METHANOL
http://www.purificationtech.com/techmtmsds.htm
Potential Health Effects:
Eye: May cause mild eye irritation. Symptoms include stinging, tearing and redness.
Skin: May cause mild skin irritation. Prolonged or repeated contact may dry the skin. Symptoms may include redness, burning, drying and cracking of skin, and skin burns. Passage of this material into the body through the skin is possible, and may add to toxic effects from breathing or swallowing.
Swallowing: Swallowing this material may be harmful. Inhalation: Breathing of vapor or mist is possible. Breathing small amounts of this material during normal handling is not likely to cause harmful effects. Breathing large amounts may be harmful. Symptoms usually occur at air concentrations higher than the recommended exposure limits.....
Symptoms of Exposure: Signs and symptoms of exposure to this material through breathing, swallowing, and/or passage of the material through the skin may include: stomach or intestinal upset (nausea, vomiting, diarrhea), irritation (nose, throat, airways), central nervous system depression (dizziness, drowsiness, weakness, fatigue, nausea, headache, unconsciousness), leg cramps, pain in the abdomen and lower back, blurred vision, shortness of breath, cyanosis (causes blue coloring of the skin and nails from lack of oxygen), visual impairment (including blindness), coma, and death.
http://www.epa.gov/opptintr/chemfact/s_methan.txt
HUMAN HEALTH EFFECTS
Pharmacokinetics
Absorption - Methanol is readily absorbed after oral, inhalation, or dermal exposure. Oral doses in humans of 71 to 84 mg/kg resulted in blood levels of 4.7 to 7.6 mg/100 mL of blood within 3 hours (Rowe and McCollister 1981). Inhalation of 500 to 1000 ppm methanol for 3 to 4 hours gave urine concentrations of 1 to 3 mg methanol/100 mL of urine at the end of exposure (Rowe and McCollister 1981). Based on urinary methanol levels, the rate of absorption of the chemical appears to be proportional to the concentration of vapor inhaled (HSDB 1994). The rate of dermal absorption increased for 35 minutes then decreased over the next 25 minutes (no other details given) (HSDB 1994).
Distribution - Methanol distributes rapidly in dogs exposed to 4000 to 15,000 ppm for 12 hours to 5 days; the highest concentrations of the chemical were found in blood, eye fluid, bile, and urine (HSDB 1994).
Metabolism - Methanol is oxidized in the human liver by the enzyme alcohol dehydrogenase (Rowe and McCollister 1981). Metabolic products include formaldehyde and formic acid (HSDB 1994). The rate of metabolism for methanol (25 mg/kg/hr) is much slower than for ethanol (175 mg/kg/hr) and is independent of concen- trations in the blood (HSDB 1994). Formic acid is responsible for the toxic effects of methanol (ACGIH 1991).
Excretion - Methanol is excreted either as parent compound in the urine or expired air, or as the formic acid metabolite in urine (Rowe and McCollister 1981; HSDB 1994). The amount of formic acid excreted varies greatly with species from 1% in rabbits to 20% in dogs; humans are intermediate (HSDB 1994). In humans, the half-life of methanol elimination in expired air after oral or dermal exposure is 1.5 hours (HSDB 1994).
Acute Toxicity
Acute methanol intoxication is manifested initially by signs of narcosis. This is followed by a latent period in which formic acid accumulates in the body causing metabolic acidosis. Severe abdominal, leg, and back pain occur and visual degeneration can lead to blindness.
Humans - Ingestion of 80 to 150 mL of methanol is usually fatal to humans (HSDB 1994). One worker died from exposure to vapor ranging from 4000 to 13,000 ppm over 12 hours (ACGIH 1991). The concentration of 4000 ppm is roughly equivalent to a total of 1140 mg/kg over the 12 hour period (see end note 2). Poisoning by nonlethal doses can be described in three stages: (1) narcotic stage similar to ethanol; (2) latent period of 10-15 hours; (3) visual disturbances and central nervous system lesions (Rowe and McCollister 1981). Visual disturbances can lead to blindness due to edema of the retina and atrophy of the optic nerve head (HSDB 1994). Third-stage CNS lesions include headache, dizziness, abdominal, back, and leg pain, delirium that can lead to coma, and nausea (HSDB 1994). Formic acid production causes severe metabolic acidosis (Rowe and McCollister 1981).
Animals - Oral LD50 values for methanol in animals are 0.4 g/kg in the mouse, 6.2 to 13 g/kg in the rat, 14.4 g/kg in the rabbit, and 2 to 7 g/kg in the monkey (Rowe and McCollister 1981). The LD50 for dermal application to rabbits is 20 mL/kg (approximately 16 g/kg) (Rowe and McCollister 1981). Dose-response data for inhalation vary with species, dose, and duration (8800 ppm for 8 hours to 152,800 ppm for 94 minutes). Symptoms of intoxication include incoordination, salivation, lethargy, narcosis, and death (Rowe and McCollister 1981).
Subchronic/Chronic Toxicity
Chronic exposure to methanol, either orally or by inhalation, causes headache, insomnia, gastrointestinal problems, and blindness in humans and hepatic and brain alterations in animals. EPA has derived an oral RfD (reference dose) (see end note 3) for methanol of 0.5 mg/kg/day, based on the absence of liver and brain effects in animals exposed by mouth to 500 mg/kg/day.
Humans - "Chronic" exposure to methanol vapors (no time or dose given) caused conjunctivitis, headache, giddiness, insomnia, gastric disturbances, and bilateral blindness (ACGIH 1991). Marked vision loss occurred in one worker exposed to 1200 to 8000 ppm vapor for 4 years (ACGIH 1991).
Animals - No effects were seen in rats given 1% (approximately 140 mg/kg/day) methanol in drinking water for 6 months (Rowe and McCollister 1981). Hepatic abnormalities (proteinic degeneration, altered RNA metabolism) occurred in rhesus monkeys given 3 to 6 g/kg for 3 to 20 weeks and in rats given 10, 100, or 500 mg/kg/day for one month (Rowe and McCollister 1981). Rabbits chronically fed methanol (no dose or time given) had increasing blood levels, brain and eye edema, and myelin thinning (HSDB 1994). Male and female rats were gavaged with 100, 500, or 2500 mg/kg/day for 90 days (U.S. EPA 1994). Increased levels of SGPT and SAP as well as decreased brain weights were seen in both sexes at the highest dose; a no- observed-adverse effect level (NOAEL) for the study was 500 mg/kg/day. Based on these data, the U.S. EPA (1994) calculated a chronic RfD (see end note 4) for methanol of 0.5 mg/kg/day. No toxic effects were seen in dogs exposed by inhalation to either 10,000 ppm for 3 minutes, 3x/day, for 100 days or to 450 or 500 ppm, 8 hours/day for 379 days (Rowe and McCollister 1981). Ultrastructural changes were observed in the photoreceptor cells of rabbits exposed to 46.6 ppm for 6 months (Rowe and McCollister 1981). Rowe and McCollister (1981) concluded that the effects of combined oral and inhalation exposure appear to be additive. Rats exposed by inhalation to 16.8 ppm, 4 hours/day, for 6 months and administered 0.7 mg/kg/day orally had changes in blood morphology, oxidation-reduction processes, and liver function (Rowe and McCollister 1981).
Animals - Rats were exposed by inhalation, 7 hours/day, to 5000 or 10,000 ppm methanol on gestation days 1-19 or to 20,000 ppm on days 7-15. Maternal intoxication (unsteadiness) occurred at the highest dose and coincided with extra or rudimentary ribs and urinary or cardiovascular defects in the fetuses (ACGIH 1991). Male rats had significantly lowered testosterone levels after inhalation exposure to 200 ppm methanol for 6 weeks; at 10,000 ppm a change in luteinizing hormone was also observed (HSDB 1994).
Neurotoxicity
Methanol causes central nervous system depression in humans and animals as well as degenerative changes in the brain and visual system.
Humans - Methanol causes narcosis similar to ethanol intoxication and nonlethal doses can lead to blindness. Autopsy of individuals after lethal doses revealed edema and hyperemia of the brain and degeneration of the ganglion cells of the retina (Rowe and McCollister 1981).
Animals - Acute methanol intoxication in animals causes CNS depression as observed by narcosis, incoordination, lethargy, drowsiness, and prostration (Rowe and McCollister 1981).
Toxicity to Aquatic Organisms
Methanol has low acute toxicity to aquatic organisms; lethal concentrations are much greater than 100 mg/L. Ninety-six hour LC50 values for fish are 28,100 mg/L for Pimephales promelas (fathead minnow), 20,100 mg/L for Oncorhynchus mykiss (rainbow trout), and >28,000 mg/L for Alburnus alburnus (bleak) (AQUIRE 1994). Forty-eight hour LC50 values for Cyprinus carpio (common carp) and Carassius auratus (goldfish) are 28,000 mg/L and 1,700 mg/L, respectively (AQUIRE 1994). Growth inhibition occurred for 4 strains of Anabaena (blue-green algae) over a range of EC50's of 2.57-3.13% for 10-14 days (AQUIRE 1994). The LC50 for Artemia salina (brine shrimp) is >10,000 mg/L in 24 hours and that for Culex restuans (mosquito) is 20,000 mg/L in 18 hours (AQUIRE 1994).
http://www.epa.gov/opptintr/chemfact/f_methan.txt
Methanol enters the body when breathed in with contaminated air or when consumed
with contaminated food or water. It can also be absorbed through skin contact.
It does not remain in the body due to its breakdown and removal in expired air
or urine.
Methanol evaporates when exposed to air. It dissolves completely when mixed with water. Most direct releases of methanol to the environment are to air. Methanol also evaporates from water and soil exposed to air. Once in air, it breaks down to other chemicals. Microorganisms that live in water and in soil can also break down methanol. Because it is a liquid that does not bind well to soil, methanol that makes its way into the ground can move through the ground and enter groundwater. Plants and animals are not likely to store methanol.
People have died as a result of drinking large amounts of methanol. Drinking smaller, non lethal amounts of methanol adversely affects the human nervous system. Effects range from headaches to incoordination similar to that associated with drunkenness. Delayed effects such as severe abdominal, leg, and back pain can follow the inebriation effects of methanol. Loss of vision and even blindness can also occur after exposure to amounts of methanol causing inebriation. These effects are not likely to occur at levels of methanol that are normally found in the environment. Human health effects associated with breathing or otherwise consuming smaller amounts of methanol over long periods of time are not known. Workers repeatedly exposed to methanol have experienced several adverse effects. Effects range from headaches to sleep disorders and gastrointestinal problems to optic nerve damage. Laboratory studies show that repeat exposure to large amounts of methanol in air or in drinking water cause similar adverse effects in animals.
http://www.healtheffects.org/Pubs/st74.htm
...inhaling low levels of methanol vapors could pose health risks for
potentially susceptible populations. Because of the known effects of ethanol on
developing fetuses, this population is one that is considered to be potentially
susceptible to the neurotoxic effects of methanol. In fact, some animal studies
have shown that exposure to high concentrations of methanol (5,000 to 20,000 ppm)
can have negative effects on fetal development. In order to evaluate the
possible risks of methanol exposure for developing fetuses...
http://ntp-server.niehs.nih.gov/htdocs/liason/
MethanolCERHRFR.html
There is a large toxicity database on reproductive and developmental effects of
methanol, including a recently completed study in primates.
http://www.embbs.com/cr/alc/alc6.html
Methanol is well absorbed from the gastrointestinal tract mucosa as well as
through the skin and lungs. Both inhalation and transdermal exposure can result
in toxicity. The exact lethal dose for a human is not known. Doses as low as 25
cc of 40% methanol have been reported as causing toxicity. In other cases doses
up to 500 cc have occurred with no side effects. Most sources consider the
minimal lethal dose to be around 100 cc (1 g/kg). Poisoning with methanol may be
accidental or intentional. There have been epidemics of methanol toxicity in
cases where illicit whiskey has been sold to large populations or when the less
expensive methanol was substituted for ethanol in drinks.
Clinical Presentation: The presentation within the first 1-2 hours may be similar to ethanol intoxication in that the patient may have drowsiness, vertigo, and uninhibited behavior. There is typically a delay of the toxic symptoms anywhere from six-30 hours and longer if ethanol has been co-ingested. In cases of methanol ingestion a lack of symptoms early on does not mean that the patient has not ingested a toxic amount of methanol.
Aside from the symptoms of intoxication patients may also present with gastrointestinal symptoms due to acute gastritis or pancreatitis. The gastritis may be severe and is occasionally hemorrhagic. Symptoms include anorexia, severe abdominal pain, vomiting, diarrhea, increased transaminases or increased amylase. Early visual disturbances are the classic findings that are associated with methanol intoxication and include decreased vision or blurred vision. Patients may complain of a 'snowstorm' in front of the eyes or photophobia. The pupils may be fixed and dilated with the funduscopic exam revealing retinal edema with hyperemia of the optic disc. In severe cases there may be papilledema and engorged retinal vessels. Other complications of severe methanol intoxication include coma, seizures, blindness, oliguric renal failure, cardiac failure, and pulmonary edema. Death may be rapid or may occur several hours after coma. Death is associated with inspiratory apnea, terminal opisthotonos and convulsions.
http://www.cec.org/takingstock/highlights/index.cfm?varlan
=english&report=7
Health effects from exposure to high concentrations of methanol, usually in
occupational settings or from accidental exposure, include visual disturbances,
permanent blindness, damage to the nervous system, nausea, vomiting, cardiac
depression, liver damage and eye, nose and mouth irritation.
http://www.nsc.org/library/chemical/methanol.htm
Methanol can cause permanent blindness when breathed, ingested, or passed
through the skin. Exposure to high concentrations can cause death. A coma
resulting from massive exposures may last as long as two to four days.
Because of the slowness with which it is eliminated by the human body, methanol should be regarded as a cumulative poison.
Exposure can damage the liver and cause headaches, cardiac depression, nausea, vomiting, blurred vision, dizziness, a feeling of intoxication, and irritations of the eyes, nose, mouth, and throat. Repeated or prolonged contact can cause dryness and cracking of the skin.
http://www.jtbaker.com/msds/m2015.htm
Potential Health Effects
Inhalation: A slight irritant to the mucous membranes. Toxic effects exerted upon nervous system, particularly the optic nerve. Once absorbed into the body, it is very slowly eliminated. Symptoms of overexposure may include headache, drowsiness, nausea, vomiting, blurred vision, blindness, coma, and death. A person may get better but then worse again up to 30 hours later.
Ingestion: Toxic. Symptoms parallel inhalation. Can intoxicate and cause blindness. Usual fatal dose: 100-125 milliliters.
Skin Contact: Methyl alcohol is a defatting agent and may cause skin to become dry and cracked. Skin absorption can occur; symptoms may parallel inhalation exposure.
Eye Contact: Irritant. Continued exposure may cause eye lesions.
Chronic Exposure: Marked impairment of vision has been reported. Repeated or prolonged exposure may cause skin irritation.
Aggravation of Pre-existing Conditions: Persons with pre-existing skin disorders or eye problems or impaired liver or kidney function may be more susceptible to the effects of the substance.
http://www.camd.lsu.edu/msds/m/methanol.htm#HealthInhalation: This substance is harmful and may be fatal. May cause headache, nausea, vomiting, dizziness, narcosis, respiratory failure, low blood pressure, central nervous system depression.
Skin: May cause irritation. Prolonged contact may cause dermatitis.Eye: May cause irritation and temporary corneal damage.
Ingestion: This material is harmful and may be fatal. May cause blindness, headache, nausea, vomiting, dizziness, gastrointestinal irritation, central nervous system depression, and hearing loss.
Medical conditions aggravated by exposure: eye disorders, skin disorders, liver and kidney disorders.
Primary routes of entry: inhalation, ingestion, eye contact, skin contact, absorption.
http://www.methanol.org/hse/
Health, Safety and the Environment
Special Reports, Speeches/Testimony, Press Releases, Technical Info
METHANOL
CASRN: 67-56-1
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~AAAC2aaaS:1
Human Health Effects:
Toxicity Summary:
Methanol occurs
naturally in humans, animals and plants. It is a natural constituent in blood,
urine, saliva and expired air. ... The two most important sources of background
body burdens for methanol and formate are diet and
metabolic processes. Methanol is available in the diet
principally from fresh fruits and vegetables, fruit juices ... fermented
beverages ... and diet foods (principally soft drinks). The artificial sweetner
aspartame is widely used and, on hydrolysis, 10% (by weight) of the molecule is
converted to free methanol, which is available for
absorption. ... Exposures to methanol can occur in
occupational settings through inhalation or dermal contact. ... Methanol
is readily absorbed by inhalation, ingestion and dermal exposure, and it is
rapidly distributed to tissues according to the distribution of body water. A
small amount of methanol is excreted unchanged by the
lungs and kidneys. ... Methanol is metabolized
primarily in the liver by sequential oxidative steps to formaldehyde, formic
acid and carbon dioxide. The initial step involves oxidation to formaldehyde by
hepatic alcohol dehydrogenase ... In step 2, formaldehyde is oxidized by
formaldehyde dehydrogenase to formic acid/or formate depending on the pH. In
step 3, formic acid is detoxified to carbon dioxide by folate-dependent
reactions. Elimination of methanol from the blood via
the urine and exhaled air and by metabolism appears to be slow in all species,
especially when compared to ethanol. ... It is the rate of metabolic
detoxification, or removal of formate that is vastly different between rodents
and primates and is the basis for the dramatic differences in methanol
toxicity observed between rodents and primates. The acute and short term
toxicity of methanol varies greatly between different
species, toxicity being highest in species with a relatively poor ability to
metabolize formate. In such cases of poor metabolism of formate, fatal methanol
poisoning occurs as a result of metabolic acidosis and neuronal toxicity,
whereas, in animals that readily metabolize formate, consequences of CNS
depression (coma, respiratory failure, etc.) are usually the cause of death.
Sensitive primate species (humans and monkeys) develop increased blood formate
concentrations following methanol exposure, while
resistant rodents, rabbits and dogs do not. Humans and non-human primates are
uniquely sensitive to the toxic effects of methanol.
Overall methanol has a low acute toxicity to
non-primate animals. ... In the rabbit, methanol is a
moderate irritant to the eye. It was not skin sensitizing ... There is no
evidence from animal studies to suggest that methanol
is a carcinogen ... The inhalation of methanol by
pregnant rodents throughout the period of embryogenesis induces a wide range of
concentration-dependent teratogenic and embryolethal effects. Treatment-related
malformations, primarily extra or rudimentary cervical ribs and urinary or
cardiovascular defects, were found in fetuses of rats ... Increased incidences
of exencephaly and cleft palate were found in the offspring of ... mice ...
There was increased embryo/fetal death ... and an increasing incidence of full
litter resorptions. Reduced fetal weight was observed ... Fetal malformations
... included neural and ocular defects, cleft palate, hydronephrosis and limb
anomalies. Humans (and non-human primates) are uniquely sensitive to methanol
poisoning and the toxic effects in these species are characterized by formic
acidemia, metabolic acidosis, ocular toxicity, nervous system depression,
blindness, coma and death. Nearly all of the available information on methanol
toxicity in humans relates to the consequences of acute rather than chronic
exposures. A vast majority of poisonings involving methanol
have occurred from drinking adulterated beverages and from methanol-containing
products. Although ingestion dominates as the most frequent route of poisoning,
inhalation of high concentrations of methanol vapor and
percutaneous absorption of methanolic liquids are as effective as the oral route
in producing acute toxic effects. The most noted health consequences of longer
term exposure to lower levels of methanol is a broad
range of ocular effects. ... The toxicity is manifest if formate generation
continues at a rate that exceeds its rate of metabolism. ... The minimum lethal
dose of methanol in the absence of medical treatment is
between 0.3 and 1 g/kg. The minimum dose causing permanent visual defects is
unknown. ... Wide interindividual variability of the toxic dose is a prominent
feature in acute methanol poisoning. Two important
determinants of human susceptibility to methanol
toxicity appear to be (1) concurrent ingestion of ethanol, which slows the
entrance of methanol into the metabolic pathway, and
(2) hepatic folate status, which governs the rate of formate detoxification. The
symptoms and signs of methanol poisoning, which may not
appear until after an asymptomatic period ... include visual disturbances,
nausea, abdominal and muscle pain, dizziness, weakness and disturbances of
consciousness ranging from coma to clonic seizures. Visual 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.
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).
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.
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)
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. Some may polymerize (P) 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 on Shipping Paper first. If Shipping Paper not available or no
answer, refer to appropriate telephone number listed on the inside back cover.
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 is
recommended for fire situations only; it is not effective in spill situations.
Evacuation: Spill: See the Table of Initial
Isolation and Protective Action Distances for highlighted substances. For
non-highlighted substances, increase, in the downwind direction, as necessary,
the isolation distance shown under "Public safety". 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. 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 the ends of
tanks. 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
emergency medical care. 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.
Recommendations for respirator selection. Max
concn for use: 5000 ppm. Respirator Class(es): Any supplied-air respirator
operated in a continuous flow mode.
Recommendations for respirator selection. Max
concn for use: 6000 ppm. Respirator Class(es): Any supplied-air respirator that
has a tight-fitting facepiece and is operated in a continuous-flow mode. Any
self-contained breathing apparatus with a full facepiece. Any supplied-air
respirator with a full facepiece.
Recommendations for respirator selection.
Condition: Emergency or planned entry into unknown concn or IDLH conditions:
Respirator Class(es): Any self-contained breathing apparatus that has a full
facepiece and is operated in a pressure-demand or other positive-pressure mode.
Any supplied-air respirator that has a full facepiece and is operated in a
pressure-demand or other positive-pressure mode in combination with an auxiliary
self-contained breathing apparatus operated in pressure-demand or other
positive-pressure mode.
Recommendations for respirator selection.
Condition: Escape from suddenly occurring respiratory hazards: Respirator
Class(es): Any appropriate escape-type, self-contained breathing apparatus.
Wear appropriate personal protective clothing
to prevent skin contact.
Wear appropriate eye protection to prevent eye
contact.
Preventive Measures:
Skin that becomes wet with liquid methyl
alcohol should be promptly washed or showered. Eating and smoking should
not be permitted in areas where liquid methyl alcohol is
handled, processed, or stored.
Contact lenses should not be worn when working
with this chemical.
SRP: The scientific literature for the use of
contact lenses in industry is conflicting. The benefit or detrimental effects of
wearing contact lenses depend not only upon the substance, but also on factors
including the form of the substance, characteristics and duration of the
exposure, the uses of other eye protection equipment, and the hygiene of the
lenses. However, there may be individual substances whose irritating or
corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn.
In any event, the usual eye protection equipment should be worn even when
contact lenses are in place.
If material not on fire and not involved in
fire: Keep sparks, flames, and other sources of ignition away. Keep material out
of water sources and sewers. Build dikes to contain flow as necessary. Attempt
to stop leak if without undue personnel hazard. Use water spray to disperse
vapors and dilute standing pools of liquid.
Before welding or cutting a vessel that has
contained methyl alcohol, the vessel should be emptied
and purged to remove every trace of the flammable liquid.
A major concern in the painting studio is
solvents, /including methanol/. ... Precautions include
... use of dilution and local exhaust ventilation, control of storage areas,
disposal of solvent soaked rags in covered containers, minimizing skin exposure,
and the use of respirators and other personal protective equipment. The control
of fire hazards is also important, since many of the solvents are highly
flammable.
Personnel protection: Avoid breathing vapors.
Keep upwind. Do not handle broken packages unless wearing appropriate personal
protective equipment. Wash away any material which may have contacted the body
with copious amounts of water or soap and water.
The worker should immediately wash the skin
when it becomes contaminated.
Work clothing that becomes wet should be
immediately removed due to its flammability hazard.
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a
hazardous material for transportation in commerce unless that person is
registered in conformance ... and the hazardous material is properly classed,
described, packaged, marked, labeled, and in condition for shipment as required
or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA)
Dangerous Goods Regulations are published by the IATA Dangerous Goods Board
pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry
carrier regulations to be followed by all IATA Member airlines when transporting
hazardous materials.
The International Maritime Dangerous Goods
Code lays down basic principles for transporting hazardous chemicals. Detailed
recommendations for individual substances and a number of recommendations for
good practice are included in the classes dealing with such substances. A
general index of technical names has also been compiled. This index should
always be consulted when attempting to locate the appropriate procedures to be
used when shipping any substance or article.
Cleanup Methods:
General Spill Actions: Stop or reduce
discharge of material if this can be done without risk. Eliminate all sources of
ignition. Avoid skin contact and inhalation. A fluorocarbon water foam can be
applied to the spill to diminish vapor and fire hazard. Hycar and carbopol,
which are absorbent materials, have shown possible applicability for vapor
suppression and/or containment of methanol in spill
situations. Leaking containers should be removed to the outdoors or to an
isolated, well-ventilated area and the contents transferred to other suitable
containers. The following materials are recommended for plugging leaks of methanol:
polyester (eg Glad bag), imid polyester (eg brown-in-bag), stafoam urethane
foam, sea-going epoxy putty, and MSA urethane.
Spills on Land: Contain if possible by forming
mechanical or chemical barriers to prevent spreading. Absorb on sand,
vermiculite or other absorbent and shovel into metal containers for disposal.
Application of universal gelling agent to immobilize the spill, or the use of
fly ash or cement powder to absorb the liquid bulk should also be considered.
Other recommended sorbent materials are activated carbon and a universal sorbent
material.
Spills in Water: After containment, a
universal gelling agent can be injected to solidify trapped mass to increase the
effectiveness of berms. Activated carbon can be applied at 10% the spilled
amount over region occupied by 10 mg/l or greater concentrations. Then use
mechanical dredges or lifts to remove immobilized masses of pollutants.
If the spilled material is known to be methanol:
Response personnel should be provided with and required to use impervious
clothing, gloves, face shields (eight-inch minimum), and other appropriate
protective clothing necessary to prevent repeated or prolonged skin contact with
liquid methyl alcohol. Splash-proof and chemical safety
goggles are recommended for eye protection. Polyvinyl plastic, neoprene or
rubber is recommended for protective clothing and gloves. Chemical suit
materials recommended for protection against methanol,
include butyl, neoprene and polyvinyl chloride.
Environmental considerations- Land spill: Dig
a pit, pond, lagoon, holding area to contain liquid or solid material. /SRP: If
time permits, pits, ponds, lagoons, soak holes, or holding areas should be
sealed with an impermeable flexible membrane liner./ Dike surface flow using
soil, sand bags, foamed polyurethane, or foamed concrete.
Environmental considerations- Water spill:
Allow to aerate. Use natural barriers or oil spill control booms to limit spill
travel. Remove trapped material with suction hoses.
Environmental considerations- Air spill: Apply
water spray or mist to knock down vapors.
Disposal Methods:
SRP: At the time of review, criteria for land
treatment or burial (sanitary landfill) disposal practices are subject to
significant revision. Prior to implementing land disposal of waste residue
(including waste sludge), consult with environmental regulatory agencies for
guidance on acceptable disposal practices.
Disposal: Waste methanol
must never be discharged directly into sewers or surface waters. Large
quantities of waste methanol can either be disposed of
at licensed waste solvent disposal company or reclaimed by filtration and
distillation. It can also be incinerated.
A good candidate for rotary kiln incineration
at a temperature range of 820 to 1,600 deg C and residence times of seconds for
liquids and gases, and hours for solids. A good candidate for liquid injection
incineration at a temperature range of 650 to 1,600 deg C and a residence time
of 0.1 to 2 seconds. A good candidate for fluidized bed incineration at a
temperature range of 450 to 980 deg C and residence times of seconds for liquids
and gases, and longer for solids.
The following wastewater treatment
technologies have been investigated for methanol
biological treatment, reverse osmosis, and activated carbon.
Spray into a furnace. Incineration will become
easier by mixing with a more flammable solvent. Recommendable methods:
Incineration, evaporation, & discharge to sewer. Peer-review: Evaporation
and discharge to sewer may be recommendable for small amt only. (Peer-review
conclusions of an IRPTC expert consultation (May 1985))
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr
Time Weighted Avg: 200 ppm (260 mg/cu m).
Vacated 1989 OSHA PEL TWA 200 ppm (260 mg/cu
m); STEL 250 ppm (325 mg/cu m), skin designation, is still enforced in some
states.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA) 200 ppm; Short
Term Exposure Limit (STEL) 250 ppm, skin
Notice of Intended Changes (1998): A4. A4= Not
classifiable as a human carcinogen.
Biological Exposure Index (BEI) adoption (1995
edition): Determinant: Methanol in urine; Sampling
Time: end of shift; BEI: 15 mg/L. The determinant is usually present in a
significant amt in biological specimens collected from subjects who have not
been occupationally exposed. Such background levels are incl in the BEI value.
The determinant is nonspecific, since it is observed after exposure to some
other chemicals. These nonspecific tests are preferred because they are easy to
use and usually offer a better correlation with exposure than specific tests. In
such instances, a BEI for a specific, less quantitative biological determinant
is recommended as a confirmatory test.
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr
Time-Weighted Avg: 200 ppm (260 mg/cu m).
Recommended Exposure Limit: 15 Min Short-Term
Exposure Limit: 250 ppm (325 mg/cu m)[skin].
Immediately Dangerous to Life or Health:
6000 ppm
Other Occupational Permissible Levels:
Emergency Response Planning Guidelines (ERPG):
ERPG(1) 200 ppm (no more than mild, transient effects) for up to 1 hr exposure;
ERPG(2) 1000 ppm (without serious, adverse effects) for up to 1 hr exposure;
ERPG(3) 5000 ppm (not life threatening) up to 1 hr exposure.
Manufacturing/Use Information:
Major Uses:
INDUSTRIAL SOLVENT; RAW MATERIAL FOR
FORMALDEHYDE, METHYL ESTERS, ORG & INORG ACIDS, ANTIFREEZE, FUEL; EXTRACTANT
FOR ANIMAL & VEGETABLE OILS; TO DENATURE ETHANOL; MFR PHARMACEUTICALS;
SOLVENT IN MFR OF STREPTOMYCIN, VITAMINS, HORMONES, POLYMERS, PLASTICS.
Used in dehydrating pipelines, as a de-icing
agent, and in the production of methylamines and chlorine dioxide.
PRIMARILY AS SUBSTITUTE SOLVENT &
RUBEFACIENT FOR ETHYL ALCOHOL IN LINIMENTS (EXTERNAL USE ONLY).
Used on household contents, mortuary
instruments, bedding (human), human clothing, tissues (biological specimens),
cadavers, and human stools against animal pathogenic bacteria (gram- and gram+
vegetative) and maggots. /Eureka Products, Criosine/
Used in oil recovery packer fluid against
slime forming bacteria, deterioration and spoilage bacteria, sulfate-reducing
bacteria. /Coat-B1400/
Used on onions during soil treatment against
onion smut (urocystis cepulae). /Wilbur-Ellis Smut-Guard/
Used on elms as injection treatment against
dutch elm disease. /Freers Elm Arrester/
Used in secondary oil recovery injection water
against slime forming bacteria. /Surflo-B17/
Used on timbers, wood fence posts, wood
poles/posts, timbers (heavy wooden members), and lumber (seasoned) for soil
contact nonfumigation treatment against wood rot and decay fungi. /Ideal
Concentrated Wood-Preservative/
... Duplicating fluid (99% methyl
alcohol) used in direct-process spirit duplicating machines
Effective solvent for the removal of
2,4-dinitrotoluene from spent carbons
Removal of toxic organic pollutants from soil
with supercritical carbon dioxide and methanol or
toluene.
Methods of Manufacturing:
A) WOOD PYROLYSIS, B) NON-CATALYTIC OXIDATION
OF HYDROCARBONS, C) AS A BY-PRODUCT IN THE FISHER-TROPSCH SYNTHESIS, AND D)
REDUCTION OF CARBON MONOXIDE
Several processes for making methanol by gasification
of wood, peat and lignite have been developed but have not yet proved out
commercially; From methane with molybdenum catalyst (experimental).
General Manufacturing Information:
METHANOL USUALLY IS
BETTER SOLVENT THAN ETHANOL, DISSOLVES MANY INORG SALTS ... SODIUM IODIDE 43%,
CALCIUM CHLORIDE 22%, AMMONIUM NITRATE 14%, COPPER SULFATE 13%, SILVER NITRATE
4%, AMMONIUM CHLORIDE 3.2%, SODIUM CHLORIDE 1.4%.
METHANOL IS PURIFIED BY DISTILLATION.
Formulations/Preparations:
Formaldehyde; intrastate fungicide; 37.0%
formaldehyde, 15.0% methyl alcohol.
Wilbur-Ellis Smut-Guard; fungicide; 37.0% formaldehyde, 12.0% methyl
alcohol.
Eureka Products, Criosine; intrastate disinfectant/bacteriocide/germicide; 47.6%
methyl alcohol, 0.86% nitrobenzene, 0.54% butyl
4-hydroxybenzoate, 30.0% phenol.
Surflo-B17; microbicide/microbisat general;
32.37% formaldehyde, 10.5% methyl alcohol, 10.0% alkyl
dimethyl benzyl ammonium chloride.
Coat-B1400; solution ready to use; 25.0% methyl
alcohol, 24.0% morpholine polyethoxyethanol.
Ideal Concentrated Wood Preservative;
fungicide; 15.0% isopropanol, 15.0% methyl alcohol, 10.0%
orthodichlorobenzene, 38.4% pentachlorophenol, 20.0% aliphatic petroleum
hydrocarbons.
Freer Elm Arrester; fungicide; 0.12% mecuric
chloride, 96.65% methyl alcohol.
Eureka Products Criosine Disinfectant;
disinfectant/bacteriocide/germicide; 47.6% methyl alcohol, 0.86%
nitrobenzene, 0.54% butyl 4-hydroxybenzoate, 30.0% phenol.
X-Cide 402 Industrial Bactericide;
bacteriostat; 11.5% isopropanol, 16.4% methyl alcohol, 28.5%
alkyl amino-3-aminopropane monoacetate, 17.8% oxydiethylenebis(alkyl) dimethyl
ammonium chloride.
Impurities:
GRADE A) ACETONE AND ALDEHYDES 30 PPM MAX;
ACETIC ACID 30 PPM MAX: WATER CONTENT 1500 PPM MAX; GRADE AA) ACETONE AND
ALDEHYES 30 PPM MAX; ACETONE 20 PPM MAX; ETHANOL 10 PPM MAX; ACETIC ACID 30 PPM
MAX; WATER CONTENT 100 PPM MAX.
Water, dimethyl ether, fusel oils, and higher alcohols.
Laboratory Methods:
A quantitative method for the determination of
methanol and formic acid in urine of workers was
described. One female and 13 male workers of mean age 41 years exposed to methanol
10 +/5 years, and five female and five male workers exposed to formic acid for 6
+/4 years participated in the study. ... Urinary samples were taken after the
shift on Thursdays and on Friday mornings. The time weighted average exposure to
methanol ranged from 58 to 277 ug/l. The highest
concentrations of urinary formic acid were measured in the samples taken on
Friday morning and ranged from 26 to 98 mg/g of creatinine. The output of
urinary formic acid 16 hours after exposure was found to be linearly
proportional to the methanol concentration in air. No
correlations were found between the methanol exposure
and the urinary formic acid or methanol concentrations
in samples taken immediately after the shift. The time weighted average exposure
to formic acid ranged form 4.1 to 11.3 ug/l. The corresponding levels of the
urinary formic acid in the Friday samples were 21.2 and 118 mg/g creatinine,
respectively. A linear correlation between the formic acid in the air and in the
urine 16 hours after the exposure was observed with the correlation coefficient
of 0.88. ... Urinary sampling for formic acid provides a reliable and simple
strategy for detection of occupational exposure to methanol
and formic acid at current levels found in industry.
A study was performed among 20 workers
employed in a printing office at 3 different work places (methanol
concentration of 85, 101 and 134 ppm) to determine whether the concentration of
formic acid in blood or urine and the methanol content
of alveolar air permit the estimation of methanol
exposure. Blood, urine and end expiratory air were collected at the beginning
and the end of the shift. For comparison formic acid concentrations were
determined in the morning and in the afternoon in blood and urine of 36 and 15
control persons, respectively. The concentration of formic acid in blood
increased significantly from 3.2:2.4 mg/l before to 7.9:3.2 mg/l after the shift
in the exposed workers (mean increase 4.7:3.8 mg/l). The corresponding
concentrations in urine were 13.1:5.3 mg/l. This difference is also significant.
In the control groups there was a small but significant decrease of formic acid
concentration in blood from 5.6:4.5 mg/l in the morning to 4.9:4.2 mg/l in the
afternoon. In urine, the formic acid concentrations in the morning (11.9:6.4
mg/l) and in the afternoon (11.7:5.6 mg/l) were not significantly different. The
increase of formic acid concentration in blood during the shift is the most
useful parameter for monitoring methanol-exposed
persons. Determinations of methanol concentrations in
the ambient air or in the exhaled air are only crude estimates.
NIOSH; Criteria Document: Methyl
Alcohol (1976) DHEW Pub. NIOSH 76-148
NIOSH; Canadian Centre for Occupational Health
and Safety: Chemical Hazard Summary No.24 1986. The chemical hazards, uses,
occurrences and toxicological properties of methanol
are discussed. ...
Synonyms and Identifiers:
Synonyms:
Coat-B1400
**PEER REVIEWED**
Surflo-B17
**PEER REVIEWED**
AI3-00409
**PEER REVIEWED**
Alcohol, methyl
**PEER REVIEWED**
ALCOOL METHYLIQUE (FRENCH)
**PEER REVIEWED**
ALCOOL METILICO (ITALIAN)
**PEER REVIEWED**
CARBINOL
**PEER REVIEWED**
Caswell no 552
**PEER REVIEWED**
X-Cide 402 Industrial Bactericide
**PEER REVIEWED**
COLONIAL SPIRITS
**PEER REVIEWED**
COLUMBIAN SPIRITS
**PEER REVIEWED**
Ideal Concentrated Wood Preservative
**PEER REVIEWED**
Wilbur-Ellis Smut-Guard
**PEER REVIEWED**
Freers Elm Arrester
**PEER REVIEWED**
EPA Pesticide Chemical Code 053801
**PEER REVIEWED**
METANOLO (ITALIAN)
**PEER REVIEWED**
Metanol (Spanish)
**PEER REVIEWED**
METHYL ALCOHOL
**PEER REVIEWED**
METHYLALKOHOL
(GERMAN)
**PEER REVIEWED**
METHYL HYDROXIDE
**PEER REVIEWED**
METHYLOL
**PEER REVIEWED**
METYLOWY ALKOHOL (POLISH)
**PEER REVIEWED**
MONOHYDROXYMETHANE
**PEER REVIEWED**
Eureka Products, Criosine
**PEER REVIEWED**
Eureka Products Criosine Disinfectant
**PEER REVIEWED**
PYROXYLIC SPIRITS
**PEER REVIEWED**
WOOD ALCOHOL
**PEER REVIEWED**
WOOD NAPHTHA
**PEER REVIEWED**
WOOD SPIRIT
**PEER REVIEWED**
Formulations/Preparations:
Formaldehyde; intrastate fungicide; 37.0%
formaldehyde, 15.0% methyl alcohol.
Wilbur-Ellis Smut-Guard; fungicide; 37.0%
formaldehyde, 12.0% methyl alcohol.
Eureka Products, Criosine; intrastate
disinfectant/bacteriocide/germicide; 47.6% methyl alcohol, 0.86%
nitrobenzene, 0.54% butyl 4-hydroxybenzoate, 30.0% phenol.
Surflo-B17; microbicide/microbisat general;
32.37% formaldehyde, 10.5% methyl alcohol, 10.0% alkyl
dimethyl benzyl ammonium chloride.
Coat-B1400; solution ready to use; 25.0% methyl
alcohol, 24.0% morpholine polyethoxyethanol.
Ideal Concentrated Wood Preservative;
fungicide; 15.0% isopropanol, 15.0% methyl alcohol, 10.0%
orthodichlorobenzene, 38.4% pentachlorophenol, 20.0% aliphatic petroleum
hydrocarbons.
Freer Elm Arrester; fungicide; 0.12% mecuric
chloride, 96.65% methyl alcohol.
Eureka Products Criosine Disinfectant;
disinfectant/bacteriocide/germicide; 47.6% methyl alcohol, 0.86%
nitrobenzene, 0.54% butyl 4-hydroxybenzoate, 30.0% phenol.
X-Cide 402 Industrial Bactericide;
bacteriostat; 11.5% isopropanol, 16.4% methyl alcohol, 28.5%
alkyl amino-3-aminopropane monoacetate, 17.8% oxydiethylenebis(alkyl) dimethyl
ammonium chloride.
EPA Hazardous Waste Number:
U154; A toxic waste when a discarded
commercial chemical product or manufacturing chemical intermediate or an
off-specification commercial chemical product.
F003; A hazardous waste from nonspecific sources when a spent solvent.
RTECS Number:
NIOSH/PC1400000
Administrative Information:
Hazardous Substances Databank Number: 93
Last Revision Date: 20020513
Last Review Date: Reviewed by SRP on 3/17/1989
Great Lakes Chemical Corporation and the Pathfinders Camp