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Methanol

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Methanol-1 Litre
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Methanol <p>CH<sub>3</sub>OH</p>

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  • Methanol <p>CH<sub>3</sub>OH</p>

Details

Methanol industrial solvent, technical grade. however very high purity.

Additional Information

Molecular Formular CH4O
Aqueous solubility Very soluble
Linear Formula CH3OH
Molar Mass 32.04 g mol−1
Acidity (pKa) 15.5
Melting Point −98--97 °C, 175-176 K, -144--143 °F
Boiling Point 64.7 °C, 338 K, 148 °F
Density 0.7918 g cm−3
Dipole Moment 1.69 D
Flash Point 11–12 °C
Vapor Pressure 13.02 kPa (at 20 °C)
Refractive Index n20/D 1.329(lit.)
Viscosity 5.9×10−4 Pa s (at 20 °C
LD 50 300 mg/kg human
Synonyms Methanol, methyl alcohol, wood alcohol, wood naphtha or wood spirits, Hydroxymethane, Methyl hydrate, Methyl hydroxide, Methylic alcohol,Methylol
CAS Number 67-56-1
UN Number 1230
PubChem Substance ID 887
Beilstein Registry 1098229
EG/EC Number 200-659-6
InChI 1S/CH4O/c1-2/h2H,1H3
InChIKey OKKJLVBELUTLKV-UHFFFAOYSA-N
RTECS PC1400000
safety_statements 7-16-36/37-45
Risk Statements 11-23/24/25-39/23/24/25
Hazard statements H225-H301-H311-H331-H370
GHS precautionary statements P210-P260-P280-P301 + P310-P311
Personal Protective Equipment Eyeshields, Faceshields, full-face respirator ), Gloves, multi-purpose combination respirator cartridge
Symbol GHS GHS02, GHS06, GHS08
RIDADR UN 1230 3/PG 2
Hazard Codes F,T
Signal word Danger
Environmental Protection Autority Information NZ

Methanol

Cas Number: 67-56-1
Synonyms: Carbinol, Methyl alcohol, Methyl hydroxide, Pyroxylic Spirit, Wood alcohol, Wood naphtha, Wood spirit
Molecular Weight: 32.04
Relative Density: 0.8100
Water Solubility (mg/l): miscible
Approval Number: HSR001186
UN Class: 3.0; 6.1; PG II
UN Number:  
Classification
3.1B   Flammable Liquids: high hazard
6.1C (oral) Acutely toxic
6.1C (dermal) Acutely toxic
6.1C (inhalation) Acutely toxic
6.4A   Irritating to the eye
6.8B   Suspected human reproductive or developmental toxicants
6.9A (inhalation) Toxic to human target organs or systems
9.3C   Harmful to terrestrial vertebrates
Classification Data
3.1B Flashpoint Value :12 °C 
Test Method :Closed cup
Boiling Point :64.7 °C
6.1C (oral) SPECIES: Human 
ENDPOINT: LD50 
VALUE: 300 mg/kg 
REFERENCE SOURCE: 
1. Bennett IL, Jr., Cary FH, Mitchell GL, Jr., et al. Acute methyl alcohol poisoning: a review based on experiences in an outbreak of 323 cases. Medicine (Baltimore) 1953;32:431-463. 
2. Roe O. Species differences in methanol poisoning. Crit Rev Toxicol 1982;10:275-286. 
3. Girault C, Tamion F, Moritz F, et al. Fomepizole (4-methylpyrazole) in fatal methanol poisoning with early CT scan cerebral lesions. J Toxicol Clin Toxicol 1999;37:777-780. 
4. Kavet R, Nauss KM. The toxicity of inhaled methanol vapors. Crit Rev Toxicol 1990;21:21-50. 
6.1C (dermal) Dermal acute toxicity: In primates, the acute dermal lethal dose is 393 mg/kg bw (studies 181 and 226, IUCLID 4 Methanol, 2005). Given that humans are at least 6-10 times more susceptible to acute methanol toxicity than primates, human fatalities could be expected at 24 hour semi-occlusive dermal exposures of = 1000 mg/kg bw (classifiable as 6.1C).5 This classification is consistent with the classification of methanol under EU CLP (REGULATION (EC) No 1272/2008, Table 3.1, Annex VI).
6.1C (inhalation) Inhalation Form:vapour
Inhalation acute toxicity: The available primate data that indicates that death will occur in monkeys at around 52 mg/L for a 4 hour exposure (study 218, IUCLID 4 Methanol, 2005). Humans are around 6-10 times more susceptible to acute methanol toxicity than primates.5 Human deaths might be expected with 4 hour exposures of = 10 mg/L (classifiable as 6.1C). This classification is consistent with the classification of methanol under EU CLP (REGULATION (EC) No 1272/2008, Table 3.1, Annex VI).
6.4A SPECIES: 
RESULT: Moderate irritant 
REFERENCE SOURCE: Union Carbide Data Sheet. (Union Carbide Corp., 39 Old Ridgebury Rd., Danbury, CT 06817) (3/24/1970) [RTECS] 
6.8B Synopsis of Research Report 89 
Effects of Prenatal Exposure to Inhaled Methanol on Nonhuman Primates and Their Infant Offspring 
INTRODUCTION 
In an effort to improve air quality and decrease dependence on petroleum, the federal government, 
industry, and other groups have encouraged development of alternative fuels such as methanol to substi-tute 
for gasoline or diesel fuel. Methanol is also a candidate to provide the hydrogen for fuel cells, which 
are being developed for a variety of power sources (including motor vehicle engines). Before people are 
exposed to increased concentrations of methanol, the potential health effects of such exposures require 
study. 
Methanol, a simple alcohol containing one carbon atom, occurs naturally in plants and animals and par-ticipates 
in human metabolism. People regularly consume low doses of methanol in fruits, vegetables, and 
fermented beverages as well as soft drinks and foods sweetened with aspartame (which breaks down to 
methanol in the gastrointestinal tract). Despite its ubiquitous presence, methanol can be highly toxic if suf-ficient 
quantities are consumed. Ingestion of methanol (usually in the form of wood alcohol or tainted alco-holic 
beverages) can result in metabolic acidosis, blindness, and even death. Although the body has the 
capacity to metabolize the low doses of methanol to which people are regularly exposed, it cannot handle 
high doses because too much methanol overwhelms the bodys ability to remove a toxic metabolite (for-mate). 
When formate accumulates, methanol poisoning occurs. One factor that regulates the rate at which 
formate is removed is the liver level of a derivative of the vitamin folic acid. People who are deficient in 
folic acid (including 15% to 30% of pregnant women) may be particularly susceptible to the toxic effects of 
methanol. 
If methanol were to be widely adopted as a fuel, environmental exposures would increase through inges-tion 
of contaminated drinking water, inhalation of vapors from evaporative and other emissions, and dermal 
contact. Current concentrations of methanol in ambient air are very low, 1 to 30 parts per billion (ppb). If all 
motor vehicles in the United States were converted to 100% methanol fuel, methanol levels in ambient air 
are estimated to increase approximately 1,000-fold (to 1 to 10 ppm in cities) and in a worst-case situation 
could occasionally reach concentrations as high as 200 ppm in enclosed spaces (HEI 1987). Inhaling these 
concentrations of methanol for short periods of time is not predicted to affect formate production and thus 
should not present a health risk. However, little is known about the consequences of long-term inhalation of 
methanol vapors, especially in susceptible populations of pregnant women and developing fetuses. HEI, 
therefore, developed a research program to address this information gap. 
APPROACH 
Dr. Thomas Burbacher and colleagues of the University of Washington studied the effects of long-term 
exposure to methanol vapors on metabolism and reproduction in adult female monkeys (Macaca fascicu-laris) 
and developmental effects in their offspring, who were exposed prenatally to methanol. 
The investigators exposed adult female monkeys (11 to 12 animals/group) to one of four concentrations 
of methanol vapors (0, 200, 600, and 1,800 ppm) for 2.5 hours a day, seven days a week during the fol-lowing 
periods: (1) before breeding, (2) during breeding, and (3) during pregnancy. They collected blood 
from the adults at regular intervals to monitor methanol levels (which served as a marker of internal dose) 
and formate concentrations. They also conducted pharmacokinetic studies to determine whether methanol 
disposition (which includes absorption, distribution, metabolism, and excretion) was altered as a result of Synopsis of Research Report 89 
Effects of Prenatal Exposure to Inhaled 
Methanol on Nonhuman Primates and 
Their Infant Offspring 
INTRODUCTION 
In an effort to improve air quality and decrease dependence on petroleum, the federal government, 
industry, and other groups have encouraged development of alternative fuels such as methanol to substi-tute 
for gasoline or diesel fuel. Methanol is also a candidate to provide the hydrogen for fuel cells, which 
are being developed for a variety of power sources (including motor vehicle engines). Before people are 
exposed to increased concentrations of methanol, the potential health effects of such exposures require 
study. 
Methanol, a simple alcohol containing one carbon atom, occurs naturally in plants and animals and par-ticipates 
in human metabolism. People regularly consume low doses of methanol in fruits, vegetables, and 
fermented beverages as well as soft drinks and foods sweetened with aspartame (which breaks down to 
methanol in the gastrointestinal tract). Despite its ubiquitous presence, methanol can be highly toxic if suf-ficient 
quantities are consumed. Ingestion of methanol (usually in the form of wood alcohol or tainted alco-holic 
beverages) can result in metabolic acidosis, blindness, and even death. Although the body has the 
capacity to metabolize the low doses of methanol to which people are regularly exposed, it cannot handle 
high doses because too much methanol overwhelms the bodys ability to remove a toxic metabolite (for-mate). 
When formate accumulates, methanol poisoning occurs. One factor that regulates the rate at which 
formate is removed is the liver level of a derivative of the vitamin folic acid. People who are deficient in 
folic acid (including 15% to 30% of pregnant women) may be particularly susceptible to the toxic effects of 
methanol. 
If methanol were to be widely adopted as a fuel, environmental exposures would increase through inges-tion 
of contaminated drinking water, inhalation of vapors from evaporative and other emissions, and dermal 
contact. Current concentrations of methanol in ambient air are very low, 1 to 30 parts per billion (ppb). If all 
motor vehicles in the United States were converted to 100% methanol fuel, methanol levels in ambient air 
are estimated to increase approximately 1,000-fold (to 1 to 10 ppm in cities) and in a worst-case situation 
could occasionally reach concentrations as high as 200 ppm in enclosed spaces (HEI 1987). Inhaling these 
concentrations of methanol for short periods of time is not predicted to affect formate production and thus 
should not present a health risk. However, little is known about the consequences of long-term inhalation of 
methanol vapors, especially in susceptible populations of pregnant women and developing fetuses. HEI, 
therefore, developed a research program to address this information gap. 
APPROACH 
Dr. Thomas Burbacher and colleagues of the University of Washington studied the effects of long-term 
exposure to methanol vapors on metabolism and reproduction in adult female monkeys (Macaca fascicu-laris) 
and developmental effects in their offspring, who were exposed prenatally to methanol. 
The investigators exposed adult female monkeys (11 to 12 animals/group) to one of four concentrations 
of methanol vapors (0, 200, 600, and 1,800 ppm) for 2.5 hours a day, seven days a week during the fol-lowing 
periods: (1) before breeding, (2) during breeding, and (3) during pregnancy. They collected blood 
from the adults at regular intervals to monitor methanol levels (which served as a marker of internal dose) 
and formate concentrations. They also conducted pharmacokinetic studies to determine whether methanol 
disposition (which includes absorption, distribution, metabolism, and excretion) was altered as a result of 
repeated methanol exposures and to assess pregnancy-related changes. Because high doses of methanol 
damage the central nervous system, the infants (8 to 9 animals/group) were examined at regular intervals 
during the first nine months of life to assess their growth and neurobehavioral development. 
RESULTS 
Exposure to methanol vapors did not affect the health of the adult monkeys prior to or during pregnancy. 
Single 2.5-hour exposures to methanol vapors caused short-term elevations in blood methanol concentra-tions 
of approximately 0- to 2-fold in the 200 ppm exposure group, 3- to 4-fold in the 600 ppm group, and 
13- to 16-fold in the 1,800 ppm group. After long-term exposures, peak blood methanol concentrations 
declined slightly over the first month and remained constant thereafter. The concentrations of plasma for-mate 
(the toxic intermediate) remained at baseline levels during the entire course of the study in all expo-sure 
groups. Pregnancy had no effect on methanol disposition. Serum folate concentrations were not 
affected by pregnancy and methanol exposure. 
Methanol exposure had no effect on most measures of reproductive performance, including menstrual 
cycles, conception rate, and live-birth delivery rate. However, all methanol-exposed animals had a decrease 
of about six to eight days in the duration of pregnancy compared to the control animals. It is not clear 
whether this decrease was related to methanol exposure as there was no dose response and no differences 
among offspring groups in body weight or other physical parameters. Prenatal exposure to methanol had no 
effect on infant growth and physical development for the first year of life. An unexplained wasting syn-drome, 
characterized by growth retardation, malnutrition, and gastroenteritis, occurred after one year of age 
in two female offspring exposed in utero to 1,800 ppm methanol. 
The investigators reported no systematic effects of prenatal methanol exposure on most of the measures 
used to test infant neurobehavioral development (neonatal behavior, early reflex responses, infant gross 
motor development, spatial memory, and social behavior). The investigators reported two possible meth-anol- 
related effects, one on visually directed reaching in male infants (a test of sensorimotor development), 
and one on novelty preference (a test of memory and cognitive function). Care must be taken in interpreting 
these results because a large number of neurobehavioral endpoints were analyzed and these results were 
based on a small number of subjects. Random fluctuations in the data may have appeared to be statistically 
significant. At the same time, however, both observations warrant further investigation as these central ner-vous 
system functions are complex perceptual processes that take time to develop and may be subject to 
latent neurotoxic effects. 
CONCLUSIONS 
This study adds substantially to our understanding of the effects of long-term exposure to inhaled meth-anol 
vapors. Because of the high quality of the study, the relevance of the animal model, the opportunities 
for dose-response analyses, and the availability of a marker of internal methanol dose, the results are 
appropriate for use in risk assessment. They can be readily used to predict the response of nutritionally 
competent people; they do not necessarily apply to women who are folate deficient. 
The investigators findings suggest that repeated inhalation exposure to concentrations of methanol vapors 
as high as 1,800 ppm would not result in accumulation of blood formate above baseline levels. With the 
exception of an unexplained shortening of gestation, methanol exposure had no effect on reproductive perfor-mance. 
The most significant result to emerge from this study was the wasting observed in two monkeys 
exposed in utero to 1,800 ppm methanol. Although this observation raises concern for prenatal exposures of 
this magnitude, pregnant women are unlikely to be exposed to such extremely high concentrations of meth-anol 
for prolonged periods of time. 
Overall, the results provide no evidence of a robust effect of prenatal methanol exposure on the neurobe-havioral 
development of nonhuman primate infants during the first nine months of life. However, 
improved understanding of methanol neurobehavioral toxicity will result from evaluation at later stages of 
development when more sophisticated tests of cognitive performance can be conducted and when latent 
effects may emerge. Such studies are now under way in the same monkeys at 4 to 5 years of age. 
REFERENCE 
Health Effects Institute. 1987. Automotive Methanol Vapors and Human Health: An Evaluation of 
Existing Scientific Information and Issues for Future Research. A Special Report of the Institutes Health 
Research Committee. Health Effects Institute, Cambridge, MA. 
[http://www.healtheffects.org/Pubs/BurbacherState.pdf]
6.9A (inhalation) EndPoint: 
Primary Organ: 
Acute inhalation of methanol vapour concentrations below 260 mg/m3 or ingestion of up to 20 mg methanol/kg by healthy or moderately folate-deficient humans should not result in formate accumulation above endogenous levels. 
Visual disturbances of several types (blurring, constriction of the visible field, changes in colour perception, and temporary or permanent blindness) have been reported in workers who experienced methanol air levels of about 1500 mg/m3 (1200 ppm) or more. 
A widely used occupational exposure limit for methanol is 260 mg/m3 (200 ppm), which is designed to protect workers from any of the effects of methanol-induced formic acid metabolic acidosis and ocular and nervous system toxicity. 
No other adverse effects of methanol have been reported in humans except minor skin and eye irritation at exposures well above 260 mg/m3 (200 ppm). 
WHO Environmental Health Criteria 
[INCHEM] 
9.3C SPECIES: Mouse 
ENDPOINT: LD50 
VALUE: 870 mg/kg 
REFERENCE SOURCE: H&S: METHYL ALCOHOL 67-56-1 [NTP] 

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