See Occupational Exposure Standards
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
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.
Human Toxicity Excerpts:
... CHRONIC POISONING FROM REPEATED EXPOSURE TO ... VAPOR WERE MANIFESTED BY
CONJUNCTIVITIS, HEADACHE, GIDDINESS, INSOMNIA, GASTRIC DISTURBANCES, &
FAILURE OF VISION. ... ONE FATAL CASE OF OCCUPATIONAL ... INTOXICATION BY
INHALATION. ...
POISONING ... RESULTS FROM A COMBINATION OF THE FOLLOWING: 1) A MINOR FACTOR
OF CNS DEPRESSION, SIMILAR TO THAT PRODUCED BY ETHYL ALCOHOL; 2) A MAJOR FACTOR
OF ACIDOSIS DUE TO FORMATION OF FORMIC & OTHER ORG ACIDS ... SPECIFIC
TOXICITY OF OXIDATION PRODUCTS ... (PROBABLY FORMALDEHYDE) FOR RETINAL CELLS.
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 PT,
& BRADYCARDIA CONSTITUTES GRAVE PROGNOSTIC SIGN.
VISUAL DISTURBANCE CAN PROCEED TO BLINDNESS ... PUPILS THEN DO NOT REACT TO
LIGHT. RESTLESSNESS & DELIRIUM ... COMA CAN DEVELOP WITH ... RAPIDITY ...
RESP IS SLOW, SHALLOW, GASPING. ... DEATH MAY BE SUDDEN, OR ... AFTER MANY HR OF
COMA. DEATH OCCURS IN INSPIRATORY APNEA, WITH TERMINAL OPISTHOTONUS &
CONVULSIONS ... DEATH ... NEARLY ALWAYS PRECEDED BY BLINDNESS. AS LITTLE AS 4 ML
OF METHANOL HAS CAUSED BLINDNESS, AND
INGESTION OF 80-150 ML IS USUALLY FATAL. ... NEUROLOGICAL DAMAGE, GIVING RISE TO
PERMANENT MOTOR DYSFUNCTION, MAY FOLLOW METHANOL POISONING.
OPHTHALMOSCOPIC EXAM ... SHOWING HYPEREMIA ... OF OPTIC NERVEHEADS ... THEN
... EDEMA OF DISC MARGINS & ADJACENT RETINA. ... EDEMA ... APPEARING CHIEFLY
IN NERVE FIBER LAYER & ... FOLLOW COURSE OF MAJOR RETINAL VESSELS. ...
PERSISTING EDEMA OF RETINA ... WITH ATROPHY OF OPTIC NERVEHEAD ... & VISION
COMPLETELY & PERMANENTLY GONE.
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 & SHEATHING,
DIMINISHED PUPILLARY LIGHT REACTION, DIMINISHED VISUAL ACUITY, CENTRAL SCOTOMA,
OTHER NERVE FIBER BUNDLE EFFECTS. COMPLETE BLINDNESS IN 2, SEVERE VISUAL DEFICIT
IN 4.
SYMPTOMATOLOGY: 1. A latency usually of 12-18 hours, during which time the
only clinical signs are those of a generally mild and transient state of
inebriation as after ethanol. 2. Headache, anorexia, weakness, fatigue, leg
cramps, vertigo, restlessness. 3. Nausea, occasionally vomiting and diarrhea.
Violent abdominal pain, back pain, leg pain. 4. Apathy or delirium progressing
sometimes rapidly to coma. Rarely excitement, mania, and convulsions. 5. 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. 6. Breathing is rapid and shallow,
not usually deep and labored as seen in other types of metabolic acidosis. 7.
Mild tachycardia is common, but the blood pressure is usually well maintained.
8. Death in coma is due to respiratory failure or rarely to circulatory
collapse. 9. Protracted convalescence with asthenia. Blindness is usually
permanent.
The NIOSH review of the literature failed to reveal any epidemiologic surveys
sufficiently comprehensive to bear significantly on the workplace environmental
limit. A report ... indicated severe recurrent headaches in workers exposed to
methyl alcohol in concentrations between
200-375 ppm. Diminution of vision was reported from airborne methyl alcohol concentrations of 1200 to 8300
ppm.
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.
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. In summary, researchers commented upon a postulated "greater
susceptibility of the ganglion cells of the retina" to poisoning by methyl alcohol.
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.
A case of methyl alcohol poisoning in
a worker who was involved in varnishing the inside of beer vats /is described/.
Work was 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.
At high concn methanol may cause
optic atrophy and blindness, as well as dermatitis.
Skin, Eye and Respiratory Irritations:
/Methanol/ is a skin and eye
irritant.
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.
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.
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.
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 hygience limit (5 ppm) caused 90 mg/g
creatinine. The similarity of these figures may indicate a common toxicological
foundation of these empirically set values.
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 less than 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 error estimate was 0.32 mg/l. This large scatter precludes
making reliable estimates of blood-methanol concentrations are definitely
associated with higher blood-ethanol in ths 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.
Populations at Special Risk:
Persons with existing skin, kidney, liver, or eye disorders may be at an
increased risk when exposed to methanol.
Probable Routes of Human Exposure:
... eye contact
The general population is exposed to methanol through inhalation of air, through
consumption of various drinking waters and foods, and through dermal contact of
various consumer products such as paint thinners and strippers, adhesives,
cleaners, and inks. Widespread occupational exposure occurs through inhalation
and dermal contact. (SRC)
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. ...
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.
2,062,431 Workers are potentially exposed to methanol based on statistical estimates
derived from the NIOSH Survey conducted between 1972-74 in the USA(1). In a
survey conducted between 1978-1982 of solvent products used in industrial
workplaces and having worker exposure, methanol was identified in 9.8% of the 275
solvent samples collected by factory inspectors(2); the products represented
solvent classes such as thinners, degreasers, paints, inks, and adhesives(2).
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).
Average Daily Intake:
AIR INTAKE: assume 1.0-25.0 ppb (0.76-19 ug/cu m)(1): 15.2-380 ug(2); WATER
INTAKE: insufficient data; FOOD INTAKE: insufficient data.
Minimum Fatal Dose Level:
The minimum lethal dose of methanol
in the absence of medical treatment is between 0.3 and 1 g/kg.
Emergency Medical Treatment:
Emergency Medical Treatment:
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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: |
SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
o Methanol is highly toxic, producing metabolic acidosis,
blindness, and death. Evidence of metabolism and/or
symptoms may be delayed for 18 to 24 hours (Range 1-72
hours). Toxicity is related to the degree of acidosis
and thus the time between exposure and specific
treatment. Prognosis is poor in patients with coma or
seizure and severe metabolic acidosis (pH <7).
o Toxic exposure may occur by ingestion, inhalation, or
dermal routes.
o Acute poisoning causes initial drowsiness, confusion
and ataxia. These symptoms are similar to mild
ethanol inebriation. Because methanol must be
metabolized, additional clinical signs and laboratory
findings of metabolic acidosis may be delayed for 18
to 24 hours. Then the patient may experience
nonspecific malaise, headache, vomiting, abdominal
pain, nausea, vomiting, and visual changes. If
untreated, CNS depression progresses to encephalopathy,
rapid respirations, wide anion gap metabolic acidosis
with hypokalemia. Coma and death follow. Visual
defects are described as blurred or "snowfield" like
vision.
1. If untreated, methanol poisoning progresses to coma,
metabolic acidosis, and finally respiratory or
circulatory arrest.
o The most common permanent sequelae following severe
poisoning are optic neuropathy, blindness,
Parkinsonism, toxic encephalopathy, and polyneuropathy.
HEENT
0.2.4.1 ACUTE EXPOSURE
o 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.
1. 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.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Tachycardia or bradycardia may develop in fatal
poisonings. Cardiac failure and severe hypotension may
occur.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Tachypnea from metabolic acidosis is common. Sudden
respiratory failure may occur in the terminal stages.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o Seizures, coma, and symptoms similar to ethanol
"hangover" may occur.
o Permanent sequelae may include basal ganglia infarcts,
Parkinsonism, toxic encephalopathy, polyneuropathy,
optic atrophy and blindness.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Abdominal pain, anorexia, nausea, and vomiting may
occur. In severe poisonings, acute necrotizing
pancreatitis has been reported.
GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
o Acute renal failure and hematuria have been reported.
ACID-BASE
0.2.11.1 ACUTE EXPOSURE
o Metabolic acidosis is classic. Acidosis may be delayed
for 18 to 24 hours, or longer with concurrent ethanol
ingestion.
FLUID-ELECTROLYTE
0.2.12.1 ACUTE EXPOSURE
o Hypomagnesemia, hypokalemia, and hypophosphatemia have
been reported.
MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE
o Rhabdomyolysis may occur in severe poisonings.
REPRODUCTIVE HAZARDS
o 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 to be a human reproductive hazard because of
mixed or poorly documented exposures.
CARCINOGENICITY
0.2.21.1 IARC CATEGORY
o At the time of this review, no studies were found on
the possible carcinogenic activity of methanol in
humans or experimental animals. |
| Laboratory: |
o Obtain CBC, electrolytes, urinalysis, and arterial blood
gases in symptomatic patients or those with a history of
significant exposure.
o Measure serum pH and electrolytes. A wide anion gap
metabolic acidosis suggests the possibility of methanol
overdose.
o Obtain serum methanol and ethanol levels. If a methanol
level cannot be obtained rapidly, an approximation may be
calculated from the difference between a measured (using
freezing point depression) and calculated serum
osmolarity. An elevated osmolal gap suggests methanol
poisoning but a normal osmolal gap does NOT reliably
exclude methanol poisoning. |
| Treatment Overview: |
ORAL EXPOSURE
o Life support measures should be provided because CNS
depression, cardiopulmonary failure, and metabolic
acidosis have been reported with massive exposures.
o Because of the potential for aspiration and CNS
depression, DO NOT induce emesis.
o GASTRIC ASPIRATION - Large volumes of ingested methanol
may produce delayed gastric emptying; thus, there may be
significant recovery of methanol even hours after
ingestion. Insert a nasogastric tube and aspirate
gastric contents after significant ingestion.
o Significant esophageal or gastrointestinal tract
irritation or burns may occur following ingestion. The
possible benefit of early removal of some ingested
material by cautious gastric lavage must be weighed
against potential complications of bleeding or
perforation.
o ACTIVATED CHARCOAL: Administer charcoal as a slurry
(240 mL water/30 g charcoal). Usual dose: 25 to 100 g
in adults/adolescents, 25 to 50 g in children (1 to 12
years), and 1 g/kg in infants less than 1 year old.
o GASTRIC LAVAGE: Consider after ingestion of a
potentially life-threatening amount of poison if it can
be performed soon after ingestion (generally within 1
hour). Protect airway by placement in Trendelenburg and
left lateral decubitus position or by endotracheal
intubation. Control any seizures first.
1. CONTRAINDICATIONS: Loss of airway protective reflexes
or decreased level of consciousness in unintubated
patients; following ingestion of corrosives;
hydrocarbons (high aspiration potential); patients at
risk of hemorrhage or gastrointestinal perforation; and
trivial or non-toxic ingestion.
o SEIZURES: Administer a benzodiazepine IV; DIAZEPAM
(ADULT: 5 to 10 mg, repeat every 10 to 15 min as
needed. CHILD: 0.2 to 0.5 mg/kg, repeat every 5 min
as needed) or LORAZEPAM (ADULT: 2 to 4 mg; CHILD: 0.05
to 0.1 mg/kg).
1. Consider phenobarbital if seizures recur after diazepam
30 mg (adults) or 10 mg (children > 5 years).
2. Monitor for hypotension, dysrhythmias, respiratory
depression, and need for endotracheal intubation.
Evaluate for hypoglycemia, electrolyte disturbances,
hypoxia.
o ACUTE LUNG INJURY: Maintain ventilation and oxygenation
and evaluate with frequent arterial blood gas or pulse
oximetry monitoring. Early use of PEEP and mechanical
ventilation may be needed.
o Monitor arterial blood gases, electrolytes, acid-base
status, CBC (especially increased MCV), and renal
function tests. Monitor blood levels of methanol,
ethanol, concomitant ingestants, and formate if
available.
o ACIDOSIS - May not develop until 18 to 48 hours
post-ingestion. Temporize with IV sodium bicarbonate;
monitor arterial blood gases to guide dosing. Patients
with metabolic acidosis need antidotal therapy (ethanol
or fomepizole) and hemodialysis.
o ETHANOL THERAPY - partially inhibits the formation of
toxic metabolites. LOADING DOSE - 10 mL/kg of 10
percent ethanol in D5W IV over 30 minutes. MAINTENANCE
DOSE - 1 to 2 mL/kg/hr of 10 percent ETHANOL in D5W by
IV infusion. Maintain blood ethanol levels at 100 to
130 mg/dL. Monitor blood glucose and blood ethanol
levels. INDICATIONS: metabolic acidosis or blood
methanol level greater than 20 mg/dL.
o FOMEPIZOLE - specific alcohol dehydrogenase antagonist.
FDA approved for methanol poisoning in the USA; LOADING
DOSE - 15 mg/kg IV over 30 minutes. INDICATIONS - for
methanol poisoning or suspected methanol ingestion,
either alone or in combination with hemodialysis.
o HEMODIALYSIS - Maintenance ethanol dose must be
increased during dialysis. Fomepizole dosing should be
increased to every 4 hr during hemodialysis.
INDICATIONS - 1) blood methanol level greater than 50
mg/dL (15 mmol/L); 2) severe acid-base and/or
fluid-electrolyte abnormalities despite conventional
therapy; 3) renal failure.
o LEUCOVORIN/FOLIC ACID - If symptomatic - IV leucovorin 1
mg/kg once (up to 50 mg/dose) followed by IV folic acid
1 mg/kg (up to 50 mg/dose) every 4 hours for 6 doses.
o Prognosis should be based upon the clinical
presentation, severity of acidosis, blood methanol and
formate levels (if available), and response to
treatment.
INHALATION EXPOSURE
o 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
beta2 agonist and corticosteroid aerosols.
o Treatment should include recommendations listed in the
ORAL EXPOSURE section when appropriate.
EYE EXPOSURE
o DECONTAMINATION: Irrigate exposed eyes with copious
amounts of tepid water for at least 15 minutes. If
irritation, pain, swelling, lacrimation, or photophobia
persist, the patient should be seen in a health care
facility.
DERMAL EXPOSURE
o 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: |
o Serious toxicity may occur from ingestion of 0.25 mL/kg of
100 percent methanol. Fatalities might occur from
ingestion of 0.5 mL/kg of 100 percent methanol. Mortality
is related to the time interval between exposure and the
institution of specific therapy. |
Antidote and Emergency Treatment:
EXPTL USE: IN RABBITS, PYRAZOLE ONLY MARGINALLY PROTECTED AGAINST METHANOL TOXICITY.
Animal Toxicity Studies:
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.
Non-Human Toxicity Excerpts:
ITS CONSUMPTION LEADS TO ATROPHY OF THE OPTIC NERVE, CAUSING PERMANENT
BLINDNESS, AND TO DEPRESSION OF CARDIAC AND VOLUNTARY MUSCLE, RESULTING IN
DEATH.
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
TEMP, LOSS IN WT & DEATH.
... THERE MAY BE IRREVERSIBLE BRAIN DAMAGE.
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.
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 ... .
... NOTED IN BLOOD OF ANIMALS INHALING METHYL ALCOHOL
AN INCREASE IN ERYTHROCYTES, HEMOGLOBIN & POLYMORPHONUCLEAR
LEUCOCYTES.
WITHIN 48 HR OF ADMIN SINGLE LD50 DOSE TO RATS, BRAIN ENZYME ACTIVITIES
UNDERWENT CHANGES, GLYCOGEN LEVELS INCR, BRAIN LACTIC ACID LEVELS INCR 1 HR
AFTER ADMIN, DECR 48 HR AFTER.
METHANOL BLOOD LEVELS IN CHRONICALLY
FED RABBITS INCR WITH TIME. CUMULATIVE LEVELS ALSO SEEN IN ACUTE STUDIES. BRAIN
EDEMA, EYE EDEMA, & MYELIN THINNING OR LOSS WERE OBSERVED IN ACUTE &
CHRONIC STUDIES.
AFTER METHANOL ADMIN, MACACA MULATTA
SHOWED OPTIC EDEMA, ACIDOSIS, & FORMATE ACCUMULATION IN BLOOD.
@ 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; @ EMERGENCE, LIMB DEFECTS OR HEMORRHAGES
WERE OBSERVED. 250 MG/L CAUSE MORPHOLOGICAL CHANGES IN LARVAL DEVELOPMENT.
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.
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
concn being 32% of the controls. A significant change in luteinizing hormone
concn 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.
Rats /were exposed/ during their entire gestation for 7 hr daily to 5000,
10,000, and 20,000 ppm. Significant increases in fetal defects occurred at the
highest level. The defects involved the skeletal, cardiac, and urinary system.
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 immediated danger in monkeys was below the minimum lethal dose.
A negative consensus resulted from all sister chromatid exchange tests when
no exogenous metabolic activation system was used.
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.
A negative consensus resulted from all Neurospera crassa tests when no
exogenous metabolic activation system was used.
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, alkalinity= 46.6
calcium carbonate, tank volume= 6.3 l, additions= 5.71 V/D, pH= 7.66 (0.03).
/Conditions of bioassay not specified/
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
METHANOL (LABELED WITH (14)C) IS
SLOWLY METABOLIZED BY RAT & IN 2 DAYS IS EXCRETED AS CARBON DIOXIDE (65% OF
DOSE), & UNCHANGED METHANOL (14%) IN
EXPIRED AIR, & AS FORMATE (3%) & METHANOL (3%) IN URINE.
... 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 AMT OF METHYLGLUCURONIDE.
OXIDN OF METHANOL APPEARS TO OCCUR BY
COUPLED PEROXIDATIVE REACTIONS CATALYZED BY HEPATIC CATALASE, & IN RATS
OCCURS @ A MUCH SLOWER RATE (25 MG/KG/HR) THAN OXIDN OF ETHANOL (175 MG/KG/HR).
METHYL ALCOHOL IS OXIDIZED IN BODY TO
FORMALDEHYDE & FORMIC ACID. ... OXIDATION ... PROCEEDS INDEPENDENTLY OF
CONCN IN BLOOD. RATE ... IS ONLY ONE SEVENTH THAT OF ETHANOL, SO THAT COMPLETE
OXIDATION & EXCRETION OF METHYL ALCOHOL
USUALLY REQUIRE SEVERAL DAYS. OXIDATION OCCURS MAINLY IN LIVER
& KIDNEY. ... EXPT WITH ISOLATED RAT-LIVER SLICES ... EMPHASIZED ... LIVER
CATALASE IN OXIDIZING METHANOL ... IN
MONKEY & IN MAN ALCOHOL DEHYDROGENASE IS INVOLVED IN FIRST STEP OF OXIDN.
SEVERAL PRIMARY ALCOHOLS ... YIELD MODERATE AMT OF MONOSULFATE ESTERS. THIS
PATHWAY HAS BEEN DETECTED FOR METHANOL
... IN RATS.
... Asparatame is broken down in the small intestine into three moieties,
aspartic acid, methanol, and
phenylalanine. Acute loading studies have been performed in human beings, ...
who received up to 200 mg/kg. No evidence of risk to the fetus was detected.
Small elevations of blood methanol
following such abuse doses of asparatame did not lead to measureable increases
in blood formic acid ... the product responsible for acidosis and ocular
toxicity.
Absorption, Distribution & Excretion:
METHYL ALCOHOL IS READILY ABSORBED
FROM GI & RESPIRATORY TRACTS.
DISTRIBUTION OF METHYL ALCOHOL WITHIN
TISSUES OF DOGS EXPOSED TO 4000 & 15000 PPM IN AIR OVER PERIODS RANGING FROM
12 HR TO 5 DAYS WAS FOUND TO BE RAPID. ... HIGHEST CONCN WERE FOUND IN BLOOD,
EYE FLUID, BILE, & URINE, & LOWEST IN BONE MARROW & FATTY TISSUE.
... 1-7 MG OF METHYL ALCOHOL/G OF BLOOD
(100-700 MG/100 ML) WAS FOUND ... IN BLOOD OF RATS FOLLOWING ORAL ADMIN OF 4 G
OF METHYL ALCOHOL/KG OF BODY WEIGHT.
... UNDER ... EXPTL CONDITIONS IN MAN FOLLOWING INGESTION & 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 CONCN RATIO WAS ... CONSTANT @ ABOUT 1.3. ...
INHALATION OF ... 500-1000 PPM ... FOR ... 3-4 HR GAVE URINE CONCN OF ABOUT 1-3
MG/100 ML. ...
IN RABBIT ONLY 1% IS EXCRETED AS FORMIC ACID IN URINE, COMPARED WITH 20% IN
DOG; INTERMEDIATE VALUE IS OBTAINED IN MAN.
METHANOL SKIN ABSORPTION SHOWED INCR
RATE IN 1ST 35 MIN OF APPLICATION, FOLLOWED BY DECR @ 35-60 MIN. BIOLOGICAL
HALF-LIFE OF METHANOL ELIM IN EXPIRED
AIR IS 1.5 HR AFTER EITHER ORAL OR DERMAL APPLICATION.
70% OF METHYL ALCOHOL LOST BY ANIMALS
WAS ELIMINATED IN EXPIRED AIR.
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.
Biological Half-Life:
BIOLOGICAL HALF-LIFE OF METHANOL ELIM
IN EXPIRED AIR IS 1.5 HR AFTER EITHER ORAL OR DERMAL APPLICATION.
... 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. ...
Mechanism of Action:
... 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 oxide
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.
Current understanding of the metabolic mechanisms of methanol toxicity is 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 metabolic disposition of one carbon moieties.
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.
Interactions:
... PYRAZOLE & 3-AMINO-1,2,4-TRIAZOLE ... ARE POTENT INHIBITORS OF
ALCOHOL DEHYDROGENASE & CATALASE ... BOTH ARE ACTIVE IN VIVO. ... ADMIN
SEPARATELY OR TOGETHER ... /TO RATS/. FINDINGS CONFIRMED ... THAT
3-AMINO-1,2,4-TRIAZOLE ... DECR RATE OF CARBON DIOXIDE PRODUCTION. ... PYRAZOLE
... SUBSTANTIALLY REDUCED OXIDN OF METHANOL TO CARBON DIOXIDE.
COMMON BIOCHEMICAL PATHWAY OF OXIDATION OF /ETHANOL & METHANOL/ ACCOUNTS, ALSO FOR CLINICAL
OBSERVATION THAT SIMULTANEOUS ADMIN OF ETHANOL MAY AMELIORATE TOXIC SEQUELAE OF
METHANOL POISONING. ... PRODUCTS OF
OXIDN OF METHANOL ARE TOXIC ...
THEREFORE ... POISONING IS MINIMIZED IF RATE OF OXIDN OF METHANOL IS REDUCED.
Chronic combined exposure to methanol
and carbon monoxide has been reported as a causative factor of cerebral
atherosclerosis.
Pharmacology:
Interactions:
... PYRAZOLE & 3-AMINO-1,2,4-TRIAZOLE ... ARE POTENT INHIBITORS OF
ALCOHOL DEHYDROGENASE & CATALASE ... BOTH ARE ACTIVE IN VIVO. ... ADMIN
SEPARATELY OR TOGETHER ... /TO RATS/. FINDINGS CONFIRMED ... THAT
3-AMINO-1,2,4-TRIAZOLE ... DECR RATE OF CARBON DIOXIDE PRODUCTION. ... PYRAZOLE
... SUBSTANTIALLY REDUCED OXIDN OF METHANOL TO CARBON DIOXIDE.
COMMON BIOCHEMICAL PATHWAY OF OXIDATION OF /ETHANOL & METHANOL/ ACCOUNTS, ALSO FOR CLINICAL
OBSERVATION THAT SIMULTANEOUS ADMIN OF ETHANOL MAY AMELIORATE TOXIC SEQUELAE OF
METHANOL POISONING. ... PRODUCTS OF
OXIDN OF METHANOL ARE TOXIC ...
THEREFORE ... POISONING IS MINIMIZED IF RATE OF OXIDN OF METHANOL IS REDUCED.
Chronic combined exposure to methanol
and carbon monoxide has been reported as a causative factor of cerebral
atherosclerosis.
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 Fate & Exposure:
Environmental Fate/Exposure Summary:
Methanol has been identified as a
natural emission product from various plants and as a biological decomposition
product of biological wastes and sewage. The largest anthropogenic source of
methanol release to the environment is
evaporation from solvent uses (1.1 billion lb/yr). If released to the
atmosphere, methanol degrades via
reaction with photochemically produced hydroxyl radicals with an approximate
half-life of 17.8 days. Physical removal from air can occur via rainfall. If
released to water, decomposition via biodegradation is expected to occur. If
released to soil, methanol is expected
to degrade via biodegradation and be susceptible to significant leaching.
Relatively rapid evaporation from dry surfaces is likely to occur. Occupational
and general exposure occurs through inhalation and dermal contact. Exposure also
occurs through consumption of various foods and waters. (SRC)
Probable Routes of Human Exposure:
... eye contact
The general population is exposed to methanol through inhalation of air, through
consumption of various drinking waters and foods, and through dermal contact of
various consumer products such as paint thinners and strippers, adhesives,
cleaners, and inks. Widespread occupational exposure occurs through inhalation
and dermal contact. (SRC)
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. ...
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.
2,062,431 Workers are potentially exposed to methanol based on statistical estimates
derived from the NIOSH Survey conducted between 1972-74 in the USA(1). In a
survey conducted between 1978-1982 of solvent products used in industrial
workplaces and having worker exposure, methanol was identified in 9.8% of the 275
solvent samples collected by factory inspectors(2); the products represented
solvent classes such as thinners, degreasers, paints, inks, and adhesives(2).
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).
Average Daily Intake:
AIR INTAKE: assume 1.0-25.0 ppb (0.76-19 ug/cu m)(1): 15.2-380 ug(2); WATER
INTAKE: insufficient data; FOOD INTAKE: insufficient data.
Natural Pollution Sources:
Methanol is found in wood.
A small amount of methanol is found
in the expired breath of normal subjects, possibly by endogenous metabolic
production.
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).
Some distilled fruit spirits contain, normally, high quantities of methanol. ...
Artificial Pollution Sources:
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(1). Annual emission releases from methanol production, end-product mfg, and
storage/handling have been estimated to be 68, 49, and 12 million lb,
respectively(1). Methanol is emitted in
exhaust from gasoline and diesel engines(2). Other artificial sources include
combustion of biomass, refuse and plastics; manufacture of petroleum, charcoal,
plastics, and starch; rendering; and wood pulping(3).
Air pollution from gasoline blended with methanol.
Environmental Fate:
TERRESTRIAL FATE: Methanol is
expected to be biodegradable in soil based on the results of a large number of
biological screening studies, which include soil microcosm studies. Its
miscibility in water and log Kow (-0.77) suggest high mobility in soil. Based on
a vapor pressure of 92 mm Hg at 20 deg C(1), evaporation from dry surfaces can
be expected to occur(SRC).
AQUATIC FATE: The important environmental fate process for methanol in water is biodegradation. A large
number of screening studies have found methanol to be significantly biodegradable.
Volatilization half-lifes of 4.8 days and 51.7 days have been estimated for a
model river (1 m deep) and an environmental pond, respectively. Aquatic
hydrolysis, oxidation, photolysis, adsorption to sediment, and bioconcentration
are not significant. (SRC)
ATMOSPHERIC FATE: Methanol is
expected to exist almost entirely in the vapor-phase in the ambient atmosphere,
based on a vapor pressure of 92 mm Hg at 20 deg C(1,2,SRC). It is degraded by
reaction with photochemically produced hydroxyl radicals with an estimated
half-life of 17.8 days in a typical ambient atmosphere. Atmospheric methanol can also react with nitrogen dioxide
in polluted air to yield methyl nitrite. Because of methanol's water solubility, rain would be
expected to physically remove some from the air(3); the detection of methanol in a thunderstorm water tends to
confirm this supposition(SRC).
Environmental Biodegradation:
Biological oxygen demand: 0.6 to 1.12 lb/lb in 5 days
Standard dilution BOD water, 5-day 48% BOD Theoretical, sewage inocula(1).
Warburg respirometer, 2-day 93% BOD Theoretical, activated sludge inocula(2).
Warburg respirometer, 1-day 21% BOD Theoretical, activated sludge inocula(3).
Standard dilution BOD water, 5-day 53.4% BOD Theoretical, 50-day 97.7% BOD
Theoretical, sewage inocula(4). Warburg respirometer, 0.96-day 55% BOD
Theoretical, activated sludge inocula acclimated to methanol(5). Standard dilution BOD water,
5-day 76% BOD Theoretical, 20-day 97% BOD Theoretical, sewage inocula(6).
Respirometric dilution, 5-day 82.9% BOD Theoretical, sewage inocula(7). Sewage
die-away, 0.4 day half-life, sewage inocula(8). Anaerobic-water, 75-80%
degradation, sewage inocula(9). Biological treatment simulation, 80%
degradation, adapted activated sludge(10).
Anaerobic-water die-away, marinewater and sediment from the San Francisco Bay
inocula, 3-day incubation, 83-91% degradation(1). Standard dilution, 5-day 88.7%
BOD Theoretical; seawater dilution, 5-day 70.7% BOD Theoretical(2). Significant
biodegradation of organic waste (methanol and acetic acid and formic acid)
observed when injected into wells (850-1000 ft depth) as determined by concn
monitoring and microbial population count(3). Methanol found to be susceptible to
biodegradation in subsurface regions in microcosm studies simulating subsurface
conditions; complete degradation within one year or less(4). Methanol degraded readily in test tube
microcosms simulating subsurface soils and groundwaters from sites in VA and
NY(5). Soil-sediment suspensions, aerobic conditions, 5-day CO2 evolution (14-C)
of 53.4%(6); soil-sediment suspensions, anaerobic conditions, 5-day CO2
evolution (14-C) of 46.3%(6).
Environmental Abiotic Degradation:
The experimentally recommended rate constant for the vapor-phase reaction of
methanol with photochemically produced
hydroxyl radicals has been reported to be 0.9X10-12 cu cm/molecule-sec at 25 deg
C(1); the atmospheric half-life for this reaction can be estimated to be 17.8
days, assuming an average atmospheric hydroxyl radical concn of 5X10+5
molecules/cu cm(1,SRC). Formaldehyde is formed from the reaction of methanol with hydroxyl radicals in the
atmosphere(1). The reaction of methanol
with nitrogen dioxide may be the major source of methyl nitrite found in
polluted atmospheres(2).
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).
Environmental Bioconcentration:
The biconcentration factor of methanol experimentally measured in fish
(golden ide) was less than 10(1). Based on a log Kow of -0.77(2), the BCF value
for methanol can be estimated to be 0.2
from a recommended regression-derived equation(3,SRC).
Soil Adsorption/Mobility:
Methanol is completely miscible in
water and has a log Kow of -0.77(1,2). These properties are indicative of high
mobility in soil(SRC).
Volatilization from Water/Soil:
Methanol has an y measured Henry's
Law Constant of 4.4X10-6 atm-cu m/mole at 25 ). This value of Henry's Law
Constant indicates that volatilization from environmental waters may be
significant(2). The volatilization half-life from a iver (1 meter deep flowing 1
m/sec with a wind speed of 3 m/sec) has been be 4.8 days(2,SRC). The
volatilization half-life from model pond has been estimated to be 51.7
days(3,SRC).
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).
RAIN WATER: Methanol was detected at
a mean level of 22 ppb in thunderstorm water collected from Santa Rita, AZ in
Sept, 1982(1).
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).
Atmospheric Concentrations:
Methanol was detected at mean ambient
atmospheric concn 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). Avg ambient concn of
3.83-26.7 ppb detected at 5 sites in and around Stockholm, Sweden(3). Methanol has been detected (concn not
reported) in indoor air of residential and office buildings(4,5).
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(1,2,3).
Plant Concentrations:
Methanol has been identified as a
volatile emission product from evergreen cypress trees(1) and alfalfa(2).
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).
Environmental Standards & Regulations:
FIFRA Requirements:
Unless designated as an active ingredient in accordance with paragraph (b) or
(c) of this section, this substance, when used in antimicrobial products, is
considered inert, having no independent pesticidal activity. The percentage of
such an ingredient shall be included on the label in the total percentage of
inert ingredients.
Methyl alcohol is exempted from the
requirement of a tolerance when used in accordance with good agricultural
practice as inert (or occasionally active) ingredients in pesticide formulations
applied to growing crops only.
Methyl alcohol is exempted from the
requirement of a tolerance when used in accordance with good agricultural
practice as inert (or occasionally active) ingredients in pesticide formulations
applied to animals.
Residues of methyl alcohol are
exempted from the requirement of a tolerance when used 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.
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 telephone number of the
NRC is (800) 424-8802; in the Washington metropolitan area (202) 426-2675. The
rule for determining when notification is required is stated in 40 CFR 302.6.
RCRA Requirements:
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).
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.
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 final product, by process units covered under this subpart.
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.
State Drinking Water Guidelines:
(FL) FLORIDA 5,000 ug/l
(MN) MINNESOTA 3000 ug/l
(WI) WISCONSIN 5000 ug/l
FDA Requirements:
Methyl alcohol is an indirect food
additive for use only as a component of adhesives.
Chemical/Physical Properties:
Molecular Formula:
C-H4-O
Molecular Weight:
32.04
Color/Form:
Colorless liquid
Odor:
ALCOHOLIC ODOR; PUNGENT ODOR WHEN CRUDE
Characteristic pungent odor.
Boiling Point:
64.7 DEG C @ 760 MM HG
Melting Point:
-97.8 DEG C
Critical Temperature & Pressure:
CRITICAL TEMP: 240.0 DEG C; CRITICAL PRESSURE: 78.5 ATM
Density/Specific Gravity:
0.8100 @ 0 DEG C/4 DEG C
Dissociation Constants:
pKa = 15.3
Heat of Combustion:
723 KJ/mole
Heat of Vaporization:
39.2 KJ/mole
Octanol/Water Partition Coefficient:
log Kow= -0.77
Solubilities:
MISCIBLE WITH ETHANOL, ETHER, BENZENE, MOST ORGANIC SOLVENTS AND KETONES.
Sol in acetone, chloroform
Completely miscible in water @ 20 deg C
Water solubility = miscible
Spectral Properties:
INDEX OF REFRACTION: 1.3292 @ 20 DEG C/D
MAX ABSORPTION (GAS): 183.3 NM (LOG E= 2.18)
IR: 287 (Sadtler Research Laboratories IR Grating Collection)
UV: 1-3 (Organic Electronic Spectral Data, Phillips et al, John Wiley &
Sons, New York)
NMR: 1 (Varian Associates NMR Spectra Catalogue)
MASS: 6 (Atlas of Mass Spectral Data, John Wiley & Sons, New York)
Surface Tension:
22.61 mN/m (at 20 deg C)
Vapor Density:
1.11
Vapor Pressure:
127 mm Hg at 25 deg C
Viscosity:
0.614 mPa sec
Other Chemical/Physical Properties:
DIPOLE MOMENT: 1.69; SPECIFIC HEAT: 0.595-0.605 AT 20-25 DEG C, FORMS
AZEOTROPES WITH MANY CMPD; BURNS WITH NONLUMINOUS BLUISH FLAME ...
1 MG/L= 764 PPM; 1 PPM= 1.31 MG/CU M @ 25 DEG C, 760 MM HG
Heat of fusion: 23.70 cal/g
Partition coefficients at 37 deg C for methanol into blood= 2,100; into oil= 56.
VAPOR PRESSURE= 100 MM HG @ 21.2 DEG C
Henry's Law constant = 4.55X10-6 atm-cu m/mol at 25 deg C
Chemical Safety & Handling:
DOT Emergency Guidelines:
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.
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.
Public safety: Call Emergency Response Telephone Number. ... Isolate spill or
leak area immediately for at least 100 to 200 meters (330 to 660 feet) in all
directions. Keep unauthorized personnel away. Stay upwind. Keep out of low
areas. Ventilate closed spaces before entering.
Protective clothing: Wear positive pressure self-contained breathing
apparatus (SCBA). Wear chemical protective clothing which 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.
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.
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 let fire burn.
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.
First aid: Move victim to fresh air. Call 911 or emergency medical service.
Apply artificial respiration if victim is not breathing. Do not use
mouth-to-mouth method if victim ingested or inhaled the substance; induce
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.
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.
Odor Threshold:
METHYL ALCOHOL DOES NOT HAVE SUITABLE
WARNING ODOR ... PROPERTIES EXCEPT @ HIGH CONCN. ... A LEVEL OF 2,000 PPM ... IS
BARELY DETECTABLE BY ODOR.
Low threshold= 13.1150 mg/cu m; High threshold= 26840 mg/cu m; Irritating
concn= 22875 mg/cu m.
Skin, Eye and Respiratory Irritations:
/Methanol/ is a skin and eye
irritant.
Fire Potential:
DANGEROUS, WHEN EXPOSED TO HEAT OR FLAME
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.
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.
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.
Flammable Limits:
Lower limits is 6.0%; Upper limits is 36%
Flash Point:
12 DEG C (CLOSED CUP)
Autoignition Temperature:
464 DEG F (464 DEG C)
Explosive Limits & Potential:
LOWER 7.3 VOL%; UPPER 36 VOL%
MODERATE, WHEN EXPOSED TO FLAME
Hazardous Reactivities & Incompatibilities:
CAN REACT VIGOROUSLY WITH OXIDIZING MATERIALS.
Strong oxidizers.
Immediately Dangerous to Life or Health:
6000 ppm
Protective Equipment & Clothing:
Wear appropriate chemical protective gloves, boots, and goggles.
There is some data suggesting that the breakthrough times of methanol through natural rubber are
approximately an hour or more.
Breakthrough times of methanol
through nitrile or Viton are greater than one hour reported by (normally) two or
more testers.
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.
Recommendations for respirator selection. Max concn for use: 2000 ppm.
Respirator Class(es): Any supplied-air respirator.