soap and water. A 

 physician may need to examine the area if irritation or 

 pain persists. 

RANGE OF TOXICITY: 

 A) TOXICITY: Most experts agree that a methanol 

 concentration of 25 mg/dL is the threshold for treatment. 

 An ingestion of 0.25 mL/kg of 100% methanol would 

 theoretically (assuming 100% absorption) result in a 

 toxic methanol concentration. 

ANTIDOTE AND EMERGENCY TREATMENT: 

 The drug 4-methylpyrazole (4-MP; fomepizole) is a competitive ADH 

 inhibitor and an effective antidote for methanol and ethylene glycol 

 poisoning. The concentration at which 4-MP inhibits 50% of ADH is 0.1 

 umol/L. The drug is used iv and orally and is eliminated by 

 Michaelis-Menten kinetics. [Sullivan, J.B., Krieger G.R. (eds). Clinical 

 Environmental Health and Toxic Exposures. Second edition. Lippincott 

 Williams and Wilkins, Philadelphia, Pennsylvania 1999., p. 1179] **PEER 

 REVIEWED** 

 Although clinical data are limited, folate or folinic acid (leucovorin, 

 citrovorum factor) commonly is given during the first 24 hours and is 

 believed to hasten formate metabolism to carbon dioxide and water. 

 [Sullivan, J.B., Krieger G.R. (eds). Clinical Environmental Health and 

 Toxic Exposures. Second edition. Lippincott Williams and Wilkins, 

 Philadelphia, Pennsylvania 1999., p. 1179] **PEER REVIEWED** 

 Sodium bicarbonate has two important roles in treating toxic alcohol 

 ingestions. As an immediate temporizing measure, administration of sodium 

 bicarbonate may reverse the life-threatening acidemia associated with 

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 methanol... ingestions. ...The second role for bicarbonate in the 

 treatment of toxic alcohol poisoning involves its ability to favorably 

 alter the distribution and elimination of certain toxic metabolites. In 

 cases of methanol poisoning, the proportion of ionized formic acid can be 

 increased by administering bicarbonate, thereby trapping formate in the 

 blood compartment. Consequently, decreased visual toxicity may result from 

 the removal of the toxic metabolites for the optic nerve. ...Further 

 investigation is required to delineate the beneficial effects of sodium 

 bicarbonate in the treatment of toxic alcohol ingestions. [Goldfrank, L.R. 

 (ed). Goldfrank's Toxicologic Emergencies. 7th Edition McGraw-Hill New 

 York, New York 2002., p. 523] **PEER REVIEWED** 

 ...Fomepizole, administered early in ethylene glycol (EG) intoxication, 

 prevents renal injury. In the absence of renal failure, EG clearance is 

 rapid, avoiding the need for prolonged fomepizole administration. The long 

 elimination half-life of methanol poisonings, with absent hemodialysis, 

 necessitates prolonged administration of fomepizole. ... However, 

 EG-poisoned patients treated with fomepizole prior to the onset of 

 significant acidosis may not require hemodialysis. Indeed, fomepizole may 

 also obviate the need for hemodialysis in selected methanol-poisoned 

 patients, in the absence of neurological and ocular impairment or severe 

 acidosis. ... [Megarbane B et al; Intensive Care Med 31 (2): 189-95 

 (2004)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15627163&query_hl=52" 

 target=new>PubMed Abstract 

 Basic treatment: Establish a patent airway. Suction if necessary. Watch 

 for signs of respiratory insufficiency and assist ventilations if 

 necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. 

 Monitor for shock and treat if necessary ... . Anticipate seizures and 

 minimize all external stimuli. Treat seizures if necessary ... . For eye 

 contamination, flush eyes immediately with water. Irrigate each eye 

 continuously with normal saline during transport ... . Do not use emetics. 

 For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water 

 for dilution if the patient can swallow, has a strong gag reflex, and does 

 not drool. Administer activated charcoal ... . /Methyl Alcohol and Related 

 Compounds/ [Bronstein, A.C., P.L. Currance; Emergency Care for Hazardous 

 Materials Exposure. 2nd ed. St. Louis, MO. Mosby Lifeline. 1994., p. 

 203-4] **PEER REVIEWED** 

 Advanced treatment: Consider orotracheal or nasotracheal intubation for 

 airway control in the patient who is unconscious or in respiratory arrest. 

 Start an IV with lactated Ringer's to support vital signs. Watch for signs 

 of fluid overload. Treat seizures with diazepam ... . For hypotension with 

 signs of hypovolemia, administer fluid cautiously. Watch for signs of 

 fluid overload ... . Hyperventilation may be beneficial for treating 

 acidosis. Use proparacaine hydrochloride to assist eye irrigation ... . 

 /Methyl Alcohol and Related Compounds/ [Bronstein, A.C., P.L. Currance; 

 Emergency Care for Hazardous Materials Exposure. 2nd ed. St. Louis, MO. 

 Mosby Lifeline. 1994., p. 204] **PEER REVIEWED** 

 Emergency and supportive measures. 1. Maintain ann open airway and assist 

 ventilation if necessary. 2. Treat coma and seizures if they occur. 3. 

 Treat metabolic acidosis with iv sodium bicarbonate. Correction of 

 acidosis should be guided by arterial blood gases. [Olson, K.R. (Ed.); 

 Poisoning & Drug Overdose. 4th ed. Lange Medical Books/McGraw-Hill. 

 New York, N.Y. 2004., p. 261] **PEER REVIEWED** 

 Specific drugs and antidotes. 1. Administer fomepizole or ethanol to 

 saturate the enzyme alcohol dehydrogenase and prevent the formation of 

 methanol's toxic metabolites. Therapy is indicated in patients with the 

 following: a. A history of significant methanol ingestion, when methanol 

 serum levels are not immediately available and the osmolar gap is > 10 

 mOsm/L. b. Metabolic acidosis and an osmolar gap > 10 mOsm/L not 

 accounted for by ethanol. c. A methanol blood concentration > 20 mg/dL. 

 2. Folic or folinic acid may enhance the conversion of formate to carbon 

 dioxide and water. [Olson, K.R. (Ed.); Poisoning & Drug Overdose. 4th 

 ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2004., p. 261] 

 **PEER REVIEWED** 

 Decontamination. 1. Prehospital. Do not induce vomiting or administer 

 charcoal. 2. Hospital. Aspirate gastric contents if this can be performed 

 within 30-60 min of ingestion. Activated charcoal is not likely to be 

 useful because the effective dose is very large and methanol is rapidly 

 absorbed from the GI tract. [Olson, K.R. (Ed.); Poisoning & Drug 

 Overdose. 4th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 

 2004., p. 261] **PEER REVIEWED** 

 Enhanced elimination. Hemodialysis rapidly removes both methanol 

 (half-life reduced to 3-6 hr) and formate. The indication for dialysis are 

 suspected methanol poisoning with significant metabolic acidosis, visual 

 abnormalities, an osmolar gap > 10 mOsm/L, or a measured serum methanol 

 concentration > 50 mg/dL. Dialysis should be continued until the 

 methanol concentration is < 20 mg/dL. [Olson, K.R. (Ed.); Poisoning 

 & Drug Overdose. 4th ed. Lange Medical Books/McGraw-Hill. New York, 

 N.Y. 2004., p. 261] **PEER REVIEWED** 

ANIMAL TOXICITY STUDIES: 

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TOXICITY SUMMARY: 

 Methanol occurs naturally in humans, animals and plants. It is a natural 

 constituent in blood, urine, saliva and expired air. ... The two most 

 important sources of background body burdens for methanol and formate are 

 diet and metabolic processes. Methanol is available in the diet 

 principally from fresh fruits and vegetables, fruit juices ... fermented 

 beverages ... and diet foods (principally soft drinks). The artificial 

 sweetner aspartame is widely used and, on hydrolysis, 10% (by weight) of 

 the molecule is converted to free methanol, which is available for 

 absorption. ... Exposures to methanol can occur in occupational settings 

 through inhalation or dermal contact. ... Methanol is readily absorbed by 

 inhalation, ingestion and dermal exposure, and it is rapidly distributed 

 to tissues according to the distribution of body water. A small amount of 

 methanol is excreted unchanged by the lungs and kidneys. ... Methanol is 

 metabolized primarily in the liver by sequential oxidative steps to 

 formaldehyde, formic acid and carbon dioxide. The initial step involves 

 oxidation to formaldehyde by hepatic alcohol dehydrogenase ... In step 2, 

 formaldehyde is oxidized by formaldehyde dehydrogenase to formic acid/or 

 formate depending on the pH. In step 3, formic acid is detoxified to 

 carbon dioxide by folate-dependent reactions. Elimination of methanol from 

 the blood via the urine and exhaled air and by metabolism appears to be 

 slow in all species, especially when compared to ethanol. ... It is the 

 rate of metabolic detoxification, or removal of formate that is vastly 

 different between rodents and primates and is the basis for the dramatic 

 differences in methanol toxicity observed between rodents and primates. 

 The acute and short term toxicity of methanol varies greatly between 

 different species, toxicity being highest in species with a relatively 

 poor ability to metabolize formate. In such cases of poor metabolism of 

 formate, fatal methanol poisoning occurs as a result of metabolic acidosis 

 and neuronal toxicity, whereas, in animals that readily metabolize 

 formate, consequences of CNS depression (coma, respiratory failure, etc.) 

 are usually the cause of death. Sensitive primate species (humans and 

 monkeys) develop increased blood formate concentrations following methanol 

 exposure, while resistant rodents, rabbits and dogs do not. Humans and 

 non-human primates are uniquely sensitive to the toxic effects of 

 methanol. Overall methanol has a low acute toxicity to non-primate 

 animals. ... In the rabbit, methanol is a moderate irritant to the eye. It 

 was not skin sensitizing ... There is no evidence from animal studies to 

 suggest that methanol is a carcinogen ... The inhalation of methanol by 

 pregnant rodents throughout the period of embryogenesis induces a wide 

 range of concentration-dependent teratogenic and embryolethal effects. 

 Treatment-related malformations, primarily extra or rudimentary cervical 

 ribs and urinary or cardiovascular defects, were found in fetuses of rats 

 ... Increased incidences of exencephaly and cleft palate were found in the 

 offspring of ... mice ... There was increased embryo/fetal death ... and 

 an increasing incidence of full litter resorptions. Reduced fetal weight 

 was observed ... Fetal malformations ... included neural and ocular 

 defects, cleft palate, hydronephrosis and limb anomalies. Humans (and 

 non-human primates) are uniquely sensitive to methanol poisoning and the 

 toxic effects in these species are characterized by formic acidemia, 

 metabolic acidosis, ocular toxicity, nervous system depression, blindness, 

 coma and death. Nearly all of the available information on methanol 

 toxicity in humans relates to the consequences of acute rather than 

 chronic exposures. A vast majority of poisonings involving methanol have 

 occurred from drinking adulterated beverages and from methanol-containing 

 products. Although ingestion dominates as the most frequent route of 

 poisoning, inhalation of high concentrations of methanol vapor and 

 percutaneous absorption of methanolic liquids are as effective as the oral 

 route in producing acute toxic effects. The most noted health consequences 

 of longer term exposure to lower levels of methanol is a broad range of 

 ocular effects. ... The toxicity is manifest if formate generation 

 continues at a rate that exceeds its rate of metabolism. ... The minimum 

 lethal dose of methanol in the absence of medical treatment is between 0.3 

 and 1 g/kg. The minimum dose causing permanent visual defects is unknown. 

 ... Wide interindividual variability of the toxic dose is a prominent 

 feature in acute methanol poisoning. Two important determinants of human 

 susceptibility to methanol toxicity appear to be (1) concurrent ingestion 

 of ethanol, which slows the entrance of methanol into the metabolic 

 pathway, and (2) hepatic folate status, which governs the rate of formate 

 detoxification. The symptoms and signs of methanol poisoning, which may 

 not appear until after an asymptomatic period ... include visual 

 disturbances, nausea, abdominal and muscle pain, dizziness, weakness and 

 disturbances of consciousness ranging from coma to clonic seizures. Visual 

 disturbances ... range from mild photophobia and misty or blurred vision 

 to markedly reduced visual acuity and complete blindness. In extreme cases 

 death results. The principal clinical feature is severe metabolic acidosis 

 of the anion-gap type. The acidosis is largely attributed to the formic 

 acid produced when methanol is metabolized. ... Visual disturbances of 

 several types (blurring, constriction of the visible field, changes in 

 color perception, and temporary or permanent blindness) have been reported 

 in workers ... No other adverse effects of methanol have been reported in 

 humans except minor skin and eye irritation. ... Methanol is of low 

 toxicity to aquatic organisms, and effects due to environmental exposure 

 to methanol are unlikely to be observed, except in the case of a spill. 

 [Environmental Health Criteria 196: Methanol pp. 1-9 (1997) by the 

 International Programme on Chemical Safety (IPCS) under the joint 

 sponsorship of the United Nations Environment Programme, the International 

 Labour Organisation and the World Health Organization.] **PEER REVIEWED** 

NON-HUMAN TOXICITY EXCERPTS: 

 /LABORATORY ANIMALS: Acute Exposure/ Under acute inhalation conditions, 

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 folate-deficient Long-Evans male rats exposed to 4000 mg/cu m (3000 ppm) 

 methanol for 20 hr/day did not survive more than 4 days. Rhesus monkeys 

 exposed to 4000 mg/cu m (3000 ppm) methanol for 21 hr/day survived the 

 20-day exposure period and rhesus monkeys exposed to 13,000 mg/cu m 

 (10,000 ppm) methanol for 21 hr/day survived for more than 4 days. [WHO; 

 Environ Health Criteria 196: Methanol p.10 (1997). Available from, as of 

 July 14, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ Oxygen free radicals are generated 

 during methanol-induced liver injury, as was shown for ethanol. The effect 

 of methanol intoxication (6 g/kg bw) on protein modification in the liver 

 of rats was investigated. Electron spin resonance determination indicated 

 an increase in the free radical signal 6 and 12 hr after intoxication. 

 After 7 days of treatment, the contents of malondialdehyde and carbonyl 

 groups in proteins were significantly increased. The level of amino groups 

 and sulphydryl groups and the amount of tryptophan in proteins were 

 decreased, whereas the amount of bi-tyrosine was increased significantly. 

 Changes in protein structure resulted both from free radical action and 

 formaldehyde generation during methanol intoxication. [Skrzydlewska E et 

 al; J Appl Toxicol 20 (3): 239-43 (2000)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10797478&query_hl=42" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Acute Exposure/ An approximate intraperitoneal 

 methanol LD50 of 3-4 g/kg for pigtail monkeys (Macaca nemestrina) was 

 reported... . Doses of 2 and 3 g/kg produced metabolic acidosis in the 

 animals, while monkeys given 4 g/kg became severely acidotic and exhibited 

 signs of toxicity that were remarkably similar to those reported in human 

 poisoning. These animals displayed a sharp decrease in blood pH (7.03) at 

 7.5-21 hr after methanol administration. Bicarbonate was the single blood 

 electrolyte observed to change during the course of methanol acidosis. 

 There was a latent period of 15-18 hr prior to the onset of overt signs of 

 toxicity, followed by a sequence of signs beginning with behavioral 

 distress, coma within 24-30 hr and death. This time-course parallels that 

 reported for humans suffering from methanol poisoning. [WHO; Environ 

 Health Criteria 196: Methanol p.78 (1997). Available from, as of July 18, 

 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ Methanol is irritating to the eye 

 and causes conjunctivitis, chemosis, iritis, and corneal opacity. Methanol 

 was reported to be a mild eye irritant. However, in another study, 

 undiluted methanol caused moderate corneal opacity in three of six rabbits 

 and conjunctival redness in all six rabbits. A 50% aqueous methanol 

 solution caused minimal to no effects, and a 25% aqueous solution caused 

 no effects. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology 

 Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 

 p.372] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ In a sensory irritation test, 

 methanol produced sensory irritation in mice at very high vapor 

 concentrations with a RD50 (concentration that decreases respiration rate 

 by 50%) of 25,300 ppm and 41,514. [Bingham, E.; Cohrssen, B.; Powell, 

 C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New 

 York, N.Y. (2001)., p. V6 p.372] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ Its consumption leads to atrophy of 

 the optic nerve, causing permanent blindness, and to depression of cardiac 

 and voluntary muscle, resulting in death. [Garner's Veterinary Toxicology. 

 3rd ed., rev. by E.G.C. Clarke and M.L. Clarke. Baltimore: Williams and 

 Wilkins, 1967., p. 285] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ Exposure of animals /to methanol in 

 air/ ... may induce ... increased rate of respiration ... nervous 

 depression followed by excitation, irritation of mucous membranes, ataxia, 

 partial paralysis, agony, prostration, CNS depression, convulsions, 

 decrease in rectal temperature, loss in weight and death. [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V6 p.372] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ The pathologic changes found in the 

 tissues of animals exposed by inhalation to methyl alcohol are quite 

 similar to those observed in animals following ingestion of this compound. 

 In the eyes of the dog ... hyperemia of the choroid and edema of the 

 ocular tissue with early signs of degeneration of the ganglionic cells of 

 the retina and nerve fibers /were found/ ... Vessels of the choroid of 

 poisoned animals were markedly congested, the entire retina was edematous, 

 and the ganglion cells were degenerated. ... Hemorrhage, edema, 

 congestion, and pneumonia were observed in the lung of the various species 

 that were exposed to vapors containing methyl alcohol. The livers and 

 kidneys showed congestion, albuminous and fatty degeneration and fatty 

 infiltration. Cardiac dilation and myocardial degeneration were observed 

 in the hearts of animals. Degenerative injuries of the central nervous 

 system have been described ... . [Clayton, G. D. and F. E. Clayton (eds.). 

 Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 

 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4531] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ Within 48 hr of administering a 

 single LD50 dose to rats, brain enzyme activities underwent changes, 

 glycogen levels increased, brain lactic acid levels increased 1 hr after 

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 administration, decreased 48 hr after. [Mikulich SG; Biol Akt Veshchestva 

 (Mikroelem, Vitam Drugie) Rastenievod Zhivotnovod Med 109-11 (1975)] 

 **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ After methanol administration, Macaca 

 mulatta showed optic edema, acidosis, and formate accumulation in blood. 

 [Martin-Amat et al; Toxicol Appl Pharmacol 45 (1): 201-8 (1978)] **PEER 

 REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=99844" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Acute Exposure/ The effects of alcohol on audition 

 were studied in the rat by examining the modification of acoustic startle 

 reflexes by pure tone pulses and by gaps in white noise. Groups of rats 

 received four injections of 0.0, 0.25, 1, and 2 g/kg of either methyl or 

 ethyl alcohol in increasing order at 1 hr intervals. One-half hour after 

 the administration of each dose, loudness perception or temporal acuity 

 was measured. Blood alcohol levels (mM) for the two alcohols obtained in 

 control animals were equivalent following the final dose. Both alcohols 

 produced a dose dependent reduction in baseline startle amplitude that was 

 greater during exposure to ethanol than methanol. Loudness functions 

 associated with pulse intensity were not diminished by the alcohols, 

 however inhibition produced by a gap in noise was reduced following the 

 highest dose of either alcohol. These data are consistent with behavioral 

 study results that have suggested that alcohol does not affect loudness 

 perception, and with electrophysical experiment results which indicate 

 that alcohol disrupts temporal relationships along the primary auditory 

 pathway. [Wecker JR, Ison JR; Toxicol Appl Pharm 74 (2): 258-66 (1984)] 

 **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ The results of the skin absorption 

 experiments were described by stating that all animals subjected to the 

 action of any amount of methyl alcohol by skin absorption had died. The 

 lowest lethal dose was 0.5 mL/kg for one monkey. It was reported that 

 rabbits were far less susceptible to methyl alcohol poisoning by this 

 route than monkeys and rats. In a study of the effects of continuous 

 administration of methyl alcohol, a known amount was dropped onto or 

 injected into the gauze pads 4 times/day. All such treated monkeys 

 displayed dilated pupils within 2 hr after one such administration of 1.3 

 mg/kg of methyl alcohol. The minimum lethal dose was a total of 4 

 administrations of 0.5 mL/kg methyl alcohol in one day, and it was 

 concluded that sufficient methyl alcohol could be absorbed through the 

 skin to cause death and that the threshold for immediate danger in monkeys 

 was below the minimum lethal dose. [McCord CP; Ind Eng Chem 23: 931-6 

 (1931) as cited in NIOSH; Criteria Document: Methyl Alcohol p.59-60 (1976) 

 DHEW Pub. NIOSH 76-148] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ Methanol administered by gavage or 

 intraperitoneally induced hypothermia in Fischer and Long-Evans rats, eg, 

 brain temperature decreased 1.5 deg C within 35 min and colonic 

 temperature was significantly lower. This occurred at dose levels of 2-3 

 g/kg, which is about 20% of the reported LD50 value of 10 g/kg in rats. 

 [WHO; Environ Health Criteria 196: Methanol p.74 (1997). Available from, 

 as of July 14, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] 

 **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ Female minipigs (Minipig YU, Charles 

 River) treated with a single oral dose of methanol at 1, 2.5 and 5.0 g/kg 

 body weight by gavage showed dose-dependent signs of acute methanol 

 intoxication, including mild CNS depression, tremors, ataxia and 

 recumbency, which developed within 0.5-2.0 hr and resolved by 52 hr. 

 Methanol- and formate-dosed minipigs did not develop optic nerve lesions, 

 toxicologically significant formate accumulation or metabolic acidosis. 

 [WHO; Environ Health Criteria 196: Methanol p.10 (1997). Available from, 

 as of July 14, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] 

 **PEER REVIEWED** 

 /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Rats received 3.25 

 mL methanol/kg bw for 6 months. The treatment caused a decline in the 

 heart contraction rate and in skin temperature by the end of the 

 experiment. Myocardial hypoxia developed. [Sheftel, V.O.; Indirect Food 

 Additives and Polymers. Migration and Toxicology. Lewis Publishers, Boca 

 Raton, FL. 2000., p. 751] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Mice exposed to 

 air containing 48,000 ppm for 3.5-4 hr daily up to cumulative total of 24 

 hr were in state of CNS depression, but survived, whereas they succumbed 

 in coma when correspondingly exposed for 54 hr to air containing 54,000 

 ppm. [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene 

 and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John 

 Wiley Sons, 1981-1982., p. 4533] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ In an oral study, 

 Sprague-Dawley rats were dosed by oral gavage with 0, 100, 500, or 2500 

 mg/kg of methanol for 90 days. There were no differences between dosed 

 animals and controls in body weight gain and food consumption. Brain 

 weights were decreased in both sexes in the 2500 mg/kg dose group. 

 Elevated serum glutamic pyruvate transaminase and alkaline phosphatase 

 were noted in the 2500 mg/kg dose group, but there were no adverse 

 treatment related effects in the gross pathology and histopathological 

 evaluation. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology 

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 Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 

 p.374] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Cynomolgus 

 monkeys or Sprague-Dawley rats were exposed by inhalation to 0, 500, 2000, 

 or 5000 ppm of methanol 6 hr/day, 5 day/week for 4 weeks. No 

 treatment-related effects in the nasal turbinates, trachea, lungs, 

 esophagus, liver, eye, or optic nerve were observed. Increased discharges 

 around the eyes and nose were observed and were attributed to upper 

 respiratory tract irritation. Groups of four male rats were exposed by 

 inhalation to 0, 200, 2000, or 10,000 ppm of methanol 6 hr/day, 5 

 days/week for 1, 2, 4, or 6 weeks. Evaluation of a number of parameters 

 including lung weights, surfactant levels, and enzyme activities did not 

 reveal any adverse effects in the lung. No histopathological examinations 

 were performed. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.373] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Rats exposed to 

 ...0.022 mg methanol/L of air 4 hr/day for 6 months and simultaneously 

 administered 0.7 mg methanol/kg daily by gavage exhibited changes in blood 

 morphology, oxidation-reduction processes and liver function. [WHO; 

 Environ Health Criteria 196: Methanol p.79 (1997). Available from, as of 

 July 18, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

 /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ When ... repeated 

 doses of 3 to 6 g/kg /were administered/ by gavage to rhesus monkeys 

 (Macaca mulata) for 3-20 weeks, average serum levels of methanol of 4750 

 mg/L were attained within a few hours. Animals were killed at the end of 

 treatment and livers examined histologically. Hepatocytes showed nucleolar 

 segregation (zoning of nucleus), hyperplasia of endoplasmic reticulum and 

 swelling of mitochondria. These changes were also found in one monkey 

 sacrificed 12 weeks after the end of treatment. [WHO; Environ Health 

 Criteria 196: Methanol p.93 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ It is unlikely 

 that methanol is carcinogenic to mouse skin. In an experiment using four 

 strains of female mice (Balb/c, Sencar, CD-1 and Swiss) to study 

 N-nitrosomethylurea carcinogenesis, methanol was used as a solvent 

 control. Four groups of 20 mice of each strain received 25 uL methanol 

 twice weekly for 50 weeks followed by observation for lifespan. Only one 

 skin tumor was observed among the 80 control animals. [WHO; Environ Health 

 Criteria 196: Methanol p.74 (1997). Available from, as of July 14, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Rats and mice 

 were exposed to 0, 10, 100, or 1000 ppm of methanol 20 hr/day for 18 

 months (mice) or 24 months (rats). There was no evidence of 

 carcinogenicity at 1000 ppm. Lung papillary adenomas and adrenal 

 pheochromocytomas were observed and reported as "biologically 

 insignificant." [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.378] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Groups of eight 

 monkeys were exposed to 0, 10, 100, or 1000 ppm of methanol 22 hr/day for 

 up to 2.5 years. Slight changes in the liver and kidney at 1000 ppm and 

 some pathological changes in the nervous system of all animals at 1000 ppm 

 were observed but were considered transient in nature and probably 

 reversible. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology 

 Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 

 p.378] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ 

 ...Developmental neurotoxicity of pregnant Long-Evans rats and their 

 newborn offspring exposed to 5900 mg/cu m (4500 ppm) of methanol by 

 inhalation for 6 hr daily /was studied/, beginning on gestation day 6, 

 with both dams and pups then being exposed through postnatal day 21. 

 Although findings suggested significant functional consequences in rats 

 resulting from this exposure, these consequences were considered subtle in 

 character. Exposure to 5900 mg methanol/cu m did not affect the suckling 

 time and conditioned olfactory aversion test of newborn rats. Methanol 

 exposed newborn pups were less active on postnatal day 18 and more active 

 on postnatal day 25 than control newborn pups (motor activity test). The 

 study found only isolated positive results that were small and variable. 

 The two adult assays, the fixed-ratio wheel-running test and the 

 stochastic discrimination test, yielded evidence of a significant methanol 

 effect. No evidence of brain damage emerged on the basis of 

 neuropathology, although differences in neural cell adhesion molecules 

 (NCAMs) arising from methanol exposure were observed in neonatal 

 cerebella. Methanol treatment caused a decrease in expression in both NCAM 

 140 and NCAM 180. [WHO; Environ Health Criteria 196: Methanol p.87 (1997). 

 Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ There have 

 been conflicting reports on the effect of methanol on testicular hormones 

 in rats. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology 

 Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 

Iris Camacho, 6308MM Page 20 of 69

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 p.378] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ In 

 Long-Evans rats dosed by oral gavage with 0, 0.8, or 1.6 g/kg of methanol 

 for 21 days, serum testosterone levels were unaffected, but serum /lactate 

 dehydrogenase/ was increased. Testis weights were decreased as were the 

 number of morphologically normal caput and cauda epididymal sperm. 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.378] **PEER 

 REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Transient 

 neurological signs and reduced body weights were found in up to 20% of 

 CD-1 dams exposed to 19,500 mg/cu m (15,000 ppm) methanol 6 hr/day 

 throughout organogenesis (gestational days 6-15). Near-term fetuses 

 revealed embryotoxicity (increased resorptions, reduced fetal weights 

 and/or fetal malformations) at 13,000 and 19,500 mg/cu m (10,000 and 

 15,000 ppm) methanol while 3-day exposures at 6500 mg/cu m (5000 ppm) for 

 6 hr/day yielded no observable adverse effects. In the studies..., terata 

 included neural and ocular defects, cleft palate, hydronephrosis, deformed 

 tails and limb (paw and digit) anomalies. Neural tube defects and ocular 

 lesions occurred after methanol inhalation by pregnant CD-1 mice between 

 gestational days 7 and 9, while limb anomalies were induced only during 

 gestational days 9-11; cleft palate and hydronephrosis were observed after 

 exposure during either period. The spectrum of teratogenic effects 

 depended upon both the stage of embryonic development and the number of 

 methanol exposures. [WHO; Environ Health Criteria 196: Methanol p.85 

 (1997). Available from, as of July 14, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Methanol was 

 shown to impair uterine decidualization during early pregnancy in Holtzman 

 rats administered 1.6, 2.4 or 3.2 g methanol/kg/day by gavage during days 

 1-8. Reductions in pregnant uterine and implantation site weights seen on 

 day 9 were the result of methanol impedance of normal uterine 

 decidualization as demonstrated by effects on decidual cell response 

 technique. Methanol (3.2 g/kg/day) produced a non-specific maternal 

 toxicity (reduction in body weight) by day 9, but no effect on days 11 or 

 20 on embryo and fetal survival or development were found. [WHO; Environ 

 Health Criteria 196: Methanol p.86 (1997). Available from, as of July 18, 

 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ No effects on 

 reproductive performance were reported in a two-generation reproductive 

 study in F-344 rats administered 13, 130 or 1300 mg/cu m (10, 100 or 1000 

 ppm) methanol by inhalation for 18-20 hr/day. A statistically significant 

 decrease in brain weight was found at the 1300 mg/cu m level in 3-, 6- and 

 8-week-old pups of the F1 generation. In the F2 generation reduced brain 

 thymus and hypophysis weight was observed. [WHO; Environ Health Criteria 

 196: Methanol p.86 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Depending on 

 the concentration and duration of methanol exposure (0-20 mg/mL for 6 hr, 

 12 hr, or 1 or 4 days) on embryonic CD-1 mouse palate in serum-free organ 

 culture, the medial epithelium either degenerated completely or remained 

 intact in unfused palates (either condition would interfere with fusion). 

 Cellular proliferation appeared to be a specific and sensitive target for 

 methanol as craniofacial tissues responded to methanol with reduction in 

 DNA content at an exposure that did not affect total protein. However both 

 DNA and protein levels decreased with increasing exposure to methanol. 

 Methanol selectively altered the morphological fate of the medial palatal 

 epithelium cells and the specific effect on cell survival was exposure 

 dependent. [WHO; Environ Health Criteria 196: Methanol p.89 (1997). 

 Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Ethanol and 

 methanol were compared with respect to their teratogenic activity on the 

 brain /in C57BL mice/. /Mice were given doses of 1.7 or 2.45 g/kg bw by 2 

 ip injections 4 hours apart on gestational day 7 up to day 17./ ...1.7 

 g/kg methanol induced 30% resorptions and midfacial deficiencies and 

 micro-anophthalmia in over 50% of live fetuses. 2.45 g/kg resulted in 55% 

 resorptions and 100% of live fetuses having malformations of the 

 holoprosencephaly spectrum (micro/anophthalmia, cebocephaly, absence of 

 forebrain, premaxillary agenesis). [European Chemicals Bureau; IUCLID 

 Dataset, Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of 

 July 19, 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The present 

 study was designed to characterize maternal reproductive performance and 

 early offspring effects following exposure to methanol (MeOH) vapor in a 

 nonhuman primate model. The two-cohort study design used 48 adult female 

 Macaca fascicularis (24/cohort) monkeys exposed to 0, 200, 600, or 1800 

 ppm MeOH vapor for approximately 2.5 hr/day, 7 days/week prior to breeding 

 and throughout pregnancy. Maternal body weight measurement, clinical 

 observations and health assessments were conducted routinely throughout 

 the study. Menstrual cyclicity was monitored during the pre-breeding and 

 breeding periods and timed matings were conducted with nonexposed males. 

 Females were monitored closely during the last month of pregnancy. At 

Iris Camacho, 6308MM Page 21 of 69

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 birth, infant physical characteristics were measured and a newborn health 

 assessment was conducted. Methanol exposure did not alter menstrual 

 cycles, the number of breedings to conception or conception rate. A total 

 of 34 live-born infants were delivered (control=8, 200 ppm=9, 600 ppm=8, 

 1800 ppm=9). One female each in the control and 600-ppm group delivered a 

 stillborn infant and a cesarean section (C-section) was required to 

 deliver a hydrocephalic infant who died in utero in the maternal 1800-ppm 

 group. Although not statistically significant, five MeOH-exposed females 

 were C-sectioned due to pregnancy complications such as uterine bleeding 

 and prolonged unproductive labor. These complications were not observed in 

 the control group. The mean length of pregnancy in the MeOH-exposed groups 

 was significantly decreased by 6 to 8 days when compared to controls. 

 There were no MeOH-related effects on offspring birthweight or newborn 

 health status. The consistent reduction in length of pregnancy observed in 

 the MeOH females may reflect a treatment effect on the fetal 

 neuroendocrine system. Given that the fetal 

 hypothalamic--pituitary-adrenal axis controls pregnancy length in most 

 species, these results suggest a modest but significant effect of MeOH on 

 the biochemical events that control the timing of birth. [Burbacher TM et 

 al; Neurotoxicol Teratol 26 (5): 639-50 (2004)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15315813&query_hl=6" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Methanol 

 causes axial skeleton and craniofacial defects in both CD-1 and C57BL/6J 

 mice during gastrulation, but C57BL/6J embryos are more severely affected. 

 We evaluated methanol-induced pathogenesis in CD-1 and C57BL/6J embryos 

 exposed during gastrulation in whole embryo culture. Conceptuses with 5-7 

 somites were exposed to 0, 1, 2, 3, 4, or 6 mg methanol/mL culture medium 

 for 24 hr and embryonic morphology was assessed. Cell death was evaluated 

 by histology and LysoTracker red staining, and cell-cycle distribution was 

 evaluated by flow cytometry. In C57BL/6J embryos, craniofacial defects 

 were observed at 3 mg methanol/mL and greater. The response for CD-1 

 embryos was different, with increased dysmorphology only at 6 mg/mL. 

 However, protein content in CD-1 embryos was reduced at 3 mg methanol/mL 

 and above, indicating growth retardation. Yolk sac toxicity occurred only 

 at 6 mg methanol/mL in both strains. Methanol caused only small changes in 

 cell-cycle distribution, while cell death was induced at 4 and 6 mg 

 methanol/mL in both strains after 8 hr. The extent of cell death after 8 

 hr was greater in C57BL/6J embryos, and increased over time through 18 hr; 

 in contrast, CD-1 embryos showed less cell death at 18 than at 8 hr, 

 suggesting recovery. [Degitz SJ et al; Birth Defects Res A Clin Mol 

 Teratol 70 (4): 179-84 (2004)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15108244&query_hl=14" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Mouse embryos 

 are more sensitive than rat embryos in response to methanol (CH(3)OH) and 

 its ability to elicit developmental abnormalities. Intrinsic differences 

 in the metabolism of CH(3)OH to formaldehyde (HCHO) and formic acid 

 (HCOOH) by the enzymes alcohol dehydrogenase (ADH1), formaldehyde 

 dehydrogenase (ADH3), and catalase may contribute to the observed species 

 sensitivity. Specific activities for enzymes involved in CH(3)OH 

 metabolism were determined in rat and mouse conceptuses during the 

 organogenesis period of 8-25 somites. Spatial activity relationships were 

 also compared separately in heads, hearts, trunks, and the visceral yolk 

 sac (VYS) from early (7-12 somites) and late (20-22 somites) 

 organogenesis-stage rat and mouse embryos. Catalase activities were 

 similar between rat and mouse conceptuses. In the mouse heart, catalase 

 activities were consistently lower when compared to other tissues. 

 Specific activities for catalase were consistently highest in the VYS of 

 both species when compared to other tissues of the embryo. These 

 activities were highly significant in the 6-12 somite VYS. ADH1 activities 

 were significantly higher in embryos when compared to VYS in both species, 

 except for a 27% lower activity in the early 8-10 somite mouse embryo. 

 Mouse ADH1 activities in the VYS were significantly lower throughout the 

 organogenesis period when compared to the rat VYS or embryos of either 

 species. Mouse activities were lower overall in specific tissues of the 

 embryo but maintained the same relative proportions as in the rat. ADH3 

 activities in the rat VYS were significantly higher by 20% than those in 

 the mouse. Mouse embryo ADH3 activities were slow to mature, starting at a 

 level 42% below rat, and failed to reach optimal levels until the 

 14-16-somite stage. Heart ADH3 activities were also significantly lower in 

 the mouse embryo at the 7-12-somite stage. Both species have lower ADH3 

 activities in the early heart, relative to other embryonic tissues. These 

 results show a more slowly maturing capacity of the mouse embryo to remove 

 HCHO, which provides a rationale for increased sensitivity of this species 

 to CH(3)OH-induced embryotoxicity and teratogenicity. [Harris C et al; 

 Reprod Toxicol 17 (3): 349-57 (2003)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12759105&query_hl=22" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The 

 teratogenic effects of methanol were determined in rats. Pregnant 

 Long-Evans-rats were gavaged on gestation day ten with a methanol dose of 

 0 to 5.2 mL/kg bw. The rats were pretreated with equal volumes of 

 mineral-oil in order to prevent local gastric irritation. The rats were 

 observed for signs of acute toxicity. Body weight was determined from 

 gestation days zero to 20. On gestation day 20, the rats were sacrificed. 

 Upon necropsy, both gross and microscopic histopathological changes were 

 investigated. The fetuses were also examined for physical abnormalities. 

Iris Camacho, 6308MM Page 22 of 69

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 Compared to the controls, food intake and body weight gain were 

 significantly reduced in maternal rats treated with 5.2 mL/kg of methanol. 

 No other indications of maternal toxicity were observed in any of the 

 exposure groups. Among the groups, there were no significant differences 

 in the number of postimplantation deaths or in the total loss per litter. 

 Relative to controls, exposed male fetuses exhibited significantly 

 decreased body weight. Among the exposed fetuses, undescended testes, eye 

 defects, wavy thoracic cage, polycystic kidney, and missing appendages 

 were noted. The number of total anomalies increased in a dose dependent 

 manner following exposure to methanol. The number of eye defects and 

 undescended testes each displayed a dose dependent relationship with 

 methanol exposure. The methanol treated fetuses had a significantly 

 increased frequency of hemorrhage in the nose and other areas, compared to 

 controls. When corrected for body weight, the biparietal diameter of the 

 fetal cranium was significantly increased in the methanol treated fetuses, 

 compared to controls. [Youssef AF et al; Repro Toxicol 11 (4): 503-10 

 (1997)] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Mature male 

 rats were examined for alterations in circulating free testosterone, 

 luteinizing hormone and follicle stimulating hormone after inhalation of 

 methanol vapor in a dynamic system for up to six weeks at doses ranging 

 from 200 to 10,000 ppm. The most extensive effects were noticed after 

 exposure to 200 ppm of methanol for 6 weeks, with serum testosterone 

 concentration being 32% of the controls. A significant change in 

 luteinizing hormone concentration after exposure to 10,000 ppm of methanol 

 for six wk was also demonstrated while follicle stimulating and the 

 elimination rate of testosterone from the blood (which indicates effects 

 on the testicular synthesis of testosterone) remained unchanged throughout 

 the experiments. [Cameron AM et al; Arch Toxicol 7: 441-3 (1984)] **PEER 

 REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Methanol was 

 administered via inhalation to groups of pregnant rats at 10000 ppm, 5000 

 ppm, or 0 ppm (control) for 7 hr/day on days 1 to 19 of gestation. Another 

 group of rats was exposed similarly at 20000 ppm on days 7 to 15. The rats 

 exposed at 20000 ppm exhibited slight maternal toxicity (a slightly 

 unsteady gait), and a high incidence of congenital malformations (p < 

 0.001) (predominately extra or rudimentary cervical ribs), and urinary or 

 cardiovascular effects were observed in fetuses taken from rats sacrificed 

 on day 20. Similar malformations were seen in the 10000 ppm group; 

 however, the incidence was not significantly different from the controls. 

 No adverse effects were noted in the 5000 ppm group [American Conference 

 of Governmental Industrial Hygienists. Documentation of Threshold Limit 

 Values for Chemical Substances and Physical Agents and Biological 

 Exposure Indices for 2001. Cincinnati, OH. 2001., p. 2] **PEER REVIEWED** 

 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Methanol 

 administered to C57BL/6J mice during gastrulation causes severe 

 craniofacial dysmorphology. ...Dysmorphogenesis, cell death, cell cycle 

 assessment, and effects on development of cranial ganglia and nerves 

 observed following administration of methanol to pregnant C57BL/6J mice on 

 gestation day (GD) 7 /are described/. Mice were injected (ip) on GD 7 with 

 0, 2.3, 3.4, or 4.9 g/kg methanol, split into two doses. In embryos of 

 mice treated with 0 or 4.9 g/kg methanol, we used histology and 

 LysoTracker red staining on GD 8 0 hr through GD 8 18 hr to examine cell 

 death and dysmorphogenesis, and we also evaluated cell-cycle distribution 

 and proliferation using flow cytometry (FCM) and /bromodeoxyuridine/ 

 (BrdU) immunohistochemistry. On GD 10, ...the effect of GD 7 exposure to 

 0, 2.3, 3.4, or 4.9 g/kg methanol on cranial ganglia and nerve development 

 using neurofilament immunohistochemistry /was evaluated/. Methanol 

 treatment on GD 7 resulted in reduced mesenchyme surrounding the fore- and 

 midbrain, and in the first branchial arches, by GD 8 12 hr. There were 

 disruptions in the forebrain neuroepithelium and optic pit. Neural crest 

 cell emigration from the mid- and hindbrain region was reduced in 

 methanol-exposed embryos. Methanol had no apparent effect on BrdU 

 incorporation or cell-cycle distribution on GD 8. Cell death was observed 

 in the hindbrain region along the path of neural crest migration and in 

 the trigeminal ganglion on GD 8 18 hr. Development of the cranial ganglia 

 and nerves was adversely affected by methanol. Development of ganglia V, 

 VIII, and IX was decreased at all dosage levels; ganglion VII was reduced 

 at 3.4 and 4.9 g/kg, and ganglion X was reduced at 4.9 g/kg. [Degitz SJ et 

 al; Birth Defects Res A Clin Mol Teratol 70 (4): 172-8 (2004)] **PEER 

 REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15108243" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ...Pregnant 

 C57BL/6J mice were administered two ip injections totaling 3.4 or 4.9 g/kg 

 methanol or distilled water four hrs apart on gestation day 'GD' 7. On GD 

 17, litters were examined for numbers of live, dead and resorbed 

 conceptuses, fetuses were weighed as a litter and examined externally, and 

 all fetuses were double stained for skeletal analysis. No maternal 

 intoxication was apparent, but the high dosage level caused a transient 

 deficit in maternal weight gain. The number of live fetuses per litter was 

 reduced at both dosages of methanol, and fetal weight was lower in the 

 high dosage group. Craniofacial defects were observed in 55.8% of fetuses 

 in the low dosage group and 91.0% of fetuses in the high dosage group, 

 including micro/anophthalmia, holoprosencephaly, facial clefts and gross 

 facial angenesis. Skeletal malformations, particularly of the cervical 

 vertebrae, were observed at both dosages of methanol, and were similar to 

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 those previously reported in the CD-1 mouse following methanol exposure. 

 [Rogers JM et al; Birth Defects Res B Dev Reprod Toxicol 71 (2): 80-8 

 (2004)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15098201&query_hl=18" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Female 

 Sprague-Dawley rats were exposed by inhalation to 0, 5000, and 10,000 ppm 

 for 7 hr/day during gestational days 1 to 19 and to 20,000 ppm 7 hr/day 

 during gestational days 7 to 15. At 20,000 ppm, methanol produced slight 

 maternal toxicity (unsteady gait only). Fetal body weights were decreased 

 in the 10,000- and 20,000-ppm groups with a high incidence of 

 malformations. The malformations were predominantly extra or rudimentary 

 cervical ribs and urinary or cardiovascular defects. Similar malformations 

 were observed at 10,000 ppm, but the incidence was not statistically 

 significant from controls. No maternal or developmental effects were noted 

 at 5,000 ppm. The blood methanol concentrations in female rates at the end 

 of the first 7 hr of exposure were 100 mg/mL at 5,000 ppm, 2240 mg/mL at 

 10,000 ppm, and 8650 mg/mL at 20,000 ppm. [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V6 p.376] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Female CD-1 

 mice were exposed by inhalation to 0, 2000, 5000, and 15,000, ppm of 

 methanol 7 hr/day during gestational days 6 to 15. A food-deprived 

 nonexposed group was added. Methanol exposure did not produce maternal 

 toxicity, but all exposure groups gained less weight than fed or 

 food-deprived controls. Most of the litters of dams exposed to 15,000 ppm 

 were completely resorbed and 38% of fetuses that survived to day 17 had 

 exencephaly. Exposure to 5000 ppm resulted in exencephaly in about 

 one-third of the litters and in 5 to 10% of the fetuses. At 2000 ppm, 1 of 

 220 fetuses had exencephaly, and there was none in the controls. The 

 maternal plasma methanol level in exposed pregnant female CD-1 mice was 

 2000 and 8000 mg/mL after the first 7 hr of exposure at 5000 and 15,000 

 ppm, respectively. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.376] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ A spectrum of 

 cephalic neural tube defects was found in near-term (gestation day 17) 

 CD-1 mouse fetuses following maternal inhalation of methanol at high 

 concentration (19,500 mg/cu m; 15,000 ppm) for 6 hr/day during neurulation 

 (gestation days 7-9). Dysraphism, chiefly exencephaly, occurred in 15% of 

 the fetuses, usually in association with reduction or absence of multiple 

 bones in the craniofacial skeleton and ocular anomalies (prematurely open 

 eyelids, cataracts, retinal folds). Exposure to a high concentration of 

 methanol (19,500 mg/cu m) injured the multiple stem populations in the 

 neuralating mouse embryo. Significant neural pathology may remain in older 

 conceptuses even in the absence of gross lesions. [WHO; Environ Health 

 Criteria 196: Methanol p.85 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ In a single 

 oral exposure, pregnant female Long-Evans rats were dosed by gavage with 

 0,1.3, 2.6, and 5.2 mL/kg of methanol on gestational day 10. At 5.2 mL/kg, 

 maternal weight loss was > 10%. A significant decrease in fetal body 

 weight (11 to 21%) was noted. Both internal and external examination of 

 the fetuses showed a dose-related increase in total anomalies of 0.6, 4.8, 

 6.7, and 17.3% at doses of 0, 1.3, 2.6, and 5.2 mL/kg of methanol 

 respectively. Those dose-related anomalies involved undescended testes and 

 the eye. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology 

 Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 

 p.377] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ In whole-rat 

 embryo culture, day 9 embryos were explanted and cultured in 0, 4000, 

 6000, 8000, 12,000, or 16,000 mg of methanol/mL serum for 24 hr and then 

 transferred to rat serum alone for 24 hr. Methanol concentrations of 8000 

 mg/mL and higher resulted in a dose-related decrease in somite number and 

 overall development. The 12,000-mg/mL concentration resulted in embryo 

 lethality, as well as dysmorphogenesis, and 16,00 mg/mL was embryolethal. 

 Head length and crown-rump length were not affected by methanol exposure 

 below embryolethal concentrations. [Bingham, E.; Cohrssen, B.; Powell, 

 C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New 

 York, N.Y. (2001)., p. V6 p.377] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Pregnant 

 Long-Evans rats were exposed to 2% methanol in drinking water on 

 gestational days 15 to 17 or 17 to 19. The animals were allowed to 

 deliver, and the postnatal behavior of the pups was assessed. Methanol 

 consumption averaged 2.5 g/kg/day. Methanol had no effect on maternal 

 weight gain, gestational duration, water consumption, litter size, birth 

 weight, neonatal mortality, postnatal growth, or the time until eye 

 opening. However, compared to nonexposed rats, prenatal exposure impaired 

 suckling behavior, as well as homing behavior, as determined by increased 

 time to return to the nest area. No significant behavioral effects were 

 noted in the offspring of female rats exposed to 15,000 ppm of methanol 

 for 7 hr/day during gestational days 7 to 19. Maternal blood methanol 

 levels, measured from samples taken within 15 minutes after removal from 

 the exposure chamber, declined from about 3800 ug/mL to 3100 ug/mL on the 

 12th day of exposure. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

Iris Camacho, 6308MM Page 24 of 69

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 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.377] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Neurotoxicity/ Rats exposed to 1.0, 2.0 and 3.0 g 

 methanol/kg by gavage exhibited an altered response in an operant 

 conditioning paradigm designed to assess motor deficits produced by 

 neurotoxicants. Methanol decreased the rate of response in a dose-related 

 fashion that suggested impaired coordination and/or reduced endurance. 

 [WHO; Environ Health Criteria 196: Methanol p.74 (1997). Available from, 

 as of July 14, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] 

 **PEER REVIEWED** 

 /LABORATORY ANIMALS: Neurotoxicity/ In contrast to many studies of 

 methanol toxicity that reported no effect of low doses, two Russian 

 studies reported evidence of neurobehavioral toxicity at low doses as 

 shown by altered chronaximetry (chronaximetry is the ratio of the minimum 

 time necessary for a stimulus of twice the absolute threshold intensity to 

 evoke a response measured as muscle contractions in response to an 

 electric current applied to an animal's hind leg). Normally, the flexor 

 chronaxia is shorter than the extensor chronaxia, and their ratio is 

 stated to be relatively stable. /One study/... reported that the average 

 chronaxia ratio for rats exposed in the high-dose group (49.77 mg/cu m) 

 for 12 hr/day, 5 days/wk for 3 months, differed significantly from that in 

 the control group of animals at week 8 of exposure. The average chronaxia 

 ratio returned to normal during the recovery period and the effects in the 

 low-dose group (1.77 mg/cu m) were insignificant. Histopathological 

 changes found in the high-dose group, but not in the low-dose group, 

 included poorly defined changes in the mucous membranes of the trachea and 

 bronchi, hyperplasia of the submucosa of the trachea, slight lymphoid 

 infiltration, swelling and hypertrophy of the muscle layer of arteries, 

 slight degenerative changes to the liver and changes in the neurons of the 

 cerebral cortex. /The second study/... reported that male rats exposed 

 continuously for 90 days to a concentration of 5.3 mg/cu m (4 ppm) of 

 methanol vapor, exhibited changes in chronaxia ratio between antagonistic 

 muscles, in whole blood cholinesterase activity, in urinary excretion of 

 coproporphyrin and in albumin-globulin ratio of the serum. Male rats 

 exposed to 0.57 mg/cu m (0.4 ppm) of methanol vapor continuously for 90 

 days showed no changes. It should be noted, however, that an analysis of 

 these studies... indicated that, due to flaws in the study designs, these 

 studies do not provide adequate evidence of an association between 

 neurobehavioral effects and low-level exposure to methanol. Both studies 

 were limited by the use of small numbers of animals per dose group, as 

 well as insufficient reporting of experimental methods, study results and 

 statistical analysis. /It was/... also stated that the biological 

 significance of changes in the chronaxia ratio is uncertain. [WHO; Environ 

 Health Criteria 196: Methanol p.74 (1997). Available from, as of July 14, 

 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

 /LABORATORY ANIMALS: Neurotoxicity/ ...In the presence of 4% methanol, 

 approximately 35% of embryos die and methanol exposure leads to severe CNS 

 defects in about half those embryos, where the longitudinal connectives 

 are dorsally displaced and commissure formation is severely reduced. In 

 addition, a range of morphological defects in other germ layers is seen, 

 and cell movement is adversely affected by methanol exposure. Although we 

 did not find any evidence to suggest that methanol exposure affects the 

 capacity of neuroblasts to divide or induces inappropriate apoptosis in 

 these cells, in the CNS of germ band retracted embryos, the number of 

 apoptotic nuclei is significantly increased in methanol-exposed embryos in 

 comparison to controls, particularly in and adjacent to the ventral 

 midline. Apoptosis contributes significantly to methanol neurotoxicity 

 because embryos lacking the cell death genes grim, hid, and reaper have 

 milder CNS defects resulting from methanol exposure than wild-type 

 embryos. Our data suggest that when neurons and glia are severely 

 adversely affected by methanol exposure, the damaged cells are cleared by 

 apoptosis, leading to embryonic death. [Mellerick DM, Liu H; J Neurobiol 

 60 (3): 308-13 (2004)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15281069&query_hl=8" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Neurotoxicity/ ...In the present work, a chronic 

 methanol intoxication scheme (2 g/kg/day ip for 2 weeks) was carried out 

 in Sprague-Dawley rats previously depleted of folates with methotrexate. 

 Taurine (2%) in drinking water was also administered in two groups of 

 animals. Blood formate levels were increased in 

 methotrexate-methanol-treated animals with respect to controls (0.98 +/- 

 0.09 and 0.30 +/- 0.03 mM, respectively). Amino acids and monoamines were 

 determined in plasma and in retina, optic nerve, hippocampus, and 

 posterior cortex by HPLC with fluorescence or electrochemical detection. 

 The main finding was an increased aspartate content in the optic nerve in 

 methotrexate methanol-treated animals. Methanol alone increased glutamate, 

 aspartate, glutamine, taurine, 5-hydroxytryptamine, and 

 5-hydroxyindoleacetic acid levels in the hippocampus and 

 5-hydroxytryptamine in the retina. Taurine administration had no 

 significant effect on changes induced by methanol treatment. ...Chronic 

 methanol administration produced accumulation of aspartate, an excitotoxic 

 amino acid, in the optic nerve. [Gonzalez-Quevedo A et al; Toxicol Appl 

 Pharmacol 185 (2): 77-84 (2002)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12490131" 

 target=new>PubMed Abstract 

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 /LABORATORY ANIMALS: Neurotoxicity/ Role of folic acid on methanol-induced 

 neurotoxicity was studied in pups at Postnatal Day (PND) 45 exposed to 

 methanol (1%, 2% and 4%, v/v) during lactation through mothers maintained 

 on folic acid-deficient (FD) and folic acid-sufficient (FS) diet. A 

 gradual loss in the body weight gain was observed in the pups exposed to 

 2% and 4% methanol in the FD group, while FS group exhibited this 

 alteration only at 4% exposure. The assessment of spontaneous locomotor 

 activity (SLA) showing a significant increase in the distance travelled 

 was observed in the 2% and 4% methanol-exposed groups in both the FS and 

 FD animals when compared with their respective controls, but the effect 

 was more marked in the FD group. A significant decrease in the conditioned 

 avoidance response (CAR) was observed in pups exposed to 2% and 4% 

 methanol in the FD group at PND 45. The results also suggest that 

 disturbances in dopaminergic and cholinergic receptors were more 

 pronounced in the FD group as compared to the FS group. A significant 

 decrease in striatal dopamine levels was also observed in the FD group at 

 2% and 4% methanol exposure, while in the FS group, a significant decrease 

 was exhibited only at 4% methanol exposure. An aberrant increase in the 

 expression of Growth-Associated Protein (GAP-43), a neuron-specific 

 growth-associated protein was observed in pups in the FD group exposed to 

 2% and 4% methanol, while an increase in the expression of GAP-43 in the 

 FS group was found only at 4% methanol exposure in the hippocampal region 

 as compared to their respective controls. [Aziz MH et al; Neurotoxicol and 

 Teratol 24 (4): 519-27 (2002)] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Neurotoxicity/ Behavioral effects induced by 

 perinatal methanol vapor exposure were studied in neonatal and adult rats. 

 Pregnant Long-Evans-hooded-rats were exposed to 0 or 4,500 ppm methanol 

 vapor 6 hr/day starting on gestational day six in 2 cubic meter hexagonal 

 Rochester chambers. At delivery, the litters culled to four offspring of 

 each sex, were kept in the exposure chambers with the dams up to weaning, 

 postnatal day (PND) 21. The offspring were evaluated as neonates for their 

 ability to find a dam's nipple in the suckling test administered on PND5 

 and olfactory aversion using orange-oil and methyl-salicylate as odorants 

 on PND10. Motor activity was evaluated on PND18 and PND25. The offspring 

 were evaluated as adults by measuring their performance in two operant 

 conditioning paradigms: running a specific number of revolutions in a 

 rotating field for a feed pellet reward (running wheel test) and 

 performing a complex lever pressing task for a feed pellet reward 

 (stochastic spatial discrimination learning (SSDL) test). Methanol 

 exposure did not affect performance in the suckling or odor aversion test. 

 The exposed rats showed lower levels of motor activity on PND18, but 

 higher levels of activity on PND25. When tested as adults, methanol 

 exposed male rats showed decreases in the rate of running in the running 

 wheel test compared to their baseline performance. Exposed females showed 

 increased rates of running. Methanol exposed rats of both sexes showed 

 impaired performance on the SSDL test at asymptotic levels of performance. 

 /It was concluded/... that exposure to 4,500ppm methanol vapor during 

 early development produces subtle changes in behavior in both neonatal and 

 adult rats. [Stern S et al; Fundam and Appl Toxicol 36 (2): 163-76 (1997)] 

 **PEER REVIEWED** 

 /GENOTOXICITY/ In mice exposed by inhalation to 800 or 4000 ppm of 

 methanol for 5 days, there were no increased frequencies of micronuclei in 

 blood cells; sister chromatid exchanges, chromosomal aberrations, or 

 micronuclei in lung cells; or synaptosomal complex damage in 

 spermatocytes. The frequency of micronucleated erythrocytes in normal or 

 folate-deficient mice treated with four daily intraperitoneal injections 

 of up to 2500 mg/kg of methanol was not increased. No increase in 

 micronuclei was observed in the bone marrow of mice exposed to methanol. 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.379] **PEER 

 REVIEWED** 

 /GENOTOXICITY/ Methanol did not induce micronuclei in Chinese hamster 

 lung V79 cells in vitro. Methanol was mutagenic in the mouse lymphoma 

 assay, in a Basc test, or in Drosophila, sex-linked, recessive lethal 

 mutation assay. Treatment of primary cultures of Syrian golden hamster 

 embryo cells with methanol did not lead to cell transformation. [Bingham, 

 E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. 

 John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.379] **PEER 

 REVIEWED** 

 /GENOTOXICITY/ Methanol was not mutagenic to Salmonella strains TA97, 

 TA98, TA1535, TA 1537, and TA1538 in Ames tests with or without metabolic 

 activation. Equivocal results were obtained with Salmonella strain TA102 

 in the presence of metabolic activation. Methanol was not mutagenic in a 

 DNA-repair test using various strains of E. coli WP2 and in a forward 

 mutation assay using Schizosaccharomyces pombe. [Bingham, E.; Cohrssen, 

 B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V6 p.379] **PEER REVIEWED** 

 /GENOTOXICITY/ Methanol was negative for gene mutation at the ade 6 locus 

 in the yeast Schizosaccharomyces pombe with or without the 

 postmitochondrial fraction from mouse liver. It was also negative in a 

 mutagenicity test for n+1 aneuploidy arising from meiotic disfunction of 

 linkage group I in the fungus Neurospora crassa. [WHO; Environ Health 

 Criteria 196: Methanol p.90 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /GENOTOXICITY/ Urine from mice administered five daily doses of methanol 

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 (5 g/kg total) showed no mutagenic activity, and no increase in the 

 incidence of abnormal sperm was reported. Oral administration of 1 g 

 methanol/kg to mice increased the incidence of chromosomal aberrations, 

 particularly aneuploidy and SCEs, as well as the incidence of micronuclei 

 in polychromatic erythrocytes. [WHO; Environ Health Criteria 196: Methanol 

 p.91 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /GENOTOXICITY/ A negative consensus resulted from all sister chromatid 

 exchange tests when no exogenous metabolic activation system was used. 

 [Latt SA et al; Mutation Res (1) 87: 17-62 (1981)] **PEER REVIEWED** 

 /GENOTOXICITY/ A negative consensus resulted from both cell transformation 

 in primary cells using limited lifetime strains and cell transformation 

 via viral enhancement tests when no exogenous metabolic activation system 

 was used. [Heidelberger C et al; Mutation Res (3) 114: 283-385 (1983)] 

 **PEER REVIEWED** 

 /GENOTOXICITY/ A negative consensus resulted from all Neurospora crassa 

 tests when no exogenous metabolic activation system was used. [Brockman HE 

 et al; Mutation Res (2) 133: 87-134 (1984)] **PEER REVIEWED** 

 /ALTERNATIVE IN VITRO TESTS/ Crude methanol extracts of red and white 

 wines were added to diethyl ether in order to divide them into the 

 anthocyanin fraction (insoluble in diethyl ether) and fractions containing 

 other flavonoids and their derivatives (soluble in diethyl ether). 

 However, the white wine did not contain anthocyanins (all of the methanol 

 extract was soluble in diethyl ether). When HCT-15 cells, derived from 

 human colon cancer or AGS cells, derived from human gastric cancer, were 

 cultured with these fractions, the anthocyanin fraction from the red wine 

 and the non-anthocyanic substances extracted from red and white wines 

 suppressed the growth of the cells, and the suppression rate by the 

 anthocyanin fraction was significantly higher than that of the other 

 fractions. Thin-layer chromatographic analysis revealed mostly delphinidin 

 in the anthocyanin fraction. The other fractions contained mostly 

 flavonoids and their derivatives. The sugars in all fractions were mainly 

 glucose, fucose, and fructose. Flow cytometric study suggested that the 

 anthocyanin fraction blocked mostly S, G2, and M phase, and the 

 non-anthocyanic flavonoids also blocked these phases, although the 

 histographic pattern varied depending on the fractions. Methanol insoluble 

 but water soluble fractions (mostly free sugars) of red and white wines 

 did not show such suppressive effects. [Kamei H et al; Cancer Biother 

 Radiopharm 13 (6): 447-52 (1998)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10851437&query_hl=40" 

 target=new>PubMed Abstract 

 /ALTERNATIVE IN VITRO TESTS/ Methanol was tested for cytotoxicity 

 (inhibition of cell growth in cultures of Ascites Sarcoma BP8 cells) as a 

 screening system for acute toxicity in humans. The IC50 value (growth 

 inhibition for 50%) was 673 mM. [European Chemicals Bureau; IUCLID 

 Dataset, Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of 

 July 19, 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 /ALTERNATIVE IN VITRO TESTS/ ...The potential of administered methanol to 

 incorporate into and/or alter the methylation of embryonal DNA or to 

 affect specific protein methylation /was investigated/. Gestational day 8 

 CD-1 mouse embryos were grown for 24 hr in culture medium (CM) with 0, 4, 

 or 8 mg MeOH + 20 uCi 14C-MeOH/mL. At the end of the culture period, yolk 

 sacs and embryos were separated for each treatment group. The DNA was 

 purified by cesium chloride gradient centrifugation in the presence of 

 ethidium bromide and 14C incorporation was determined. Methylation of a 

 selected gene, Hoxc-8, was assessed by using methylation-specific 

 restriction enzymes. The 14C activity was found superimposed over the 

 DNA-containing fraction, indicating incorporation. DNA from embryos 

 treated with 4 mg MeOH/mL CM gave the highest incorporation of 14C-MeOH (8 

 mg/mL was growth inhibiting). Methylation of Hoxc-8 appeared to be 

 increased in embryos treated with 4 mg MeOH/mL CM, but not in embryos 

 treated with 8 mg MeOH/mL. Lack of incorporation of methylation at the 

 higher concentration may be due to the failure of embryos to grow at this 

 concentration of MeOH. The incorporation of 14C-MeOH into embryo proteins 

 was investigated by polyacrylamide gel electrophoresis (PAGE) and 

 autoradiography. Incorporation of 14C-MeOH into specific proteins was 

 observed but the labeling specificity was not methanol dose-related. These 

 results indicate that methyl groups from 14C-MeOH are incorporated into 

 mouse embryo DNA and protein. [Huang YS et al; Repro Toxicol 15 (4): 

 429-35 (2001)] **PEER REVIEWED** 

 /OTHER TOXICITY INFORMATION/ Several factors may contribute to the unique 

 vulnerability of the retina and optic nerve to the cytotoxic actions of 

 formate. One component of this selectivity is related to the differences 

 in the distribution of formate in the eye and the brain. Formate 

 concentrations measured in the vitreous humor and retinas of 

 methanol-intoxicated rats were equivalent to or greater than corresponding 

 blood formate concentrations. In contrast, the concentrations of formate 

 in the brain were significantly lower than blood formate concentrations. 

 These data suggest that the toxic actions of methanol on the visual system 

 may be due to the selective accumulation of formate in the vitreous humor 

 and the retina as compared with other regions of the CNS. Secondly, the 

 retina has a very limited metabolic capacity to oxidize and thus detoxify 

 formate. Thirdly, cytochrome oxidase activity and ATP concentrations have 

 been shown to be selectively reduced in the retina, optic nerve and brain 

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 in methanol-intoxicated rats, suggesting that there may be tissue- and 

 cell-specific differences in mitochondrial populations and in the actions 

 of formate on mitochondrial function. Finally, in vitro studies in 

 isolated retinal and cardiac mitochondria have shown that formate 

 selectively inhibits retinal mitochondrial ATP synthesis. These findings 

 support the hypothesis that formate acts as a selective mitochondrial 

 toxin in the retina and establish a link between the effects of formate in 

 vitro and the retinal toxicity associated with formate accumulation in 

 methanol intoxication. [WHO; Environ Health Criteria 196: Methanol p.99 

 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

ECOTOXICITY EXCERPTS: 

 /AQUATIC SPECIES/ At 40,000-80,000 mg/L, methanol killed Chironomus 

 dorsalis meig larvae within 2 days; 500-20,000 mg/L within 26 days. 50-200 

 mg/L delayed imago emergence; at emergence, limb defects or hemorrhages 

 were observed. 250 mg/L cause morphological changes in larval development. 

 [Puzikova NB; Tr Sarat Otd Gosniorkh 13: 151-3 (1975)] **PEER REVIEWED** 

 /AQUATIC SPECIES/ Cyprinus carpio /(Common carp) were exposed to methanol 

 for up to/ 72 hr. ...Methanol treatment did not affect serum glucose but 

 led to increased serum cortisol, decreased serum protein, decreased serum 

 cholesterol, decreased liver glycogen, and increased muscle glycogen. 

 /The effective concentration was/ > /=790 mg/L. [European Chemicals 

 Bureau; IUCLID Dataset, Methanol (67-56-1) (2000 CD-ROM edition). 

 Available from, as of July 15, 2005: http://ecb.jrc.ec.europa.eu/esis/] 

 **PEER REVIEWED** 

 /AQUATIC SPECIES/ ...The mussel, Mytilus edulis, /was exposed/ to methanol 

 concentrations of 1, 2, 3, 5 and 10% (v/v) for 96 hr. All the mussels in 

 both the 5 and 10% exposure groups died within 13.5 hr. Sublethal narcotic 

 effects such as slow movement and sporadic filter feeding were reported in 

 mussels exposed to 2 and 3%. Mussels exposed to 1% methanol exhibited no 

 adverse effects during the 96-hr exposure period. [WHO; Environ Health 

 Criteria 196: Methanol p.115 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /AQUATIC SPECIES/ ...The effect of methanol on the embryonic development 

 of the medaka fish (Oryzias latipes) /was determined/. The eggs were 

 exposed to methanol in both Petri dishes and vials. No effects on 

 embryonic development were reported at a methanol concentration of 0.5%. 

 [WHO; Environ Health Criteria 196: Methanol p.123 (1997). Available from, 

 as of July 19, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] 

 **PEER REVIEWED** 

 /AQUATIC SPECIES/ The effect of methanol on the fertilization of chum 

 salmon (Oncorhynchus keta) ova was examined at methanol exposure levels of 

 0.001% to 10% by volume (7.9 to 79 000 mg/lL). Both gametes (sperm and 

 unfertilized ova) and fertilized eggs were exposed to methanol for brief 

 periods. Exposures up to and including 1% methanol did not significantly 

 affect fertilization, survival to hatching, hatching time, alevin size at 

 hatch or physical deformities among alevins, although a methanol 

 concentration of 10% was lethal in most cases. [WHO; Environ Health 

 Criteria 196: Methanol p.123 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 /AQUATIC SPECIES/ Static renewal bioassays were conducted in the 

 laboratory and in outdoor artificial enclosures to evaluate toxic effects 

 of methanol to one teleost fish and two aquatic invertebrates and to 

 limnological variables of aquatic ecosystem. Ninety-six-hour acute 

 toxicity tests revealed cladoceran crustacea Moina micrura as the most 

 sensitive to methanol (LC50, 4.82 g/L), followed by freshwater teleost 

 Oreochromis mossambicus (LC50, 15.32 g/L) and oligochaete worm Branchiura 

 sowerbyi (LC50, 54.89 g/L). The fish, when exposed to lethal 

 concentrations of methanol, showed difficulties in respiration and 

 swimming. The oligochaete body wrinkled and fragmented under lethal 

 exposure of methanol. Effects of five sublethal concentrations of methanol 

 (0, 23.75, 47.49, 736.10, and 1527.60 mg/L) on the feeding rate of the 

 fish and on its growth and reproduction were evaluated by separate 

 bioassays. Ninety-six-hour bioassays in the laboratory showed significant 

 reduction in the appetite of fish when exposed to 736.10 mg/L or higher 

 concentrations of methanol. Chronic toxicity bioassays (90 days) in 

 outdoor enclosures showed a reduction in growth, maturity index and 

 fecundity of fish at 47.49 mg/L or higher concentrations of methanol. 

 Primary productivity, phytoplankton population, and alkalinity of water 

 were also reduced at these concentrations. Chronic exposure to 1527.60 

 mg/L methanol resulted in damages of the epithelium of primary and 

 secondary gill lamellae of the fish. The results revealed 23.75 mg/L as 

 the no-observed-effect concentration (NOEC) of methanol to freshwater 

 aquatic ecosystem. [Kaviraj A et al; Int J Toxicol 23 (1): 55-63 (2004)] 

 **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15162848&query_hl=12" 

 target=new>PubMed Abstract 

 /AQUATIC SPECIES/ ...The dehydrated /Artemia salina (Brine shrimp)/ cysts 

 were directly exposed for 48 hr to the action of three alcohols, methanol, 

 ethanol, and n-propanol. No teratogenic or lethal effects on larvae were 

 found at any methanol or ethanol concentrations. Predicted values of 

 effect concentration, EC1, EC10 and EC50 were calculated from the 

 estimated probit models for larva growth inhibition, GI, and for cyst 

 lethal concentration, LC. At concentrations of 0.21 M methanol and 0.13 M 

Iris Camacho, 6308MM Page 28 of 69

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 ethanol, there were no signs of alterations in Artemia salina cyst 

 development; these concentrations show a NOEC (No Observed Effect 

 Concentration) value, and properly employed do not interfere with effects 

 due to a given chemical. [Vismara C; Chemosphere 37 (14-15): 3027-3034 

 (1998)] **PEER REVIEWED** 

NON-HUMAN TOXICITY VALUES: 

 LD50 Rat oral 5628 mg/kg [Lewis, R.J. Sax's Dangerous Properties of 

 Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 LC50 Rat inhalation 64000 ppm/4 hr [Lewis, R.J. Sax's Dangerous 

 Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van 

 Nostrand Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 LC50 Rat inhalation 87.5 mg/L/6 hr [European Chemicals Bureau; IUCLID 

 Dataset, Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of 

 July 19, 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LD50 Rat ip 7529 mg/kg [Lewis, R.J. Sax's Dangerous Properties of 

 Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 LD50 Rat iv 2131 mg/kg [Lewis, R.J. Sax's Dangerous Properties of 

 Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 LD50 Mouse oral 7300 mg/kg [Lewis, R.J. Sax's Dangerous Properties of 

 Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 LD50 Mouse ip 10765 mg/kg [Lewis, R.J. Sax's Dangerous Properties of 

 Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 LD50 Mouse sc 4100 mg/kg bw [European Chemicals Bureau; IUCLID Dataset, 

 Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of July 19, 

 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LD50 Mouse iv 4710 mg/kg [Lewis, R.J. Sax's Dangerous Properties of 

 Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 LD50 Rabbit oral 14.4 g/kg [Bingham, E.; Cohrssen, B.; Powell, C.H.; 

 Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, 

 N.Y. (2001)., p. V6 p.372] **PEER REVIEWED** 

 LD50 Rabbit dermal 15,800 mg/kg bw [European Chemicals Bureau; IUCLID 

 Dataset, Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of 

 July 19, 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LD50 Rabbit ip 1826 mg/kg bw [European Chemicals Bureau; IUCLID Dataset, 

 Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of July 19, 

 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LD50 Rabbit iv 8907 mg/kg bw [European Chemicals Bureau; IUCLID Dataset, 

 Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of July 19, 

 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LD50 Monkey oral 2-3 g/kg [Bingham, E.; Cohrssen, B.; Powell, C.H.; 

 Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, 

 N.Y. (2001)., p. V6 p.372] **PEER REVIEWED** 

 LD50 Macaca nemestrina (Pigtail monkey) ip 3-4 g/kg [WHO; Environ Health 

 Criteria 196: Methanol p.78 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LD50 Dog oral 8000 mg/kg bw [European Chemicals Bureau; IUCLID Dataset, 

 Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of July 19, 

 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LC50 Cat inhalation 85.41 mg/L/4.5 hr [European Chemicals Bureau; IUCLID 

 Dataset, Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of 

 July 19, 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LC50 Cat inhalation 43.68 mg/L/6 hr [European Chemicals Bureau; IUCLID 

 Dataset, Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of 

 July 19, 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LD50 Guinea pig ip 3556 mg/kg bw [European Chemicals Bureau; IUCLID 

 Dataset, Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of 

 July 19, 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LD50 Hamster ip 8555 mg/kg bw [European Chemicals Bureau; IUCLID Dataset, 

 Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of July 19, 

 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

ECOTOXICITY VALUES: 

 LC50 Pimephales promelas (fathead minnows) 29.4 g/L/96 hr, (28-29 days 

 old), confidence limit= 28.5-30.4; Test conditions: Water temp= 25 deg C, 

 dissolved oxygen= 7.3 mg/L, water hardness= 43.5 mg/l calcium carbonate, 

Iris Camacho, 6308MM Page 29 of 69

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 alkalinity= 46.6 calcium carbonate, tank volume= 6.3 L, additions= 5.71 

 V/D, pH= 7.66 (0.03). [Brooke, L.T., D.J. Call, D.T. Geiger and C.E. 

 Northcott (eds.). Acute Toxicities of Organic Chemicals to Fathead Minnows 

 (Pimephales Promelas). Superior, WI: Center for Lake Superior 

 Environmental Studies Univ. of Wisconsin Superior, 1984., p. 19] **PEER 

 REVIEWED** 

 LC50 Pimephales promelas (Fathead minnow, 28-32 day old, 0.126 g) 29,700 

 mg/L/24 hr; flow-through, 23.3+/-1.7 deg C, hardness 46.4 mg/L CaCO3, pH 

 7.0-8.0 /from table/ [WHO; Environ Health Criteria 196: Methanol p.119 

 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Pimephales promelas (Fathead minnow, 30 day old 0.12 g) 28,100 

 mg/L/96 hr; flow-through, 24-26 deg C, hardness 45.5 mg/L CaCO3, pH 7.5 

 /from table/ [WHO; Environ Health Criteria 196: Methanol p.120 (1997). 

 Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Artemia salina (Brine shrimp, 24 hr old) 1578.84 mg/L/24 hr; static, 

 25 deg C, seawater /from table/ [WHO; Environ Health Criteria 196: 

 Methanol p.117 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Artemia salina (Brine shrimp, 48 hr old) 1101.46 mg/L/24 hr; static, 

 25 deg C, seawater /from table/ [WHO; Environ Health Criteria 196: 

 Methanol p.117 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Artemia salina (Brine shrimp, 72 hr old) 900.73 mg/L/24 hr; static, 

 25 deg C, seawater /from table/ [WHO; Environ Health Criteria 196: 

 Methanol p.117 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Oncorhynchus mykiss (Rainbow trout, 0.8 g) 19,000 mg/L/96 hr; static, 

 12 deg C, hardness 44 mg/L CaCO3, pH 7.4 /from table/ [WHO; Environ Health 

 Criteria 196: Methanol p.119 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Oncorhynchus mykiss (Rainbow trout, juvenile 0.813 g) 20,300 mg/L/24 

 hr; flow-through, 12.7+/-1 deg C, hardness 46.4 mg/L CaCO3, pH 7.0-8.0 

 /from table/ [WHO; Environ Health Criteria 196: Methanol p.119 (1997). 

 Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Oncorhynchus mykiss (Rainbow trout, juvenile 0.813 g) 20,100 mg/L/96 

 hr; flow-through, 12.7+/-1 deg C, hardness 46.4 mg/L CaCO3, pH 7.0-8.0 

 /from table/ [WHO; Environ Health Criteria 196: Methanol p.119 (1997). 

 Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Lepomis macrochirus (Bluegill) 15,400 mg/L/96 hr; flow-through 

 [European Chemicals Bureau; IUCLID Dataset, Methanol (67-56-1) (2000 

 CD-ROM edition). Available from, as of July 15, 2005: 

 http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LC50 Lepomis macrochirus (Bluegill) 19,230 mg/L/24 hr; flow-through 

 [European Chemicals Bureau; IUCLID Dataset, Methanol (67-56-1) (2000 

 CD-ROM edition). Available from, as of July 15, 2005: 

 http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LC50 Lepomis macrochirus (Bluegill sunfish, juvenile 3.07 g) 19,100 

 mg/L/24 hr; flow-through, 19.8+/-2.3 deg C, hardness 46.4 mg/L CaCO3, pH 

 7.0-8.0 /from table/ [WHO; Environ Health Criteria 196: Methanol p.120 

 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Lepomis macrochirus (Bluegill sunfish, juvenile 3.07 g) 15,400 

 mg/L/96 hr; flow-through, 19.8+/-2.3 deg C, hardness 46.4 mg/L CaCO3, pH 

 7.0-8.0 /from table/ [WHO; Environ Health Criteria 196: Methanol p.120 

 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Nitocra spinipes (Harpacticoid copepod, adult) 12,000 mg/L/96 hr; 

 static, 21+/-1 deg C, pH 7.9 /from table/ [WHO; Environ Health Criteria 

 196: Methanol p.118 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Poecilia reticulata (Guppy) 11.5 mg/L/14 days; semistatic [European 

 Chemicals Bureau; IUCLID Dataset, Methanol (67-56-1) (2000 CD-ROM 

 edition). Available from, as of July 15, 2005: 

 http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LC50 Poecilia reticulata (Guppy, 2-3 months) 10,860 mg/L/7 days; 

 semistatic (test solutions renewed every 24 hours), 21-23 deg C, hardness 

 25 mg/L CaCO3 /from table/ [WHO; Environ Health Criteria 196: Methanol 

 p.121 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Alburnus alburnus (Bleak, 8 cm) 28,000 mg/L/96 hr; static, 10 deg C, 

 pH 7.9 /from table/ [WHO; Environ Health Criteria 196: Methanol p.121 

Iris Camacho, 6308MM Page 30 of 69

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 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Leuciscus idus melanotus (Golden orfe) > 10,000 mg/L/48 hr; static 

 [European Chemicals Bureau; IUCLID Dataset, Methanol (67-56-1) (2000 

 CD-ROM edition). Available from, as of July 15, 2005: 

 http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 EC50 Daphnia magna (Water flea; immobilizaiton) > 10,000 mg/L/24 hr; 

 static, 20 deg C, total hardness 2.5 mmol/L CaCO3, pH 7.8-8.2 /from table/ 

 [WHO; Environ Health Criteria 196: Methanol p.116 (1997). Available from, 

 as of July 19, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] 

 **PEER REVIEWED** 

 LC50 Gammarus fasciatus > 100 mg/L/96 hr /Conditions of bioassay not 

 specified in source examined/ [European Chemicals Bureau; IUCLID Dataset, 

 Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of July 15, 

 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LC50 Helisoma trivolvis (aquatic mollusk) > 100 mg/L/96 hr /Conditions 

 of bioassay not specified in source examined/ [European Chemicals Bureau; 

 IUCLID Dataset, Methanol (67-56-1) (2000 CD-ROM edition). Available from, 

 as of July 15, 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LC50 Dugesia tigrina (aquatic worm) > 100 mg/L/96 hr /Conditions of 

 bioassay not specified in source examined/ [European Chemicals Bureau; 

 IUCLID Dataset, Methanol (67-56-1) (2000 CD-ROM edition). Available from, 

 as of July 15, 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LC50 Ceriodaphnia dubia 11 mg/L/48 hr /Conditions of bioassay not 

 specified in source examined/ [European Chemicals Bureau; IUCLID Dataset, 

 Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of July 15, 

 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LC50 Lumbriculus variegatus (aquatic worm) > 100 mg/L/96 hr /Conditions 

 of bioassay not specified in source examined/ [European Chemicals Bureau; 

 IUCLID Dataset, Methanol (67-56-1) (2000 CD-ROM edition). Available from, 

 as of July 15, 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 EC50 Photobacterium posphoreum (marine bacterium; inhibition of 

 luminescence) 14,700 mg/L/15 min /Conditions of bioassay not specified in 

 source examined/ [WHO; Environ Health Criteria 196: Methanol p.114 (1997). 

 Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Photobacterium posphoreum (marine bacterium) 7690 mg/L/4 hr 

 /Conditions of bioassay not specified in source examined/ [WHO; Environ 

 Health Criteria 196: Methanol p.114 (1997). Available from, as of July 19, 

 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

 LC50 Paramecium caudatum (Ciliate protozoan) 44,860 mg/L/10 min 

 /Conditions of bioassay not specified in source examined/ [WHO; Environ 

 Health Criteria 196: Methanol p.114 (1997). Available from, as of July 19, 

 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

 LC50 Daphnia pulex (Water flea, < 24 hr old) 19,500 mg/L/18 hr; static, 

 22 deg C, hardness 23+/-2 mg/L CaCO3 /from table/ [WHO; Environ Health 

 Criteria 196: Methanol p.116 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 EC50 Daphnia obtusa (Water flea, < 24 hr old; immobilization) 23,500 

 mg/L/24 hr; static, 20+/-2 deg C, hardness 250 mg/L CaCO3, pH 7.8+/-0.2 

 /from table/ [WHO; Environ Health Criteria 196: Methanol p.116 (1997). 

 Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 EC50 Daphnia obtusa (Water flea, < 24 hr old; immobilization) 22,200 

 mg/L/48 hr; static, 20+/-2 deg C, hardness 250 mg/L CaCO3, pH 7.8+/-0.2 

 /from table/ [WHO; Environ Health Criteria 196: Methanol p.116 (1997). 

 Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Crangon crangon (Brown shrimp, adult) 1975 mg/L/48 hr; static, 15 deg 

 C, seawater /from table/ [WHO; Environ Health Criteria 196: Methanol p.117 

 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Crangon crangon (Brown shrimp, adult) 1340 mg/L/96 hr; semistatic 

 (test solutions renewed every 24 hr), 15 deg C, seawater /from table/ 

 [WHO; Environ Health Criteria 196: Methanol p.117 (1997). Available from, 

 as of July 19, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] 

 **PEER REVIEWED** 

 LC50 Crangon crangon (Brown shrimp, adult) 10,000 mg/L/24 hr; static, 24.5 

 deg C, seawater /from table/ [WHO; Environ Health Criteria 196: Methanol 

 p.117 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Mytilus edulis (Mussel, 5-7 cm) 15,900 mg/L/96 hr; flow-through, 

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 15+/-0.5 deg C, seawater /from table/ [WHO; Environ Health Criteria 196: 

 Methanol p.118 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Palaemonetes kadiakensis (Glass shrimp, juvenile) 21,900 mg/L/18 hr; 

 static, 23+/-2 deg C /from table/ [WHO; Environ Health Criteria 196: 

 Methanol p.117 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Cardium edule (Cockle, adult) 7900 mg/L/48 hr; static, 15 deg C, 

 seawater /from table/ [WHO; Environ Health Criteria 196: Methanol p.118 

 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Hyallela azteca (Scud, juvenile) 19,350 mg/L/18 hr; static, 23+/-2 

 deg C /from table/ [WHO; Environ Health Criteria 196: Methanol p.118 

 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 LC50 Agonus cataphractus (Armed bullhead, adult) 7900-26,070 mg/L/96 hr; 

 semistatic (test solutions renewed every 24 hours), 15 deg C, seawater 

 /from table/ [WHO; Environ Health Criteria 196: Methanol p.122 (1997). 

 Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 EC50 Tetrahymena pyriformis (Protozoa; population growth inhibition test) 

 18756.34 mg/L/48 hr /Conditions of bioassay not specified in source 

 examined/ /95% pure/ [European Chemicals Bureau; IUCLID Dataset, 

 Methanol (67-56-1) (2000 CD-ROM edition). Available from, as of July 19, 

 2005: http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 LC50 Anodonta imbecilis (Mussel) 37.02 mg/L/48 hr; static [Keller AE; Bull 

 Environ Contam Toxicol 51 (5): 696-702 (1993). ECOTOX database on Methanol 

 (67-56-1). Available from, as of July 20, 2005: 

 http://cfpub.epa.gov/ecotox/quick_query.htm] **PEER REVIEWED** 

 LC50 Oryzias latipes (Medaka) > 10,000 mg/L/24 hr; static /formulated 

 product/ [Tsuji S et al; Eisei Kagaku 32 (1): 46-53 (1986). ECOTOX 

 database on Methanol (67-56-1). Available from, as of July 20, 2005: 

 http://cfpub.epa.gov/ecotox/quick_query.htm] **PEER REVIEWED** 

METABOLISM/PHARMACOKINETICS: 

METABOLISM/METABOLITES: 

 Methanol (labeled with (14)C) is slowly metabolized by rat and in 2 days 

 is excreted as carbon dioxide (65% of dose), and unchanged methanol (14%) 

 in expired air, and as formate (3%) and methanol (3%) in urine. [Parke, D. 

 V. The Biochemistry of Foreign Compounds. Oxford: Pergamon Press, 1968., 

 p. 212] **PEER REVIEWED** 

 ...Methanol is... metabolized by pathways of 1-carbon metabolism, giving 

 rise to methyl group of choline, etc. In the rabbit it may also result 

 in... a small amount of methylglucuronide. [Parke, D. V. The Biochemistry 

 of Foreign Compounds. Oxford: Pergamon Press, 1968., p. 213] **PEER 

 REVIEWED** 

 Oxidation of methanol appears to occur by coupled peroxidative reactions 

 catalyzed by hepatic catalase, and in rats occurs at a much slower rate 

 (25 mg/kg/hr) than oxidation of ethanol (175 mg/kg/hr). [Parke, D. V. The 

 Biochemistry of Foreign Compounds. Oxford: Pergamon Press, 1968., p. 213] 

 **PEER REVIEWED** 

 ... Methanol is metabolized in human beings by the same enzymes that 

 metabolize ethanol, alcohol dehydrogenase and aldehyde dehydrogenase, to 

 toxic intermediates, formaldehyde and formic acid. Oxidation of methanol, 

 like that of ethanol, proceeds at a rate that is independent of its 

 concentration in the blood. However, the rate is only one-seventh that of 

 the oxidation of ethanol, and complete oxidation and excretion of methanol 

 thus usually require several days. [Hardman, J.G., L.E. Limbird, P.B., 

 A.G. Gilman. Goodman and Gilman's The Pharmacological Basis of 

 Therapeutics. 10th ed. New York, NY: McGraw-Hill, 2001., p. 1886] **PEER 

 REVIEWED** 

 Several primary alcohols... yield moderate amounts of monosulfate esters. 

 This pathway has been detected for methanol... in rats. [Testa, B. and P. 

 Jenner. Drug Metabolism: Chemical & Biochemical Aspects. New York: 

 Marcel Dekker, Inc., 1976., p. 188] **PEER REVIEWED** 

 The first step in the metabolism of methanol is oxidation to formaldehyde. 

 In rats, a catalase-peroxidase system is primarily responsible for the 

 initial step, whereas in humans and monkeys, alcohol dehydrogenase plays a 

 major role. Despite the difference, the initial metabolic step proceeds at 

 similar rates. The third possible pathway in methanol oxidation is hepatic 

 microsomal oxidation involving the cytochrome P450 system. [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V6 p.374] **PEER REVIEWED** 

 Following a 2 mg/kg oral dose of methanol to primates and rats, about 90% 

 is metabolized. Even after a high dose of 1 g/kg of radiolabeled methanol 

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 to monkeys, 78% of the activity was recovered within 24 hr as exhaled CO2. 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.375] **PEER 

 REVIEWED** 

 In the liver, alcohol dehydrogenase (ADH) metabolizes approximately 75-85% 

 of methanol to formaldehyde, which is then oxidized by aldehyde 

 dehydrogenase to formic acid. In the presence of folate, formic acid is 

 converted to carbon dioxide and water. This beneficial aspect of folate 

 has been demonstrated both in mice and in nonhuman primates. 

 Folate-deficient rats were more susceptible to methanol toxicity than were 

 folate-rich rats. Monkeys treated with folate after methanol 

 administration were relatively resistant to methanol toxicity, and when 

 methanol toxicity was allowed to develop, it was reversed after folate 

 treatment. ...At low concentrations methanol metabolism follows zero-order 

 kinetics at a rate of 8.5 mg/dL/hr. At much higher methanol concentrations 

 first-order kinetics occur, possibly because of increased pulmonary 

 elimination. In the presence of therapeutic levels of ethanol, the 

 half-life ranges from 30-52 hours with a median of 43 hours. In the 

 presence of fomepizole, the mean half-life is 54 hours. [Goldfrank, L.R. 

 (ed). Goldfrank's Toxicologic Emergencies. 7th Edition McGraw-Hill New 

 York, New York 2002., p. 982] **PEER REVIEWED** 

 Methanol is ... released during the metabolism of food additives such as 

 the artificial sweetener, aspartame, and /dimethyl dicarbonate/ (DMDC), a 

 yeast inhibitor added to a variety of beverages. [DHHS/NTP; NTP-CERHR 

 Expert Panel Report on the Reproductive and Developmental Toxicity of 

 Methanol p.7 (April 2002) NTP-CERHR-MeOH-02. Available from, as of July 

 20, 2005: http://cerhr.niehs.nih.gov/news/methanol/methanol_final.pdf] 

 **PEER REVIEWED** 

 The disposition of methanol and its putative toxic metabolite formate has 

 been studied in humans, non-human primates, and rodents after exposure to 

 high, neurotoxic doses. The rate at which rodents detoxify formate is more 

 rapid than that of primates. Formate, an endogenous biological substrate, 

 is detoxified by metabolism to /carbon dioxide/ via a 

 tetrahydrofolate-(THF) dependent pathway. Species with high hepatic THF 

 levels, such as rodents, are less sensitive to the neurotoxic effects of 

 large methanol doses compared with species with low THF levels, such as 

 primates. Data on the capacity of primates to detoxify formate derived 

 from inhalation of low levels of methanol are critical for assessing human 

 risk from methanol fuels. Female cynomolgus monkeys exposed to low 

 concentrations of [14C]methanol (10-200 ppm) for 2 hr have blood levels of 

 methanol-derived formate that are 100-to 1000-fold lower than endogenous 

 levels of formate. Healthy human volunteers exposed at rest or during 

 exercise to 200 ppm methanol for 6 hr or exposed to 20 mg/kg orally have 

 elevated blood levels of methanol, but blood formate concentrations are 

 not significantly increased above endogenous concentrations. Deficiencies 

 in THF may prolong blood levels of formate and increase the likelihood of 

 toxic effects. Limited studies in non-human primates with low THF levels 

 exposed to 900 ppm methanol for 2 hr have shown that concentrations of 

 methanol-derived formate in blood remain below endogenous levels. 

 [Medinsky MA, Dorman DC; Toxicology Letters 82-83: 707-11 (1995)] **PEER 

 REVIEWED** 

 Wistar male rats were exposed to methanol and toluene vapors by inhalation 

 individually and simultaneously. Blood was sampled from the tail of the 

 rats at 0, 1.5 and 3 hr after a 6-hr exposure and the methanol and/or 

 toluene concentrations were measured by the headspace-gas 

 chromatography-mass spectrometry (GC). Major metabolites of methanol and 

 toluene, that is, formic acid and hippuric acid in urine were measured at 

 0, 18 and 42 hr after the end of the exposure. The toluene concentration 

 in blood in the simultaneous exposure group was lower than that in the 

 toluene exposure one. The biological half time of toluene in blood in the 

 simultaneous exposure group was shorter than that in the single exposure 

 one. The excretion rate of hippuric acid in urine in the simultaneous 

 exposure group was significantly lower than that in the toluene exposure 

 one when both the methanol and toluene concentrations were 300 ppm. These 

 results suggest that the metabolic rate of toluene was enhanced by 

 methanol. On the other hand, the biological half time of methanol in blood 

 and the formic acid concentration in urine were not significantly 

 different in the single and simultaneous exposure groups, although the 

 methanol concentration in blood in the simultaneous exposure group was 

 lower than that in the methanol exposure one. [Hori H et al; J of Occup 

 Health 41 (3): 149-153 (1999)] **PEER REVIEWED** 

ABSORPTION, DISTRIBUTION & EXCRETION: 

 Methanol is absorbed following inhalation or ingestion, and inhalation is 

 the major route of absorption in the occupational environment. There is no 

 agreement on the potential risk of dermal exposure to methanol. Methanol 

 is uniformly distributed according to the relative water content of the 

 tissue. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology 

 Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 

 p.374] **PEER REVIEWED** 

 Methyl alcohol is readily absorbed from GI and respiratory tracts. 

 [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial 

 Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-275] 

 **PEER REVIEWED** 

 The rate of absorption /of methanol from the gastrointestinal tract is 

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 approximately/... 8.4 mg/sq cm/hr. Time to peak serum concentration... 

 after ingestion /is/... 30-60 minutes for methanol... . [Goldfrank, L.R. 

 (ed). Goldfrank's Toxicologic Emergencies. 7th Edition McGraw-Hill New 

 York, New York 2002., p. 982] **PEER REVIEWED** 

 Distribution of methyl alcohol within tissues of dogs exposed to 4000 and 

 15000 ppm in air over periods ranging from 12 hr to 5 days was found to be 

 rapid. ... Highest concentrations were found in blood, eye fluid, bile, 

 urine, and lowest in bone marrow and fatty tissue. ... 1-7 mg of methyl 

 alcohol/g of blood (100-700 mg/100 mL) was found ... in blood of rats 

 following oral administration of 4 g of methyl Alcohol/kg of body weight. 

 [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and 

 Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley 

 Sons, 1981-1982., p. 4534] **PEER REVIEWED** 

 ... Under ... experimental conditions in man following ingestion and 

 inhalation, dosages of 71-84 mg/kg orally resulted in blood levels of 

 4.7-7.6 mg/100 mL ... 2-3 hr afterward. urine/blood concentration ratio 

 was ... constant at about 1.3. ... Inhalation of ... 500-1000 ppm ... for 

 ... 3-4 hr gave urine concentration of about 1-3 mg/100 mL. ... [Clayton, 

 G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: 

 Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 

 1981-1982., p. 4537] **PEER REVIEWED** 

 70% of methyl alcohol lost by animals was eliminated in expired air. 

 [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and 

 Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley 

 Sons, 1981-1982., p. 4535] **PEER REVIEWED** 

 Two human male volunteers were exposed on several different occasions to 

 methyl alcohol vapor at concentrations of from 650 to 1,430 mg/cu m 

 (approximately 500-1,100 ppm). Concentrations were verified by analyzing 

 air samples collected at frequent intervals during and after exposures for 

 methyl alcohol content. Using urinary methyl alcohol concentrations as an 

 index of methyl alcohol absorption, it was concluded that the rate of 

 absorption was proportional to the concentration of the vapor inhaled. 

 Exposure to methyl alcohol vapor at a concentration of 1,430 mg/cu m 

 (approximately 1,100 ppm) for 2 1/2 hr resulted in a urinary methyl 

 alcohol concentration of 2.56 mg/100 mL. Exposure periods were not 

 sufficiently long to determine whether the rate of excretion would 

 increase to equal the rate of absorption. An exposure period of 3-4 hr was 

 all that could be reasonably tolerated. The threshold of intoxication was 

 calculated for these two workers as 2,800 ppm (3,670 mg/cu m) and 3,000 

 ppm (3,930 mg/cu m) respectively. [Leaf G, Zatman LJ; Br J Ind Med 9: 

 19-31 (1952) as cited in NIOSH; Criteria Document: Methyl Alcohol p.39-40 

 (1976) DHEW Pub. NIOSH 76-148] **PEER REVIEWED** 

 Pulmonary retention in humans after 8 hr of inhalation exposure to 

 methanol was 58% of the inhaled amount, regardless of the exposure level, 

 duration of the exposure, or pulmonary ventilation. The methanol blood 

 concentrations in dogs exposed repeatedly to vapor concentrations of 450 

 or 500 ppm, 8 hr/day, for 379 continuous days varied between 10 and 15 

 mg/100mL at the end of an 8 hr period, but occasional values as high as 52 

 mg/dL were obtained. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.374] **PEER REVIEWED** 

 Rabbits given a single oral dose of methanol (2 to 10 g/kg) excreted 0.1 

 to 1.1% of it as formate and 13 to 20% of it as methanol in the urine 

 within 47 to 143 hr. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.375] **PEER REVIEWED** 

 Following a 2 mL/kg oral dose of methanol to rabbits, 5.3% was excreted in 

 the expired air and 7.8% in the urine. [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V6 p.375] **PEER REVIEWED** 

 Dogs given 1 to 2 g/kg of methanol orally excreted 5 to 15% in the urine 

 as formate and 5 to 8% as unchanged methanol. Dogs excrete more formate 

 than rabbits after ingestion of methanol. [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V6 p.375] **PEER REVIEWED** 

 The rate of elimination for methanol from the blood is much lower than 

 that of ethanol. The rate of methanol disappearance from the blood also 

 depends on dose. Elimination follows first order kinetics. The rat and the 

 monkey have similar capabilities for eliminating methanol at low 

 inhalation exposures (200 ppm) but not at higher exposure levels. 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.375] **PEER 

 REVIEWED** 

 In rats exposed by inhalation to 200, 1200, and 2000 ppm methanol for 6 

 hr, the peak methanol concentrations in the blood were 3.3, 32.2, and 90.8 

 mg/mL, respectively, indicating a nonlinear response. [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V6 p.375] **PEER REVIEWED** 

 In Rhesus monkeys exposed to 200, 1200, and 2000 ppm of methanol for 6 hr, 

 the peak methanol concentration in the blood was 7.7, 39.3 and 66.1 mg/mL, 

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 respectively, a directly proportional response. ... Exposures did not 

 cause an elevation in blood formate levels that could be attributed to 

 methanol metabolism. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.375] **PEER REVIEWED** 

 Female Long-Evans rats were exposed by inhalation to 4500 ppm of methanol 

 6 hr/day from gestational day 6 to birth, and dams and their pups were 

 exposed until postnatal day 21. The average methanol concentrations were 

 0.35, 0.499, and 1.3 mg/mL for pregnant dams, nursing dams, and neonates, 

 respectively. In pregnant female Long-Evans rats exposed to 2% methanol in 

 drinking water on gestational day 17 and euthanized the next day 

 (approximately 2 g/kg consumed), there was a rapid equilibration of 

 methanol across placental and blood-brain barriers. [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V6 p.375] **PEER REVIEWED** 

 Low-level inhalation exposures to methanol cause small increases in blood 

 and urine formate levels. A study was conducted of 20 workers in a 

 printing office who were exposed to an estimated methanol concentration 

 between 111 and 174 mg/cu m throughout the work day. During the day, the 

 blood level of formate increased an average of 4.7 mg/L (3.2 mg/L before 

 the work shift to 7.9 mg/L when work ended), and urinary formate increased 

 an average of 7.1 mg/L. A control group maintained relatively stable 

 levels throughout the day of 5.3 mg/L of blood and 11.8 mg/L of urine. 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.381] **PEER 

 REVIEWED** 

 ... Twenty workers were exposed throughout the day to 120 mg/cu m of 

 methanol. At the end of the day, blood and urine levels of methanol were 

 8.9 and 21.8 mg/L, respectively; a control group had a mean blood and 

 urine level of < 0.6 and 1.1 mg/L, respectively. Urinary formic acid was 

 significantly higher in the workers (29.9 mg/L) than in the controls (12.7 

 mg/L). [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology 

 Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 

 p.381] **PEER REVIEWED** 

 In an inhalation study, six human volunteers were exposed to 200 ppm 

 methanol for 6 hr. At the end of the exposure, the blood methanol level 

 was increased from a mean of 1.8 mg/mL to 7.0 mg/mL. With light exercise, 

 the total amount of methanol inhaled during the exposure period was 1.8 

 times higher than inhaled at rest; however, no statistically significant 

 increase in blood methanol was observed. Formate did not accumulate in the 

 blood above the background level in subjects at rest or during excercise. 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 p.381] **PEER 

 REVIEWED** 

 The dermal uptake rate of liquid methanol applied to the forearm of human 

 volunteers was 11.5 mg/sq cm/hr. An absorption rate of 0.145 mg/sq cm/min 

 was observed after application to the forearm for 15 min, increasing to 

 0.22 and then decreasing to 0.185 mg/sq cm/min after 35 and 60 min, 

 respectively. When 15 mL of methanol was applied to the forearm skin of 

 human volunteers, there was some evidence of uptake based on increased 

 blood and urine methanol levels. The dermal flux for methanol in human 

 skin (epidermis) in vitro is 8.29 mg/sq cm/hr. [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V6 p.382] **PEER REVIEWED** 

 Background levels of methanol and formic acid in the body are derived 

 mainly from dietary and metabolic processes. A mean methanol blood level 

 of 0.73 mg/L in 31 unexposed subjects (range 0.32 to 2.61 mg/L) was 

 reported. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology 

 Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 

 p.382] **PEER REVIEWED** 

 ... 26 unexposed workers averaged 1.1 mg/L, with a range of < 0.6 to 

 2.9 mg/L. A mean of 0.25 mg/L methanol in expired breath of nine "normal" 

 people (range 0.06 to 0.45 mg/L) was reported. Urine concentrations of 

 methanol of up to 5 mg/L have been measured after ingestion of alcoholic 

 beverages by subjects not otherwise exposed to methanol. [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V6 p.382] **PEER REVIEWED** 

 Methanol is rapidly absorbed from the gastrointestinal tract with peak 

 absorption occurring in 30-60 min depending on the presence or absence of 

 food in the stomach. [WHO; Environ Health Criteria 196: Methanol p.56 

 (1997). Available from, as of July 14, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 ...The absence of formic acid accumulation in the urine of 5 volunteers 

 following 5 days of exposure to an atmosphere containing 260 mg/cu m (200 

 ppm) of methanol in a test chamber /was determined/. These results 

 indicated that there was no day-to day accumulation of formic acid in 

 urine in conjunction with 5 consecutive days of near-maximal permissible 

 airborne methanol exposure and that measurement of formic acid in urine 

 specimens collected 16 hr following cessation of exposure did not appear 

 to reflect inhalation methanol exposure on the preceding day. [WHO; 

 Environ Health Criteria 196: Methanol p.10 (1997). Available from, as of 

 July 14, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

Iris Camacho, 6308MM Page 35 of 69

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 REVIEWED** 

 Skin absorption rate studies of methanol ranging from 0.031-0.241 mg/sq cm 

 per min conducted in human volunteers showed that an average of 0.192 mg 

 methanol/sq cm per min is absorbed through direct contact of the skin to 

 methanol. [WHO; Environ Health Criteria 196: Methanol p.58 (1997). 

 Available from, as of July 14, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 After intake of small quantities of methanol (10-20 mL), human subjects 

 showed no methanol in blood after 48 hr, and the concentration of formic 

 acid in the urine was normal (6.5-12.8 mg%) within 24 hr. Following intake 

 of large amounts of methanol (50 mL), methanol was found in the blood 

 (250-1200 mg/L) after 48 hr. Formic acid was found in the blood (26-78 

 mg/L) as well as an increased excretion of formic acid in the urine 

 (540-2050 mg/L), and up to 20,500 mg/L within 24 hr. Maximum excretion of 

 formic acid was found to occur not later than the second or third day 

 after intake of methanol. [WHO; Environ Health Criteria 196: Methanol p.58 

 (1997). Available from, as of July 14, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 The rate of absorption into the skin has been found to be higher with M-85 

 (85% methanol-15% gasoline) than with pure methanol. The gasoline was 

 suggested to act by drying out the skin allowing the methanol to be more 

 readily absorbed. /M-85/ [WHO; Environ Health Criteria 196: Methanol p.58 

 (1997). Available from, as of July 14, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 In separate studies, methanol (100 or 500 mg/kg) and 3H2O (20 uCi/kg) were 

 administered intravenously on gestational days 20 and 14 to rats and on 

 gestational day 18 to mice. The methanol concentration-time data were 

 consistent with saturable maternal elimination and apparent first-order 

 transfer between maternal and conceptual compartments. At distribution 

 equilibrium, conceptual methanol concentrations exceeded those in the dam 

 by approximately 25%. The initial rate of conceptual permeation of 

 methanol was proportional to the reciprocal of maternal blood methanol 

 concentration (r2 = 0.910). The data indicated that high circulating 

 maternal methanol concentrations decrease the rate of presentation of 

 methanol and 3H2O to the conceptus, and, depending on the severity of the 

 decrease, fetal hypoxia could also result [WHO; Environ Health Criteria 

 196: Methanol p.60 (1997). Available from, as of July 14, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 A fatal case involving a 41-yr-old man who had ingested a large quantity 

 of methanol disclosed a broad distribution of methanol in postmortem 

 tissues and fluids. The highest content of methanol was found in the 

 kidney (5.13 g/kg) followed by the liver (4.18 g/kg), vitreous humor (3.9 

 g/L), heart (3.45 g/kg), urine (3.43 g/L), pericardial fluid (3.29 g/L), 

 blood (2.84 g/L) and stomach contents (2.21 g/L). [WHO; Environ Health 

 Criteria 196: Methanol p.106 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 A study in 24 one-year-old infants measured blood methanol concentrations 

 after oral exposure to aspartame. In a series of studies, 10 infants were 

 exposed to 34 mg/kg aspartame (the estimated premarketing 99th percentile 

 of adult daily ingestion), 6 infants were exposed to 50 mg/kg (termed a 

 very high dose), and 8 infants received 100 mg/kg (described as an 

 “abusive” dose). Methanol is a hydrolytic metabolite of aspartame 

 accounting for 10% of aspartame consumed. Thus, these authors estimated 

 the aspartame doses studied to be equivalent to ingestion of 3.4, 5, and 

 10 mg/kg bw methanol. Aspartame was administered via a cherry-flavored 

 beverage. A fasting blood sample and three subsequent samples were 

 obtained from each subject. The authors observed a positive correlation 

 between aspartame dose and blood methanol level in the infants that was 

 similar to that observed in a previous study of similar design and dose in 

 adults. Mean blood methanol levels were at the limit of detection (3.5 

 mg/L) in infants administered 34 mg/kg aspartame. Infants administered 

 aspartame at 50 mg/kg had peak blood methanol values of 3.0+/-1.0 mg/L 

 30-90 minutes after aspartame dosing. These values were essentially the 

 same as those seen in adults, 3.4+/-1.2 mg/L, receiving an equivalent 

 dose. The 8 infants administered the 100 mg/kg aspartame dose had a peak 

 mean blood methanol value of 10.2+/-2.8 mg/L 90 minutes post dosing. In 

 comparison, the mean blood methanol concentrations in 6 adults 

 administered an equivalent dose of aspartame was 12.7+/-2.0 mg/L 60 

 minutes after dosing. While the responses in infants and adults at this 

 dose were similar, the serum levels peaked earlier in adults and appeared 

 to persist longer when one compared the area-under-the-curve throughout a 

 2.5-hour sampling period. [DHHS/NTP; NTP-CERHR Expert Panel Report on the 

 Reproductive and Developmental Toxicity of Methanol p.10 (April 2002) 

 NTP-CERHR-MeOH-02. Available from, as of July 20, 2005: 

 http://cerhr.niehs.nih.gov/news/methanol/methanol_final.pdf] **PEER 

 REVIEWED** 

 Toxicokinetic studies were conducted following daily inhalation exposure 

 to methanol vapor prior to and throughout pregnancy in adult female Macaca 

 fascicularis monkeys. ...In a two-cohort study design, 48 females 

 (24/cohort) were assigned to parallel exposure groups at 0 (control), 200, 

 600, or 1800 ppm methanol vapor for approximately 2.5 hr/day, 7 days/wk 

 throughout breeding and pregnancy. Blood methanol at 30 min postexposure 

 was monitored biweekly. The time course for the clearance of blood MeOH 

 concentrations following exposure was characterized on four occasions: 

Iris Camacho, 6308MM Page 36 of 69

http://toxnet.nlm.nih.gov/cgi-bin/sis/download.txt 2/24/2011
 twice during the prebreeding period and during mid- and late pregnancy. 

 Average blood methanol concentrations at 30 min postexposure were 5, 11, 

 and 35 ug/mL across all four toxicokinetic studies in the 200, 600 and 

 1800 ppm groups, respectively. Blood concentrations in the 200 ppm group 

 were barely above basal (preexposure) blood methanol concentrations or 

 those observed in the control group (approximately 3 ug/mL). Nonlinear 

 elimination kinetics were observed in most of the 1800 ppm group females. 

 There was a decrease in elimination half-life (7-20%) and an increase in 

 clearance (30%) after 3-months of daily MeOH exposure compared to the 

 initial exposure. There were no statistically significant changes in the 

 first-order blood methanol half-life or clearance during pregnancy, but 

 the mean distribution volume per kilogram body weight decreased by 22% and 

 17% in the 600 and 1800 ppm groups. Plasma formate levels did not differ 

 between the methanol and control exposure groups. Plasma formate and serum 

 folate concentrations increased slightly over the course of this study in 

 both the exposed and control groups but these increases were not related 

 to methanol exposure. [Burbacher TM et al; Neurotoxicology and Teratology 

 26 (2): 201-221 (2004)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15019954" 

 target=new>PubMed Abstract 

BIOLOGICAL HALF-LIFE: 

 Biological half-life of methanol elimination in expired air is 1.5 hr 

 after either oral or dermal application. [Dutkiewicz B; Int Congr Ser- 

 Excerpta Med 440 (Ind Environ Xenobiotics): 106-9 (1978)] **PEER 

 REVIEWED** 

 ... Experiments were made during the morning after /human volunteers/ had 

 consumed 1000-1500 mL red wine (9.5% weight/volume ethanol, 100 mg/L 

 methanol) the previous evening. The washout of methanol from the body 

 coincided with the onset of hangover. The concentrations of ethanol and 

 methanol in blood were determined indirectly by analysis of end-expired 

 alveolar air. In the morning when blood-ethanol dropped below the Km of 

 liver alcohol dehydrogenase of about 100 mg/L (2.2 mM), the disappearance 

 half-life of ethanol was 21, 22, 18 and 15 min in 4 test subjects, 

 respectively. The corresponding elimination half-lives of methanol were 

 213, 110, 133 and 142 min in these same individuals. ... [Jones AW; 

 Pharmacol Toxicol 60 (3): 217-20 (1987)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3588516" 

 target=new>PubMed Abstract 

 Urinary methanol levels decreased exponentially with a half-life of about 

 2.5 to 3 hr in four volunteers exposed by inhalation to 102, 205, or 300 

 mg/cu m for 8 hr. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.381] **PEER REVIEWED** 

 In rats exposed by inhalation to 200, 1200, and 2000 ppm methanol for 6 

 hr... the blood half-lives were 0.8, 2.3, and 2.4 hr at 200, 1200, and 

 2000 ppm, respectively. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V6 p.375] **PEER REVIEWED** 

 ... The primate half lives after 200, 1200, and 2000 ppm were 2.4, 3.3, 

 and 3.5 hr, respectively. [Bingham, E.; Cohrssen, B.; Powell, C.H.; 

 Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, 

 N.Y. (2001)., p. V6 p.375] **PEER REVIEWED** 

 When methanol was administered orally to three volunteers at doses of 2.4, 

 4.0, or 5.6 g, elimination of methanol from the blood followed first-order 

 kinetics with a half-time of about 3 hr. [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V6 p.536] **PEER REVIEWED** 

MECHANISM OF ACTION: 

 ...The metabolic mechanisms of methanol toxicity /are/ reviewed. ... It is 

 noted that the most severe toxicty occurs many hours following peak blood 

 and tissue methanol concentrations so that these do not necessarily 

 provide an accurate indication of toxicity. Individual differences are 

 seen both in this latent period and in individual susceptibility to 

 methanol. This susceptibility may depend on the activity of folic acid 

 requiring metabolic reactions involved in formate metabolism, formate 

 being an intermediate produced during methanol oxidation and responsible 

 for many toxic effects of methanol. Studies of the characteristics of 

 methanol poisoning in non-primates and monkeys are examined. Despite the 

 ingestion of lethal doses of methanol, non-primates generally do not 

 develop significant metabolic acidosis nor impairment of vision, and no 

 consistent histopathology has been demonstrated in these species. In 

 monkeys, results suggest that the latent period represents a period of 

 compensated metabolic acidosis; when compensatory mechanisms are 

 exhausted, blood pH begins to drop. Formate accumulates and produces 

 acidosis in the methanol poisoned monkey, but not in the rat, apparently 

 due to a slower rate of formate metabolism to carbon dioxide in the 

 monkey. ... Studies demonstrating the role of alcohol dehydrogenase in 

 methanol metabolism in the monkey are reported; however, the 

 catalase/peroxidative system which participates in methanol metabolism in 

 rats apparently does not function in the monkey. Formaldehyde and formate 

 metabolism are also examined. The regulation of the rate of formate 

 metabolism is governed by regulation of the hepatic tetrahydrofolate 

 concentrations. ... Further research is needed to determine what step or 

 process it is which places the primate at a distinct liability in the 

Iris Camacho, 6308MM Page 37 of 69

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 metabolic disposition of one carbon moieties. [Tephly TR, Martin KE; Food 

 Sci Technol 12: 111-40 (1984)] **PEER REVIEWED** 

 Methanol toxicity is observed in monkeys and humans but is not seen in 

 rats or mice. The expression of methanol poisoning is related to the 

 ability of an animal to metabolize formate to carbon dioxide. Since the 

 rate of formate oxidation is related to hepatic tetrahydrofolate content 

 and the activites of folate dependent enzymes, studies were designed to 

 determine hepatic concentrations of hepatic tetrahydrofolate and activites 

 of folate dependent enzymes of human liver and livers of species 

 considered insensitive to methanol poisoning. An excellent correlation 

 between hepatic tetrahydrofolate and maximal rates of formate oxidation 

 has been observed. In human liver, levels were only 50% of those observed 

 for rat liver and similar to those found in monkey liver. Total folate was 

 also lower (60% decreased) in human liver than that found in rat or monkey 

 liver. Interestingly, mouse liver contains much higher hepatic 

 tetrahydrofolate and total folate than rat or monkey liver. This is 

 consistent with higher formate oxidation rates in this species. A second 

 important observation has been made. 10-Formyltetrahydrofolate 

 dehydrogenase activity, the enzyme catalyzing the final step of formate 

 oxidation to carbon dioxide, was markedly reduced in both monkey and human 

 liver. Thus, two mechanisms may be operative in explaining low formate 

 oxidation in species susceptible to methanol toxicity, low hepatic 

 tetahydrofolate levels and reduced hepatic 10-formyltetrahydrofolate 

 dehydrogenase activity. [Johlin FC et al; Mol Pharmacol 31 (5): 557-61 

 (1987)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3574297" 

 target=new>PubMed Abstract 

 Formic acid, the toxic metabolite of methanol, has been hypothesized to 

 produce retinal and optic nerve toxicity by disrupting mitochondrial 

 energy production. It has been shown in vitro to inhibit the activity of 

 cytochrome oxidase, a vital component of the mitochondrial electron 

 transport chain involved in ATP synthesis. Inhibition occurs subsequent to 

 the binding of formic acid to the ferric heme iron of cytochrome oxidase, 

 and the apparent inhibition constant is between 5 and 30 mM. 

 Concentrations of formate present in the blood and tissues of 

 methanol-intoxicated humans, non-human primates and rodent models of 

 methanol-intoxication are within this range. Studies conducted in 

 methanol-sensitive rodent models have revealed abnormalities in retinal 

 and optic nerve function and morphology, consistent with the hypothesis 

 that formate acts as a mitochondrial toxin. In these animal models, 

 formate oxidation is selectively inhibited by dietary or chemical 

 depletion of folate coenzymes, thus allowing formate to accumulate to 

 toxic concentrations following methanol administration. 

 Methanol-intoxicated rats developed formic acidemia, metabolic acidosis 

 and visual toxicity analogous to the human methanol poisoning syndrome. 

 [WHO; Environ Health Criteria 196: Methanol p.94 (1997). Available from, 

 as of July 18, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] 

 **PEER REVIEWED** 

 Visual dysfunction was measured as reduction in the flash evoked cortical 

 potential (FEP) and electroretinogram (ERG). The FEP is a measure of the 

 functional integrity of the primary visual pathway from the retina to the 

 visual cortex and the ERG is a global measure of retinal function in 

 response to illumination. The FEP was progressively diminished in methanol 

 intoxicated rats, indicative of a disruption of neuronal conduction along 

 the primary visual pathway from the retina to the visual cortex. ERG 

 analysis in methanol-intoxicated rats revealed a significant early deficit 

 in b-wave amplitude, followed by a temporally delayed lesser reduction in 

 a-wave amplitude. The b-wave of the ERG is generated by depolarization of 

 the Muller glial cells and reflects synaptic activity at the level of the 

 bipolar cells. The b-wave of the ERG is extremely sensitive to conditions 

 that interfere with retinal energy metabolism and is reduced or abolished 

 following brief ischemia or the administration of metabolic poisons. Both 

 FEP and ERG alterations occurred at the same time as accumulation of blood 

 formate, indicative of a causal relationship between formate-induced 

 metabolic and visual disturbances. Similar ERG reductions have been 

 reported in methanol-intoxicated primates and in human methanol 

 intoxication. [WHO; Environ Health Criteria 196: Methanol p.95 (1997). 

 Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 In addition to neurofunctional changes, bioenergetic and morphological 

 alterations indicative of formate-induced disruption of retinal energy 

 metabolism have been documented in methanol-intoxicated rats. 

 Morphological studies, coupled with cytochrome oxidase histochemistry, 

 revealed generalized retinal edema, photoreceptor and /retinal pigment 

 epithelium/ (RPE) vacuolation, mitochondrial swelling and a reduction in 

 cytochrome oxidase activity in photoreceptor mitochondria from methanol 

 intoxicated rats. The most striking structural alterations observed in the 

 retinas of methanol-intoxicated rats were vacuolation and mitochondrial 

 swelling in inner segments of the photoreceptor cells. Photoreceptor 

 mitochondria from methanol-intoxicated rats were swollen and expanded to 

 disrupted cristae and showed no evidence of cytochrome oxidase reaction 

 product. In contrast, photoreceptor mitochondria from control animals 

 showed normal morphology with well-defined cristae and were moderately 

 reactive for cytochrome oxidase reaction product. These findings are 

 consistent with disruption of ionic homoeostasis in the photoreceptors, 

 secondary to inhibition of mitochondrial function. Biochemical 

 measurements also showed a significant reduction in retinal and brain 

Iris Camacho, 6308MM Page 38 of 69

http://toxnet.nlm.nih.gov/cgi-bin/sis/download.txt 2/24/2011
 cytochrome oxidase activity and ATP concentrations in methanol-intoxicated 

 rats relative to control animals. Surprisingly, no differences from 

 control values were observed in hepatic, renal or cardiac cytochrome 

 oxidase activity or ATP concentrations in methanol-intoxicated rats. The 

 reduction in retinal function, inhibition of retinal, optic nerve and 

 brain cytochrome oxidase activity, depletion of retinal and brain ATP 

 concentrations, and mitochondrial disruption produced in 

 methanol-intoxicated rats are consistent with the hypothesis that formate 

 acts as a mitochondrial toxin with selectivity for the retina and brain. 

 [WHO; Environ Health Criteria 196: Methanol p.96 (1997). Available from, 

 as of July 18, 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] 

 **PEER REVIEWED** 

 Role of free radicals in methanol toxicity was evaluated in methanol 

 treated albino rats. Methanol intoxication increased lipid peroxidation 

 and depleted the free radical scavenging enzyme systems. The free radical 

 quenching effect of vitamin E protected the animals from methanol induced 

 free radical damage. [Paula EM et al; Indian J Physiol Pharmacol 47 (2): 

 207-11 (2003)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15255626&query_hl=10" 

 target=new>PubMed Abstract 

 The initiating effect in the ocular toxicity of formic acid is believed to 

 involve the inhibition of cytochrome oxidase, which is located in the 

 mitochondria and is involved in oxidative phosphorylation. [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V6 p.380] **PEER REVIEWED** 

INTERACTIONS: 

 ...Pyrazole and 3-amino-1,2,4-triazole... are potent inhibitors of alcohol 

 dehydrogenase and catalase... both are active in vivo. ...Administered 

 separately or together... /to rats/. Findings confirmed... that 

 3-amino-1,2,4-triazole... decreased rate of carbon dioxide production. 

 ...Pyrazole... substantially reduced oxidation of methanol to carbon 

 dioxide. [The Chemical Society. Foreign Compound Metabolism in Mammals 

 Volume 3. London: The Chemical Society, 1975., p. 624] **PEER REVIEWED** 

 Ethanol is used to inhibit the conversion of methanol to its highly toxic 

 metabolite, formic acid... . [Hardman, J.G., L.E. Limbird, P.B., A.G. 

 Gilman. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 

 10th ed. New York, NY: McGraw-Hill, 2001., p. 78] **PEER REVIEWED** 

 Chronic combined exposure to methanol and carbon monoxide has been 

 reported as a causative factor of cerebral atherosclerosis. [International 

 Labour Office. Encyclopedia of Occupational Health and Safety. Vols. 

 I&II. Geneva, Switzerland: International Labour Office, 1983., p. 

 1357] **PEER REVIEWED** 

 ... Dinitrogen oxide inhibited the oxidation of formate generated from the 

 metabolism of methanol resulting in the development of severe metabolic 

 acidosis and high blood formate levels in these animals compared with air 

 breathing monkeys administered the same dose of methanol. Treatment of 

 dinitrogen oxide exposed monkeys with repetitive doses of methionine (100 

 mg/kg 10, 12, and 14 hr after methanol exposure) reversed the effects of 

 dinitrogen oxide on formate oxidation resulting in a marked decrease in 

 blood formate levels and an increase in the rate of (14)carbon dioxide 

 formation from methanol. Methionine treatment also reversed the 

 development of metabolic acidosis and bicarbonate depletion observed in 

 dinitrogen oxide exposed monkeys. Thus, hepatic methionine synthetase is 

 important in the regulation of tetrahydrofolate dependent metabolism in 

 the monkey and the generation of this enzyme is a major factor in 

 determining the sensitivity of a species to methanol poisoning. [Eells JT 

 et al; J Pharm Exp Ther 227 (2): 349-53 (1983)] **PEER REVIEWED** 

 Inhaled methanol potentiated the hepatotoxicity produced by carbon 

 tetrachloride in adult male F-344 rats. Rats were exposed to methanol (0 

 or 13,000 mg/cu m) 10000 ppm for 6 hr, then treated 24 hr later with oral 

 CCl4 (0.075 mL/kg). CCl4 alone produced a low level of hepatotoxicity 

 within 3 days. Methanol plus CCl4 resulted in marked increases in serum 

 aspartate aminotransferase and alanine aminotransferase that lasted for 7 

 days. Methanol also exacerbated the histological evidence of CCl4-induced 

 centrilobular degeneration and necrosis. Methanol exposure by inhalation 

 induced cytochrome P4502E1 (CYP2E1), which appeared to be the principal 

 toxicokinetic mechanism underlying methanol potentiation of carbon 

 tetrachloride hepatotoxicity. [WHO; Environ Health Criteria 196: Methanol 

 p.93 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 When dichloromethane (DCM) is metabolized carbon monoxide is formed, 

 leading to increased carboxyhemoglobin (COHb) levels in blood. ...In rats 

 pretreated with methanol, methanol doses of 790-6330 mg/kg (24.7-198 

 mmol/kg) stimulated increased metabolism of DCM, as seen by further 

 increases in COHb levels. When methanol was administered simultaneously 

 with DCM, a decrease in COHb formation was seen at methanol doses of 4736 

 to 7900 mg/kg (148-247 mmol/kg) but not at 3162 mg/kg (98.8 mmol/kg). Thus 

 methanol can interact with DCM metabolism both by induction and by 

 competitive inhibition, the latter only at very high doses. [WHO; Environ 

 Health Criteria 196: Methanol p.93 (1997). Available from, as of July 18, 

 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

Iris Camacho, 6308MM Page 39 of 69

http://toxnet.nlm.nih.gov/cgi-bin/sis/download.txt 2/24/2011
 This research was undertaken to determine potential interactions among 

 chemical and physical agents. Radiofrequency (RF) radiation is used in 

 numerous workplaces, and many workers are concurrently exposed to RF 

 radiation and various chemicals. The developmental toxicity of RF 

 radiation is associated with the degree and duration of hyperthermia 

 induced by the exposure. Previous animal research indicates that 

 hyperthermia induced by an elevation in ambient temperature can potentiate 

 the toxicity and teratogenicity of some chemical agents. We previously 

 demonstrated that combined exposure to RF radiation (10 MHz) and the 

 industrial solvent, 2-methoxyethanol (2ME), enhanced teratogenicity in 

 rats. Interactions were noted at even the lowest levels of 2ME tested, but 

 only at hyperthermic levels of RF radiation. The purpose of the present 

 research is to investigate if the interactive effects noted for RF 

 radiation and 2ME are unique to these agents, or if similar interactions 

 might be seen with other chemicals. Because methanol is widely used as a 

 solvent as well as fuel additive, and, at high levels, is teratogenic in 

 animals, we selected methanol as a chemical to address generalizability. 

 Based on the literature and our pilot studies, 0, 2, or 3 g/kg methanol 

 (twice, at 6-hr intervals) were administered on gestation day 9 or 13 to 

 groups of 10 Sprague-Dawley rats. Dams treated on day 9 were given 

 methanol and exposed to RF radiation sufficient to maintain colonic 

 temperature at 41 deg C for 60 minutes (or sham). Those treated on day 13 

 were given methanol plus either 0 or 100 mg/kg 2ME. Because we observed 

 that methanol produced hypothermia, some groups were given the initial 

 dose of methanol concurrently with the RF or 2ME, and others were given 

 the first dose of methanol 1.5 hours prior to RF or 2ME. Dams were 

 sacrificed on gestation day 20, and the fetuses were examined for external 

 malformations. The results indicate that RF radiation or methanol on day 9 

 increased the incidence of resorbed fetuses, but no interactive effects 

 were observed. The resorptions were highest in groups given the 

 experimental treatments 1.5 hours apart. The higher dose of methanol also 

 reduced fetal weights. Administration of 2ME or methanol on day 13 

 increased the rate of malformations, and there was evidence of a positive 

 interaction between 2ME and methanol. Fetal weights were reduced by 2ME 

 and methanol alone, but no interaction was observed. Also, separation of 

 the dosing with the teratogens did not affect the results. [Nelson BK et 

 al; Int J Toxicol 20 (2): 89-100 (2001)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11354470&query_hl=46" 

 target=new>PubMed Abstract 

 An attempt has been made to study the histological and ultrastructural 

 changes in the liver of rats caused by individual and combined treatment 

 of three industrial solvents viz. xylene, toulene and methyl alcohol. 

 Results show that methyl alcohol is more hepatotoxic than xylene and 

 toluene. A mixture of these solvents is also hepatotoxic. It causes 

 peculiar ultrastructural changes viz. involution of nuclear membrane and 

 irregular arrangement of mitochondrial cristae. It is concluded that a 

 weak interaction takes place at the site of their metabolism expressed as 

 weak antagonism. Histological changes thus noted do not strictly 

 correspond with functional changes as observed during earlier 

 investigations. [Rana S VS, Kumar S; J of Environ Biol 18 (2): 185-90 

 (1997)] **PEER REVIEWED** 

 The drug 4-methylpyrazole (4-MP; fomepizole) is a competitive ADH 

 inhibitor and an effective antidote for methanol and ethylene glycol 

 poisoning. [Sullivan, J.B., Krieger G.R. (eds). Clinical Environmental 

 Health and Toxic Exposures. Second edition. Lippincott Williams and 

 Wilkins, Philadelphia, Pennsylvania 1999., p. 1179] **PEER REVIEWED** 

 It has been suggested that the metabolic acidosis due to methanol might be 

 exacerbated in individuals with diabetes since it is well known that these 

 patients suffer from diabetic ketoacidosis. However, there are no clinical 

 or experimental data on any interaction between methanol acidosis and 

 diabetic ketoacidosis. [WHO; Environ Health Criteria 196: Methanol p.113 

 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

PHARMACOLOGY: 

INTERACTIONS: 

 ...Pyrazole and 3-amino-1,2,4-triazole... are potent inhibitors of alcohol 

 dehydrogenase and catalase... both are active in vivo. ...Administered 

 separately or together... /to rats/. Findings confirmed... that 

 3-amino-1,2,4-triazole... decreased rate of carbon dioxide production. 

 ...Pyrazole... substantially reduced oxidation of methanol to carbon 

 dioxide. [The Chemical Society. Foreign Compound Metabolism in Mammals 

 Volume 3. London: The Chemical Society, 1975., p. 624] **PEER REVIEWED** 

 Ethanol is used to inhibit the conversion of methanol to its highly toxic 

 metabolite, formic acid... . [Hardman, J.G., L.E. Limbird, P.B., A.G. 

 Gilman. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 

 10th ed. New York, NY: McGraw-Hill, 2001., p. 78] **PEER REVIEWED** 

 Chronic combined exposure to methanol and carbon monoxide has been 

 reported as a causative factor of cerebral atherosclerosis. [International 

 Labour Office. Encyclopedia of Occupational Health and Safety. Vols. 

 I&II. Geneva, Switzerland: International Labour Office, 1983., p. 

 1357] **PEER REVIEWED** 

Iris Camacho, 6308MM Page 40 of 69

http://toxnet.nlm.nih.gov/cgi-bin/sis/download.txt 2/24/2011
 ... Dinitrogen oxide inhibited the oxidation of formate generated from the 

 metabolism of methanol resulting in the development of severe metabolic 

 acidosis and high blood formate levels in these animals compared with air 

 breathing monkeys administered the same dose of methanol. Treatment of 

 dinitrogen oxide exposed monkeys with repetitive doses of methionine (100 

 mg/kg 10, 12, and 14 hr after methanol exposure) reversed the effects of 

 dinitrogen oxide on formate oxidation resulting in a marked decrease in 

 blood formate levels and an increase in the rate of (14)carbon dioxide 

 formation from methanol. Methionine treatment also reversed the 

 development of metabolic acidosis and bicarbonate depletion observed in 

 dinitrogen oxide exposed monkeys. Thus, hepatic methionine synthetase is 

 important in the regulation of tetrahydrofolate dependent metabolism in 

 the monkey and the generation of this enzyme is a major factor in 

 determining the sensitivity of a species to methanol poisoning. [Eells JT 

 et al; J Pharm Exp Ther 227 (2): 349-53 (1983)] **PEER REVIEWED** 

 Inhaled methanol potentiated the hepatotoxicity produced by carbon 

 tetrachloride in adult male F-344 rats. Rats were exposed to methanol (0 

 or 13,000 mg/cu m) 10000 ppm for 6 hr, then treated 24 hr later with oral 

 CCl4 (0.075 mL/kg). CCl4 alone produced a low level of hepatotoxicity 

 within 3 days. Methanol plus CCl4 resulted in marked increases in serum 

 aspartate aminotransferase and alanine aminotransferase that lasted for 7 

 days. Methanol also exacerbated the histological evidence of CCl4-induced 

 centrilobular degeneration and necrosis. Methanol exposure by inhalation 

 induced cytochrome P4502E1 (CYP2E1), which appeared to be the principal 

 toxicokinetic mechanism underlying methanol potentiation of carbon 

 tetrachloride hepatotoxicity. [WHO; Environ Health Criteria 196: Methanol 

 p.93 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

 When dichloromethane (DCM) is metabolized carbon monoxide is formed, 

 leading to increased carboxyhemoglobin (COHb) levels in blood. ...In rats 

 pretreated with methanol, methanol doses of 790-6330 mg/kg (24.7-198 

 mmol/kg) stimulated increased metabolism of DCM, as seen by further 

 increases in COHb levels. When methanol was administered simultaneously 

 with DCM, a decrease in COHb formation was seen at methanol doses of 4736 

 to 7900 mg/kg (148-247 mmol/kg) but not at 3162 mg/kg (98.8 mmol/kg). Thus 

 methanol can interact with DCM metabolism both by induction and by 

 competitive inhibition, the latter only at very high doses. [WHO; Environ 

 Health Criteria 196: Methanol p.93 (1997). Available from, as of July 18, 

 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

 This research was undertaken to determine potential interactions among 

 chemical and physical agents. Radiofrequency (RF) radiation is used in 

 numerous workplaces, and many workers are concurrently exposed to RF 

 radiation and various chemicals. The developmental toxicity of RF 

 radiation is associated with the degree and duration of hyperthermia 

 induced by the exposure. Previous animal research indicates that 

 hyperthermia induced by an elevation in ambient temperature can potentiate 

 the toxicity and teratogenicity of some chemical agents. We previously 

 demonstrated that combined exposure to RF radiation (10 MHz) and the 

 industrial solvent, 2-methoxyethanol (2ME), enhanced teratogenicity in 

 rats. Interactions were noted at even the lowest levels of 2ME tested, but 

 only at hyperthermic levels of RF radiation. The purpose of the present 

 research is to investigate if the interactive effects noted for RF 

 radiation and 2ME are unique to these agents, or if similar interactions 

 might be seen with other chemicals. Because methanol is widely used as a 

 solvent as well as fuel additive, and, at high levels, is teratogenic in 

 animals, we selected methanol as a chemical to address generalizability. 

 Based on the literature and our pilot studies, 0, 2, or 3 g/kg methanol 

 (twice, at 6-hr intervals) were administered on gestation day 9 or 13 to 

 groups of 10 Sprague-Dawley rats. Dams treated on day 9 were given 

 methanol and exposed to RF radiation sufficient to maintain colonic 

 temperature at 41 deg C for 60 minutes (or sham). Those treated on day 13 

 were given methanol plus either 0 or 100 mg/kg 2ME. Because we observed 

 that methanol produced hypothermia, some groups were given the initial 

 dose of methanol concurrently with the RF or 2ME, and others were given 

 the first dose of methanol 1.5 hours prior to RF or 2ME. Dams were 

 sacrificed on gestation day 20, and the fetuses were examined for external 

 malformations. The results indicate that RF radiation or methanol on day 9 

 increased the incidence of resorbed fetuses, but no interactive effects 

 were observed. The resorptions were highest in groups given the 

 experimental treatments 1.5 hours apart. The higher dose of methanol also 

 reduced fetal weights. Administration of 2ME or methanol on day 13 

 increased the rate of malformations, and there was evidence of a positive 

 interaction between 2ME and methanol. Fetal weights were reduced by 2ME 

 and methanol alone, but no interaction was observed. Also, separation of 

 the dosing with the teratogens did not affect the results. [Nelson BK et 

 al; Int J Toxicol 20 (2): 89-100 (2001)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11354470&query_hl=46" 

 target=new>PubMed Abstract 

 An attempt has been made to study the histological and ultrastructural 

 changes in the liver of rats caused by individual and combined treatment 

 of three industrial solvents viz. xylene, toulene and methyl alcohol. 

 Results show that methyl alcohol is more hepatotoxic than xylene and 

 toluene. A mixture of these solvents is also hepatotoxic. It causes 

 peculiar ultrastructural changes viz. involution of nuclear membrane and 

 irregular arrangement of mitochondrial cristae. It is concluded that a 

 weak interaction takes place at the site of their metabolism expressed as 

Iris Camacho, 6308MM Page 41 of 69

http://toxnet.nlm.nih.gov/cgi-bin/sis/download.txt 2/24/2011
 weak antagonism. Histological changes thus noted do not strictly 

 correspond with functional changes as observed during earlier 

 investigations. [Rana S VS, Kumar S; J of Environ Biol 18 (2): 185-90 

 (1997)] **PEER REVIEWED** 

 The drug 4-methylpyrazole (4-MP; fomepizole) is a competitive ADH 

 inhibitor and an effective antidote for methanol and ethylene glycol 

 poisoning. [Sullivan, J.B., Krieger G.R. (eds). Clinical Environmental 

 Health and Toxic Exposures. Second edition. Lippincott Williams and 

 Wilkins, Philadelphia, Pennsylvania 1999., p. 1179] **PEER REVIEWED** 

 It has been suggested that the metabolic acidosis due to methanol might be 

 exacerbated in individuals with diabetes since it is well known that these 

 patients suffer from diabetic ketoacidosis. However, there are no clinical 

 or experimental data on any interaction between methanol acidosis and 

 diabetic ketoacidosis. [WHO; Environ Health Criteria 196: Methanol p.113 

 (1997). Available from, as of July 19, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

MINIMUM FATAL DOSE LEVEL: 

 The minimum lethal dose of methanol in the absence of medical treatment is 

 between 0.3 and 1 g/kg. [Environmental Health Criteria 196: Methanol pp. 8 

 (1997) by the International Programme on Chemical Safety (IPCS) under the 

 joint sponsorship of the United Nations Environment Programme, the 

 International Labour Organisation and the World Health Organization.] 

 **PEER REVIEWED** 

ENVIRONMENTAL FATE & EXPOSURE: 

ENVIRONMENTAL FATE/EXPOSURE SUMMARY: 

 Methanol's production and use as a solvent, fuel additive, and in the 

 production of formaldehyde, acetic acid, and methyl tertiary butyl ether 

 (MTBE) may result in its release to the environment through various waste 

 streams. Methanol has been identified as a natural emission product from 

 various plants and as a biological decomposition product of biological 

 wastes and sewage. If released to the atmosphere, a vapor pressure of 127 

 mm Hg at 25 deg C indicates that methanol will exist solely in the vapor 

 phase. Vapor phase methanol is degraded in the atmosphere by reaction with 

 photochemically-produced hydroxyl radicals; the half-life for this 

 reaction in air is estimated to be 17 days. If released to soil, methanol 

 is expected to have very high mobility based upon an estimated Koc of 1. 

 Volatilization from moist soil surfaces is expected to be an important 

 fate process based upon a Henry's Law constant of 4.55X10-6 atm-cu m/mole. 

 Methanol may also volatilize from dry soils based upon it vapor pressure. 

 Biodegradation of methanol in soils is expected to occur rapidly based on 

 half-lives in a sandy silt loam from Texas and a sandy loam from 

 Mississippi of 1 and 3.2 days, respectively. If released into water, 

 methanol is not expected to adsorb to suspended solids and sediment based 

 upon the estimated Koc. Volatilization from water surfaces is expected to 

 be an important fate process based upon this compound's Henry's Law 

 constant. Estimated volatilization half-lives for a model river and model 

 lake are 3 and 35 days, respectively. Biodegradation is expected to occur 

 in natural waters since methanol is degraded quickly in soils and was 

 biodegraded rapidly in various aqueous screening tests using sewage seed 

 or activated sludge. BCF values of less than 10, measured in fish suggests 

 bioconcentration in aquatic organisms is low. Hydrolysis of methanol and 

 photolysis in sunlit surface waters are not expected since methanol lacks 

 functional groups that are susceptible to hydrolysis or photolysis under 

 environmental conditions. Occupational exposure to methanol may occur 

 through inhalation and dermal contact with this compound at workplaces 

 where methanol is produced or used. Monitoring data indicate that the 

 general population may be exposed to methanol via inhalation of ambient 

 air, and ingestion of food and drinking water. (SRC) **PEER REVIEWED** 

PROBABLE ROUTES OF HUMAN EXPOSURE: 

 STUDY OF WOOD HEEL INDUSTRY IN MA SHOWED AVG METHANOL VAPOR CONCN RANGING 

 FROM 160-170 PPM, WITH NO DEFINITE EVIDENCE OF INJURY TO EXPOSED WORKERS 

 ... CONCN BETWEEN 400 & 1000 PPM IN SPIRIT DUPLICATING PROCESSES /WERE 

 REPORTED/. NO MENTION WAS MADE OF SYMPTOMS OR COMPLAINTS, BUT THESE CONCN 

 WERE CONSIDERED EXCESSIVE. ... [American Conference of Governmental 

 Industrial Hygienists. Documentation of the Threshold Limit Values and 

 Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference 

 of Governmental Industrial Hygienists, 1986., p. 372] **PEER REVIEWED** 

 ALTHOUGH INDIVIDUAL RESPONSES OF MAN TO METHYL ALCOHOL MAY VARY 

 CONSIDERABLY, INDUSTRIAL EXPOSURES ARE NOT VERY HAZARDOUS IF CONCN ARE 

 MAINTAINED WITHIN UPPER LIMIT OF 200 PPM BY PROPER VENTILATION. [Clayton, 

 G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: 

 Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 

 1981-1982., p. 4541] **PEER REVIEWED** 

 NIOSH (NOES Survey 1981-1983) has statistically estimated that 1,219,371 

 workers (295,849 of these are female) are potentially exposed to methanol 

 in the US(1). Occupational exposure to methanol may occur through 

 inhalation and dermal contact with this compound at workplaces where 

 methanol is produced or used(SRC). Monitoring data indicate that the 

 general population may be exposed to methanol via inhalation of ambient 

 air, ingestion of food and drinking water(SRC). [(1) NIOSH; International 

 Safety Cards. Methanol. 67-56-1. Available at 

Iris Camacho, 6308MM Page 42 of 69

http://toxnet.nlm.nih.gov/cgi-bin/sis/download.txt 2/24/2011
 http://www.cdc.gov/niosh/ipcs/nicstart.html as of Jul 1, 2005.] **PEER 

 REVIEWED** 

BODY BURDEN: 

 Methanol was detected in 1 of 12 samples of human milk collected from 

 volunteers in 4 USA cities(1). Methanol has been detected in expired human 

 air(2,3,4); in one study, it was detected in 3.6% of 387 expired air 

 samples collected from 54 volunteers at a geometric mean concn of 0.549 

 ng/l(4). [(1) Pellizzari ED et al; Bull Environ Contam Toxicol 28: 322-8 

 (1982) (2) Krotosynski B; J Chromat Sci 15: 239-44 (1977) (3) Krotosynski 

 BK, O'Neill HJ; J Environ Sci Health Part A-Environ Sci Eng 17: 855-83 

 (1982) (4) Krotosynski BK et al; J Anal Toxicol 3: 255-43 (1979)] **PEER 

 REVIEWED** 

NATURAL POLLUTION SOURCES: 

 Methanol is found in wood. [Verschueren, K. Handbook of Environmental Data 

 of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 

 1983., p. 430] **PEER REVIEWED** 

 A small amount of methanol is found in the expired breath of normal 

 subjects, possibly by endogenous metabolic production. [Haddad, L.M. and 

 Winchester, J.F. Clinical Management of Poisoning and Drug Overdosage. 

 Philadelphia, PA: W.B. Saunders Co., 1983., p. 393] **PEER REVIEWED** 

 Methanol has been identified as a volatile emission product from evergreen 

 cypress trees(1). Methanol is formed during biological decomposition of 

 biological wastes, sewage, and sludges(2). Natural emission sources 

 include volcanic gases, vegetation, microbes, and insects(3). [(1) 

 Isidorov VA et al; Atmos Environ 19: 1-8 (1985) (2) Abrams EF et al; 

 Identification of Organic Compounds in Effluents from Industrial Sources 

 EPA- 560/3-75-002 p. 102 (1975) (3) Graedel TE et al; Atmospheric Chemical 

 Compounds. Sources, Occurrence, and Bioassay. Orlando, FL: Academic Press 

 p. 232 (1986)] **PEER REVIEWED** 

 Some distilled fruit spirits contain, normally, high quantities of 

 methanol. ... [Bindler F et al; Food Addit Contam 5 (3): 343-51 (1988)] 

 **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3396738" 

 target=new>PubMed Abstract 

ARTIFICIAL POLLUTION SOURCES: 

 Methanol's production and use as a solvent, fuel additive, and in the 

 production of formaldehyde, acetic acid, and methyl tertiary butyl ether 

 (MTBE)(1) may result in its release to the environment through various 

 waste streams(SRC). The largest anthropogenic source of methanol release 

 to the environment is evaporation from solvent uses which amounts to an 

 estimated 1.1 billion lb annually(2). Annual emission releases from 

 methanol production, end-product mfg, and storage/handling have been 

 estimated to be 68, 49, and 12 million lb, respectively(2). [(1) English A 

 et al; in Kirk-Othmer Encycl Cheml Technol 4th ed Kroschwitz JI, ed. NY, 

 NY John Wiley and Sons 16: 537-56 (1995) (2) USEPA; Chemical Hazard 

 Information Profiles (CHIPS). USEPA-560/11-80-011 p. 196-7 (1980)] **PEER 

 REVIEWED** 

ENVIRONMENTAL FATE: 

 TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc 

 value of 1(SRC), determined from a structure estimation method(2), 

 indicates that methanol is expected to have very high mobility in 

 soil(SRC). Volatilization of methanol from moist soil surfaces is expected 

 to be an important fate process(SRC) given a Henry's Law constant of 

 4.55X10-6 atm-cu m/mole(3). The potential for volatilization of methanol 

 from dry soil surfaces may exist(SRC) based upon a vapor pressure of 127 

 mm Hg(4). Biodegradation is expected to be an important fate process for 

 methanol based on half-lives of 1 and 3.2 days measured in a sandy silt 

 loam and sandy loam from Texas and Mississippi, respectively(5). [(1) 

 Swann RL et al; Res Rev 85: 17-28 (1983) (2) Meylan WM et al; Environ Sci 

 Technol 26: 1560-67 (1992) (3) Gaffney JS et al; Environ Sci Technol 21: 

 519-23 (1987) (4) Boublik T et al, eds; The Vapour Pressures of Pure 

 Substances. 2nd rev ed. Amsterdam: Elsevier (1984) (5) Loehr RC; 

 Treatability potential for EPA listed hazardous wastes in soil. USEPA. 

 Robert S. Kerr Environ. Res. Lab., ADA, OK. EPA/600/2-89/011 (1989)] 

 **PEER REVIEWED** 

 AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value 

 of 1(SRC), determined from a structure estimation method(2), indicates 

 that methanol is not expected to adsorb to suspended solids and 

 sediment(SRC). Volatilization from water surfaces is expected(3) based 

 upon a Henry's Law constant of 4.55X10-6 atm-cu m/mole(4). Using this 

 Henry's Law constant and an estimation method(3), volatilization 

 half-lives for a model river and model lake are 3 and 35 days, 

 respectively(SRC). According to a classification scheme(5), a BCF of less 

 than 10 measured in fish(6), suggests bioconcentration in aquatic 

 organisms is low(SRC). Hydrolysis and photolysis in sunlit surface waters 

 is not expected to be an important environmental fate process for methanol 

 since this compound lacks functional groups that hydrolyze or absorb light 

 under environmentally relevant conditions. Methanol has been shown to 

 undergo rapid biodegradation in a variety of screening studies using 

 sewage seed and activated sludge inoculum(7-9), which suggests that 

 biodegradation will occur in aquatic environments. [(1) Swann RL et al; 

 Res Rev 85: 17-28 (1983) (2) Meylan WM et al; Environ Sci Technol 26: 

 1560-67 (1992) (3) Lyman WJ et al; Handbook of Chemical Property 

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 Estimation Methods. Washington, DC: Amer Chem Soc pp. 4-9, 15-1 to 15-29 

 (1990) (4) Gaffney JS et al; Environ Sci Technol 21: 519-23 (1987) (5) 

 Franke C et al; Chemosphere 29: 1501-14 (1994) (6) Freitag D et al; 

 Chemosphere 14: 1589-1616 (1985) (7) Dore M et al; Trib Cebedeau 28: 3-11 

 (1975) (8) Gellman I, Heukelekian H; Sew Indust Wastes 27: 793-801 (1955) 

 (9) Gerhold RM, Malaney GW; J Water Pollut Control Fed 38: 562-79 (1966)] 

 **PEER REVIEWED** 

 ATMOSPHERIC FATE: According to a model of gas/particle partitioning of 

 semivolatile organic compounds in the atmosphere(1), methanol, which has a 

 vapor pressure of 127 mm Hg at 25 deg C(2), is expected to exist solely as 

 a vapor in the ambient atmosphere. Vapor-phase methanol is degraded in the 

 atmosphere by reaction with photochemically-produced hydroxyl 

 radicals(SRC); the half-life for this reaction in air is estimated to be 

 17 days(SRC), calculated from its rate constant of 9.4X10-13 cu 

 cm/molecule-sec at 25 deg C(3). [(1) Bidleman TF; Environ Sci Technol 22: 

 361-367 (1988) (2) Boublik T et al, eds; The Vapour Pressures of Pure 

 Substances. 2nd rev ed. Amsterdam: Elsevier (1984) (3) Kwok ESC, Atkinson 

 R; Estimation of hydroxyl radical reaction rate constants for gas-phase 

 organic compounds using a structure-reactivity relationship: an update. 

 Riverside, CA: Univ CA, Statewide Air Pollut Res CTR., CMA Contract No. 

 AFC-8.0-OR-8.0-OR (1994)] **PEER REVIEWED** 

ENVIRONMENTAL BIODEGRADATION: 

 AEROBIC: The half-life for methanol applied to a sandy loam from 

 Mississippi (68% sand, 23.4% silt, 8.6% clay, 0.94% organic carbon, pH 

 4.8) was 3.2 days(1). The half-life of methanol applied to a sandy silt 

 loam from Texas (61.5% sand, 31.1% silt, 7.4% clay, 3.28% organic carbon, 

 pH 7.8) was 1 day(1). The moisture content of each soil was maintained at 

 approximately 80% of its field capacity over the 64 day incubation period, 

 and the half-lives did not account for any potential volatilization loss. 

 [(1) Loehr RC; Treatability potential for EPA listed hazardous wastes in 

 soil. USEPA. Robert S. Kerr Environ. Res. Lab., ADA, OK. EPA/600/2-89/011 

 (1989)] **PEER REVIEWED** 

 AEROBIC: Methanol, present at 0.050 mg/L, reached 48% of its theoretical 

 BOD in 5 days using a sewage inoculum(1). Using activated sludge as 

 inoculum, methanol achieved 93%(2) and 21%(3) of its theoretical BOD in 2 

 day and 1 day Warburg respirometer studies, respectively. Using a standard 

 dilution technique, methanol reached 53.4% of its theoretical BOD in 5 

 days, and 97.7% of the theoretical BOD was achieved in 50 days using 

 sewage seed(4). Using an activated sludge acclimated to methanol, 55% of 

 the theoretical BOD was achieved in 23 hours(5). Methanol had a half-life 

 of 0.4 days in a sewage die-away test(6). [(1) Dore M et al; Trib Cebedeau 

 28: 3-11 (1975) (2) Gellman I, Heukelekian H; Sew Indust Wastes 27: 

 793-801 (1955) (3) Gerhold RM, Malaney GW; J Water Pollut Control Fed 38: 

 562-79 (1966) (4) Lamb CB, Jenkins GF; Proc 8th Industrial Waste Conf,. 

 Purdue Univ p. 326-9 (1952) (5) McKinney RE, Jeris JS; Sew Indust Wastes 

 27: 728-35 (1955) (6) Wagner R; Vom Wasser 42: 271-305 (1974)] **PEER 

 REVIEWED** 

 AEROBIC: Using a starting concentration of 2.56 ppm, methanol achieved 

 88.7% of its theoretical BOD over a 5 day incubation period using a 

 freshwater standard dilution technique, and 70.7% of its theoretical BOD 

 over a 5 day incubation period using a sea water dilution technique(1). 

 Significant biodegradation of organic waste (methanol and acetic acid and 

 formic acid) was observed when injected into wells (850-1000 ft depth) as 

 determined by concentration monitoring and microbial population count(2). 

 Soil-sediment suspensions, maintainted under aerobic conditions, resulted 

 in a 5-day CO2 evolution (14-C) of 53.4%(3). [(1) Takemoto S et al; 

 Suishitsu Odaku Kenkyu 4: 80-90 (1981) (2) Ditommaso A, Elkan GH; 

 Underground Waste Manage Artif Recharge, Prepr Pap Int Symp, 2nd 1: 585-99 

 (1973) (3) Scheunert I et al; Chemosphere 16: 1031-41 (1987)] **PEER 

 REVIEWED** 

 ANAEROBIC: Approximately 83-91% biodegradation was observed in an 

 anaerobic die-away test, using marine water and sediment from the San 

 Francisco Bay during a 3-day incubation period(1). Methanol was found to 

 be susceptible to biodegradation in low oxygen subsurface regions in 

 microcosm studies simulating subsurface conditions; complete degradation 

 was observed within one year or less(2). Methanol degraded readily in test 

 tube microcosms simulating subsurface soils and groundwaters from sites in 

 VA and NY(3). Soil-sediment suspensions, maintained under anaerobic 

 conditions, resulted in a 5-day CO2 evolution (14-C) of 46.3%(4). [(1) 

 Oremland RL et al; Nature 296: 143-5 (1982) (2) Novak JT et al; Wat Sci 

 Tech 17: 71-85 (1985) (3) Goldsmith CD; Diss Abstr Int B 46: 3767 (1985) 

 (4) Scheunert I et al; Chemosphere 16: 1031-41 (1987)] **PEER REVIEWED** 

ENVIRONMENTAL ABIOTIC DEGRADATION: 

 The rate constant for the vapor-phase reaction of methanol with 

 photochemically-produced hydroxyl radicals has been measured as 9.4X10-13 

 cu cm/molecule-sec at 25 deg C(1). This corresponds to an atmospheric 

 half-life of about 17 days at an atmospheric concentration of 5X10+5 

 hydroxyl radicals per cu cm(1). Methanol is not expected to undergo 

 hydrolysis in the environment due to the lack of hydrolyzable functional 

 groups nor to directly photolyze due to the lack of absorption in the 

 environmental UV spectrum ( > 290 nm)(2). [(1) Kwok ESC, Atkinson R; 

 Estimation of hydroxyl radical reaction rate constants for gas-phase 

 organic compounds using a structure-reactivity relationship: an update. 

 Riverside, CA: Univ CA, Statewide Air Pollut Res CTR., CMA Contract NO. 

 AFC-8.0-OR-8.0-OR (1994) (2) Lyman WJ et al; Handbook of Chemical Property 

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 Estimation Methods. Washington, DC: Amer Chem Soc pp. 7-4, 7-5 (1990)] 

 **PEER REVIEWED** 

 The rate constant for the reaction of methanol with hydroxyl radicals in 

 aqueous solution is approximately 1X10+9 l/mol-sec(1); if the hydroxyl 

 radical concn of sunlit natural water is assumed to be 1X10-17 moles/l(2), 

 the half-life would be approximately 2.2 years(SRC). Methanol in aqueous 

 solution exhibited no degradation when exposed to sunlight using an EPA 

 test protocol(3). Sediment and clay suspensions solution did not 

 photocatalyze the degradation of methanol in aqueous solution during 

 irradiation with UV light(4). Alcohols are generally resistant to 

 environmental aqueous hydrolysis(5). [(1) Guesten H et al; Atmos Environ 

 15: 1763-5 (1981) (2) Mill T et al; Science 207: 886-7 (1980) (3) Hustert 

 K et al; Chemosphere 10: 995-8 (1981) (4) Oliver BG et al; Environ Sci 

 Technol 13: 1075-7 (1979) (5) Lyman WJ et al; Handbook of Chemical 

 Property Estimation Methods NY: McGraw-Hill p. 7-4 (1982)] **PEER 

 REVIEWED** 

ENVIRONMENTAL BIOCONCENTRATION: 

 Fish (golden ide) exposed to 0.05 mg/L of methanol for three days in an 

 aquatic tank had measured BCF values of less than 10(1). Based on a 

 classification scheme(2), this BCF value suggests that bioconcentration in 

 aquatic organisms is low(SRC). [(1) Freitag D et al; Chemosphere 14: 

 1589-1616 (1985) (2) Franke C et al; Chemosphere 29: 1501-14 (1994)] 

 **PEER REVIEWED** 

SOIL ADSORPTION/MOBILITY: 

 Using a structure estimation method based on molecular connectivity 

 indices(1), the Koc for methanol can be estimated to be 1(SRC). According 

 to a classification scheme(2), this estimated Koc value suggests that 

 methanol is expected to have very high mobility in soil(SRC). [(1) Meylan 

 WM et al; Environ Sci Technol 26: 1560-67 (1992) (2) Swann RL et al; Res 

 Rev 85: 17-28 (1983)] **PEER REVIEWED** 

VOLATILIZATION FROM WATER/SOIL: 

 The Henry's Law constant for methanol is 4.55X10-6 atm-cu m/mole(SRC)(1). 

 This Henry's Law constant indicates that methanol is expected to 

 volatilize from water surfaces(2). Based on this Henry's Law constant, the 

 volatilization half-life from a model river (1 m deep, flowing 1 m/sec, 

 wind velocity of 3 m/sec)(2) is estimated as 3 days(SRC). The 

 volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, 

 wind velocity of 0.5 m/sec)(2) is estimated as 35 days(SRC). Methanol's 

 Henry's Law constant indicates that volatilization from moist soil 

 surfaces may occur(SRC). The potential for volatilization of methanol from 

 dry soil surfaces may exist(SRC) based upon a vapor pressure of 127 mm 

 Hg(3). [(1) Gaffney JS et al; Environ Sci Technol 21: 519-23 (1987) (2) 

 Lyman WJ et al; Handbook of Chemical Property Estimation Methods. 

 Washington, DC: Amer Chem Soc pp. 15-1 to 15-29 (1990) (3) Boublik T et 

 al, eds; The Vapour Pressures of Pure Substances. 2nd rev ed. Amsterdam: 

 Elsevier (1984)] **PEER REVIEWED** 

ENVIRONMENTAL WATER CONCENTRATIONS: 

 DRINKING WATER: Methanol has been qualitatively detected in drinking water 

 from Miami, FL, Seattle, WA, Philadelphia, PA, Cincinnati, OH, and New 

 Orleans, LA(1,2). As part of the USEPA National Organics Reconnaissance 

 Survey (NORS), methanol was detected in 6 of 10 drinking waters from USA 

 cities(3). [(1) USEPA; Preliminary Assessment of Suspected Carcinogens in 

 Water. Interim Report to Congress, June, 1975. Washington DC (1975) (2) 

 USEPA; New Orleans Area Water Supply Draft Analytical Report by the Lower 

 Mississippi River Facility, Sliddell, LA. Dallas, TX (1974) (3) Bedding ND 

 et al; Sci Total Environ 25: 143-67 (1982)] **PEER REVIEWED** 

 RAIN WATER: Methanol was detected at a mean level of 22 ppb in 

 thunderstorm water collected from Santa Rita, AZ in Sept, 1982(1). [(1) 

 Snider JR, Dawson GA; J Geophys Res, D2, 90: 3797-805 (1985)] **PEER 

 REVIEWED** 

EFFLUENT CONCENTRATIONS: 

 Methanol levels of 18-70 ppm were detected in wastewater effluents from a 

 chemical mfg facility (near the Brackish River), but none was detected in 

 associated river water or sediments(1). Methanol has been identified in 

 wastewater effluents from chemical, paper, and latex manufacturing plants 

 and from sewage treatment plants(2). Concn of 42.4 ppm detected in 

 leachate from the Love Canal in Niagara Falls, NY(3). Concn of 1050 ppm 

 detected in condensate waters from a coal-gasification plant(4). Levels of 

 0.1-0.6 ppm were found in exhausts from engines using simple hydrocarbon 

 fuels(5). Methanol has been identified in exhausts from both gasoline and 

 diesel engines(6). [(1) Jungclaus GA et al; Environ Sci Technol 12: 88-96 

 (1978) (2) Shackelford WM, Keith LH; Frequency of Organic Compounds 

 Identified in Water EPA-600/4-76- 062 p. 169 (1976) (3) Venkataramani ES 

 et al; CRC Crit Rev Environ Control 14: 333-76 (1984) (4) Mohr DH, King J; 

 Environ Sci Technol 19: 929-35 (1985) (5) Seizinger DE, Dimitriades B; J 

 Air Pollut Control Assoc 22: 47-51 (1972) (6) Jonsson A et al; Environ 

 International 11: 383-92 (1985)] **PEER REVIEWED** 

ATMOSPHERIC CONCENTRATIONS: 

 URBAN/SUBURBAN: Avg ambient concns of methanol in the range of 3.83-26.7 

 ppb were detected at 5 sites in and around Stockholm, Sweden(1). Methanol 

 was detected at levels of 0.10 to 2.21 ng/cu m in urban atmospheric 

 particulates in Kobe City, Japan in 1999(2). [(1) Jonsson A et al; Environ 

 International 11: 383-92 (1985) (2) Suzuki Y et al; Environ Sci Technol 

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 35: 2656-64 (2001)] **PEER REVIEWED** 

 INDOOR: Methanol has been detected (concn not reported) in indoor air of 

 residential and office buildings(1,2). [(1) Jarke FH et al; ASHRAE Trans 

 87: 153-66 (1981) (2) Tsuchiya Y; Volatile Organic Compounds in Indoor 

 Air. Am Chem Soc Div Environ Chem Preprint, New Orleans, LA 27: 183-5 

 (1987)] **PEER REVIEWED** 

 RURAL/REMOTE: Methanol was detected at mean ambient atmospheric concns of 

 7.9 and 2.6 ppb at two remote AZ locations during 1982 monitoring(1). 

 Concns of 0.0-1.2 ppb (ave 0.77 ppb methanol and ethanol) were identified 

 in Arctic air from Point Barrows, Alaska in Sept 1967(2). Methanol was 

 detected in the atmosphere above the Arapaho National Forest in Colorado 

 at levels of approximately 2-12 ppb in July and August 1999(3). [(1) 

 Snider JR, Dawson GA; J Geophys Res, D2, 90: 3797-805 (1985) (2) Cavanagh 

 LA et al; Environ Sci Technol 3: 251-7 (1969) (3) Baker B et al; Environ 

 Sci Technol 35: 1701-9 (2001)] **PEER REVIEWED** 

FOOD SURVEY VALUES: 

 Methanol has been identified as a volatile component of dried legumes 

 (concn 1.5-7.9 ppm), baked potatoes, and roasted filbert nuts(1-3). 

 Methanol was identified, not quantified, in the volatile flavor components 

 of fresh grapefruit(4). Methanol was detected at levels of 7-126 ppm in 

 fresh squeezed orange juice(5). [(1) Coleman EC et al; J Agric Food Chem 

 29: 42-8 (1981) (2) Kinlin TE et al; J Agric Food Chem 20: 1021-8 (1972) 

 (3) Lovegren NV et al; J Agric Food Chem 27: 851-3 (1979) (4) Cadwallader 

 KR, Xu Y; J Agric Food Chem 42: 782-4 (1994) (5) Moshonas NG, Shaw PE; J 

 Agric Food Chem 42: 1525-8 (1994)] **PEER REVIEWED** 

PLANT CONCENTRATIONS: 

 Methanol has been identified as a volatile emission product from evergreen 

 cypress trees(1) and alfalfa(2). [(1) Isidorov VA et al; Atmos Environ 19: 

 1-8 (1985) (2) Owens LD et al; Phytopathology 59: 1468-72 (1969)] **PEER 

 REVIEWED** 

OTHER ENVIRONMENTAL CONCENTRATIONS: 

 Methanol was identified as a component of several industrial paint 

 strippers(1). Engine exhausts from both gasoline and diesel vehicles have 

 been found to contain methanol(2). Methanol has been identified as a 

 constituent of tobacco smoke(3). [(1) Hahn WJ, Werschulz PO; Evaluation of 

 Alternatives to Toxic Organic Paint Strippers. USEPA-600/S2-86-063 (1986) 

 (2) Jonsson A et al; Environ International 11: 383-92 (1985) (3) Graedel 

 TE et al; Atmospheric Chemical Compounds. Sources, Occurrence, and 

 Bioassay. Orlando, FL: Academic Press p. 232 (1986)] **PEER REVIEWED** 

ENVIRONMENTAL STANDARDS & REGULATIONS: 

FIFRA REQUIREMENTS: 

 Residues of methanol are exempted from the requirement of a tolerance when 

 used as a solvent in accordance with good agricultural practice as inert 

 (or occasionally active) ingredients in pesticide formulations applied to 

 growing crops or to raw agricultural commodities after harvest. [40 CFR 

 180.910; U.S. National Archives and Records Administration's Electronic 

 Code of Federal Regulations. Available from, as of June 1, 2005: 

 http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

 Residues of methanol are exempted from the requirement of a tolerance when 

 used as a synergist in accordance with good agricultural practice as inert 

 (or occasionally active) ingredients in pesticide formulations applied to 

 growing crops only. [40 CFR 180.920; U.S. National Archives and Records 

 Administration's Electronic Code of Federal Regulations. Available from, 

 as of June 1, 2005: http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

 Residues of methanol are exempted from the requirement of a tolerance when 

 used as a solvent, cosolvent in accordance with good agricultural practice 

 as inert (or occasionally active) ingredients in pesticide formulations 

 applied to animals. [40 CFR 180.930; U.S. National Archives and Records 

 Administration's Electronic Code of Federal Regulations. Available from, 

 as of June 1, 2005: http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

 As the federal pesticide law FIFRA directs, EPA is conducting a 

 comprehensive review of older pesticides to consider their health and 

 environmental effects and make decisions about their future use. Under 

 this pesticide reregistration program, EPA examines health and safety data 

 for pesticide active ingredients initially registered before November 1, 

 1984, and determines whether they are eligible for reregistration. In 

 addition, all pesticides must meet the new safety standard of the Food 

 Quality Protection Act of 1996. Pesticides for which EPA had not issued 

 Registration Standards prior to the effective date of FIFRA '88 were 

 divided into three lists based upon their potential for human exposure and 

 other factors, with List B containing pesticides of greater concern and 

 List D pesticides of less concern. Methyl alcohol is found on List D. Case 

 No: 4003; Pesticide type: insecticide, fungicide, herbicide, 

 antimicrobial; Case Status: RED Approved 3/95; OPP has made a decision 

 that some/all uses of the pesticide are eligible for reregistration, as 

 reflected in a Reregistration Eligibility Decision (RED) document .; 

 Active ingredient (AI): methyl alcohol; AI Status: The active ingredient 

 is no longer contained in any registered products. Thus, we characterize 

 it as "cancelled." [United States Environmental Protection Agency/ 

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 Prevention, Pesticides and Toxic Substances; Status of Pesticides in 

 Registration, Reregistration, and Special Review. (1998) EPA 

 738-R-98-002, p. 290] **PEER REVIEWED** 

CERCLA REPORTABLE QUANTITIES: 

 Persons in charge of vessels or facilities are required to notify the 

 National Response Center (NRC) immediately, when there is a release of 

 this designated hazardous substance, in an amount equal to or greater 

 than its reportable quantity of 5000 lb or 2270 kg. The toll free number 

 of the NRC is (800) 424-8802. The rule for determining when notification 

 is required is stated in 40 CFR 302.4 (section IV. D.3.b). [40 CFR 

 302.4; U.S. National Archives and Records Administration's Electronic Code 

 of Federal Regulations. Available from, as of June 1, 2005: 

 http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

RCRA REQUIREMENTS: 

 U154; As stipulated in 40 CFR 261.33, when methanol, as a commercial 

 chemical product or manufacturing chemical intermediate or an 

 off-specification commercial chemical product or a manufacturing chemical 

 intermediate, becomes a waste, it must be managed according to Federal 

 and/or State hazardous waste regulations. Also defined as a hazardous 

 waste is any residue, contaminated soil, water, or other debris resulting 

 from the cleanup of a spill, into water or on dry land, of this waste. 

 Generators of small quantities of this waste may qualify for partial 

 exclusion from hazardous waste regulations (40 CFR 261.5). [40 CFR 261.33; 

 U.S. National Archives and Records Administration's Electronic Code of 

 Federal Regulations. Available from, as of June 1, 2005: 

 http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

 F003; When methanol is a spent solvent, it is classified as a hazardous 

 waste from a nonspecific source (F003), as stated in 40 CFR 261.31, and 

 must be managed according to State and/or Federal hazardous waste 

 regulations. [40 CFR 261.31; U.S. National Archives and Records 

 Administration's Electronic Code of Federal Regulations. Available from, 

 as of June 1, 2005: http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

ATMOSPHERIC STANDARDS: 

 This action promulgates standards of performance for equipment leaks of 

 Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical 

 Manufacturing Industry (SOCMI). The intended effect of these standards is 

 to require all newly constructed, modified, and reconstructed SOCMI 

 process units to use the best demonstrated system of continuous emission 

 reduction for equipment leaks of VOC, considering costs, non air quality 

 health and environmental impact and energy requirements. Methanol is 

 produced, as an intermediate or a final product, by process units covered 

 under this subpart. [40 CFR 60.489; U.S. National Archives and Records 

 Administration's Electronic Code of Federal Regulations. Available from, 

 as of June 1, 2005: http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

 Listed as a hazardous air pollutant (HAP) generally known or suspected to 

 cause serious health problems. The Clean Air Act, as amended in 1990, 

 directs EPA to set standards requiring major sources to sharply reduce 

 routine emissions of toxic pollutants. EPA is required to establish and 

 phase in specific performance based standards for all air emission sources 

 that emit one or more of the listed pollutants. Methanol is included on 

 this list. [Clean Air Act as amended in 1990, Sect. 112 (b) (1) Public Law 

 101-549 Nov. 15, 1990] **PEER REVIEWED** 

STATE DRINKING WATER GUIDELINES: 

 (FL) FLORIDA 5,000 ug/L [USEPA/Office of Water; Federal-State Toxicology 

 and Risk Analysis Committee (FSTRAC). Summary of State and Federal 

 Drinking Water Standards and Guidelines (11/93) To Present] **PEER 

 REVIEWED** 

 (MN) MINNESOTA 3000 ug/L [USEPA/Office of Water; Federal-State Toxicology 

 and Risk Analysis Committee (FSTRAC). Summary of State and Federal 

 Drinking Water Standards and Guidelines (11/93) To Present] **PEER 

 REVIEWED** 

 (NH) NEW HAMPSHIRE 4,000 ug/L [USEPA/Office of Water; Federal-State 

 Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and 

 Federal Drinking Water Standards and Guidelines (11/93) To Present] 

 **QC REVIEWED** 

 (WI) WISCONSIN 5000 ug/L [USEPA/Office of Water; Federal-State Toxicology 

 and Risk Analysis Committee (FSTRAC). Summary of State and Federal 

 Drinking Water Standards and Guidelines (11/93) To Present] **PEER 

 REVIEWED** 

FDA REQUIREMENTS: 

 Methyl alcohol is an indirect food additive for use only as a component of 

 adhesives. [21 CFR 175.105; U.S. National Archives and Records 

 Administration's Electronic Code of Federal Regulations. Available from, 

 as of June 1, 2005: http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

 Methyl alcohol may be present in the following foods under the conditions 

 specified: (a) In spice oleoresins as a residue from the extraction of 

 spice, at a level not to exceed 50 parts per million. (b) In hops extract 

 as a residue from the extraction of hops, at a level not to exceed 2.2 

 percent by weight; Provided, that: (1) The hops extract is added to the 

 wort before or during cooking in the manufacture of beer. (2) The label 

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 of the hops extract specifies the presence of methyl alcohol and provides 

 for the use of the hops extract only as prescribed by paragraph (b)(1) of 

 this section. [21 CFR 173.250; U.S. National Archives and Records 

 Administration's Electronic Code of Federal Regulations. Available from, 

 as of June 1, 2005: http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

ALLOWABLE TOLERANCES: 

 Residues of methanol are exempted from the requirement of a tolerance when 

 used as a solvent in accordance with good agricultural practice as inert 

 (or occasionally active) ingredients in pesticide formulations applied to 

 growing crops or to raw agricultural commodities after harvest. [40 CFR 

 180.910; U.S. National Archives and Records Administration's Electronic 

 Code of Federal Regulations. Available from, as of June 1, 2005: 

 http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

 Residues of methanol are exempted from the requirement of a tolerance when 

 used as a synergist in accordance with good agricultural practice as inert 

 (or occasionally active) ingredients in pesticide formulations applied to 

 growing crops only. [40 CFR 180.920; U.S. National Archives and Records 

 Administration's Electronic Code of Federal Regulations. Available from, 

 as of June 1, 2005: http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

 Residues of methanol are exempted from the requirement of a tolerance when 

 used as a solvent, cosolvent in accordance with good agricultural practice 

 as inert (or occasionally active) ingredients in pesticide formulations 

 applied to animals. [40 CFR 180.930; U.S. National Archives and Records 

 Administration's Electronic Code of Federal Regulations. Available from, 

 as of June 1, 2005: http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

CHEMICAL/PHYSICAL PROPERTIES: 

MOLECULAR FORMULA: 

 C-H4-O [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 

 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 2174] 

 **PEER REVIEWED** 

MOLECULAR WEIGHT: 

 32.04 [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of 

 Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: 

 Merck and Co., Inc., 2001., p. 1065] **PEER REVIEWED** 

COLOR/FORM: 

 Colorless liquid [NIOSH. NIOSH Pocket Guide to Chemical Hazards & 

 Other Databases CD-ROM. Department of Health & Human Services, Centers 

 for Disease Prevention & Control. National Institute for Occupational 

 Safety& Health. DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER 

 REVIEWED** 

ODOR: 

 Alcoholic odor; pungent odor when crude [O'Neil, M.J. (ed.). The Merck 

 Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th 

 Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1065] 

 **PEER REVIEWED** 

 Characteristic pungent odor [NIOSH. NIOSH Pocket Guide to Chemical Hazards 

 & Other Databases CD-ROM. Department of Health & Human Services, 

 Centers for Disease Prevention & Control. National Institute for 

 Occupational Safety& Health. DHHS (NIOSH) Publication No. 2004-103 

 (2003).] **PEER REVIEWED** 

BOILING POINT: 

 64.7 deg C at 760 mm Hg [O'Neil, M.J. (ed.). The Merck Index - An 

 Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, 

 Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1065] **PEER 

 REVIEWED** 

MELTING POINT: 

 -97.8 deg C [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of 

 Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: 

 Merck and Co., Inc., 2001., p. 1065] **PEER REVIEWED** 

CRITICAL TEMPERATURE & PRESSURE: 

 Critical temperature: 240.0 deg C; critical pressure: 78.5 atm [O'Neil, 

 M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and 

 Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 

 2001., p. 1065] **PEER REVIEWED** 

DENSITY/SPECIFIC GRAVITY: 

 0.8100 at 0 deg C/4 deg C; 0.7866 at 25 deg C/4 deg C [O'Neil, M.J. (ed.). 

 The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 

 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 

 1065] **PEER REVIEWED** 

DISSOCIATION CONSTANTS: 

 pKa = 15.3 [Serjeant, E.P., Dempsey B.; Ionisation Constants of Organic 

 Acids in Aqueous Solution. International Union of Pure and Applied 

 Chemistry (IUPAC). IUPAC Chemical Data Series No. 23, 1979. New York, New 

 York: Pergamon Press, Inc., p. 989] **PEER REVIEWED** 

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HEAT OF COMBUSTION: 

 723 kJ/mole [Environment Canada; Tech Info for Problem Spills: Methanol 

 (Draft) p.4 (1981)] **PEER REVIEWED** 

HEAT OF VAPORIZATION: 

 39.2 kJ/mole [Environment Canada; Tech Info for Problem Spills: Methanol 

 (Draft) p.4 (1981)] **PEER REVIEWED** 

OCTANOL/WATER PARTITION COEFFICIENT: 

 log Kow= -0.77 [Hansch, C., Leo, A., D. Hoekman. Exploring QSAR - 

 Hydrophobic, Electronic, and Steric Constants. Washington, DC: American 

 Chemical Society., 1995., p. 3] **PEER REVIEWED** 

SOLUBILITIES: 

 Miscible with ethanol, ether, benzene, most organic solvents and ketones. 

 [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, 

 Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and 

 Co., Inc., 2001., p. 1065] **PEER REVIEWED** 

 Sol in acetone, chloroform [Lide, D.R., G.W.A. Milne (eds.). Handbook of 

 Data on Organic Compounds. Volume I. 3rd ed. CRC Press, Inc. Boca Raton 

 ,FL. 1994., p. V4: 3388] **PEER REVIEWED** 

 Completely miscible in water @ 20 deg C [Flick, E.W. Industrial Solvents 

 Handbook. 3rd ed. Park Ridge, NJ: Noyes Publications, 1985., p. 188] 

 **PEER REVIEWED** 

 Water solubility = miscible [Riddick, J.A., W.B. Bunger, Sakano T.K. 

 Techniques of Chemistry 4th ed., Volume II. Organic Solvents. New York, 

 NY: John Wiley and Sons., 1985., p. 190] **PEER REVIEWED** 

SPECTRAL PROPERTIES: 

 Index of refraction: 1.3292 at 20 deg C/D [O'Neil, M.J. (ed.). The Merck 

 Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th 

 Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1065] 

 **PEER REVIEWED** 

 MAX ABSORPTION (GAS): 183.3 NM (LOG EPSILON= 2.18) [Weast, R.C. (ed.). 

 Handbook of Chemistry and Physics. 52nd ed. Cleveland: The Chemical Rubber 

 Co., 1972., p. C-370] **PEER REVIEWED** 

 IR: 287 (Sadtler Research Laboratories IR Grating Collection) [Lide, D.R., 

 G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. Volume I. 3rd 

 ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V4: 3388] **PEER REVIEWED** 

 UV: 1-3 (Organic Electronic Spectral Data, Phillips et al, John Wiley 

 & Sons, New York) [Lide, D.R., G.W.A. Milne (eds.). Handbook of Data 

 on Organic Compounds. Volume I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 

 1994., p. V4: 3388] **PEER REVIEWED** 

 NMR: 1 (Varian Associates NMR Spectra Catalogue) [Lide, D.R., G.W.A. Milne 

 (eds.). Handbook of Data on Organic Compounds. Volume I. 3rd ed. CRC 

 Press, Inc. Boca Raton ,FL. 1994., p. V4: 3388] **PEER REVIEWED** 

 MASS: 61305 (NIST/EPA/MSDC Mass Spectral Database, 1990 version) [Lide, 

 D.R., G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. Volume 

 I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V4: 3388] **PEER 

 REVIEWED** 

SURFACE TENSION: 

 22.61 mN/m (at 20 deg C) [Environment Canada; Tech Info for Problem 

 Spills: Methanol (Draft) p.4 (1981)] **PEER REVIEWED** 

VAPOR DENSITY: 

 1.11 [Environment Canada; Tech Info for Problem Spills: Methanol (Draft) 

 p.3 (1981)] **PEER REVIEWED** 

VAPOR PRESSURE: 

 127 mm Hg at 25 deg C [Boublik, T., Fried, V., and Hala, E., The Vapour 

 Pressures of Pure Substances. Second Revised Edition. Amsterdam: Elsevier, 

 1984.] **PEER REVIEWED** 

VISCOSITY: 

 0.614 mPa sec [Environment Canada; Tech Info for Problem Spills: Methanol 

 (Draft) p.4 (1981)] **PEER REVIEWED** 

OTHER CHEMICAL/PHYSICAL PROPERTIES: 

 Dipole moment: 1.69 /debyes/; specific heat: 0.595-0.605 at 20-25 deg C, 

 forms Azeotropes with many cmpd; burns with nonluminous bluish flame ... 

 [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, 

 Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and 

 Co., Inc., 2001., p. 1065] **PEER REVIEWED** 

 1 MG/L= 764 PPM; 1 PPM= 1.31 MG/CU M @ 25 DEG C, 760 MM HG [Clayton, G. D. 

 and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: 

 Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 

 1981-1982., p. 4530] **PEER REVIEWED** 

 Heat of fusion: 103 J/g [Kirk-Othmer Encyclopedia of Chemical Technology. 

 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. 

 V16: 538 (1995)] **PEER REVIEWED** 

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 Partition coefficients at 37 deg C for methanol into blood= 2,100; into 

 oil= 56. [Sato A, Nakajima T; Scand J Work Environ Health 13: 81-93 

 (1987)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3299685" 

 target=new>PubMed Abstract 

 Vapor pressure= 100 mm Hg at 21.2 deg C [Lewis, R.J. Sax's Dangerous 

 Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van 

 Nostrand Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 Henry's Law constant = 4.55X10-6 atm-cu m/mol at 25 deg C [Gaffney JS et 

 al; Environ Sci Technol 21: 519-23 (1987)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19994967" 

 target=new>PubMed Abstract 

 Hydroxyl radical reaction rate constant = 9.4X10-13 cu cm/molec-sec at 25 

 deg C [Kwok ESC, Atkinson R; Estimation of hydroxyl radical reaction rate 

 constants for gas-phase organic compounds using a structure-reactivity 

 relationship: an update. Riverside, CA: Univ CA, Statewide Air Pollut Res 

 CTR., CMA Contract NO. AFC-8.0-OR-8.0-OR (1994)] **PEER REVIEWED** 

CHEMICAL SAFETY & HANDLING: 

DOT EMERGENCY GUIDELINES: 

 /GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Health: TOXIC; may be fatal if 

 inhaled, ingested or absorbed through skin. Inhalation or contact with 

 some of these materials will irritate or burn skin and eyes. Fire will 

 produce irritating, corrosive and/or toxic gases. Vapors may cause 

 dizziness or suffocation. Runoff from fire control or dilution water may 

 cause pollution. [U.S. Department of Transportation. 2004 Emergency 

 Response Guidebook. A Guide book for First Responders During the Initial 

 Phase of a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 

 2004] **QC REVIEWED** 

 /GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Fire or Explosion: HIGHLY FLAMMABLE: 

 Will be easily ignited by heat, sparks or flames. Vapors may form 

 explosive mixtures with air. Vapors may travel to source of ignition and 

 flash back. Most vapors are heavier than air. They will spread along 

 ground and collect in low or confined areas (sewers, basements, tanks). 

 Vapor explosion and poison hazard indoors, outdoors or in sewers. Those 

 substances designated with a "P" may polymerize explosively when heated or 

 involved in a fire. Runoff to sewer may create fire or explosion hazard. 

 Containers may explode when heated. Many liquids are lighter than water. 

 [U.S. Department of Transportation. 2004 Emergency Response Guidebook. A 

 Guide book for First Responders During the Initial Phase of a Dangerous 

 Goods/Hazardous Materials Incident. Washington, D.C. 2004] **QC REVIEWED** 

 

 /GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Public Safety: CALL Emergency 

 Response Telephone Number ... . As an immediate precautionary measure, 

 isolate spill or leak area for at least 50 meters (150 feet) in all 

 directions. Keep unauthorized personnel away. Stay upwind. Keep out of low 

 areas. Ventilate closed spaces before entering. [U.S. Department of 

 Transportation. 2004 Emergency Response Guidebook. A Guide book for First 

 Responders During the Initial Phase of a Dangerous Goods/Hazardous 

 Materials Incident. Washington, D.C. 2004] **QC REVIEWED** 

 /GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Protective Clothing: Wear positive 

 pressure self-contained breathing apparatus (SCBA). Wear chemical 

 protective clothing that is specifically recommended by the manufacturer. 

 It may provide little or no thermal protection. Structural firefighters' 

 protective clothing provides limited protection in fire situations ONLY; 

 it is not effective in spill situations where direct contact with the 

 substance is possible. [U.S. Department of Transportation. 2004 Emergency 

 Response Guidebook. A Guide book for First Responders During the Initial 

 Phase of a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 

 2004] **QC REVIEWED** 

 /GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Evacuation: ... Fire: If tank, rail 

 car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) 

 in all directions; also, consider initial evacuation for 800 meters (1/2 

 mile) in all directions. [U.S. Department of Transportation. 2004 

 Emergency Response Guidebook. A Guide book for First Responders During the 

 Initial Phase of a Dangerous Goods/Hazardous Materials Incident. 

 Washington, D.C. 2004] **QC REVIEWED** 

 /GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Fire: CAUTION: All these products 

 have a very low flash point. Use of water spray when fighting fire may be 

 inefficient. Small fires: Dry chemical, CO2, water spray or 

 alcohol-resistant foam. Large fires: Water spray, fog or alcohol-resistant 

 foam. Move containers from fire area if you can do it without risk. Dike 

 fire control water for later disposal; do not scatter the material. Use 

 water spray or fog; do not use straight streams. Fire involving tanks or 

 car/trailer loads: Fight fire from maximum distance or use unmanned hose 

 holders or monitor nozzles. Cool containers with flooding quantities of 

 water until well after fire is out. Withdraw immediately in case of rising 

 sound from venting safety devices or discoloration of tank. ALWAYS stay 

 away from tanks engulfed in fire. For massive fire use unmanned hose 

 holders or monitor nozzles; if this is impossible, withdraw from area and 

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 let fire burn. [U.S. Department of Transportation. 2004 Emergency Response 

 Guidebook. A Guide book for First Responders During the Initial Phase of a 

 Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 2004] **QC 

 REVIEWED** 

 /GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Spill or Leak: Fully encapsulating, 

 vapor protective clothing should be worn for spills and leaks with no 

 fire. ELIMINATE all ignition sources (no smoking, flares, sparks or flames 

 in immediate area). All equipment used when handling the product must be 

 grounded. Do not touch or walk through spilled material. Stop leak if you 

 can do it without risk. Prevent entry into waterways, sewers, basements or 

 confined areas. A vapor suppressing foam may be used to reduce vapors. 

 Small spills: Absorb with earth, sand or other non-combustible material 

 and transfer to containers for later disposal. Use clean non-sparking 

 tools to collect absorbed material. Large spills: Dike far ahead of liquid 

 spill for later disposal. Water spray may reduce vapor; but may not 

 prevent ignition in closed spaces. [U.S. Department of Transportation. 

 2004 Emergency Response Guidebook. A Guide book for First Responders 

 During the Initial Phase of a Dangerous Goods/Hazardous Materials 

 Incident. Washington, D.C. 2004] **QC REVIEWED** 

 /GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ First Aid: Move victim to fresh air. 

 Call 911 or emergency medical service. Give artificial respiration if 

 victim is not breathing. Do not use mouth-to-mouth method if victim 

 ingested or inhaled the substance; give artificial respiration with the 

 aid of a pocket mask equipped with a one-way valve or other proper 

 respiratory medical device. Administer oxygen if breathing is difficult. 

 Remove and isolate contaminated clothing and shoes. In case of contact 

 with substance, immediately flush skin or eyes with running water for at 

 least 20 minutes. Wash skin with soap and water. Keep victim warm and 

 quiet. In case of burns, immediately cool affected skin for as long as 

 possible with cold water. Do not remove clothing if adhering to skin. 

 Effects of exposure (inhalation, ingestion or skin contact) to substance 

 may be delayed. Ensure that medical personnel are aware of the material(s) 

 involved and take precautions to protect themselves. [U.S. Department of 

 Transportation. 2004 Emergency Response Guidebook. A Guide book for First 

 Responders During the Initial Phase of a Dangerous Goods/Hazardous 

 Materials Incident. Washington, D.C. 2004] **QC REVIEWED** 

ODOR THRESHOLD: 

 The air odor threshold for methanol has been reported as 100 ppm. A level 

 of 2,000 ppm ... is barely detectable. [Bingham, E.; Cohrssen, B.; Powell, 

 C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New 

 York, N.Y. (2001)., p. V6 p.370] **PEER REVIEWED** 

 Low threshold= 13.1150 mg/cu m; High threshold= 26840 mg/cu m; Irritating 

 concn= 22875 mg/cu m. [Ruth JH; Am Ind Hyg Assoc J 47: A-142-51 (1986)] 

 **PEER REVIEWED** 

SKIN, EYE AND RESPIRATORY IRRITATIONS: 

 /Methanol/ is an eye and skin irritant. [Lewis, R.J. Sax's Dangerous 

 Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van 

 Nostrand Reinhold, 1996., p. 2174] **PEER REVIEWED** 

FIRE POTENTIAL: 

 Dangerous fire hazard when exposed to heat, flame or oxidizers. [Lewis, 

 R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 

 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 2175] **PEER 

 REVIEWED** 

NFPA HAZARD CLASSIFICATION: 

 Health: 1. 1= Materials that, on exposure, would cause irritation, but 

 only minor residual injury, including those requiring the use of an 

 approved air-purifying respirator. These materials are only slightly 

 hazardous to health and only breathing protection is needed. [Fire 

 Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire 

 Protection Association, 2002., p. 325-81] **PEER REVIEWED** 

 Flammability: 3. 3= This degree includes Class IB and IC flammable liquids 

 and materials that can be easily ignited under almost all normal 

 temperature conditions. Water may be ineffective in controlling or 

 extinguishing fires in such materials. [Fire Protection Guide to Hazardous 

 Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., 

 p. 325-81] **PEER REVIEWED** 

 Reactivity: 0. 0= This degree includes materials that are normally stable, 

 even under fire exposure conditions, and that do not react with water. 

 Normal fire fighting procedures may be used. [Fire Protection Guide to 

 Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection 

 Association, 2002., p. 325-81] **PEER REVIEWED** 

FLAMMABLE LIMITS: 

 Lower limits is 6.0%; Upper limits is 36% [Fire Protection Guide to 

 Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection 

 Association, 2002., p. 325-81] **PEER REVIEWED** 

FLASH POINT: 

 15.6 deg C (open cup) /from table/ [WHO; Environ Health Criteria 196: 

 Methanol p.11 (1997). Available from, as of July 14, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

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 54 deg F (12 deg C) (closed cup) [O'Neil, M.J. (ed.). The Merck Index - An 

 Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, 

 Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1065] **PEER 

 REVIEWED** 

AUTOIGNITION TEMPERATURE: 

 867 DEG F (464 DEG C) [Fire Protection Guide to Hazardous Materials. 13 

 ed. Quincy, MA: National Fire Protection Association, 2002., p. 325-81] 

 **PEER REVIEWED** 

FIRE FIGHTING PROCEDURES: 

 To fight fire use alcohol foam. [Lewis, R.J. Sax's Dangerous Properties 

 of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2175] **PEER REVIEWED** 

EXPLOSIVE LIMITS & POTENTIAL: 

 Lower explosive limit 6.0%; Upper explosive limit 36.5 % [Lewis, R.J. 

 Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. 

 New York, NY: Van Nostrand Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 Explosive in the form of vapor when exposed to heat or flame. [Lewis, 

 R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 

 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 2175] **PEER 

 REVIEWED** 

HAZARDOUS REACTIVITIES & INCOMPATIBILITIES: 

 Distillation of mixtures with C1-C3 alcohols gives highly explosive alkyl 

 perchlorates. /Barium perchlorate/ [Bretherick, L. Handbook of Reactive 

 Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 

 80] **PEER REVIEWED** 

 During hydrogenation of an unspecified substrate in methanol solution 

 under hydrogen at 100 bar with Raney nickel catalyst, sudden temperature 

 increase led to hydrogenolysis of methanol to methane, and the pressure 

 increase led to an overpressure accident. Such incidents may be avoided by 

 control of agitation, limiting the amount of catalyst, and checking 

 thermal stability of starting materials and end products beforehand. 

 [Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

 Butterworth-Heinemann Ltd., 1990, p. 174] **PEER REVIEWED** 

 Can react vigorously with oxidizing materials. [Lewis, R.J. Sax's 

 Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New 

 York, NY: Van Nostrand Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 Strong oxidizers. [NIOSH. NIOSH Pocket Guide to Chemical Hazards & 

 Other Databases CD-ROM. Department of Health & Human Services, Centers 

 for Disease Prevention & Control. National Institute for Occupational 

 Safety& Health. DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER 

 REVIEWED** 

 /Acetyl bromide/ interaction with... methanol... is violent, hydropgen 

 bromide being evolved. [Bretherick, L. Handbook of Reactive Chemical 

 Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 243] 

 **PEER REVIEWED** 

 Accidental use of methanol in place of hexane to rinse out a hypodermic 

 syringe used for a diulte alkylaluminium solution caused a violent 

 reaction which blew the plunger out of the barrel. [Bretherick, L. 

 Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

 Butterworth-Heinemann Ltd., 1990, p. 174] **PEER REVIEWED** 

 Reaction of /beryllium hydride/ with methanol... is violent, even at -196 

 deg C. [Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. 

 Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 86] **PEER REVIEWED** 

 The rapid autocatalytic dissolution of aluminum, magnesium or zinc in 9:1 

 methanol-carbon tetrachloride mixtures is sufficiently vigorous to be 

 rated as potentially hazardous. [Bretherick, L. Handbook of Reactive 

 Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 

 174] **PEER REVIEWED** 

 During attempted preparation of trimethyl orthoformate, addition of sodium 

 to an inadequately cooled chloroform-methanol mixture caused a violent 

 explosion. [Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. 

 Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 133] **PEER REVIEWED** 

 A chloroform-methanol mixture was put into a drum contaminated with sodium 

 hydroxide. A vigorous reaction set in and the drum burst. Chloroform 

 normally reacts slowly with sodium hydroxide owing to the insolublility of 

 the latter. The presence of methanol increases the rate of reaction by 

 increasing the degree of ocntact between chloroform and alkali. Addition 

 of chloroform to a 4:1 mixture of methanol and 50 w/v% sodium hydroxide 

 solution caused the drum to burst. [Bretherick, L. Handbook of Reactive 

 Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 

 133] **PEER REVIEWED** 

 A crust of residual cynauric chloride left in a reactor from a previous 

 batch reacted with the methanol (usually charged first) to form hydrogen 

 chloride. When the base was added (usually before the chloride), vigorous 

 evolution of carbon dioxide expelled some of the solvent. In a second 

 incident, accidentally boubling the charge of cyanuric chloride but not 

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 the base, led to the development of free acid (which auto-catalyses the 

 reaction with methanol), and a runaway reaction developed causing violent 

 boiling of the solvent, methyl chloride evolution and damage to the plant. 

 [Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

 Butterworth-Heinemann Ltd., 1990, p. 333] **PEER REVIEWED** 

 Dichloromethane, previously considered to be non-flammable except in 

 oxygen, becomes flammable in air... at 27 deg C/1 bar in presence of less 

 than 0.5 vol% of methanol. [Bretherick, L. Handbook of Reactive Chemical 

 Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 141] 

 **PEER REVIEWED** 

 Interaction /of diethylzinc and methanol/ is explosively violent and 

 ignition ensues. [Bretherick, L. Handbook of Reactive Chemical Hazards. 

 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 493] **PEER 

 REVIEWED** 

 /There is an/ explosive nature of mixtures of aluminum or magnesium with 

 methanol... [Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. 

 Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 28] **PEER REVIEWED** 

 The reaction of magnesium and methanol to form magnesium methoxide and 

 used to prepare dry methanol is very vigorous, but often subject to a 

 lengthy induction period. Sufficient methanol must be present to absorb 

 the violent exotherm which sometimes occurs. Mixtures of powdered 

 magnesium (or aluminum) and methanol are capable of detonation and are 

 more powerful than military explosives. [Bretherick, L. Handbook of 

 Reactive Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 

 1990, p. 1323] **PEER REVIEWED** 

 Passage of chlorine through cold recovered methanol (but not fresh 

 methanol) led to a mild explosion and ignition, formation of methyl 

 hypochlorite apparently being catalysed by an impurity. [Bretherick, L. 

 Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

 Butterworth-Heinemann Ltd., 1990, p. 1004] **PEER REVIEWED** 

 When methanol was used to rinse a pestle and mortar which had been used to 

 grind coarse chromium trioxide, immediate ignition occurred due to 

 vigorous oxidation of the solvent. [Bretherick, L. Handbook of Reactive 

 Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 

 1069] **PEER REVIEWED** 

 The explosion limits have been determined for liquid systems containing... 

 methanol... under various types of initiation. In general, explosive 

 behavior is noted where the ratio of hydrogen peroxide to water is > 1, 

 and if the overall fuel-peroxide composition is stoicheiometric... . 

 [Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

 Butterworth-Heinemann Ltd., 1990, p. 1212] **PEER REVIEWED** 

 A saturated solution of anhydrous lead perchlorate in dry methanol 

 exploded violently when disturbed. [Bretherick, L. Handbook of Reactive 

 Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 

 1030] **PEER REVIEWED** 

 Furfuryl alcohol is hypergolic with high-strength nitric acid and methanol 

 has been used as a propellant fuel. [Bretherick, L. Handbook of Reactive 

 Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 

 1150] **PEER REVIEWED** 

 Several explosions involving methanol and sodium hypochlorite were 

 attributed to formation of methyl hypochlorite, especially in presence of 

 acids or other esterification catalyst. [Bretherick, L. Handbook of 

 Reactive Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 

 1990, p. 985] **PEER REVIEWED** 

 Liquid /phosphorous (III) oxide/ (above 24 deg C) reacts very violently 

 with methanol... and charring may occur. [Bretherick, L. Handbook of 

 Reactive Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 

 1990, p. 1431] **PEER REVIEWED** 

 Contact of 1.5g portions of solid /potassium tert-butoxide/ with drops of 

 /methanol/ or with the vapors of /methanol/ caused ignition... 

 [Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

 Butterworth-Heinemann Ltd., 1990, p. 475] **PEER REVIEWED** 

 Static discharge ignited the contents of a polythene bottle being filled 

 with a 40:60 mixture of methanol and water at 30 deg C, and a later 

 similar incident in a plastics-lined metal tank involved a 30:70 mixture 

 [Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

 Butterworth-Heinemann Ltd., 1990, p. 175] **PEER REVIEWED** 

HAZARDOUS DECOMPOSITION: 

 When heated to decomposition it emits acrid smoke and irritating fumes. 

 [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. 

 Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 2175] **PEER 

 REVIEWED** 

PRIOR HISTORY OF ACCIDENTS: 

 An outbreak of acute methanol intoxication involving 28 young men in Papua 

 New Guinea in 1977, each of whom consumed an equivalent of 60-600 mL pure 

 methanol, resulted in all becoming hospitalized within 8-36 hr due to 

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 acute metabolic acidosis, severe visual impairment and acute pancreatitis. 

 Four died within 72 hr after hospitalization. Of 24 who recovered, 16 

 showed no residual complications, 6 had bilateral visual impairment and 2 

 had difficulty in speech as well as visual impairment. [WHO; Environ 

 Health Criteria 196: Methanol p.101 (1997). Available from, as of July 18, 

 2005: http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER 

 REVIEWED** 

 ...In Atlanta, Georgia, USA, in 1951, when within a 5-day period, 323 

 people consumed bootlegged whiskey contaminated with 35-40% methanol and 

 41 of them died. ...The poisoning of 18 individuals /was reported/, of 

 whom 8 died, when a diluted paint thinner containing approximately 37% (by 

 volume) methanol was used as an alcoholic beverage in Lexington, Kentucky, 

 USA. An epidemic in the State Prison of Southern Michigan in 1979 in which 

 methanol diluent used in photocopying machines was used as "home-made" 

 spirits (containing approximately 3% methanol) resulted in 46 definite 

 cases of methanol intoxication and 3 deaths. Methanol poisoning among 23 

 servicemen in an Army hospital in Korea who had ingested bootleg sake 

 contaminated with methanol was reported. ...Acute methanol poisoning in 49 

 naval personnel who consumed drinks made from duplicating fluid containing 

 a high concentration of methanol /was also reported/. [WHO; Environ Health 

 Criteria 196: Methanol p.101 (1997). Available from, as of July 18, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] **PEER REVIEWED** 

IMMEDIATELY DANGEROUS TO LIFE OR HEALTH: 

 6000 ppm [NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other 

 Databases CD-ROM. Department of Health & Human Services, Centers for 

 Disease Prevention & Control. National Institute for Occupational 

 Safety& Health. DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER 

 REVIEWED** 

PROTECTIVE EQUIPMENT & CLOTHING: 

 Wear appropriate chemical protective gloves, boots, and goggles. 

 [Association of American Railroads/Bureau of Explosives; Emergency 

 Handling of Hazardous Materials in Surface Transportation. Association of 

 American Railroads. Pueblo, CO. 2002., p. 586] **PEER REVIEWED** 

 There is some data suggesting that the breakthrough times of methanol 

 through natural rubber are approximately an hour or more. [ACGIH; 

 Guidelines Select of Chem Protect Clothing Volume #1 Field Guide p.61 

 (1983)] **PEER REVIEWED** 

 Breakthrough times of methanol through nitrile or Viton are greater than 

 one hour reported by (normally) two or more testers. [ACGIH; Guidelines 

 Select of Chem Protect Clothing Volume #1 Field Guide p.61 (1983)] **PEER 

 REVIEWED** 

 Breakthrough times of methanol through polyvinyl alcohol or polyvinyl 

 chloride are less (usually significantly less) than one hour reported by 

 (normally) two or more testers. [ACGIH; Guidelines Select of Chem Protect 

 Clothing Volume #1 Field Guide p.61 (1983)] **PEER REVIEWED** 

 Respirator Recommendations: Up to 2000 ppm: (Assigned Protection Factor = 

 10) Any supplied-air respirator. [NIOSH. NIOSH Pocket Guide to Chemical 

 Hazards & Other Databases CD-ROM. Department of Health & Human 

 Services, Centers for Disease Prevention & Control. National Institute 

 for Occupational Safety& Health. DHHS (NIOSH) Publication No. 2004-103 

 (2003).] **PEER REVIEWED** 

 Respirator Recommendations: Up to 5000 ppm: (Assigned Protection Factor = 

 25) Any supplied-air respirator operated in a continuous-flow mode. 

 [NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases 

 CD-ROM. Department of Health & Human Services, Centers for Disease 

 Prevention & Control. National Institute for Occupational Safety& 

 Health. DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER REVIEWED** 

 Respirator Recommendations: Up to 6000 ppm: (Assigned Protection Factor = 

 50) Any supplied-air respirator that has a tight-fitting facepiece and is 

 operated in a continuous-flow mode/(Assigned Protection Factor = 50) Any 

 self-contained breathing apparatus with a full facepiece/(Assigned 

 Protection Factor = 50) Any supplied-air respirator with a full facepiece. 

 [NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases 

 CD-ROM. Department of Health & Human Services, Centers for Disease 

 Prevention & Control. National Institute for Occupational Safety& 

 Health. DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER REVIEWED** 

 Respirator Recommendations: Emergency or planned entry into unknown 

 concentrations or IDLH conditions: (Assigned Protection Factor = 10,000) 

 Any self-contained breathing apparatus that has a full facepiece and is 

 operated in a pressure-demand or other positive-pressure mode/(Assigned 

 Protection Factor = 10,000) Any supplied-air respirator that has a full 

 facepiece and is operated in a pressure-demand or other positive-pressure 

 mode in combination with an auxiliary self-contained positive-pressure 

 breathing apparatus. [NIOSH. NIOSH Pocket Guide to Chemical Hazards & 

 Other Databases CD-ROM. Department of Health & Human Services, Centers 

 for Disease Prevention & Control. National Institute for Occupational 

 Safety& Health. DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER 

 REVIEWED** 

 Respirator Recommendations: Escape: Any appropriate escape-type, 

 self-contained breathing apparatus. [NIOSH. NIOSH Pocket Guide to Chemical 

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 Hazards & Other Databases CD-ROM. Department of Health & Human 

 Services, Centers for Disease Prevention & Control. National Institute 

 for Occupational Safety& Health. DHHS (NIOSH) Publication No. 2004-103 

 (2003).] **PEER REVIEWED** 

 Wear appropriate personal protective clothing to prevent skin contact. 

 [NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases 

 CD-ROM. Department of Health & Human Services, Centers for Disease 

 Prevention & Control. National Institute for Occupational Safety& 

 Health. DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER REVIEWED** 

 Wear appropriate eye protection to prevent eye contact. [NIOSH. NIOSH 

 Pocket Guide to Chemical Hazards & Other Databases CD-ROM. Department 

 of Health & Human Services, Centers for Disease Prevention & 

 Control. National Institute for Occupational Safety& Health. DHHS 

 (NIOSH) Publication No. 2004-103 (2003).] **PEER REVIEWED** 

PREVENTIVE MEASURES: 

 Skin that becomes wet with liquid methyl alcohol should be promptly washed 

 or showered. Eating and smoking should not be permitted in areas where 

 liquid methyl alcohol is handled, processed, or stored. [Mackison, F. W., 

 R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational 

 Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 

 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. 

 2] **PEER REVIEWED** 

 SRP: The scientific literature for the use of contact lenses in industry 

 is conflicting. The benefit or detrimental effects of wearing contact 

 lenses depend not only upon the substance, but also on factors including 

 the form of the substance, characteristics and duration of the exposure, 

 the uses of other eye protection equipment, and the hygiene of the lenses. 

 However, there may be individual substances whose irritating or corrosive 

 properties are such that the wearing of contact lenses would be harmful to 

 the eye. In those specific cases, contact lenses should not be worn. In 

 any event, the usual eye protection equipment should be worn even when 

 contact lenses are in place. **PEER REVIEWED** 

 If material not on fire and not involved in fire: Keep sparks, flames, and 

 other sources of ignition away. Keep material out of water sources and 

 sewers. Build dikes to contain flow as necessary. Attempt to stop leak if 

 without undue personnel hazard. Use water spray to disperse vapors and 

 dilute standing pools of liquid. [Association of American Railroads/Bureau 

 of Explosives; Emergency Handling of Hazardous Materials in Surface 

 Transportation. Association of American Railroads. Pueblo, CO. 2002., p. 

 586] **PEER REVIEWED** 

 Before welding or cutting a vessel that has contained methyl alcohol, the 

 vessel should be emptied and purged to remove every trace of the flammable 

 liquid. [International Labour Office. Encyclopedia of Occupational Health 

 and Safety. Vols. I&II. Geneva, Switzerland: International Labour 

 Office, 1983., p. 1357] **PEER REVIEWED** 

 A major concern in the painting studio is solvents, /including methanol/. 

 ... Precautions include ... use of dilution and local exhaust ventilation, 

 control of storage areas, disposal of solvent soaked rags in covered 

 containers, minimizing skin exposure, and the use of respirators and other 

 personal protective equipment. The control of fire hazards is also 

 important, since many of the solvents are highly flammable. [Hart C; J of 

 Environ Health 49 (5): 282-6 (1987)] **PEER REVIEWED** 

 Personnel protection: Avoid breathing vapors. Keep upwind. Do not handle 

 broken packages unless wearing appropriate personal protective equipment. 

 Wash away any material which may have contacted the body with copious 

 amounts of water or soap and water. [Association of American 

 Railroads/Bureau of Explosives; Emergency Handling of Hazardous Materials 

 in Surface Transportation. Association of American Railroads. Pueblo, CO. 

 2002., p. 586] **PEER REVIEWED** 

 The worker should immediately wash the skin when it becomes contaminated. 

 [NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases 

 CD-ROM. Department of Health & Human Services, Centers for Disease 

 Prevention & Control. National Institute for Occupational Safety& 

 Health. DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER REVIEWED** 

 Work clothing that becomes wet should be immediately removed due to its 

 flammability hazard. [NIOSH. NIOSH Pocket Guide to Chemical Hazards & 

 Other Databases CD-ROM. Department of Health & Human Services, Centers 

 for Disease Prevention & Control. National Institute for Occupational 

 Safety& Health. DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER 

 REVIEWED** 

 If material on fire or involved in fire: Do not extinguish fire unless 

 flow can be stopped. Use water in flooding quantities as fog. Solid 

 streams of water may be ineffective. Cool all affected containers with 

 flooding quantities of water. Apply water from as far a distance as 

 possible. Use 'alcohol' foam, dry chemical, or carbon dioxide. 

 [Association of American Railroads/Bureau of Explosives; Emergency 

 Handling of Hazardous Materials in Surface Transportation. Association of 

 American Railroads. Pueblo, CO. 2002., p. 586] **PEER REVIEWED** 

 SRP: Local exhaust ventilation should be applied wherever there is an 

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 incidence of point source emissions or dispersion of regulated 

 contaminants in the work area. Ventilation control of the contaminant as 

 close to its point of generation is both the most economical and safest 

 method to minimize personnel exposure to airborne contaminants. **PEER 

 REVIEWED** 

 SRP: Contaminated protective clothing should be segregated in such a 

 manner so that there is no direct personal contact by personnel who 

 handle, dispose, or clean the clothing. Quality assurance to ascertain the 

 completeness of the cleaning procedures should be implemented before the 

 decontaminated protective clothing is returned for reuse by the workers. 

 Contaminated clothing should not be taken home at end of shift, but should 

 remain at employee's place of work for cleaning. **PEER REVIEWED** 

SHIPMENT METHODS AND REGULATIONS: 

 No person may /transport,/ offer or accept a hazardous material for 

 transportation in commerce unless that person is registered in conformance 

 ... and the hazardous material is properly classed, described, packaged, 

 marked, labeled, and in condition for shipment as required or authorized 

 by ... /the hazardous materials regulations (49 CFR 171-177)./ [49 CFR 

 171.2; U.S. National Archives and Records Administration's Electronic Code 

 of Federal Regulations. Available from, as of February 15, 2006: 

 http://www.gpoaccess.gov/ecfr/] **PEER REVIEWED** 

 The International Air Transport Association (IATA) Dangerous Goods 

 Regulations are published by the IATA Dangerous Goods Board pursuant to 

 IATA Resolutions 618 and 619 and constitute a manual of industry carrier 

 regulations to be followed by all IATA Member airlines when transporting 

 hazardous materials. [International Air Transport Association. Dangerous 

 Goods Regulations. 47th Edition. Montreal, Quebec Canada. 2006., p. 217] 

 **PEER REVIEWED** 

 The International Maritime Dangerous Goods Code lays down basic principles 

 for transporting hazardous chemicals. Detailed recommendations for 

 individual substances and a number of recommendations for good practice 

 are included in the classes dealing with such substances. A general index 

 of technical names has also been compiled. This index should always be 

 consulted when attempting to locate the appropriate procedures to be used 

 when shipping any substance or article. [International Maritime 

 Organization. International Maritime Dangerous Goods Code. London, UK. 

 2004., p. 53] **PEER REVIEWED** 

CLEANUP METHODS: 

 General Spill Actions: Stop or reduce discharge of material if this can be 

 done without risk. Eliminate all sources of ignition. Avoid skin contact 

 and inhalation. A fluorocarbon water foam can be applied to the spill to 

 diminish vapor and fire hazard. Hycar and carbopol, which are absorbent 

 materials, have shown possible applicability for vapor suppression and/or 

 containment of methanol in spill situations. Leaking containers should be 

 removed to the outdoors or to an isolated, well-ventilated area and the 

 contents transferred to other suitable containers. The following materials 

 are recommended for plugging leaks of methanol: polyester (eg Glad bag), 

 imid polyester (eg brown-in-bag), stafoam urethane foam, sea-going epoxy 

 putty, and MSA urethane. [Environment Canada; Tech Info for Problem 

 Spills: Methanol (Draft) p.98 (1981)] **PEER REVIEWED** 

 Spills on Land: Contain if possible by forming mechanical or chemical 

 barriers to prevent spreading. Absorb on sand, vermiculite or other 

 absorbent and shovel into metal containers for disposal. Application of 

 universal gelling agent to immobilize the spill, or the use of fly ash or 

 cement powder to absorb the liquid bulk should also be considered. Other 

 recommended sorbent materials are activated carbon and a universal sorbent 

 material. [Environment Canada; Tech Info for Problem Spills: Methanol 

 (Draft) p.98 (1981)] **PEER REVIEWED** 

 Spills in Water: After containment, a universal gelling agent can be 

 injected to solidify trapped mass to increase the effectiveness of berms. 

 Activated carbon can be applied at 10% the spilled amount over region 

 occupied by 10 mg/L or greater concentrations. Then use mechanical dredges 

 or lifts to remove immobilized masses of pollutants. [Environment Canada; 

 Tech Info for Problem Spills: Methanol (Draft) p.98 (1981)] **PEER 

 REVIEWED** 

 If the spilled material is known to be methanol: Response personnel should 

 be provided with and required to use impervious clothing, gloves, face 

 shields (eight-inch minimum), and other appropriate protective clothing 

 necessary to prevent repeated or prolonged skin contact with liquid methyl 

 alcohol. Splash-proof and chemical safety goggles are recommended for eye 

 protection. Polyvinyl plastic, neoprene or rubber is recommended for 

 protective clothing and gloves. Chemical suit materials recommended for 

 protection against methanol, include butyl, neoprene and polyvinyl 

 chloride. [Environment Canada; Tech Info for Problem Spills: Methanol 

 (Draft) p.100 (1981)] **PEER REVIEWED** 

 Environmental considerations- Land spill: Dig a pit, pond, lagoon, holding 

 area to contain liquid or solid material. /SRP: If time permits, pits, 

 ponds, lagoons, soak holes, or holding areas should be sealed with an 

 impermeable flexible membrane liner./ Dike surface flow using soil, sand 

 bags, foamed polyurethane, or foamed concrete. [Association of American 

 Railroads/Bureau of Explosives; Emergency Handling of Hazardous Materials 

 in Surface Transportation. Association of American Railroads. Pueblo, CO. 

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 2002., p. 586] **PEER REVIEWED** 

 Environmental considerations- Water spill: Allow to aerate. Use natural 

 barriers or oil spill control booms to limit spill travel. Remove trapped 

 material with suction hoses. [Association of American Railroads/Bureau of 

 Explosives; Emergency Handling of Hazardous Materials in Surface 

 Transportation. Association of American Railroads. Pueblo, CO. 2002., p. 

 586] **PEER REVIEWED** 

 Environmental considerations- Air spill: Apply water spray or mist to 

 knock down vapors. [Association of American Railroads/Bureau of 

 Explosives; Emergency Handling of Hazardous Materials in Surface 

 Transportation. Association of American Railroads. Pueblo, CO. 2002., p. 

 586] **PEER REVIEWED** 

DISPOSAL METHODS: 

 Generators of waste (equal to or greater than 100 kg/mo) containing this 

 contaminant, EPA hazardous waste numbers U154 and F003, must conform with 

 USEPA regulations in storage, transportation, treatment and disposal of 

 waste. [40 CFR 240-280, 300-306, 702-799 (7/1/2004)] **PEER REVIEWED** 

 Disposal: Waste methanol must never be discharged directly into sewers or 

 surface waters. Large quantities of waste methanol can either be disposed 

 of at licensed waste solvent disposal company or reclaimed by filtration 

 and distillation. It can also be incinerated. [Environment Canada; Tech 

 Info for Problem Spills: Methanol (Draft) p.100 (1981)] **PEER REVIEWED** 

 A good candidate for rotary kiln incineration at a temperature range of 

 820 to 1,600 deg C and residence times of seconds for liquids and gases, 

 and hours for solids. A good candidate for liquid injection incineration 

 at a temperature range of 650 to 1,600 deg C and a residence time of 0.1 

 to 2 seconds. A good candidate for fluidized bed incineration at a 

 temperature range of 450 to 980 deg C and residence times of seconds for 

 liquids and gases, and longer for solids. [USEPA; Engineering Handbook for 

 Hazardous Waste Incineration p.3-14 (1981) EPA 68-03-3025] **PEER 

 REVIEWED** 

 The following wastewater treatment technologies have been investigated for 

 methanol biological treatment, reverse osmosis, and activated carbon. 

 [USEPA; Management of Hazardous Waste Leachate, EPA Contract No.68-03-2766 

 p.E-16 (1982)] **PEER REVIEWED** 

 Spray into a furnace. Incineration will become easier by mixing with a 

 more flammable solvent. Recommendable methods: Incineration... . [United 

 Nations. Treatment and Disposal Methods for Waste Chemicals (IRPTC File). 

 Data Profile Series No. 5. Geneva, Switzerland: United Nations 

 Environmental Programme, Dec. 1985., p. 209] **PEER REVIEWED** 

OCCUPATIONAL EXPOSURE STANDARDS: 

OSHA STANDARDS: 

 Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 200 ppm (260 

 mg/cu m). [29 CFR 1910.1000; U.S. National Archives and Records 

 Administration's Electronic Code of Federal Regulations. Available from, 

 as of June 1, 2005: http://www.gpoaccess.gov/ecfr] **PEER REVIEWED** 

 Vacated 1989 OSHA PEL TWA 200 ppm (260 mg/cu m); STEL 250 ppm (325 mg/cu 

 m), skin designation, is still enforced in some states. [NIOSH. NIOSH 

 Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. 

 Washington, D.C. U.S. Government Printing Office, 1997., p. 367] **PEER 

 REVIEWED** 

THRESHOLD LIMIT VALUES: 

 8 hr Time Weighted Avg (TWA): 200 ppm; 15 min Short Term Exposure Limit 

 (STEL): 250 ppm. Skin. [American Conference of Governmental Industrial 

 Hygienists TLVs and BEIs. Threshold Limit Values for Chemical Substances 

 and Physical Agents and Biological Exposure Indices. Cincinnati, OH, 2008, 

 p. 38] **QC REVIEWED** 

 Biological Exposure Index (BEI): Determinant: methanol in urine; Sampling 

 Time: end of shift; BEI: 15 mg/L. The determinant may be present in 

 biological specimens collected from subjects who have not been 

 occupationally exposed, at a concentration which could affect 

 interpretation of the result. Such background concentrations are 

 incorporated in the BEI value. The determinant is nonspecific, since it is 

 also observed after exposure to other chemicals. [American Conference of 

 Governmental Industrial Hygienists TLVs and BEIs. Threshold Limit Values 

 for Chemical Substances and Physical Agents and Biological Exposure 

 Indices. Cincinnati, OH, 2008, p. 106] **QC REVIEWED** 

NIOSH RECOMMENDATIONS: 

 Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 200 ppm (260 mg/cu 

 m), 15 Min Short-Term Exposure Limit: 250 ppm (325 mg/cu m), skin. [NIOSH. 

 NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

 Department of Health & Human Services, Centers for Disease Prevention 

 & Control. National Institute for Occupational Safety& Health. 

 DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER REVIEWED** 

IMMEDIATELY DANGEROUS TO LIFE OR HEALTH: 

Iris Camacho, 6308MM Page 57 of 69

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 6000 ppm [NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other 

 Databases CD-ROM. Department of Health & Human Services, Centers for 

 Disease Prevention & Control. National Institute for Occupational 

 Safety& Health. DHHS (NIOSH) Publication No. 2004-103 (2003).] **PEER 

 REVIEWED** 

OTHER STANDARDS REGULATIONS AND GUIDELINES: 

 Arab Republic of Egypt TWA 200 ppm (260 mg/cu m), skin [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V8 p.1284] **PEER REVIEWED** 

 Australia TWA 200 ppm (260 mg/cu m); STEL 250 ppm, skin [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V8 p.1284] **PEER REVIEWED** 

 Beligium TWA 200 ppm (260 mg/cu m); STEL 250 ppm, skin [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V8 p.1284] **PEER REVIEWED** 

 Denmark TWA 200 (260 mg/cu m), skin [Bingham, E.; Cohrssen, B.; Powell, 

 C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New 

 York, N.Y. (2001)., p. V8 p.1284] **PEER REVIEWED** 

 Finland TWA 200 (260 mg/cu m); STEL 250 ppm, skin [Bingham, E.; Cohrssen, 

 B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 France TWA 200 (260 mg/cu m); STEL 1000 ppm (1300 mg/cu m), skin 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V8 p.1285] 

 **PEER REVIEWED** 

 Germany (DFG MAK) TWA 200 (270 mg/cu m) [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 Hungary 50 mg/cu m; STEL 100 mg/cu m, skin [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 Ireland TWA 200 ppm (260 mg/cu m); STEL 250 ppm (310 mg/cu m), skin 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V8 p.1285] 

 **PEER REVIEWED** 

 Japan (JSOH) TWA 200 ppm (260 mg/cu m), skin [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 The Netherlands TWA 200 ppm (260 mg/cu m), skin [Bingham, E.; Cohrssen, 

 B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 The Philippines TWA 200 ppm (260 mg/cu m) [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 Poland TWA 100 ppm; STEL 300 mg/cu m, skin [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 Russia TWA 200 ppm; STEL 5 mg/cu m, skin [Bingham, E.; Cohrssen, B.; 

 Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & 

 Sons. New York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 Sweden TWA 200 ppm (250 mg/cu m); STEL 250 ppm (350 mg/cu m), skin 

 [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 

 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V8 p.1285] 

 **PEER REVIEWED** 

 Switzerland TWA 200 ppm (260 mg/cu m); STEL 400 ppm, skin [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 Thailand TWA 200 ppm (260 mg/cu m) [Bingham, E.; Cohrssen, B.; Powell, 

 C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New 

 York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 Turkey TWA 200 ppm (260 mg/cu m) [Bingham, E.; Cohrssen, B.; Powell, 

 C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New 

 York, N.Y. (2001)., p. V8 p.1285] **PEER REVIEWED** 

 United Kingdom TWA 200 ppm (260 mg/cu m); STEL/CEIL (C) 250 ppm (333 mg/cu 

 m) [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 

 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V8 p.1285] 

 **PEER REVIEWED** 

 Emergency Response Planning Guidelines (ERPG): ERPG(1) 200 ppm (no more 

 than mild, transient effects) for up to 1 hr exposure; ERPG(2) 1000 ppm 

 (without serious, adverse effects) for up to 1 hr exposure; ERPG(3) 5000 

 ppm (not life threatening) up to 1 hr exposure. [American Industrial 

Iris Camacho, 6308MM Page 58 of 69

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 Hygiene Association. The AIHA 2005 Emergency Response Planning Guidelines 

 and Workplace Environmental Exposure Level Handbook. AIHA. Fairfax, VA 

 2005., p. 23] **PEER REVIEWED** 

MANUFACTURING/USE INFORMATION: 

MAJOR USES: 

 For methanol (USEPA/OPP Pesticide Code: 053801) there are 0 labels match. 

 /SRP: Not registered for current use in the U.S., but approved pesticide 

 uses may change periodically and so federal, state and local authorities 

 must be consulted for currently approved uses./ [U.S. Environmental 

 Protection Agency/Office of Pesticide Program's Chemical Ingredients 

 Database on Methanol (67-56-1). Available from, as of June 1, 2005: 

 http://ppis.ceris.purdue.edu/htbin/epachem.com] **PEER REVIEWED** 

 Industrial solvent. Raw material for making formaldehyde and methyl esters 

 of organic and inorganic acids. Antifreeze for automotive radiators and 

 brakes; ingredient of gasoline and diesel oil antifreezes. Octane booster 

 in gasoline. As fuel for picnic stoves and soldering torches. Extractant 

 for animal and vegetable oils. To denature ethanol. Softening agent for 

 pyroxylin plastics. Solvent and solvent adjuvant for polymers. Solvent in 

 the manufacture of cholesterol, streptomycin, vitamins, hormones, and 

 other pharmaceuticals. [O'Neil, M.J. (ed.). The Merck Index - An 

 Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, 

 Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1065] **PEER 

 REVIEWED** 

 Used in dehydrating pipelines, as a de-icing agent, and in the production 

 of methylamines and chlorine dioxide. [Environment Canada; Tech Info for 

 Problem Spills: Methanol (Draft) p.15 (1981)] **PEER REVIEWED** 

 Primarily as substitute solvent and rubefacient for ethyl alcohol in 

 liniments (external use only). [Rossoff, I.S. Handbook of Veterinary 

 Drugs. New York: Springer Publishing Company, 1974., p. 8] **PEER 

 REVIEWED** 

 Used on household contents, mortuary instruments, bedding (human), human 

 clothing, tissues (biological specimens), cadavers, and human stools 

 against animal pathogenic bacteria (gram- and gram+ vegetative) and 

 maggots. /Eureka Products, Criosine/ [Purdue University; National 

 Pesticide Information Retrieval System (1988)] **PEER REVIEWED** 

 Used in oil recovery packer fluid against slime forming bacteria, 

 deterioration and spoilage bacteria, sulfate-reducing bacteria. 

 /Coat-B1400/ [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Used on onions during soil treatment against onion smut (urocystis 

 cepulae). /Wilbur-Ellis Smut-Guard/ [Purdue University; National Pesticide 

 Information Retrieval System (1988)] **PEER REVIEWED** 

 Used on elms as injection treatment against dutch elm disease. /Freers Elm 

 Arrester/ [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Used in secondary oil recovery injection water against slime forming 

 bacteria. /Surflo-B17/ [Purdue University; National Pesticide Information 

 Retrieval System (1988)] **PEER REVIEWED** 

 Used on timbers, wood fence posts, wood poles/posts, timbers (heavy wooden 

 members), and lumber (seasoned) for soil contact nonfumigation treatment 

 against wood rot and decay fungi. /Ideal Concentrated Wood-Preservative/ 

 [Purdue University; National Pesticide Information Retrieval System 

 (1988)] **PEER REVIEWED** 

 ... Duplicating fluid (99% methyl alcohol) used in direct-process spirit 

 duplicating machines [Frederick LJ et al; Am Ind Hyg Assoc J 45 (1): 51-55 

 (1984)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6702599" 

 target=new>PubMed Abstract 

 Effective solvent for the removal of 2,4-dinitrotoluene from spent carbons 

 [Ho PC, Daw CS; Environ Sci Technol 22 (8): 919-24 (1988)] **PEER 

 REVIEWED** 

 Removal of toxic organic pollutants from soil with supercritical carbon 

 dioxide and methanol or toluene. [USEPA; Proc Int Conf New Front Hazard 

 Waste Manage 2nd Ed. p.383-97 (1987) EPA/600/9-87/018F] **PEER REVIEWED** 

 About 70% of methanol manufactured worldwide is used as feedstock for the 

 production of chemicals such as formaldehyde, methyl tertiary butyl ether 

 (MTBE), acetic acid, methyl methacrylate, and dimethyl terephthalate. 

 [DHHS/NTP; NTP-CERHR Expert Panel Report on the Reproductive and 

 Developmental Toxicity of Methanol p.2 (April 2002) NTP-CERHR-MeOH-02. 

 Available from, as of July 20, 2005: 

 http://cerhr.niehs.nih.gov/news/methanol/methanol_final.pdf] **PEER 

 REVIEWED** 

MANUFACTURERS: 

Iris Camacho, 6308MM Page 59 of 69

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 Air Products and Chemicals, Inc., 7201 Hamilton Blvd., Allentown, PA 

 18195-1501, (610) 481-6799; Industrial Chemicals Division; Production 

 site: Pace, FL 32571 [SRI Consulting. 2004 Directory of Chemical 

 Producers. SRI International, Menlo Park, CA 2004., p. 721] **PEER 

 REVIEWED** 

 Celanese LTD., 86 Morris Avenue, Summit, NJ 07901, (872) 443-4000. 

 Production sites: Bishop, TX 78343; Clear Lake, TX 77507 [SRI Consulting. 

 2004 Directory of Chemical Producers. SRI International, Menlo Park, CA 

 2004., p. 721] **PEER REVIEWED** 

 Dakota Gasification Company, 1600 East Interstate Avenue, P.O. Box 5540, 

 Bismark, ND 58506-5540, (701) 221-4411; Production site: Beulah, ND 58523 

 [SRI Consulting. 2004 Directory of Chemical Producers. SRI International, 

 Menlo Park, CA 2004., p. 721] **PEER REVIEWED** 

 Eastman Chemical Company, PO Box 511, Kingsport, TN 37662 (423) 229-2000; 

 Production site: Kingsport, TN 37662 [SRI Consulting. 2004 Directory of 

 Chemical Producers. SRI International, Menlo Park, CA 2004., p. 721] 

 **PEER REVIEWED** 

 Lyondell Methanol Company, One Houston Center, 1221 Mckinney St., Suite 

 1600, Houston, TX 77010 (713) 652-7000 Production site: Channelview, TX 

 77530 [SRI Consulting. 2004 Directory of Chemical Producers. SRI 

 International, Menlo Park, CA 2004., p. 721] **PEER REVIEWED** 

 Millenium Petrochemicals, 11500 Northlake Drive, P.O. Box 429550, 

 Cincinnati, OH 45249, (513)530-6500; Production site: LaPorte, TX 77571 

 [SRI Consulting. 2004 Directory of Chemical Producers. SRI International, 

 Menlo Park, CA 2004., p. 721] **PEER REVIEWED** 

 Motiva Enterprises, 1100 Louisiana, Houston, TX 77002, (713) 277-8000; 

 Production site: Delaware City, DE 19706 [SRI Consulting. 2004 Directory 

 of Chemical Producers. SRI International, Menlo Park, CA 2004., p. 721] 

 **PEER REVIEWED** 

 Praxir Inc., 39 Old Ridgebury Rd., Danbury, CT 06810-5113, (716) 879-4077; 

 Production site: Geismar, LA 70734 [SRI Consulting. 2004 Directory of 

 Chemical Producers. SRI International, Menlo Park, CA 2004., p. 721] 

 **PEER REVIEWED** 

 Sterling Chemicals Inc., 1200 Smith St., Suite 1900, Houston, TX 

 77002-4312, (713) 650-3700; Production site: Texas City, TX 77590 [SRI 

 Consulting. 2004 Directory of Chemical Producers. SRI International, Menlo 

 Park, CA 2004., p. 721] **PEER REVIEWED** 

 Terra Industries Inc., Terra Centre, 600 Fourth St., Sioux City, IA 51101, 

 (712) 277-7296; Production sites: Beaumont, TX 77704; Woodward, OK 73801 

 [SRI Consulting. 2004 Directory of Chemical Producers. SRI International, 

 Menlo Park, CA 2004., p. 721] **PEER REVIEWED** 

METHODS OF MANUFACTURING: 

 Methanol is manufactured by the reaction between carbon monoxide and 

 hydrogen at 503-673 deg K and 5-60 MPa (50-600 atm). High pressure 

 processes (P greater than 150 atm) are catalyzed by copper chromite 

 catalysts. The most widely used process, however, is the low pressure 

 methanol process that is conducted at 503-523 deg K, 5-10 MPa (50-100 

 atm), space velocities of 20,000-60,000 h-1, and H2-to-CO ratios of 3. The 

 reaction is catalyzed by a copper-zinc oxide catalyst using promoters such 

 as alumina. This catalyst is more easily poisoned than the older copper 

 chromite catalysts and requires the use of sulfur-free synthesis gas. The 

 reaction between carbon monoxide and hydrogen is exothermic ... and plants 

 must be designed to remove heat efficiently. In order to control the 

 exotherm, CO conversions are typically maintained well below the 

 equilibrium conversion, 45% at 523 deg K. This necessitates a substantial 

 recycle of carbon monoxide and hydrogen. [Kirk-Othmer Encyclopedia of 

 Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 

 1991-Present., p. V5 103 (1993)] **PEER REVIEWED** 

 /The liquid-phase methanol/ ... process utilizes a catalyst such as copper 

 -zinc oxide suspended in a hydrocarbon oil. The liquid phase is used as a 

 heat-transfer medium and allows the reaction to be conducted at higher 

 conversions than conventional reactor designs. In addition, the use of the 

 liquid-phase methanol process allows the use of a coal-derived, CO-rich 

 synthesis gas. Typical reactor conditions for this process are 3.5-6.3 MPa 

 (35-60 atm) and 473-563 deg K. [Kirk-Othmer Encyclopedia of Chemical 

 Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 

 1991-Present., p. V5 103 (1993)] **PEER REVIEWED** 

 By high-pressure catalytic synthesis from carbon monoxide and hydrogen; 

 partial oxidation of natural gas hydrocarbons; Several processes for 

 making methanol by gasification of wood, peat and lignite have been 

 developed but have not yet proved out commercially; From methane with 

 molybdenum catalyst (experimental). [Lewis, R.J. Sr.; Hawley's Condensed 

 Chemical Dictionary 14th Edition. John Wiley & Sons, Inc. New York, NY 

 2001., p. 722] **PEER REVIEWED** 

GENERAL MANUFACTURING INFORMATION: 

 Methanol usually is better solvent than ethanol, dissolves many inorganic 

 salts ... sodium iodide 43%, calcium chloride 22%, ammonium nitrate 14%, 

 copper sulfate 13%, silver nitrate 4%, ammonium chloride 3.2%, sodium 

Iris Camacho, 6308MM Page 60 of 69

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 chloride 1.4%. [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of 

 Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: 

 Merck and Co., Inc., 2001., p. 1065] **PEER REVIEWED** 

 METHANOL IS PURIFIED BY DISTILLATION. [Kirk-Othmer Encyclopedia of 

 Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and 

 Sons, 1978-1984., p. 15(78) 408] **PEER REVIEWED** 

FORMULATIONS/PREPARATIONS: 

 Grade: Technical, CP (99.85%), electronic (used to clean and dry 

 componets), fuel [Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 

 14th Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 722] 

 **PEER REVIEWED** 

 Formaldehyde; intrastate fungicide; 37.0% formaldehyde, 15.0% methyl 

 alcohol. [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Wilbur-Ellis Smut-Guard; fungicide; 37.0% formaldehyde, 12.0% methyl 

 alcohol. [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Eureka Products, Criosine; intrastate disinfectant/bacteriocide/germicide; 

 47.6% methyl alcohol, 0.86% nitrobenzene, 0.54% butyl 4-hydroxybenzoate, 

 30.0% phenol. [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Surflo-B17; microbicide/microbisat general; 32.37% formaldehyde, 10.5% 

 methyl alcohol, 10.0% alkyl dimethyl benzyl ammonium chloride. [Purdue 

 University; National Pesticide Information Retrieval System (1988)] **PEER 

 REVIEWED** 

 Coat-B1400; solution ready to use; 25.0% methyl alcohol, 24.0% morpholine 

 polyethoxyethanol. [Purdue University; National Pesticide Information 

 Retrieval System (1988)] **PEER REVIEWED** 

 Ideal Concentrated Wood Preservative; fungicide; 15.0% isopropanol, 15.0% 

 methyl alcohol, 10.0% orthodichlorobenzene, 38.4% pentachlorophenol, 20.0% 

 aliphatic petroleum hydrocarbons. [Purdue University; National Pesticide 

 Information Retrieval System (1988)] **PEER REVIEWED** 

 Freer Elm Arrester; fungicide; 0.12% mecuric chloride, 96.65% methyl 

 alcohol. [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Eureka Products Criosine Disinfectant; 

 disinfectant/bacteriocide/germicide; 47.6% methyl alcohol, 0.86% 

 nitrobenzene, 0.54% butyl 4-hydroxybenzoate, 30.0% phenol. [Purdue 

 University; National Pesticide Information Retrieval System (1988)] **PEER 

 REVIEWED** 

 X-Cide 402 Industrial Bactericide; bacteriostat; 11.5% isopropanol, 16.4% 

 methyl alcohol, 28.5% alkyl amino-3-aminopropane monoacetate, 17.8% 

 oxydiethylenebis(alkyl) dimethyl ammonium chloride. [Purdue University; 

 National Pesticide Information Retrieval System (1988)] **PEER REVIEWED** 

IMPURITIES: 

 GRADE A) ACETONE AND ALDEHYDES 30 PPM MAX; ACETIC ACID 30 PPM MAX: WATER 

 CONTENT 1500 PPM MAX; GRADE AA) ACETONE AND ALDEHYES 30 PPM MAX; ACETONE 

 20 PPM MAX; ETHANOL 10 PPM MAX; ACETIC ACID 30 PPM MAX; WATER CONTENT 100 

 PPM MAX. [Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., 

 Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 15(81) 

 409] **PEER REVIEWED** 

 Water, dimethyl ether, fusel oils, and higher alcohols. [Environment 

 Canada; Tech Info for Problem Spills: Methanol (Draft) p.15 (1981)] **PEER 

 REVIEWED** 

CONSUMPTION PATTERNS: 

 39% FOR FORMALDEHYDE; 12% EXPORTED; 8% FOR SOLVENT USAGE; 6% FOR DIMETHYL 

 TEREPHTHALATE; 6% FOR METHYL HALIDES; 4% FOR METHYL METHACRYLATE; 3% FOR 

 ACETIC ACID; 3% FOR METHYLAMINES; 1% FOR FORMALDEHYDE INHIBITOR; 17% MISC 

 (1973) [SRI] **PEER REVIEWED** 

 CHEMICAL PROFILE: Methanol. Formaldehyde, 27%; MTBE /methyl tert-butyl 

 ether/, 25%; acetic acid, 11%; chloromethanes, 7%; solvents, 8%; methyl 

 halides, 4%; methyl methacrylates, 4%; methylamines, 3%; methylene 

 chloride, 2%; utility power, 1%; miscellaneous and exports, 2%. [Kavaler 

 AR; Chemical Marketing Reporter 230 (12): 70 (1986)] **PEER REVIEWED** 

 CHEMICAL PROFILE: Methanol. Demand: 1985: 1.29 billion gallons; 1986: 1.35 

 billion gallons; 1990 /projected/: 1.6 billion gallons. [Kavaler AR; 

 Chemical Marketing Reporter 230 (12): 70 (1986)] **PEER REVIEWED** 

 CHEMICAL PROFILE: Methanol. Formaldehyde, 27%; MTBE /methyl tert-butyl 

 ether/, 26%; acetic acid, 11%; chloromethanes, 7%; solvents, 7%; methyl 

 halides, 4%; methylmethacrylates, 4%; methylamines, 3%; methylene 

 chloride, 2%; miscellaneous and exports, 9%. [Kavaler AR; Chemical 

 Marketing Reporter 236 (13): 62 (1989)] **PEER REVIEWED** 

 CHEMICAL PROFILE: Methanol. Demand: 1988: 1.8 billion gallons; 1989: 1.6 

Iris Camacho, 6308MM Page 61 of 69

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 billion gallons; 1993 /projected/: 2.2 billion gallons. (Includes imports, 

 which totaled 690 million gallons last year, as well as export shipments, 

 which are negligible, totaling 36 million gallons last year.) [Kavaler AR; 

 Chemical Marketing Reporter 236 (13): 62 (1989)] **PEER REVIEWED** 

 CHEMICAL PROFILE: Methanol. Demand: 2000: 2.92 billion gallons; 2001: 

 2.838 billion gallons; 2005 /projected/: 2.7 billion gallons with MTBE 

 phase out or 3.11 billion gallons with MTBE phase out. [Kirshner M; 

 Chemical Marketing Reporter. December, 16 (2002)] **PEER REVIEWED** 

U. S. PRODUCTION: 

 This chemical is listed as a High Production Volume (HPV) (65FR81686; 

 http://www.epa.gov/opptintr/chemrtk/hpvchmlt.htm). Chemicals listed as HPV 

 were produced in or imported into the U.S. in > 1 million pounds in 

 1990. The HPV list is based on the 1990 Inventory Update Rule. (IUR) (40 

 CFR part 710 subpart B; 51FR21438; http://www.epa.gov/oppt/iur/index.htm). 

 [EPA/Office of Pollution Prevention and Toxics; High Production Volume 

 (HPV) Challenge Program's Robust Summaries and Test Plans. Available from, 

 as of December 19, 2005: http://www.epa.gov/hpv/pubs/general/opptsrch.htm] 

 **PEER REVIEWED** 

 (1984) 3.72X10+12 g [USITC. SYN ORG CHEM-U.S. PROD/SALES p.256 (1984)] 

 **PEER REVIEWED** 

 5.00X10+9 lb /Synthetic/ [USITC. SYN ORG CHEM-U.S. PROD/SALES p.266 

 (1985)] **PEER REVIEWED** 

 (1990) 8.35 billion lb [Chem & Engineering News 70 (15): 17 (4/13/92)] 

 **PEER REVIEWED** 

 (1991) 8.71 billion lb [Chem & Engineering News 71 (15): 11 (4/12/93)] 

 **PEER REVIEWED** 

 (1992)8.08 billion lb [Chem & Engineering News 72 (15): 13 (4/11/94)] 

 **PEER REVIEWED** 

 (1993) 10.54 billion lb [Chem & Engineering News 72 (15): 13 

 (4/11/94)] **PEER REVIEWED** 

 (1986) > 1 billion pounds [US EPA; Non-confidential Production Volume 

 Information Submitted by Companies for Chemicals Under the 1986-2002 

 Inventory Update Rule (IUR). Methanol (67-56-1). Available from, as of 

 July 28, 2005: http://www.epa.gov/oppt/iur/tools/data/2002-vol.html] 

 **PEER REVIEWED** 

 (1990) > 1 billion pounds [US EPA; Non-confidential Production Volume 

 Information Submitted by Companies for Chemicals Under the 1986-2002 

 Inventory Update Rule (IUR). Methanol (67-56-1). Available from, as of 

 July 28, 2005: http://www.epa.gov/oppt/iur/tools/data/2002-vol.html] 

 **PEER REVIEWED** 

 (1994) > 1 billion pounds [US EPA; Non-confidential Production Volume 

 Information Submitted by Companies for Chemicals Under the 1986-2002 

 Inventory Update Rule (IUR). Methanol (67-56-1). Available from, as of 

 July 28, 2005: http://www.epa.gov/oppt/iur/tools/data/2002-vol.html] 

 **PEER REVIEWED** 

 (1998) > 1 billion pounds [US EPA; Non-confidential Production Volume 

 Information Submitted by Companies for Chemicals Under the 1986-2002 

 Inventory Update Rule (IUR). Methanol (67-56-1). Available from, as of 

 July 28, 2005: http://www.epa.gov/oppt/iur/tools/data/2002-vol.html] 

 **PEER REVIEWED** 

 (2002) > 1 billion pounds [US EPA; Non-confidential Production Volume 

 Information Submitted by Companies for Chemicals Under the 1986-2002 

 Inventory Update Rule (IUR). Methanol (67-56-1). Available from, as of 

 July 28, 2005: http://www.epa.gov/oppt/iur/tools/data/2002-vol.html] 

 **PEER REVIEWED** 

U. S. IMPORTS: 

 (1983) 6.74X10+7 g [BUREAU OF THE CENSUS. U.S. IMPORTS FOR CONSUMPTION 

 & GENERAL IMPORTS, p.1-360 (1984)] **PEER REVIEWED** 

 (1984) 5.13X10+8 g [BUREAU OF THE CENSUS. U.S. IMPORTS FOR CONSUMPTION 

 & GENERAL IMPORTS, p.1-360 (1984)] **PEER REVIEWED** 

 17.72X10+6 gal /For producing synthetic natural gas (SNG) or for use as 

 fuel/ [BUREAU OF THE CENSUS. US IMPORTS FOR CONSUMPTION AND GENERAL 

 IMPORTS P.1-527 (1986)] **PEER REVIEWED** 

 3.59X10+8 gal /NSPF/ [BUREAU OF THE CENSUS. US IMPORTS FOR CONSUMPTION AND 

 GENERAL IMPORTS P.1-527 (1986)] **PEER REVIEWED** 

 1.421 billion gallons in 2000, 1.816 billion gallons in 2001 [Kirshner M; 

 Chemical Marketing Reporter. December 16, (2002)] **PEER REVIEWED** 

U. S. EXPORTS: 

 (1984) 1.95X10+10 g [BUREAU OF THE CENSUS. U.S. EXPORTS p.2-75 (1984)] 

 **PEER REVIEWED** 

 (1987) 1.2X10+6 gal [BUREAU OF THE CENSUS. U. S. EXPORTS, SCHEDULE E, 

Iris Camacho, 6308MM Page 62 of 69

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 P.2-76 (OCTOBER 1987)] **PEER REVIEWED** 

 32 million gallons in 2000, 52 million gallons in 2001 [Kirshner M; 

 Chemical Marketing Reporter. December 16, (2002)]] **PEER REVIEWED** 

LABORATORY METHODS: 

CLINICAL LABORATORY METHODS: 

 Ultramicro chromatographic method, incl methanol, in blood & urine. 

 [Manno BR, Manno JE; Simple Approach to Gas Chromatographic Microanalysis 

 of Alcohol in Blood & Urine By Direct-Injection Technique; J Anal Tox 

 2 (6): 257-61 (1978)] **PEER REVIEWED** 

 ... Determination in blood serum of methanol ... was accomplished by gas 

 chromatography using a Varian Model 2100 gas chromatograph equipped with 

 dual columns, dual flame ionization detectors, and a linear temp 

 programmer. Standard curves were linear ... over the concn range 1-100 

 nmol/ml and the limits of detection were 0.1 nmol/ml ethylene glycol. No 

 interference from 30 solvents studied was detected. [Cheung ST, Lin WN; J 

 Chromatogr 414 (1): 248-50 (1987)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3571391" 

 target=new>PubMed Abstract 

 A quantitative method for the determination of methanol and formic acid in 

 urine of workers was described. One female and 13 male workers of mean age 

 41 years exposed to methanol 10 +/5 years, and five female and five male 

 workers exposed to formic acid for 6 +/4 years participated in the study. 

 ... Urinary samples were taken after the shift on Thursdays and on Friday 

 mornings. The time weighted average exposure to methanol ranged from 58 to 

 277 ug/l. The highest concentrations of urinary formic acid were measured 

 in the samples taken on Friday morning and ranged from 26 to 98 mg/g of 

 creatinine. The output of urinary formic acid 16 hours after exposure was 

 found to be linearly proportional to the methanol concentration in air. No 

 correlations were found between the methanol exposure and the urinary 

 formic acid or methanol concentrations in samples taken immediately after 

 the shift. The time weighted average exposure to formic acid ranged form 

 4.1 to 11.3 ug/l. The corresponding levels of the urinary formic acid in 

 the Friday samples were 21.2 and 118 mg/g creatinine, respectively. A 

 linear correlation between the formic acid in the air and in the urine 16 

 hours after the exposure was observed with the correlation coefficient of 

 0.88. ... Urinary sampling for formic acid provides a reliable and simple 

 strategy for detection of occupational exposure to methanol and formic 

 acid at current levels found in industry. [Liesivuori J, Savolainen H; Am 

 Ind Hyg Assoc J 48 (1): 32-34 (1987)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3565260" 

 target=new>PubMed Abstract 

 A study was performed among 20 workers employed in a printing office at 3 

 different work places (methanol concentration of 85, 101 and 134 ppm) to 

 determine whether the concentration of formic acid in blood or urine and 

 the methanol content of alveolar air permit the estimation of methanol 

 exposure. Blood, urine and end expiratory air were collected at the 

 beginning and the end of the shift. For comparison formic acid 

 concentrations were determined in the morning and in the afternoon in 

 blood and urine of 36 and 15 control persons, respectively. The 

 concentration of formic acid in blood increased significantly from 3.2:2.4 

 mg/l before to 7.9:3.2 mg/l after the shift in the exposed workers (mean 

 increase 4.7:3.8 mg/l). The corresponding concentrations in urine were 

 13.1:5.3 mg/l. This difference is also significant. In the control groups 

 there was a small but significant decrease of formic acid concentration in 

 blood from 5.6:4.5 mg/l in the morning to 4.9:4.2 mg/l in the afternoon. 

 In urine, the formic acid concentrations in the morning (11.9:6.4 mg/l) 

 and in the afternoon (11.7:5.6 mg/l) were not significantly different. The 

 increase of formic acid concentration in blood during the shift is the 

 most useful parameter for monitoring methanol-exposed persons. 

 Determinations of methanol concentrations in the ambient air or in the 

 exhaled air are only crude estimates. [Baumann K, Angerer J; Int Arch 

 Occup Environ Health 42 (3-4): 241-9 (1979)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=422265" 

 target=new>PubMed Abstract 

ANALYTIC LABORATORY METHODS: 

 Method: NIOSH 2000; Procedure: Gas chromatography with flame ionization 

 detector; Analyte: methanol; Matrix: air; Detection Limit: 0.7 ug per 

 sample. [CDC; NIOSH Manual of Analytical Methods, 4th ed. Methanol 

 (67-56-1). Available from, as of June 1, 2005: 

 http://www.cdc.gov/niosh/docs/2003-154/] **PEER REVIEWED** 

 Method: NIOSH 2549, Volatile Organic Compounds (Screening); Procedure: 

 Thermal desorption, gas chromatography, mass spectrometry; Analyte: 

 methanol; Matrix: air; Detection Limit: 100 ng per tube or less. [CDC; 

 NIOSH Manual of Analytical Methods, 4th ed. Methanol (67-56-1). Available 

 from, as of June 1, 2005: http://www.cdc.gov/niosh/docs/2003-154/] **PEER 

 REVIEWED** 

 Method: OSHA 91: Procedure: Gas chromatography with flame ionization 

 detector; Analyte: methanol; Matrix: air; Detection Limit: 142 ppb (186 

 ug/cu m). [U.S. Department of Labor/Occupational Safety and Health 

 Administration's Index of Sampling and Analytical Methods. Available 

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 from: http://www.osha.gov/dts/sltc/methods/toc.html on Methanol (67-56-1) 

 as of June 1, 2005] **PEER REVIEWED** 

 Method: AOAC 972.11, Methanol in Distilled Liquors; Procedure: Gas 

 chromatographic method; Analyte: methanol; Matrix: distilled liquors; 

 Detection Limit: not provided. [Horwitz W, ed.; Official Methods of 

 Analysis of AOAC International 17th ed. (2003). CD-ROM, AOAC 

 International, Gaithersburg, MD] **PEER REVIEWED** 

 Method: AOAC 971.03, Methanol in Hazardous Substances; Procedure: Gas 

 chromatography with flame ionization detector; Analyte: methanol; Matrix: 

 applicable in presence of acetone, butyl acetate, ethyl alcohol, 

 isopropanol, hexane, methyl ethyl ketone, CH2Cl2, 2-methoxyethanol, 

 paraffin, toluene, and H2O, including many paint removers, fuels, liquid 

 sanders, antifreezes, and paint products; Detection Limit: not provided. 

 [Horwitz W, ed.; Official Methods of Analysis of AOAC International 17th 

 ed. (2003). CD-ROM, AOAC International, Gaithersburg, MD] **PEER 

 REVIEWED** 

 Method: AOAC 958.04, Methanol in Distilled Liquors; Procedure: 

 Chromotropic acid colorimetric method; Analyte: methanol; Matrix: 

 distilled liquors; Detection Limit: not provided. [Horwitz W, ed.; 

 Official Methods of Analysis of AOAC International 17th ed. (2003). 

 CD-ROM, AOAC International, Gaithersburg, MD] **PEER REVIEWED** 

 Method: AOAC 920.132; Methanol in Vanilla Extract; Procedure: Titrimetric 

 method; Analyte: methanol; Matrix: vanilla extract; Detection Limit: not 

 provided. [Horwitz W, ed.; Official Methods of Analysis of AOAC 

 International 17th ed. (2003). CD-ROM, AOAC International, Gaithersburg, 

 MD] **PEER REVIEWED** 

 Method: EPA-OSW 8015C; Procedure: Nonhalogenated Organics by GC-FID; 

 Analyte: methanol; Matrix: surface water, ground water, and solid 

 matrices; Detection Limit: 21 ug/L. [National Environmental Methods Index; 

 Analytical, Test and Sampling Methods. Methanol (67-56-1). Available from, 

 as of June 1, 2005: http://www.nemi.gov] **PEER REVIEWED** 

 Method: EPA-OSW 8260B; Procedure: Volatile Organic Compounds by GC/MS; 

 Analyte: methanol; Matrix: determines most volatile organic compounds with 

 boiling points below 200 C; Detection Limit: not provided. [National 

 Environmental Methods Index; Analytical, Test and Sampling Methods. 

 Methanol (67-56-1). Available from, as of June 1, 2005: 

 http://www.nemi.gov] **PEER REVIEWED** 

SAMPLING PROCEDURES: 

 A known volume of air is drawn through a 7 cm x 6 mm OD silica gel tube 

 containing 2 sections of 20/40 mesh silica gel separated by a 2 mm portion 

 of urethane foam. The first section contains 100 mg whereas the second 

 section contains 50 mg. A silylated glass wool plug is placed before the 

 front absorbing section. A sample size of 5 l of air sampled at 200 ml/min 

 is recommended. The silica gel tube sample is scored before the first 

 section of silica gel and broken. The larger section of silica gel is 

 transferred to a 2 ml stoppered sample container containing 1.0 ml of 

 distilled water. The same operation is performed with the back-up section. 

 The sample should be allowed to desorb for 4 hours. A 5 ul aliquot of 

 sample is injected into a gas chromatograph equipped with a flame 

 ionization detector. [Environment Canada; Tech Info for Problem Spills: 

 Methanol (Draft) p.105-6 (1981)] **PEER REVIEWED** 

 Qualitative method for the detection of methanol in soil: Acetyl chloride 

 (three to four drops) is placed in a dry test tube and the fumes resulting 

 from the reaction with atmospheric moisture are allowed to dissipate. The 

 sample is added to the test tube dropwise until a total of three drops 

 have been added. A positive indication is given by a vigorous reaction, 

 the mixture boils spontaneously, ... and hydrogen chloride gas is evolved. 

 [Environment Canada; Tech Info for Problem Spills: Methanol (Draft) p.108 

 (1981)] **PEER REVIEWED** 

 A sampling system designed to quantify compounds in a mixture of polar and 

 non-polar organic vapors was tested. Employees in a motor manufacturing 

 facility who were exposed to mixtures containing toluene, xylene, butanol, 

 ethanol, isopropanol, and methanol were studied. A personal sampling pump 

 with two charcoal tubes in series was used. The second tube was used to 

 collect vapors that passed through the first tube because of overloading 

 or selective displacement. Desorption efficiency was determined. Non-polar 

 compounds, toluene and xylene, were collected effectively by the first 

 tube until overload. When vapor concentrations were low, almost all 

 non-polar compounds were collected in the first tube. The percent of polar 

 compounds collected in the first tube was about 97%. Ethanol was not 

 collected effectively. A moderate increase in concentration caused vapors 

 to pass to the second tube. An increase in other polar compounds caused 

 ethanol to be displaced. Collection efficiency was poor in the first tube 

 when the concentrations of all vapors was high. ... Silica gel /could/ be 

 used as a collection medium in the back up or second tube when mixtures 

 contain both polar and non-polar vapors. [Goller JW; Am Ind Hyg Assoc J 46 

 (3): 170-73 (1985)] **PEER REVIEWED** 

 Two sampling methods for reliable determination of methanol concentration 

 were studied. Methanol vapor stored in glass container was found to be 

 decomposed on the glass surface. The decomposition increased as the 

 surface area of the glass container was extended. The proportion of the 

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 decomposition in the glass container was relatively high, especially when 

 the concentration of methanol vapor was low. Therefore, a reliable 

 determination by the above sampling method was impossible. In the solid 

 sorbent sampling by silica gel, the collected methanol was also 

 decomposed, but the decomposed amount was negligibly small compared to the 

 collected methanol when the amount of methanol was more than 0.1 of the 

 liquid methanol. It could be concluded from the foregoing findings that 

 the determination of methanol concentration by this method is reliable. 

 [Niisawa K et al; Sangyo Igaku 28 (3): 177-80 (1986)] **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3773296" 

 target=new>PubMed Abstract 

 A new method is described for collecting and concentrating volatile 

 compounds in the breath, in order to facilitate their assay by gas 

 chromatography. Breath was collected into sealed Mylar bags containing an 

 internal standard (isopropyl alcohol). The sample was pumped through a 

 cooled gas chromatograph column, where the volatile compounds were 

 concentrated by adsorption onto the resin packing (Porapak Q) at 35 deg C. 

 The column was then heated, and the volatilized sample was separated for 

 assay by flame ionization detection. ... This assay provided a number of 

 advantages over previously described methods. The use of breath collection 

 bags enabled the collection of samples outside the laboratory. The use of 

 an internal standard in the collection bag reduced errors that might have 

 resulted from leakage of the specimen. An on-column concentration of the 

 sample in the gas chromatograph eliminated the need for an additional 

 preconcentration device, such as cryogenic or adsorptive trapping 

 apparatus. [Phillips M, Greenberg J; Anal Biochem 163 (1): 165-69 (1987)] 

 **PEER REVIEWED** <a 

 href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3619015" 

 target=new>PubMed Abstract 

SPECIAL REFERENCES: 

SPECIAL REPORTS: 

 Environment Canada; Tech Info for Problem Spills: Methanol (Draft) (1981) 

 NIOSH; Criteria Document: Methyl Alcohol (1976) DHEW Pub. NIOSH 76-148 

 NIOSH; Canadian Centre for Occupational Health and Safety: Chemical Hazard 

 Summary No.24 1986. The chemical hazards, uses, occurrences and 

 toxicological properties of methanol are discussed. ... 

 DHHS/NTP; NTP-CERHR Expert Panel Report on the Reproductive and 

 Developmental Toxicity of Methanol p.14 (April 2002) NTP-CERHR-MeOH-02. 

 Available from: 

 http://cerhr.niehs.nih.gov/news/methanol/methanol_final.pdf as of July 20, 

 2005. 

 WHO; Environ Health Criteria 196: Methanol p.93 (1997). Available from: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm as of July 18, 2005. 

 European Chemicals Bureau; IUCLID Dataset, Methanol (67-56-1) (2000 CD-ROM 

 edition). Available from the database query page: 

 http://ecb.jrc.it/esis/esis.php as of July 15, 2005. 

SYNONYMS AND IDENTIFIERS: 

RELATED HSDB RECORDS: 

 1646 [FORMIC ACID] (metabolite) 

 164 [FORMALDEHYDE] (metabolic precursor) 

 3915 [ASPARTAME] (metabolic precursor) 

SYNONYMS: 

 Coat-B1400 [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Surflo-B17 [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 AI3-00409 **PEER REVIEWED** 

 Alcohol, methyl **PEER REVIEWED** 

 ALCOOL METHYLIQUE (FRENCH) [Lewis, R.J. Sax's Dangerous Properties of 

 Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 ALCOOL METILICO (ITALIAN) [Lewis, R.J. Sax's Dangerous Properties of 

 Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 CARBINOL [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 

 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 2174] 

 **PEER REVIEWED** 

Iris Camacho, 6308MM Page 65 of 69

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 Caswell no 552 **PEER REVIEWED** 

 X-Cide 402 Industrial Bactericide [Purdue University; National Pesticide 

 Information Retrieval System (1988)] **PEER REVIEWED** 

 COLONIAL SPIRIT [Lewis, R.J. Sax's Dangerous Properties of Industrial 

 Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 

 1996., p. 2174] **PEER REVIEWED** 

 COLUMBIAN SPIRITS [Lewis, R.J. Sax's Dangerous Properties of Industrial 

 Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 

 1996., p. 2174] **PEER REVIEWED** 

 Ideal Concentrated Wood Preservative [Purdue University; National 

 Pesticide Information Retrieval System (1988)] **PEER REVIEWED** 

 Wilbur-Ellis Smut-Guard [Purdue University; National Pesticide Information 

 Retrieval System (1988)] **PEER REVIEWED** 

 Freers Elm Arrester [Purdue University; National Pesticide Information 

 Retrieval System (1988)] **PEER REVIEWED** 

 Manhattan spirits [WHO; Environ Health Criteria 196: Methanol p.10 (1997). 

 Available from, as of July 14, 2005: 

 http://www.inchem.org/documents/ehc/ehc/ehc196.htm] 

 METANOLO (ITALIAN) [Lewis, R.J. Sax's Dangerous Properties of Industrial 

 Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 

 1996., p. 2174] **PEER REVIEWED** 

 Metanol (Spanish) **PEER REVIEWED** 

 Methilic alcohol [European Chemicals Bureau; IUCLID Dataset, Methanol 

 (67-56-1) (2000 CD-ROM edition). Available from, as of July 15, 2005: 

 http://ecb.jrc.ec.europa.eu/esis/] 

 METHYL ALCOHOL [Weast, R.C. (ed.) Handbook of Chemistry and Physics. 69th 

 ed. Boca Raton, FL: CRC Press Inc., 1988-1989., p. C-351] **PEER 

 REVIEWED** 

 METHYLALKOHOL (GERMAN) [Lewis, R.J. Sax's Dangerous Properties of 

 Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 Methyl hydrid [European Chemicals Bureau; IUCLID Dataset, Methanol 

 (67-56-1) (2000 CD-ROM edition). Available from, as of July 15, 2005: 

 http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 Methyl hydrate [European Chemicals Bureau; IUCLID Dataset, Methanol 

 (67-56-1) (2000 CD-ROM edition). Available from, as of July 15, 2005: 

 http://ecb.jrc.ec.europa.eu/esis/] **PEER REVIEWED** 

 METHYL HYDROXIDE [Lewis, R.J. Sax's Dangerous Properties of Industrial 

 Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 

 1996., p. 2174] **PEER REVIEWED** 

 METHYLOL [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 

 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 2174] 

 **PEER REVIEWED** 

 METYLOWY ALKOHOL (POLISH) [Lewis, R.J. Sax's Dangerous Properties of 

 Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand 

 Reinhold, 1996., p. 2174] **PEER REVIEWED** 

 MONOHYDROXYMETHANE [Lewis, R.J. Sax's Dangerous Properties of Industrial 

 Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 

 1996., p. 2174] **PEER REVIEWED** 

 Eureka Products, Criosine [Purdue University; National Pesticide 

 Information Retrieval System (1988)] **PEER REVIEWED** 

 Eureka Products Criosine Disinfectant [Purdue University; National 

 Pesticide Information Retrieval System (1988)] **PEER REVIEWED** 

 PYROXYLIC SPIRIT [Lewis, R.J. Sax's Dangerous Properties of Industrial 

 Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 

 1996., p. 2174] **PEER REVIEWED** 

 WOOD ALCOHOL [Lewis, R.J. Sax's Dangerous Properties of Industrial 

 Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 

 1996., p. 2174] **PEER REVIEWED** 

 WOOD NAPHTHA [Lewis, R.J. Sax's Dangerous Properties of Industrial 

 Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 

 1996., p. 2174] **PEER REVIEWED** 

 WOOD SPIRIT [Lewis, R.J. Sax's Dangerous Properties of Industrial 

 Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 

 1996., p. 2174] **PEER REVIEWED** 

 USEPA/OPP Pesticide Code: 053801 [U.S. Environmental Protection 

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 Agency/Office of Pesticide Program's Chemical Ingredients Database on 

 Methanol (67-56-1). Available from, as of June 1, 2005: 

 http://ppis.ceris.purdue.edu/htbin/epachem.com] **PEER REVIEWED** 

FORMULATIONS/PREPARATIONS: 

 Grade: Technical, CP (99.85%), electronic (used to clean and dry 

 componets), fuel [Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 

 14th Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 722] 

 **PEER REVIEWED** 

 Formaldehyde; intrastate fungicide; 37.0% formaldehyde, 15.0% methyl 

 alcohol. [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Wilbur-Ellis Smut-Guard; fungicide; 37.0% formaldehyde, 12.0% methyl 

 alcohol. [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Eureka Products, Criosine; intrastate disinfectant/bacteriocide/germicide; 

 47.6% methyl alcohol, 0.86% nitrobenzene, 0.54% butyl 4-hydroxybenzoate, 

 30.0% phenol. [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Surflo-B17; microbicide/microbisat general; 32.37% formaldehyde, 10.5% 

 methyl alcohol, 10.0% alkyl dimethyl benzyl ammonium chloride. [Purdue 

 University; National Pesticide Information Retrieval System (1988)] **PEER 

 REVIEWED** 

 Coat-B1400; solution ready to use; 25.0% methyl alcohol, 24.0% morpholine 

 polyethoxyethanol. [Purdue University; National Pesticide Information 

 Retrieval System (1988)] **PEER REVIEWED** 

 Ideal Concentrated Wood Preservative; fungicide; 15.0% isopropanol, 15.0% 

 methyl alcohol, 10.0% orthodichlorobenzene, 38.4% pentachlorophenol, 20.0% 

 aliphatic petroleum hydrocarbons. [Purdue University; National Pesticide 

 Information Retrieval System (1988)] **PEER REVIEWED** 

 Freer Elm Arrester; fungicide; 0.12% mecuric chloride, 96.65% methyl 

 alcohol. [Purdue University; National Pesticide Information Retrieval 

 System (1988)] **PEER REVIEWED** 

 Eureka Products Criosine Disinfectant; 

 disinfectant/bacteriocide/germicide; 47.6% methyl alcohol, 0.86% 

 nitrobenzene, 0.54% butyl 4-hydroxybenzoate, 30.0% phenol. [Purdue 

 University; National Pesticide Information Retrieval System (1988)] **PEER 

 REVIEWED** 

 X-Cide 402 Industrial Bactericide; bacteriostat; 11.5% isopropanol, 16.4% 

 methyl alcohol, 28.5% alkyl amino-3-aminopropane monoacetate, 17.8% 

 oxydiethylenebis(alkyl) dimethyl ammonium chloride. [Purdue University; 

 National Pesticide Information Retrieval System (1988)] **PEER REVIEWED** 

SHIPPING NAME/ NUMBER DOT/UN/NA/IMO: 

 UN 1230; Methanol 

 IMO 3.2; Methanol 

STANDARD TRANSPORTATION NUMBER: 

 49 092 30; Methanol or methyl alcohol (wood alcohol) 

 49 092 37; Methanol (contaminated, only for refining) 

 49 104 04; Methanol, solidified (alcohol, not otherwise specified) 

EPA HAZARDOUS WASTE NUMBER: 

 U154; A toxic waste when a discarded commercial chemical product or 

 manufacturing chemical intermediate or an off-specification commercial 

 chemical product. 

 F003; A hazardous waste from nonspecific sources when a spent solvent. 

ADMINISTRATIVE INFORMATION: 

HAZARDOUS SUBSTANCES DATABANK NUMBER: 93 

LAST REVISION DATE: 20060414 

LAST REVIEW DATE: Reviewed by SRP on 9/15/2005 

UPDATE HISTORY: 

 Field Update on 2010-06-02, 4 fields added/edited/deleted 

 Field Update on 2010-04-27, 1 fields added/edited/deleted 

 Field Update on 2008-09-02, 2 fields added/edited/deleted 

 Field Update on 2008-08-15, 25 fields added/edited/deleted 

 Field Update on 2007-06-07, 1 fields added/edited/deleted 

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 Field Update on 2006-04-18, 2 fields added/edited/deleted 

 Field Update on 2006-04-17, 2 fields added/edited/deleted 

 Complete Update on 2006-04-14, 84 fields added/edited/deleted 

 Complete Update on 2005-06-24, 20 fields added/edited/deleted 

 Field Update on 2005-01-27, 2 fields added/edited/deleted 

 Complete Update on 02/14/2003, 1 field added/edited/deleted. 

 Complete Update on 11/08/2002, 1 field added/edited/deleted. 

 Complete Update on 10/31/2002, 1 field added/edited/deleted. 

 Complete Update on 07/22/2002, 1 field added/edited/deleted. 

 Complete Update on 05/13/2002, 1 field added/edited/deleted. 

 Complete Update on 01/18/2002, 4 fields added/edited/deleted. 

 Field Update on 01/14/2002, 1 field added/edited/deleted. 

 Complete Update on 08/09/2001, 1 field added/edited/deleted. 

 Complete Update on 05/16/2001, 1 field added/edited/deleted. 

 Complete Update on 05/15/2001, 1 field added/edited/deleted. 

 Complete Update on 02/22/2001, 2 fields added/edited/deleted. 

 Complete Update on 02/08/2000, 1 field added/edited/deleted. 

 Complete Update on 02/02/2000, 1 field added/edited/deleted. 

 Complete Update on 11/18/1999, 1 field added/edited/deleted. 

 Complete Update on 09/27/1999, 1 field added/edited/deleted. 

 Complete Update on 09/21/1999, 1 field added/edited/deleted. 

 Complete Update on 08/26/1999, 1 field added/edited/deleted. 

 Complete Update on 07/20/1999, 5 fields added/edited/deleted. 

 Complete Update on 05/04/1999, 1 field added/edited/deleted. 

 Complete Update on 03/29/1999, 3 fields added/edited/deleted. 

 Field Update on 03/19/1999, 1 field added/edited/deleted. 

 Field Update on 03/19/1999, 1 field added/edited/deleted. 

 Complete Update on 03/01/1999, 1 field added/edited/deleted. 

 Complete Update on 01/20/1999, 1 field added/edited/deleted. 

 Complete Update on 11/12/1998, 2 fields added/edited/deleted. 

 Field Update on 10/29/1998, 1 field added/edited/deleted. 

 Complete Update on 09/11/1998, 1 field added/edited/deleted. 

 Complete Update on 06/02/1998, 1 field added/edited/deleted. 

 Complete Update on 02/25/1998, 1 field added/edited/deleted. 

 Complete Update on 10/17/1997, 1 field added/edited/deleted. 

 Complete Update on 08/13/1997, 1 field added/edited/deleted. 

 Complete Update on 05/08/1997, 1 field added/edited/deleted. 

 Complete Update on 03/27/1997, 2 fields added/edited/deleted. 

 Complete Update on 02/24/1997, 1 field added/edited/deleted. 

 Complete Update on 10/12/1996, 1 field added/edited/deleted. 

 Complete Update on 07/22/1996, 5 fields added/edited/deleted. 

 Complete Update on 06/03/1996, 1 field added/edited/deleted. 

 Complete Update on 05/10/1996, 1 field added/edited/deleted. 

 Complete Update on 04/16/1996, 8 fields added/edited/deleted. 

 Field Update on 01/18/1996, 1 field added/edited/deleted. 

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 Complete Update on 05/26/1995, 1 field added/edited/deleted. 

 Complete Update on 01/23/1995, 1 field added/edited/deleted. 

 Complete Update on 12/19/1994, 1 field added/edited/deleted. 

 Complete Update on 11/18/1994, 1 field added/edited/deleted. 

 Complete Update on 07/28/1994, 1 field added/edited/deleted. 

 Complete Update on 06/08/1994, 1 field added/edited/deleted. 

 Complete Update on 03/25/1994, 1 field added/edited/deleted. 

 Complete Update on 08/07/1993, 1 field added/edited/deleted. 

 Complete Update on 08/04/1993, 1 field added/edited/deleted. 

 Complete Update on 04/28/1993, 2 fields added/edited/deleted. 

 Complete Update on 02/05/1993, 1 field added/edited/deleted. 

 Field update on 12/10/1992, 1 field added/edited/deleted. 

 Complete Update on 11/26/1992, 1 field added/edited/deleted. 

 Complete Update on 09/03/1992, 1 field added/edited/deleted. 

 Complete Update on 05/29/1992, 1 field added/edited/deleted. 

 Complete Update on 04/27/1992, 1 field added/edited/deleted. 

 Complete Update on 01/23/1992, 1 field added/edited/deleted. 

 Field update on 01/28/1991, 1 field added/edited/deleted. 

 Complete Update on 10/10/1990, 1 field added/edited/deleted. 

 Complete Update on 05/21/1990, 1 field added/edited/deleted. 

 Complete Update on 05/04/1990, 1 field added/edited/deleted. 

 Complete Update on 01/11/1990, 2 fields added/edited/deleted. 

 Complete Update on 08/17/1989, 103 fields added/edited/deleted. 

 Field Update on 07/06/1988, 1 fields added/edited/deleted. 

 Field Update on 07/06/1988, 1 fields added/edited/deleted. 

Complete Update on 06/04/1985 

Created 19830401 by GCF 

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