METHANOL
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
ALCOHOL, METHYL ALCOHOL METILICO (Spanish) ALCOOL METHYLIQUE (French) ALCOOL METILICO (Italian) BIELESKI'S SOLUTION CARBINOL COAT-B 1400 COLONIAL SPIRITS COLUMBIAN SPIRITS EUREKA PRODUCTS, CRIOSINE EUREKA PRODUCTS CRIOSINE DISINFECTANT FREERS ELM ARRESTER HYDROXYMETHANE IDEAL CONCENTRATED WOOD PRESERVATIVE MANHATTAN SPIRITS METANOL (Spanish) METANOLO (Italian) METHANOL METHYL ALCOHOL METHYL HYDRATE METHYL HYDROXIDE METHYLALKOHOL (German) METHYLOL METYLOWY ALKOHOL (Polish) MONOHYDROXYMETHANE PYROXYLIC SPIRITS SURFLO-B17 WILBUR-ELLIS SMUT-GUARD WOOD ALCOHOL WOOD NAPHTHA WOOD SPIRIT X-CIDE 402 INDUSTRIAL BACTERICIDE COHOL METILICO (SPANISH) COLUMBIAN SPIRIT FORMALDEHYDE SOLUTIONS, FLAMMABLE FORMALIN SOLUTION METANPLO METHANAL (FORMALDEHYDE) METHYLENE GLYCOL (CAS 50-00-0) METHYLESTER KISELINY OCTOVE (CZECH) TETRAOXYMETHYLENE TRIOXANE
IDENTIFIERS
1230-Methanol 1230-Methyl alcohol
SYNONYM REFERENCE
- (HSDB , 2002; IPCS, 1997; OHM/TADS , 2002; Pohanish, 2002; RTECS , 2002)
USES/FORMS/SOURCES
Methanol is widely used in paint, varnish removers and as an industrial solvent. It is also used in the manufacture of formaldehyde, acetic acid, methyl derivatives and inorganic acids; as an antifreeze, fuel anti-icing additive, and fuel octane booster; an ethanol denaturant; an extraction agent; an extractant solvent; and as fuel for picnic stoves and soldering torches. Methanol is further used as a solvent in the manufacture of cholesterol, streptomycin, vitamins, hormones, and other pharmaceuticals (ACGIH, 1991; Ashford, 2001; Bingham et al, 2001; Budavari, 2000; Lewis, 2001; Lewis, 1998).
Methanol is the simplest of the primary alcohols and is a colorless, highly polar, flammable liquid. Pure methanol has a faintly sweet odor at ambient temperatures; crude methanol may have a repulsive, pungent odor (AAR, 2000; ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; Lewis, 2001; Lewis, 1998; Lewis, 2000).
Methanol is a volatile emission product from plants and is also naturally formed during the decomposition of biological waste, sewage, and sludge. Artificially, methanol is primarily released to the environment by evaporation from its use as an industrial solvent. Lesser emission releases also occur from methanol production, end product manufacturing, storage and handling, and as a component of gas and diesel emissions (Howard, 1990). Small amounts of methanol are produced endogenously by normal metabolism. Methanol occurs in, or is metabolically produced from fruits and is found in "hard" liquors (Lindinger et al, 1997; Taucher et al, 1995). HOME DISTILLATION OF METHYLATED SPIRITS: A common source of methanol intoxication is home distillation of methylated spirits. Some methylated spirits contain approximately 90% ethanol and 5% methanol ("purple lady"), which can produce classical signs of severe methanol poisoning (Foley & Rogers, 1999; Meyer et al, 2000). Romanian Tuica (pronounced Tsweeka), is a sweet-tasting, clear alcohol made from locally available fruits (eg; plums, apples). It has been responsible for several cases of lethal methanol toxicity. In one study, 26 of 35 Tuica samples (74%) contained detectable methanol levels (mean level, 0.66 g/dL; range, 0.06 to 8.6 g/dL) (Levy et al, 2003). Chang'aa (or kill me quick) is a brewed bootleg alcohol in Kenya. Because of its methanol content, it is believed to be responsible for hundreds of deaths each year (Levy et al, 2003) FIRE EATING: A man developed irreversible bilateral blindness following an accidental ingestion of small amounts of methanol during fire "eating" (Cursiefen & Bergua, 2002). METHYL ACETATE IN NAIL POLISH REMOVERS Many manufacturers of non-acetone nail polish removers have recently changed their formulations from ethyl acetate to methyl acetate. In acidic environments, methyl acetate is hydrolyzed to methanol and acetic acid. One retrospective study evaluated 83 cases of exposure to these methyl acetate-containing nail polish removers; 75 patients were 5 years and younger; 4 children were 6 years and older; 4 patients were adults. In most cases, the amount of nail polish remover ingested was unknown, and only 11 (13%) patients ingested more than a mouthful. Four adults ingested "a mouthful" to 150 mL of non-acetone nail polish removers. Overall, 75% (n=62) of patients were referred to a healthcare facility; 75% did not develop any effects. Minor effects developed in 25% of cases and these effects included vomiting (n=12; 14%), throat/oral irritation (n=5; 6%), drowsiness (n=1; 1.2%), abdominal pain (n=1; 1.2%), and ataxia (n=1; 1.2%). A 2-year-old boy developed mild metabolic acidosis after ingesting about 12 mL of Fung-off No Lift fungal liquid for nails. He recovered following supportive care (Minns et al, 2013).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- 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.
- 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.
- EPIDEMIOLOGY: Uncommon exposure that can result in significant morbidity and mortality.
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. 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, pancreatitis, and acute renal failure. Rhabdomyolysis may occur in severe poisonings. Hypomagnesemia, hypokalemia, and hypophosphatemia have also been reported. 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.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
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.
ACUTE CLINICAL EFFECTS
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. EPIDEMIOLOGY: Uncommon exposure that can result in significant morbidity and mortality. EXPOSURE 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. 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, pancreatitis, and acute renal failure. Rhabdomyolysis may occur in severe poisonings. Hypomagnesemia, hypokalemia, and hypophosphatemia have also been reported. 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.
METABOLIC ACIDOSIS: Metabolic acidosis is a classic adverse effect following methanol ingestion. Severe intoxication may cause cerebral edema and brain death. The acidosis may be delayed for 18 to 24 hours, or longer with concurrent ethanol ingestion (Airas et al, 2008; Askar & Al-Suwaida, 2007; Vara-Castrodeza et al, 2007). One of the most significant clinical effects of methanol poisoning is the presence of a severe anion gap metabolic acidosis. The severity of symptoms secondary to methanol poisoning appear to correlate with the degree of metabolic acidosis (Bitar et al, 2004).
TACHYCARDIA: Mild tachycardia is common in patients with significant poisoning (Airas et al, 2008; Vara-Castrodeza et al, 2007; Carpentieri et al, 2003). BRADYCARDIA: In more pronounced fatal methanol poisoning cases, marked sinus bradycardia may develop with widening of the pulse pressure (Bennett, 1953; Kinoshita et al, 1998). HEART FAILURE, CASE REPORT: Severe reversible cardiac failure with left ventricular dysfunction and diffuse T-wave abnormalities were described in severe methanol poisoning (Cavalli et al, 1987). HYPOTENSION: Blood pressure usually remains within normal limits until the terminal state is reached, when refractory hypotension occurs. Severe hypotension, requiring fluid and vasopressor therapy, occurs terminally in severe methanol intoxications (Williams et al, 1997; Kinoshita et al, 1998).
PERCUTANEOUS SKIN ABSORPTION: Toxicity following percutaneous absorption of methanol can occur, and resultant adverse effects have included coma, hypotension, severe metabolic acidosis, and even death (Adanir et al, 2005; Soysal et al, 2007).
HYPERGLYCEMIA: Elevated blood sugar levels, requiring insulin infusions, have been reported following severe methanol intoxications (Williams et al, 1997).
HYPOMAGNESEMIA: Three cases of recalcitrant hypomagnesemia have been reported in alcohol-using patients who ingested toxic doses of methanol and underwent dialysis (Harchelroad, 1993b). HYPOKALEMIA: Eleven of 15 cases of methanol toxicity had potassium levels at or below 3.5 mmol/L despite significant metabolic acidosis, with authors associating the hypokalemia with accumulations of potassium formate (Hassoun et al., 1993). HYPOPHOSPHATEMIA: Hypophosphatemia has been reported following methanol intoxication. Two women were reported with hypophosphatemia (0.11 and 0.4 mmol/L, respectively; normal range, 0.65 to 1.0 mmol/L) following ingestion of unknown amounts of methanol with ethanol (Williams et al, 1997).
NAUSEA AND VOMITING: Nausea and vomiting with severe abdominal pain have been reported (Osterloh et al, 1986; Williams et al, 1997). ABDOMINAL PAIN: Abdominal pain may occur following methanol ingestion (Williams et al, 1997; Osterloh et al, 1986). Absence of abdominal pain does not rule out a significant ingestion. DIARRHEA: Diarrhea may occur following methanol intoxication, but it is not a prominent sign of acute methanol intoxication, occurring in 10% of patients in a series of 323 cases (Bennett, 1953). CONSTIPATION: Severe constipation and obstipation (ie, intestinal blockage or obstruction) may accompany recovery from methanol poisoning (Bennett, 1953). PANCREATITIS: Acute necrotizing pancreatitis may result from severe methanol poisoning (Hantson & Mahieu, 2000; Hantson & Mahieu, 2000).
RENAL FAILURE: Rhabdomyolysis and myoglobinuric, anuric renal failure have been described in a patient with a peak blood methanol level of 410 mg/dL (Grufferman et al, 1985) and in 2 fatalities (Williams et al, 1997). In a case series review, authors concluded that the mechanism responsible for nephrotoxicity is likely multifactorial (hypotension, hemolysis, myoglobinuria, hyperosmolality) (Verhelst et al, 2004). HEMATURIA: Hematuria (blood in urine) has been reported and appears to be related to the degree of acidosis (Harchelroad, 1993a).
TRANSIENT DEFECTS: Transient visual abnormalities that develop during acute methanol intoxication may include blurred or double vision, changes in color perception, constricted visual fields, spots before the eyes, and sharply reduced visual acuity (Ingemansson, 1984; Kinney & Nauss, 1988). In a chart review of methanol poisonings (n=113) reported to a poison center, visual symptoms were reported in 24 cases (21.2%) (Kalkan et al, 2003). PERMANENT DEFECTS: Permanent ocular abnormalities may include pallor of the optic disc, attenuation and sheathing of retinal arterioles, a diminished pupillary light reaction, reduced visual acuity, central scotomata, and defects of optic nerve fiber bundles (Naeser, 1988; Sharma et al, 1999). The incidence of permanent visual defects is directly correlated with the degree of metabolic acidosis, with the volume of methanol consumed, delay in treatment, the pupillary response at presentation (Liu et al, 1998; Yang et al, 2005). BLINDNESS: Permanent blindness due to toxic effects of the methanol metabolite on the retina and optic nerve may occur. Fixed, dilated pupils on initial presentation following ingestions are an ominous sign of severe vision loss (Sullivan-Mee & Solis, 1998). SNOWFIELD BLINDNESS EFFECT: Visual abnormalities may be delayed in onset for several hours or days following acute ingestion. A whiteness in the visual field, "like stepping out into a snowfield" has been described (Becker, 1981; Williams et al, 1997). IRRITATION: Direct methanol eye contact produces mild, reversible irritation, assuming treatment is initiated promptly (Grant & Schuman, 1993).
LEUKOCYTOSIS: Leukocytosis (19,900/microliter) developed 2 days following a toxic ingestion of methanol (Yu et al, 1995). In another case, leukocytosis (21,390/mcL) was reported 2 days after a toxic ingestion in a 16-year-old (Foster & Schoenhals, 1995). COAGULOPATHY: Persistent coagulopathy, with increased prothrombin and partial thromboplastin times, has been reported after severe methanol intoxications (Foster & Schoenhals, 1995).
HEPATIC FAILURE: In fatal cases of methanol intoxications, multiple organ failure, including hepatic failure, may occur prior to death (Foster & Schoenhals, 1995; Deniz et al, 2000).
HYPERAMMONEMIA: Hyperammonemia has been reported following severe methanol intoxication. In one case, a 16-year-old had a serum ammonia level of 347 mmol/L (normal, 7 to 27 mmol/L) 2 days after a toxic ingestion of methanol. The boy had normal liver function tests, and his elevated ammonia levels persisted for at least 2 more days in spite of hemodialysis (Foster & Schoenhals, 1995).
RHABDOMYOLYSIS: Severe poisonings may result in complication of rhabdomyolysis and possibly compartment syndrome (Figueras Coll et al, 2008; Hantson & Mahieu, 2000; Williams et al, 1997) .
Neurologic symptoms of methanol intoxication can mimic those of an ethanol "hangover" and may include general malaise, headache, dizziness, vertigo, neuritis, and weakness (Proctor & Hughes, 1978). In a chart review of methanol poisonings (n=113) reported to a poison center, central nervous system symptoms were reported in 51 cases (45.1%) (Kalkan et al, 2003). A retrospective study of 30 patients poisoned by methanol reported that the occurrence of neurologic signs was significantly increased with greater amounts of methanol ingested, greater time between ingestion and beginning of treatment at the hospital, and decreased blood pH. Risk factors for permanent neurologic sequelae and death were decreased blood pH and greater delay in treatment (Anderson et al, 1989). COMA: In severe methanol intoxication, profound coma and seizures may develop. When coma or seizures and severe acidosis are present on admission to the ED, prognosis is poor (Vara-Castrodeza et al, 2007; Hovda et al, 2005; Salzman, 2006; Liu & Daya, 1997). EXTRAPYRAMIDAL DISEASE: Multiple cases have been reported showing evidence of extrapyramidal disease and Parkinson-like syndrome (some permanent) following acute methanol ingestion. Symptoms included: muscle rigidity, hypokinesia, intention tremor, masked face, moderate cogwheel rigidity, shuffling gait, and impairment of postural reflexes (Arora et al, 2007; Airas et al, 2008; Guggenheim et al, 1971; Bitar et al, 2004). CEREBELLAR INFARCTION: Infarcts and necrosis of the basal ganglia, particularly the putamina, may occur after severe methanol poisoning (Rosenberg, 1987; Yu et al, 1995). CEREBRAL HEMORRHAGE: Methanol toxicity involving the optic nerve and brain may result in basal ganglia hemorrhage, evidenced on CT scan (Askar & Al-Suwaida, 2007; Ganguly et al, 1996). Abrupt onset of blindness and loss of consciousness may occur with basal ganglia bleeding (Ganguly et al, 1996). NEUROPATHY: Paresthesias and tingling of the extremities may occasionally develop during the first few days of recovery from acute methanol poisoning (Bennett, 1953).
DYSPNEA: Dyspnea may occur during the early stages of methanol poisoning, but is unusual (Bennett, 1953). TACHYPNEA: Tachypnea secondary to metabolic acidosis is common following methanol exposure (Vara-Castrodeza et al, 2007; Adanir et al, 2005; Carpentieri et al, 2003). RESPIRATORY ARREST: Respiratory arrest may develop with severe poisoning (Bennett, 1953; Williams et al, 1997) and is a strong prognostic indicator of poor outcome if present on hospital admission (Hovda et al, 2005). PULMONARY EDEMA: Severe pulmonary edema, seen at autopsy and histological examination in 2 fatalities, was reported following methanol ingestion of 97g and 107g, respectively (Kinoshita et al, 1998). INHALATION: Inhalation exposure to methanol-containing substances may cause severe toxicity (Frenia & Schauben, 1992). Tachypnea (as well as visual, neurologic, and metabolic toxicity) has been reported in deliberate inhalational abusers of methanol-containing products (Frenia & Schauben, 1992). In a retrospective study of 22 patients with inhalation exposure, 14 (63.6%) presented with vomiting, and all patients developed neurologic abnormalities (ataxia, lethargy). Significant toxicities were rare (LoVecchio et al, 2004).
CHRONIC CLINICAL EFFECTS
- Because methanol is eliminated from the body more slowly than ethanol, it can have CUMULATIVE TOXICITY with repeated exposures (ACGIH, 1992). Repeated skin contact can cause a defatting dermatitis with dryness and cracking (Sax, 1984). Other symptoms of chronic exposure include eye irritation, headache, giddiness, insomnia, gastric disturbances, and visual difficulties. Repeated exposure to airborne concentrations in the range of 200 to 375 parts per million (ppm) have been associated with headaches, and at 1200 to 8300 ppm with damaged vision (Clayton & Clayton, 1994; Von Burg, 1994).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
- There is no role for prehospital decontamination.
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
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.
FIRST AID EYE EXPOSURE: Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection. DERMAL EXPOSURE: Flush the contaminated skin with water promptly. If this chemical penetrates the clothing, immediately remove the clothing and flush the skin with water promptly. If irritation persists after washing, get medical attention. INHALATION EXPOSURE: Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible. ORAL EXPOSURE: If this chemical has been swallowed, get medical attention immediately. TARGET ORGANS: Eyes, skin, respiratory system, central nervous system, and gastrointestinal (GI) tract (National Institute for Occupational Safety and Health, 2007; Chemsoft(R) , 2000)..
INHALATION EXPOSURE 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 an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
DERMAL EXPOSURE EYE EXPOSURE DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
ORAL EXPOSURE If methanol has been swallowed, seek medical assistance immediately. Because of the potential for CNS depression and seizures, do NOT induce emesis.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
- Lethal exposure to methanol usually results from ingestion. The fatal dose in humans is between 2 and 8 ounces (ACGIH, 1991).
- Death has occurred after ingestion of about 15 mL of 40% methanol (Bennett, 1953).
- A fatality was reported in a 35-year-old chronic alcoholic woman who drank approximately 500 mL of windshield washing liquid containing 20% methanol (about 100 mL of pure methanol) 12 to 18 hours before medical management (Girault et al, 1999).
- In the absence of medical treatment, the minimum lethal dose of methanol is between 0.3 and 1 g/kg (HSDB , 2002).
- An amount of 100 to 200 mL is fatal to most adults (Baselt, 2000; Budavari, 2000).
- Ingestion of less than 30 mL has been reported to cause death (Budavari, 2000).
- The minimum lethal dose for human beings is 0.3 to 1.0 g/kg (Grant & Schuman, 1993).
MAXIMUM TOLERATED EXPOSURE
Most exposures to methanol result from ingestion; however, symptoms may also occur from inhalation, skin absorption, or intravenous injection. Patients develop nausea, abdominal pain, headache, abnormally slow, deep breathing, and visual symptoms ranging from blurred or double vision and changes in color perception to constricted visual fields and complete blindness within 18 to 48 hours of ingestion. Chronic exposures to airborne concentrations of 1200 to 8300 parts per million (ppm) can lead to impaired vision. Exposure to airborne vapor concentrations ranging from 365 to 3080 ppm may result in blurred vision, headache, dizziness, and nausea (Grant & Schuman, 1993; Hathaway et al, 1996). On a scale of 1 to 6 (1 is practically nontoxic; 6 is super toxic), methanol is rated as 3 (moderately toxic) (Gosselin et al, 1984). Note: The metabolism of methanol in rats is different than in humans. This might lead to a discrepancy between the experimental animal findings and the actual toxicity of methanol in humans. In particular, rats can assimilate higher levels of methanol than humans without serious physical effects (Kinney & Kavet, 1988). Methanol toxicity in humans should probably be upgraded to level 4, highly toxic.
The range of toxicity of methanol is extremely variable. Blindness has followed ingestion of about 4 mL of absolute methanol (Bennett, 1953). Extremely high exposures (greater than 25,000 ppm) are necessary to produce sensory irritation (Bingham et al, 2001).
INHALATIONAL EXPOSURE: In a retrospective study of 22 patients with inhalational exposure to methanol-containing carburetor cleaners (mean serum methanol concentration of 28 mg/dL obtained at a mean of 3.5 hours postexposure; range 0 to 34), all patients presented with neurotoxicity. Vomiting and metabolic acidosis developed in 14 (63.6%) and 17 (77%) patients, respectively. Overall, significant toxicity was rare, with symptoms improving without aggressive care (dialysis, alcohol dehydrogenase blockade). Visual disturbances or neurological sequelae did not develop in any patients (LoVecchio et al, 2004). A 24-year-old man presented unconscious (Glasgow Coma score 10) about 2 hours after ingesting about 100 mL of methanol and 50 g of sodium ferrocyanide. His vital signs included a blood pressure of 78/34 mmHg, heart rate of 56 beats/min, irregular respiratory rate, and pulse oxygen saturation of 65%. Laboratory results revealed increased leukocytes, respiratory failure, acute kidney injury, and metabolic acidosis. Serum concentrations of sodium ferrocyanide, methanol, and its product formic acid at 2 hours postingestion were 361.2 mg/L, 1244.1 mg/L, and 728.6 mg/L, respectively. Following supportive care, including endotracheal intubation and mechanical ventilation, gastric lavage, sodium bicarbonate, ethanol, plasmapheresis (plasma exchange), and continuous renal replacement therapy (CRRT), his condition gradually improved and he was discharged on day 6 without further sequelae (Liu et al, 2015). One patient survived after drinking 500 mL of 40% methanol (Martens et al, 1982). The occurrence of severe methanol poisoning with fatal outcome or ocular sequelae appeared to be related to the time between ingestion and initiation of treatment. All of 4 patients admitted before 10 hours postingestion had a favorable outcome. Of 6 patients admitted 20 hours or more after ingestion, 4 had ocular sequelae and 1 died (Mahieu et al, 1989). In a letter to the editor, 1 case of intravenous injection of approximately 250 mg of methanol was reported to result in optic papillitis and retinal edema with subsequent blindness in a 20-year-old man (Wang et al, 1999). Sivilotti et al (2000) question whether this small dose of methanol could cause serious methanol toxicity and suggest that the patient may have had an additional source of methanol (Sivilotti et al, 2000).
- Carcinogenicity Ratings for CAS67-56-1 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methanol EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Methanol IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; 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 Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Methyl alcohol MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS67-56-1 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 5x10(-1) mg/kg-day
Inhalation: Drinking Water:
References: IPCS, 1997 ITI, 1995 Lewis, 2000 OHM/TADS, 2002 RTECS, 2002 LC50- (INHALATION)RAT: LCLo- (INHALATION)CAT: LCLo- (INHALATION)MOUSE: LCLo- (INHALATION)PRIMATE: LD50- (ORAL)DOG: LD50- (INTRAPERITONEAL)GUINEA_PIG: LD50- (INTRAPERITONEAL)HAMSTER: LD50- (INTRAPERITONEAL)MOUSE: LD50- (INTRAVENOUS)MOUSE: LD50- (ORAL)MOUSE: LD50- (SUBCUTANEOUS)MOUSE: 4100 mg/kg (ITI, 1995) 9800 mg/kg
LD50- (ORAL)PRIMATE: LD50- (INTRAPERITONEAL)RABBIT: LD50- (INTRAVENOUS)RABBIT: LD50- (ORAL)RABBIT: LD50- (SKIN)RABBIT: LD50- (INTRAPERITONEAL)RAT: LD50- (INTRAVENOUS)RAT: LD50- (ORAL)RAT: 6.2 g/kg (IPCS, 1997) 9.1 g/kg (IPCS, 1997) 12.9 g/kg (IPCS, 1997) 13.0 g/kg (IPCS, 1997) 5628 mg/kg Young, 5300 mg/kg (OHM/TADS, 2002) 6200 mg/kg (OHM/TADS, 2002) 12,880 mg/kg for 14D (OHM/TADS, 2002)
LDLo- (INTRAVENOUS)CAT: LDLo- (ORAL)DOG: 7500 mg/kg 6300 mg/kg (ITI, 1995)
LDLo- (ORAL)HUMAN: 143 mg/kg -- optic nerve neuropathy; dyspnea; nausea or vomiting 340 mg/kg (ITI, 1995) 428 mg/kg -- headache; lung, thorax, or respiration changes 6422 mg/kg -- circulation changes in brain and brain coverings; dyspnea; nausea or vomiting
LDLo- (ORAL)MOUSE: LDLo- (ORAL)PRIMATE: LDLo- (SKIN)PRIMATE: LDLo- (ORAL)RABBIT: LDLo- (INTRAPERITONEAL)RAT: MLD- (ORAL)PRIMATE: 2-3 g/kg (IPCS, 1997) 7.0 g/kg (IPCS, 1997)
MLD- (ORAL)RABBIT: MLD- (ORAL)RAT: TCLo- (INHALATION)HUMAN: 86,000 mg/m(3) -- lacrimation, cough, changes of the lung, thorax, or respiration 300 ppm -- visual changes, headache; lung, thorax or respiration changes
TCLo- (INHALATION)MOUSE: Female, 15,000 ppm at 7-9D of pregnancy -- postimplantation mortality; fetotoxicity (except death) Female, 2000 ppm for 7H at 6-15D of pregnancy -- developmental abnormalities of musculoskeletal system Female, 7500 ppm for 7H at 6-15D of pregnancy -- postimplantation mortality; fetal death Female, 5000 ppm for 7H at 6-15D of pregnancy -- craniofacial and central nervous system effects Female, 1500 ppm for 6H at 7-9D of pregnancy -- central nervous system effects
TCLo- (INHALATION)RAT: Female, 10,000 ppm for 7H at 7-19D day of pregnancy -- fetotoxicity (except death) 50 mg/m(3) for 12H/13W - intermittent -- degenerative changes of brain and coverings; muscle contraction or spasticity 2610 ppm for 6H/4W - intermittent -- changes in spleen weight Female, 20,000 ppm for 7H at 7-15D of pregnancy -- developmental abnormalities in musculoskeletal and endocrine systems Female, 20,000 ppm for 7H at 1-22D of pregnancy -- developmental abnormalities in musculoskeletal, cardiovascular, and urogenital systems
TDLo- (ORAL)HUMAN: 100 mg/kg (ITI, 1995) 9450 mcL/kg -- mydriasis; general anesthetic; body temperature decrease 3429 mg/kg -- visual field changes 3571 mcL/kg -- visual field changes; dyspnea; blood changes 4 g/kg -- visual field changes; dyspnea; nausea or vomiting
TDLo- (INTRAPERITONEAL)MOUSE: TDLo- (ORAL)MOUSE: Female, 4 g/kg at 7D of pregnancy -- craniofacial and musculoskeletal system abnormalities Female, 40 g/kg at 6-15D of pregnancy -- fetotoxicity (except death); craniofacial abnormalities
TDLo- (INTRAPERITONEAL)RAT: TDLo- (ORAL)RAT: 2885 mg/kg for 3D - intermittent -- changes in urine composition 7 mL/kg for 7D - intermittent -- liver and B vitamin changes 12 g/kg for 8W - intermittent -- ataxia; changes in operant conditioning Female, 7500 mg/kg at 7-19D of pregnancy (Lewis, 2000) Female, 35,295 mg/kg at 1-15D of pregnancy -- fetotoxicity (except death); biochemical and metabolic effects on newborn Female, 35,295 mg/kg at 1-15D of pregnancy -- effects on female fertility index; pre- and postimplantation mortality Female, 5200 mcL/kg at 10D of pregnancy -- fetotoxicity (except death); eye, ear, and urogenital system abnormalities Female, 20 g/kg at 6-15D of pregnancy -- postimplantation mortality; affected litter size Female, 7500 mg/kg at 17-19D of pregnancy -- behavioral effects on newborn Male, 200 ppm for 20H at 78W prior to mating -- effects on testes, epididymis, sperm duct
CALCULATIONS
1 mg/L = 764 ppm (Bingham et al, 2001) 1 mg/m(3) = 0.764 ppm (Verschueren, 2001) 1 ppm = 1.33 mg/m(3) (Verschueren, 2001) 1 ppm = 1.31 mg/m(3) (at 25 degrees C; 1013 hPa) (IPCS, 1997) 1 mmol/L = 32 mg/L (IPCS, 1997) 1 mg/m(3) = 0.763 ppm (at 25 degrees C; 1013 hPa) (IPCS, 1997) 1 mg/L = 31.2 umol/L (IPCS, 1997) 1 ppm = 1.31 mg/m(3) (Bingham et al, 2001; NIOSH , 2002)
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS67-56-1 (American Conference of Governmental Industrial Hygienists, 2010):
Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
- AIHA WEEL Values for CAS67-56-1 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS67-56-1 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS67-56-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS67-56-1 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS67-56-1 (U.S. Environmental Protection Agency, 2010):
Listed as: Methanol Final Reportable Quantity, in pounds (kilograms): Additional Information: The following spent non-halogenated solvents and the still bottoms from the recovery of these solvents. (F003) Listed as: Methanol Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: Methyl alcohol Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS67-56-1 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS67-56-1 (U.S. Environmental Protection Agency, 2010b):
Listed as: Methanol P or U series number: U154 Footnote: Listed as: Methyl alcohol P or U series number: U154 Footnote: Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.
- EPA SARA Title III, Extremely Hazardous Substance List for CAS67-56-1 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS67-56-1 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS67-56-1 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS67-56-1 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1230 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1230 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS67-56-1 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
Methanol is a human poison by ingestion, and it is moderately toxic by inhalation. It is irritating to the eyes and skin; avoid skin contact and wear solvent-resistant personal protective clothing. Methanol may accumulate static electrical charges that may cause ignition of its vapors; sources of ignition such as smoking and open flames are prohibited wherever methanol is handled, used, or stored. Use only nonsparking tools and equipment, especially when opening and closing containers of methanol (Lewis, 2000; Pohanish, 2002; Pohanish & Greene, 1997).
HANDLING
- Only nonsparking tools and equipment should be used around containers of methanol, particularly when opening or closing the containers. All sources of ignition are prohibited wherever methanol is handled, stored, or used (Lewis, 2000; Pohanish, 2002).
STORAGE
Store in tightly-closed containers. All drums must be equipped with self-closing valves, pressure vacuum bungs, and flame arresters. All metal containers should be grounded and bonded (Pohanish, 2002).
- ROOM/CABINET RECOMMENDATIONS
Store in a cool, well-ventilated area, away from heat. Storage of large volumes of methanol should be remote from inhabited buildings or structures (ITI, 1995; Pohanish, 2002).
Methanol may accumulate static electrical charges that may cause ignition of its vapors. It forms an explosive mixture with air. Methanol is incompatible with strong acids, strong oxidizers, caustics, aliphatic amines, isocyanates, chromic anhydride, lead perchlorate, perchloric acid, and phosphorus trioxide. It may react with metallic aluminum at high temperature, and it attacks some plastics, rubber, and coatings (Pohanish, 2002; Pohanish & Greene, 1997).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective 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.
- Methanol is a human poison by ingestion, and it is moderately toxic by inhalation. It is irritating to the eyes and skin; avoid skin contact and wear solvent-resistant personal protective clothing. All protective clothing should be clean before use. Do not handle broken containers or spilled methanol unless wearing appropriate protective clothing and equipment. Wash away any methanol that contacts the body with copious amounts of water or soap and water (AAR, 2000; Lewis, 2000; Pohanish, 2002).
EYE/FACE PROTECTION
- Wear splash-proof chemical goggles and a face shield when working with methanol unless wearing full facepiece respiratory protection (Pohanish, 2002).
RESPIRATORY PROTECTION
- Avoid breathing vapors; keep upwind (AAR, 2000).
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 67-56-1.
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004) 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.
If methanol is on fire or involved in a fire, do not extinguish the fire unless the flow of methanol 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 away as possible. Use "alcohol" foam, dry chemical, or carbon dioxide to extinguish the fire (AAR, 2000; ITI, 1995; Pohanish, 2002).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS67-56-1 (NFPA, 2002):
- INITIATING OR CONTRIBUTING PROPERTIES
Methanol's low flash point (12 degrees C; 54 degrees F) indicates that it can be easily ignited over a wide range of ambient temperature conditions. Methanol vapors may also be ignited by accumulated static electrical charges (AAR, 2000; Pohanish & Greene, 1997).
- FIRE CONTROL/EXTINGUISHING AGENTS
- FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
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.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
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 let fire burn.
- NFPA Extinguishing Methods for CAS67-56-1 (NFPA, 2002):
When heated to decomposition, methanol emits acrid smoke and irritating fumes, including formaldehyde (Lewis, 2000; Pohanish, 2002).
EXPLOSION HAZARD
- Methanol's low flash point (12 degrees C; 54 degrees F) indicates that it can be easily ignited over a wide range of ambient temperature conditions. Methanol vapors may also be ignited by accumulated static electrical charges. Additionally, the vapors are slightly heavier than air and in warm weather they may travel some distance to a source of ignition and flash back. Accumulations of vapors in confined spaces (such as buildings or sewers) may explode if ignited (AAR, 2000; Pohanish & Greene, 1997).
DUST/VAPOR HAZARD
- Methanol vapors may be ignited by accumulated static electrical charges. Additionally, the vapors are slightly heavier than air and in warm weather they may travel some distance to a source of ignition and flash back. Accumulations of vapors in confined spaces (such as buildings or sewers) may explode if ignited (AAR, 2000; Pohanish & Greene, 1997).
- Methanol is mildly toxic by inhalation. Avoid breathing vapors; stay upwind (AAR, 2000; Lewis, 2000).
- When heated to decomposition, methanol emits acrid smoke and irritating fumes, including formaldehyde (Lewis, 2000; Pohanish, 2002).
- Methanol is toxic and may be fatal if inhaled (HSDB , 2002).
- Methanol vapors mix well with air. Explosive mixtures are easily formed (ILO , 1998).
REACTIVITY HAZARD
- Methanol forms an explosive mixture with air due to its low flash point (Lewis, 2000; Pohanish & Greene, 1997; Urben, 2000).
- It has an explosive reaction with chloroform + sodium methoxide, and diethyl zinc (Lewis, 2000; Urben, 2000).
Solid sodium methoxide, methanol, and chloroform were mixed together; the mixture boiled violently and then exploded (Urben, 2000). The interaction of methanol and diethyl zinc is explosively violent and ignites (Urben, 2000).
- Methanol has a violent reaction with alkyl aluminum salts (up to C4), acetyl bromide, chloroform + sodium hydroxide, chromic anhydride, cyanuric chloride, lead perchlorate, percloric acid, phosphorus trioxide, and nitric acid (Lewis, 2000; Pohanish & Greene, 1997; Urben, 2000).
Methanol accidentally used to rinse out a hypodermic syringe used for a dilute alkyl aluminum solution caused a violent reaction which blew the plunger out of the barrel (Urben, 2000). An exothermic reaction occurred when 1 g of sodium hydroxide was added to a mixture of 1 mL methanol and 1 mL chloroform (NFPA, 2002a). An explosion and fire resulted when methanol was contacted by chromic anhydride in a laboratory preparation (NFPA, 2002a). A saturated solution of anhydrous lead perchlorate dissolved in methanol exploded when it was disturbed (NFPA, 2002a).
- Methanol is incompatible with beryllium dihydride, metals (such as potassium and magnesium), oxidants (such as barium perchlorate, bromine, sodium hypochlorite, chlorine, and hydrogen peroxide), potassium tert-butoxide, carbon tetrachloride + metals (such as aluminum, magnesium, and zinc), and dichloromethane (Lewis, 2000; Pohanish & Greene, 1997; Urben, 2000).
The reaction between magnesium and methanol is very vigorous, but often subject to a lengthy induction period. Mixtures of powdered magnesium (or aluminum) and methanol are capable of detonation (Urben, 2000). The rapid autocatalytic dissolution of aluminum, magnesium, or zinc in a 9:1 methanol - carbon tetrachloride mixture is sufficiently vigorous to be rated as potentially hazardous (Urben, 2000).
- It may react with metallic aluminum at high temperature (Pohanish & Greene, 1997; Urben, 2000).
- It attacks some plastics, rubber, and coatings (Pohanish & Greene, 1997).
- Methanol can have vigorous reactions with oxidizing materials (HSDB , 2002).
- Phosphorus trioxide and methanol will react very violently, often charring (NFPA, 2002a).
- When 1 molar ethyl alcohol (instead of 0.11 molar) was added to 15 grams of mercuric oxide and 25 mL of methanol, a violent explosion occurred (NFPA, 2002a).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
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.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131(ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. 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.
- AIHA ERPG Values for CAS67-56-1 (AIHA, 2006):
Listed as Methanol ERPG-1 (units = ppm): 200 ERPG-2 (units = ppm): 1000 ERPG-3 (units = ppm): 5000 Under Ballot, Review, or Consideration: No Definitions: ERPG-1: The ERPG-1 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing more than mild, transient adverse health effects or perceiving a clearly defined objectionable odor. ERPG-2: The ERPG-2 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing irreversible or other serious health effects or symptoms that could impair an individual's ability to take protective action. ERPG-3: The ERPG-3 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing life-threatening health effects.
- DOE TEEL Values for CAS67-56-1 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Methyl alcohol; (Methanol) TEEL-0 (units = ppm): 200 TEEL-1 (units = ppm): 530 TEEL-2 (units = ppm): 2100 TEEL-3 (units = ppm): 7200 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS67-56-1 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
Listed as: Methanol Proposed Value: AEGL-1 10 min exposure: ppm: 670 ppm mg/m3: 880 mg/m(3)
30 min exposure: ppm: 670 ppm mg/m3: 880 mg/m(3)
1 hr exposure: ppm: 530 ppm mg/m3: 690 mg/m(3)
4 hr exposure: ppm: 340 ppm mg/m3: 450 mg/m(3)
8 hr exposure: ppm: 270 ppm mg/m3: 350 mg/m(3)
Definitions: AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling, are transient, and are reversible upon cessation of exposure.
Listed as: Methanol Proposed Value: AEGL-2 10 min exposure: ppm: 4000 ppm mg/m3: 5200 mg/m(3)
30 min exposure: ppm: 4000 ppm mg/m3: 5200 mg/m(3)
1 hr exposure: ppm: 2100 ppm mg/m3: 2800 mg/m(3)
4 hr exposure: ppm: 720 ppm mg/m3: 940 mg/m(3)
8 hr exposure: ppm: 510 ppm mg/m3: 670 mg/m(3)
Definitions: AEGL-2 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape.
Listed as: Methanol Proposed Value: AEGL-3 10 min exposure: ppm: 15000 ppm mg/m3: 20,000 mg/m(3)
30 min exposure: ppm: 15000 ppm mg/m3: 20000 mg/m(3)
1 hr exposure: ppm: 7900 ppm mg/m3: 10,000 mg/m(3)
4 hr exposure: ppm: 2500 ppm mg/m3: 3300 mg/m(3)
8 hr exposure: ppm: 1600 ppm mg/m3: 2100 mg/m(3)
Definitions: AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening health effects or death.
- NIOSH IDLH Values for CAS67-56-1 (National Institute for Occupational Safety and Health, 2007):
IDLH: 6000 ppm Note(s): Not Listed
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004) 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.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective 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.
If methanol is spilled on land, dig a pit, pond, lagoon, or other holding area to contain the spill. Dike surface flow using soil, sandbags, foamed polyurethane, or foamed concrete (AAR, 2000). If methanol is spilled onto water, allow it to aerate. Use natural barriers or oil spill control booms to limit travel of the spill and remove the trapped methanol with suction hoses (AAR, 2000). If methanol is released into the air, apply water spray or mist to knock down the vapors (AAR, 2000).
SMALL SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004) 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.
Restrict people not wearing appropriate protective equipment from the spill area until clean-up is complete. Ventilate the spill area and remove all sources of ignition. Keep methanol out of confined spaces to avoid the possibility of an explosion. Absorb spilled methanol in vermiculite, dry sand, earth, or a similar material and store in sealed containers (Pohanish, 2002).
LARGE SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004) If methanol is not on fire and is not involved in a fire, keep sparks, flames and other sources of ignition away from it. Keep methanol out of water sources and sewers; build dikes to contain the flow of methanol as necessary. Attempt to stop the leak if this is possible without undue personnel hazard. Use water spray to knock down vapors and dilute standing pools of methanol (AAR, 2000; Pohanish, 2002).
Biological treatment, reverse osmosis, and activated carbon have all been investigated as wastewater treatment technologies (HSDB , 2002). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Methanol is primarily released to the environment by evaporation during its use as a solvent; it is also released during its manufacture, and storage and handling. Methanol is emitted in gasoline and diesel exhaust, from the combustion of biomass, refuse, and plastics, from the manufacture of petroleum, charcoal, plastics, and starch, rendering, and wood pulping. Methanol is also released to the environment as a volatile emission from plants, volcanic gasses, microbes, and insects. It is formed during the decomposition of biological wastes, sewage, and sludges (Howard, 1990).
- Methanol vapor in the air can be oxidized to formaldehyde; incomplete combustion in fuel systems will yield formaldehyde and formic acid. All these products, along with methanol vapor, form a significant health hazard (Posner, 1975; Kinney & Kavet, 1988).
ENVIRONMENTAL FATE AND KINETICS
Based on its vapor pressure, methanol exists almost entirely in the vapor phase in the ambient atmosphere. It is degraded by reaction with photochemically produced hydroxyl radicals and has an estimated half-life of 17.8 days. Methanol is physically removed from the air by rain due to its solubility. Methanol can react with nitrogen dioxide in polluted air to form methyl nitrate (Howard, 1990). The half-life of methanol in air ranges from 71 hours (3 days) to 713 hours (29.7 days) based on its photooxidation half-life in air (Howard et al, 1991).
SURFACE WATER Methanol in water is rapidly biodegraded and volatilized. Aquatic hydrolysis, oxidation, photolysis, adsorption to sediment, and bioconcentration are not significant fate processes (Howard, 1990). The estimated half-life of methanol in surface water ranges from 24 hours (1 day) to 168 hours (7 days) based on estimated unacclimated aqueous aerobic biodegradation (Howard et al, 1991). The estimated half-life of methanol in ground water ranges from 24 hours (1 day) to 168 hours (7 days) based on an unacclimated grab sample of aerobic soil/water suspensions from ground water aquifers (Howard et al, 1991). Volatilization half-life estimate for a model river, 1 meter deep, is 4.8 days. The estimate for an environmental pond is 51.7 days (HSDB , 2002). Other estimates for these model are 5.3 hours (for the river) and 2.6 days (for the pond) (Howard, 1990).
TERRESTRIAL Methanol biodegrades significantly in the soil. It is highly mobile in soil based on its solubility and low octanol/water partion coefficient. It evaporates from dry surfaces based on its relatively high vapor pressure (Howard, 1990). The estimated half-life of methanol in soil ranges from 24 hours (1 day) to 168 hours (7 days) based on an unacclimated grab sample of aerobic soil/water suspensions from ground water aquifers (Howard et al, 1991).
ABIOTIC DEGRADATION
- The rate constant for the vapor-phase reaction of methanol with photochemically produced hydroxyl radicals has been reported to be 0.9 x 10(-12)cm(3)/molecule-sec at 25 degrees C. The atmospheric half-life for this reaction is estimated to be 17.8 days, assuming an average hydroxyl radical concentration of 5 x 10(5) molecules/cm(3) (Howard, 1990).
- The photooxidation half-life of methanol in water ranges from 4728 hours (197 days) to 22 years based on the measured rate data for hydroxyl radicals in aqueous solution (Howard et al, 1991).
- The photooxidation half-life of methanol in the air ranges from 6.2 hours (0.26 days) to 72 hours (3 days) based on measured rate data for the vapor phase reaction with hydroxyl radicals (Howard et al, 1991).
- The reaction of methanol with hydroxyl radicals in aqueous solution has a rate constant of approximately 1 x 10(9) l/mol-sec. The half-life is expected to be approximately 2.2 years if the hydroxyl radical concentration of sunlit natural water is assumed to be 1 x 10(-17) moles/l(2) (HSDB , 2002).
- When methanol in aqueous solution was exposed to sunlight using an EPA test protocol, the methanol exhibited no degradation (HSDB , 2002).
- When methanol in aqueous solution was irradiated with ultraviolet light, sediment and clay suspensions solution did not photocatalyze the degradation of the methanol (HSDB , 2002).
BIODEGRADATION
- Test results suggest that methanol biodegrades rapidly in soil, water, and air (Howard, 1990).
- The scientific judgement for aerobic half-life of methanol ranges from 24 hours (1 day) to 168 hours (7 days) based on an unacclimated grab sample of aerobic soil/water suspensions from ground water aquifers (Howard et al, 1991).
- The scientific judgement for anaerobic half-life of methanol ranges from 24 hours (1 day) to 120 hours (5 days) based on an unacclimated grab sample of anaerobic marine water/sediment and soil/water suspensions (Howard et al, 1991).
- Removal of methanol in secondary treatment ranges between 86% and 99% based on the percent degraded under acclimated aerobic semi-continuous flow conditions (Howard et al, 1991).
- Traces of cobalt in a culture medium greatly increased the rate of methanogenesis of methanol and acetate produced in an anaerobic digester. Cobalt sufficient reactors converted 87% of the COD at an organic loading rate of 8 g COD/L/D (Florencio et al, 1993).
- An 8-membered bacteria consortium, isolated from methanol-contaminated soil samples, was immobilized and packed in a 5 cm diameter x 60 cm high column bioreactor. The unit effectively removed up to 112.8 g/H methanol/m(3) of packing. The methanol biofiltration process was limited by oxygen diffusion and methanol degradation kinetics (Shareefdeen et al, 1993).
- The biological oxygen demand for methanol is 0.6 to 1.12 lb/lb in 5 days (CHRIS , 2002).
BIOACCUMULATION
The bioconcentration factor of methanol may be estimated to be 0.2 based on the octanol/water partition coefficient and a recommended regression-derived equation (Howard, 1990). An experimentally measured BCF in fish (golden ide) was less than 10 (HSDB , 2002).
ENVIRONMENTAL TOXICITY
- LC50 - Pimephales promelas/fathead minnow: 29.4 g/L for 96H -- 28-29D old, confidence limit = 28.5-30.4; test conditions: water temperature = 25 degrees C, dissolved oxygen = 7.3 mg/L, water hardness = 43.5 mg/L calcium carbonate, alkalinity = 46.6 calcium carbonate, tank volume = 6.3 L, additions = 5.71 V/D, pH = 7.66(0.03), other conditions of bioassay not specified (HSDB , 2002)
- LC50 values for aquatic invertebrates have ranged from 1300 mg/L (48 hour exposure) to 15,900 mg/l (96 hour exposure). Values for fish range from 13,000 to 29,000 mg/L (96 hour exposure) (IPCS, 1997).
- References: (IPCS, 1997; OHM/TADS , 2002)
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Methanol is the simplest of the primary alcohols and is a colorless, highly polar, flammable liquid. Pure methanol has a faintly sweet odor at ambient temperatures; crude methanol may have a repulsive, pungent odor (AAR, 2000; ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; Lewis, 2001; Lewis, 1998; Lewis, 2000).
PH
VAPOR PRESSURE
- 92 mmHg (at 20 degrees C) (Howard, 1990; Lewis, 2001; Verschueren, 2001)
- 100 mmHg (at 21.2 degrees C) (Lewis, 2000)
- 127 mmHg (at 25 degrees C) (HSDB , 2002)
- 160 mmHg (at 30 degrees C) (Bingham et al, 2001; Verschueren, 2001)
- 96 mmHg (at 20 degrees C) (ACGIH, 1991)
- 128 hPa (at 20 degrees C) (Verschueren, 2001)
SPECIFIC GRAVITY
- NORMAL TEMPERATURE AND PRESSURE
(25 degrees C; 77 degrees F and 760 mmHg) 0.7866 (at 25/4 degrees C) (Budavari, 2000; IPCS, 1997)
- STANDARD TEMPERATURE AND PRESSURE
- OTHER TEMPERATURE AND/OR PRESSURE
0.7960 (at 15/4 degrees C) (Budavari, 2000) 0.7915 (at 20/4 degrees C) (Budavari, 2000; IPCS, 1997; Lewis, 2000) 0.792 (at 20 degrees C) (ACGIH, 1991) 0.8 (at 15 degrees C) (OHM/TADS , 2002; Verschueren, 2001)
- TEMPERATURE AND/OR PRESSURE NOT LISTED
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
FREEZING/MELTING POINT
-97.8 degrees C (Lewis, 2001; Lewis, 2000) -98 degrees C (Ashford, 2001; Pohanish, 2002) -97.68 degrees C (IPCS, 1997) -144.0 degrees F; -97.8 degrees C; 175.4 K (CHRIS , 2002)
-97.8 degrees C (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; Howard, 1990) -98 degrees C (ILO , 1998; Pohanish, 2002; Verschueren, 2001)
BOILING POINT
- -44.0 degrees C (at 1 mmHg) (Budavari, 2000)
- -25.3 degrees C (at 5 mmHg) (Budavari, 2000)
- -16.2 degrees C (at 10 mmHg) (Budavari, 2000)
- -6.0 degrees C (at 20 mmHg) (Budavari, 2000)
- 5.0 degrees C (at 40 mmHg) (Budavari, 2000)
- 12.1 degrees C (at 60 mmHg) (Budavari, 2000)
- 21.2 degrees C (at 100 mmHg) (Budavari, 2000)
- 34.8 degrees C (at 200 mmHg) (Budavari, 2000)
- 49.9 degrees C (at 400 mmHg) (Budavari, 2000)
- 64 degrees C; 147 degrees F (NFPA, 2002a)
- 64.5 degrees C (ACGIH, 1991; Lewis, 2001)
- 64.7 degrees C (at 760 mmHg) (Budavari, 2000; Howard, 1990)
- 65 degrees C (Ashford, 2001; Bingham et al, 2001; Verschueren, 2001)
- 64.8 degrees C (Lewis, 2000)
- 148.1 degrees F; 64.5 degrees C; 337.7 K (all at 1 atm) (CHRIS , 2002)
FLASH POINT
- 6 degrees C (closed cup) (Ashford, 2001)
- 11 degrees C; 52 degrees F (NFPA, 2002a)
- 16 degrees C (open cup) (ACGIH, 1991)
- 12.2 degrees C; 54 degrees F (open cup) (Lewis, 2001)
- 12 degrees C; 54 degrees F (closed cup) (ACGIH, 1991; Budavari, 2000)
- 12 degrees C (NFPA, 2002a)
- 15.6 degrees C (open cup) (IPCS, 1997)
- 12.2 degrees C (closed cup) (IPCS, 1997)
- 54 degrees F (closed cup); 61 degrees F (open cup) (CHRIS , 2002)
AUTOIGNITION TEMPERATURE
- 464 degrees C; 867 degrees F (ACGIH, 1991; Lewis, 2001; NFPA, 2002a)
- 470 degrees C; 878 degrees F (Budavari, 2000; Lewis, 2000)
- 385 degrees C (ILO , 1998; NFPA, 2002a)
EXPLOSIVE LIMITS
6.0% (ACGIH, 1991; Bingham et al, 2001; Budavari, 2000; NFPA, 2002a) 5.5% (IPCS, 1997)
SOLUBILITY
Methanol is miscible in water (ACGIH, 1991; Ashford, 2001; Budavari, 2000; Howard, 1990; Lewis, 2001; Lewis, 2000; Lewis, 1998; NFPA, 2002a). Methanol is completely miscible in water (at 20 degrees C) (HSDB , 2002). Methanol is fully soluble in water (AAR, 2000). Methanol is miscible in water (at 25 degrees C; 760 mmHg) (Bingham et al, 2001).
It is also miscible in ethanol, ether, benzene, ketones, and most other organic solvents (ACGIH, 1991; Ashford, 2001; Budavari, 2000; Lewis, 2001; Lewis, 2000; Lewis, 1998). Methanol is soluble in acetone and chloroform (HSDB , 2002). Methanol is miscible with ethanol, ether, benzene, ketones, and most organic solvents (HSDB , 2002).
OCTANOL/WATER PARTITION COEFFICIENT
- log Kow = -0.77 (Howard, 1990; HSDB , 2002)
- log Kow = -0.82; -0.77; -0.68 (IPCS, 1997)
HENRY'S CONSTANT
- 1.1x10(-6) atm-m(3)/mol (Ehrenfeld et al, 1986)
- 1.35x10(-4) atm-m(3)/mol (at 25 degrees C) (Howard, 1990; IPCS, 1997)
- 4.55x10(-6) atm-m(3)/mol (at 25 degrees C) (HSDB , 2002)
- 4.4x10(-6) atm-m(3)/mole (measured) (at 25 degrees C) (HSDB , 2002)
SPECTRAL CONSTANTS
OTHER/PHYSICAL
100 ppm (Bingham et al, 2001; Pohanish, 2002) 2000-5900 ppm (Bingham et al, 2001) Threshold for unadapted panelists: 2000 ppm (Verschueren, 2001) After adaptation with pure odorant: 20,000 ppm (Verschueren, 2001) Low: 13.1 mg/m(3) (HSDB , 2002) Distinct odor: 8800 ppm; 11,700 mg/m(3) (Verschueren, 2001) 13.1150 mg/m(3) (low) (HSDB , 2002) 26840 mg/m(3) (high) (HSDB , 2002) 22875 mg/m(3) (irritating concentration) (HSDB , 2002) A range from 100 ppm to 1500 ppm has been reported (ACGIH, 1991) Mild odor threshold of around 8-10 ppm (Baxter, 2000).
22.6 dynes/dm (at 20 degrees C) (Lewis, 2001) 22.61 mN/m (at 20 degrees C) (HSDB , 2002)
78.5 atm (Budavari, 2000) 1142.0 psia; 77.7 atm; 7.87 MN/m(2) (CHRIS , 2002)
240 degrees C (Budavari, 2000) 464 degrees F; 240 degrees C; 513 K (CHRIS , 2002)
pKa = 15.3 (HSDB , 2002) Poct = -0.82/-0.66 (Verschueren, 2001) log H = -3.72 (at 25 degrees C) (Verschueren, 2001)
723 kJ/mole (HSDB , 2002) -8419 Btu/lb; -4677 cal/g; -195.8x10(5) J/kg (CHRIS , 2002)
1.33066 (at 15 degrees C) (Budavari, 2000) 1.3285 (at 20 degrees C) (Bingham et al, 2001) 1.3292 (at 20 degrees C) (Budavari, 2000; Lewis, 2001) 1.3284 (IPCS, 1997)
- NUCLEAR MAGNETIC RESONANCE
0.00593 cP (at 20 degrees C) (Lewis, 2001) 0.614 mPa sec (HSDB , 2002)
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