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*This document is like a lab demo—an example Certificate of Analysis (COA) that showcases what a COA looks like but may not match the latest batch in all its glory. Think of it as a chemistry experiment: close, but not quite the final reaction!
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Bulk Quote| Molecular Weight: | 32.042 g/mol |
| XLogP3: | -0.5 |
| Hydrogen Bond Donor Count: | 1 |
| Hydrogen Bond Acceptor Count: | 1 |
| Rotatable Bond Count: | 0 |
| Exact Mass: | 32.026214747 g/mol |
| Monoisotopic Mass: | 32.026214747 g/mol |
| Topological Polar Surface Area: | 20.2 Ų |
| Heavy Atom Count: | 2 |
| Formal Charge: | 0 |
| Complexity: | 2 |
| Isotope Atom Count: | 0 |
| Defined Atom Stereocenter Count: | 0 |
| Undefined Atom Stereocenter Count: | 0 |
| Defined Bond Stereocenter Count: | 0 |
| Undefined Bond Stereocenter Count: | 0 |
| Covalently-Bonded Unit Count: | 1 |
| Compound Is Canonicalized: | Yes |
| Related Compounds |
| hazard signal | Danger |
| hazard classes and categories | |
| precautionary statement codes | P210, P233, P240, P241, P242, P243, P260, P261, P262, P264, P270, P271, P280, P301+P316, P302+P352, P303+P361+P353, P304+P340, P308+P316, P316, P321, P330, P361+P364, P370+P378, P403+P233, P403+P235, P405, and P501 |
| hazard statements |
| toxicity summary | IDENTIFICATION AND USE: Methanol is a clear colorless liquid, used in hydraulic fracturing mixtures. It is also used as dehydrator of natural gas; fuel for utility plants ; feedstock for manufacture of synthetic proteins by continuous fermentation; source of hydrogen for fuel cells, home-heating-oil extender. HUMAN STUDIES: Humans are uniquely sensitive to methanol poisoning. 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. The minimum lethal dose of methanol in the absence of medical treatment is between 0.3 and 1 g/kg. 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 concurrent ingestion of ethanol, which slows the entrance of methanol into the metabolic pathway, and 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. ANIMAL STUDIES: The rate of metabolic detoxification, or removal of formate 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 are usually the cause of death. 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. The association between methanol exposure and lymphoma in some animal studies is weak, and is better interpreted as due to confounding factors or to a mechanism not relevant in humans. 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. No increase in micronuclei was observed in the bone marrow of mice exposed to methanol. Methanol did not induce micronuclei in Chinese hamster lung V79 cells in vitro. Methanol was mutagenic in the mouse lymphoma assay, in a Basc test, or in Drosophila, sex-linked, recessive lethal mutation assay. Treatment of primary cultures of Syrian golden hamster embryo cells with methanol did not lead to cell transformation. Methanol was not mutagenic to Salmonella strains TA97, TA98, TA1535, TA 1537, and TA1538 in Ames tests with or without metabolic activation. Equivocal results were obtained with Salmonella strain TA102 in the presence of metabolic activation. Methanol was not mutagenic in a DNA-repair test using various strains of E. coli WP2 and in a forward mutation assay using Schizosaccharomyces pombe. ECOTOXICITY STUDIES: 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.The target of methanol in the eye is the retina, specifically the optic disk and optic nerve. Muller cells and rod and cone cells are altered functionally and structurally, because cytochrome oxidase activity in mitochondria is inhibited, resulting in a reduction in ATP. |
| hazards summary | Methanol is released to the environment during industrial uses and naturally from volcanic gases, vegetation, and microbes. Exposure may occur from ambient air and during the use of solvents. Acute (short-term) or chronic (long-term) exposure of humans to methanol by inhalation or ingestion may result in blurred vision, headache, dizziness, and nausea. No information is available on the reproductive, developmental, or carcinogenic effects of methanol in humans. Birth defects have been observed in the offspring of rats and mice exposed to methanol by inhalation. EPA has not classified methanol with respect to carcinogenicity.Methanol poisoning can cause blindness and death. The lethal oral dose in humans is 2 to 8 ounces. Most cases have occurred after ingestion. Methanol poisoning after inhalation or skin absorption in the workplace has been reported. Symptoms of methanol poisoning include initial CNS depression and vomiting followed by metabolic acidosis and severe vision impairment 8-24 hours later. Coma, respiratory failure, and death may ensue. In high-dose reproductive studies in animals, methyl alcohol causes testicular damage and birth defects. Patients may present with inebriation and gastritis. There is a characteristic latency of 6-30 hours after exposure. Combined osmolar and anion gaps suggest poisoning by methanol or ethylene glycol, but also may occur in severe alcoholic ketoacidosis or diabetic ketoacidosis. |
| symptoms | irritation eyes, skin, upper respiratory system. headache, drowsiness, dizziness, nausea, vomiting. visual disturbance, optic nerve damage . dermatitisMethanol can produce sensory irritation and narcosis at airborne concentrations below those which produce organ system pathology. |
| health effects | Acute methanol poisoning in humans is characterized by an asymptomatic period of 12h to 24h followed by formic acidemia, ocular toxicity, coma, and in extreme cases death. Visual disturbances develop between 18h to 48h after ingestion and range from mild photophobia and blurred vision to markedly reduced visual acuity and complete blindness. |
| carcinogen classification | default_key: No indication of carcinogenicity to humans . |
