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Results for “METHYL ALCOHOL”

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At least 19 recordsLinked to original sources
PubMed2001

Final report on the safety assessment of Methyl Alcohol.

Methyl Alcohol is an aliphatic alcohol with use in a few cosmetic formulations as a solvent and denaturant. Concentrations up to 5% are typically used to denature ethyl alcohol in cosmetic products. Methyl Alcohol is readily absorbed through the skin and from the gastrointestinal and respiratory tracts, is distributed throughout all organs and tissues (in direct relation to the body's water distribution), and is eliminated primarily via the lungs. Undiluted Methyl Alcohol is an ocular and skin irritant. Inhalation studies showed a no-effect level for maternal damage of 10,000 ppm and for teratogenic effects of 5,000 ppm. Overall, Methyl Alcohol is not considered mutagenic. Carcinogenicity data were unavailable. The toxicity of Methyl Alcohol in humans results from the metabolism of the alcohol to formate and formic acid through a formaldehyde intermediate. Formate accumulation causes metabolic acidosis and inhibits cellular respiration. Methyl Alcohol toxicity is time and concentration dependent, and its toxic effect is competitively inhibited with ethyl alcohol. Because of the moderating effect of ethyl alcohol, it was concluded that Methyl Alcohol is safe as used to denature ethyl alcohol used in cosmetic products. No conclusion was reached regarding any other use of Methyl Alcohol.

Animals↗
PubMed1977

Methyl alcohol poisoning. II. Development of a model for ocular toxicity in methyl alcohol poisoning using the rhesus monkey.

Rhesus monkeys were intoxicated with methyl alcohol, using an initial dose of 2 gm/kg and subsequent doses were administered in order to maintain an attenuated and prolonged state of intoxication. Arterial blood samples were drawn for methyl alcohol, formate, PO2, PCO2, and pH, which were monitored periodically throughout the course of the experiment. With the use of these procedures monkeys developed metabolic acidosis with the accumulation of formic acid in the blood and a corresponding decrease in blood bicarbonate. These animals served as models, which allowed for ocular evaluation for early signs related to methyl alcohol poisoning. A mechanism to explain toxicity is proposed and discussed.

Acidosis↗
PubMed2002

Results of long-term experimental studies on the carcinogenicity of methyl alcohol and ethyl alcohol in rats.

Methyl alcohol was administered in drinking water supplied ad libitum at doses of 20,000, 5,000, 500, or 0 ppm to groups of male and female Sprague-Dawley rats 8 weeks old at the start of the experiment. Animals were kept under observation until spontaneous death. Ethyl alcohol was administered by ingestion in drinking water at a concentration of 10% or 0% supplied ad libitum to groups of male and female Sprague-Dawley rats; breeders and offspring were included in the experiment. Treatment started at 39 weeks of age (breeders), 7 days before mating, or from embryo life (offspring) and lasted until their spontaneous death. Under tested experimental conditions, methyl alcohol and ethyl alcohol were demonstrated to be carcinogenic for various organs and tissues. They must also be considered multipotential carcinogenic agents. In addition to causing other tumors, ethyl alcohol induced malignant tumors of the oral cavity, tongue, and lips. These sites have been shown to be target organs in man by epidemiologic studies.

Animals↗
PubMed1986

Hyperamylasemia following methyl alcohol intoxication. Source and significance.

Methyl alcohol intoxication has been reported to cause hyperamylasemia and pancreatitis. We describe a patient with severe, nonfatal methyl alcohol intoxication who had a rise in serum amylase activity with the level peaked on the second hospital day at tenfold the upper limit of normal. However, isoamylase analysis showed that this striking hyperamylasemia was due to salivary-type amylase. Furthermore, the serum lipase activity remained entirely normal during the peak amylase elevation. Thus, in cases of methyl alcohol intoxication, as in other clinical situations, hyperamylasemia, even when striking, should not be equated with pancreatitis. More specific laboratory tests for pancreatitis should be used before embarking on extensive investigations of the pancreas.

Acute Disease↗
PubMed1990

[Accidental methyl alcohol poisoning].

An accidental poisoning due to drinking methyl alcohol in Chaoyang county is reported, analysing the accident. The poison came from the "retail white spirit" which was contaminated with methyl alcohol. Twenty-nine persons drank the wine, fourteen of them died, two of them became blind. After drinking this "retail white spirit" the drinkers showed symptoms of vertigo, headache, weakness, vomiting, night sweat, dyspnea and blurring of vision etc. within 6-120 hours. On examining the remaining spirit, we found the content of methyl alcohol to be between 16.6 and 40.69 g/100 ml. Some of the patients' urine and blood also contained methyl alcohol. We reckoned that each one of the twenty patients had taken more than 27 g of methyl alcohol and each of the ten dead drank more than 40 ml of the alcohol.

Adult↗
PubMed2003

Fatalities due to methyl alcohol intoxication in Turkey: an 8-year study.

The aim of this study is to examine methyl alcohol poisoning cases from the medico-legal point of view. The records of the Morgue Department of Council of the Forensic Medicine were reviewed retrospectively for all methyl alcohol poisonings for the period of 27.10.1992 and 30.05.2001. The victim's age, sex, death year, death place, methyl alcohol blood levels, the source of methyl alcohol, accompanying laboratory results and histopathologic tissue changes were recorded. The number of deaths due to the methyl alcohol poisoning was 271 during that period of time. Two hundred and forty-two of the (89.3%) total 271 methyl alcohol fatalities were men and 29 (10.7%) of were women. The largest age group was 36-40 years old, followed by 41-45. The methyl alcohol blood concentrations ranged widely from 50 to 755 mg for per 100 ml. There were 222 cases (81.9%) with the methyl alcohol blood concentrations over 100 mg/dl. Twenty-nine (10.7%) victims were poisoned through the consumption of cologne and three of them with alcoholic beverage named "Raki". Consumed products were not known in all other cases because of insufficient patient history and data. As a conclusion, regarding the distribution according to years, mortality due to methyl alcohol intoxication in our country have been proceeding on a certain level. In order to decrease the mortality due to methyl alcohol intoxication, some precautions should be developed that could prevent the production and consumption of alcoholic beverages illegally produced.

Adolescent↗
PubMed1979

An outbreak of acute methyl alcohol intoxication.

An outbreak of acute methyl alcohol intoxication occurred in Port Moresby, Papua New Guinea, in March 1977. Twenty-eight young men attended a drinking party and drank methyl alcohol. The amount consumed by each individual ranged from an equivalent of 60--600 ml of pure methanol. Three had prior ethanol ingestion. All 28 became ill 8--36 hours after drinking and were hospitalized. The most commonly observed clinical syndromes were: acute metabolic acidosis, severe visual impairment and acute pancreatitis. Four died within 72 hours after admission to the hospital. All had severe metabolic acidosis and visual impairment and three pancreatitis. Of 24 who recovered, 16 showed no residual complications, six had bi-lateral visual impairment and two had difficulty in speech as well as visual impairment. A three month follow-up examination showed no change in the findings. Coma, seizures and prolonged acidosis were poor prognostic signs. The estimated amount of consumed methanol and the rapidity of the appearance of signs of toxicity following methanol ingestion did not seem to influence the outcome of poisoning. The treatment of acute methyl alcohol intoxication in centres where dialysis is not available is discussed.

Adolescent↗
PubMed1989

Spectrophotometric determination of methyl alcohol in the atmosphere.

Spectrophotometric method for determination of methyl alcohol in the atmosphere has been developed. The method is based on adsorption of methyl alcohol on activated charcoal, desorption with carbon tetrachloride, oxidation of methyl alcohol to formaldehyde and spectrophotometric determination with chromotropic acid. Good precision has been obtained. Coefficient of variation was found to be +/- 4.96% for n = 24. The minimum determinable amount of methyl alcohol in the atmosphere was found to be 0.005 mg/m3 by passing 720 l of air.

Air Pollutants, Occupational↗
PubMed2006

Stability of benzoyl peroxide in methyl alcohol.

The purpose of this study was to clarify the stability of benzoyl peroxide (BPO) in some solvents. BPO was dissolved in acetone, acetonitrile (AcCN), 50% acetonitrile-50% distilled water (50% AcCN), ethyl alcohol (EtOH), and methyl alcohol (MeOH). Solutions containing BPO were incubated for eight days at 25 degrees C. In MeOH, BPO rapidly decomposed into benzoic acid (BA) and methyl benzoate (MeBA) time-dependently, whereas BPO in acetone, AcCN, and 50% AcCN was relatively stable. Although BPO in EtOH was slightly stable within the first 24 hours, it decomposed time-dependently such that BA and EtBA as decomposition products of BPO were produced. These results indicated that the stability of BPO in a solution was dependent on the solvent and the decomposition rate of BPO dissolved in MeOH was the fastest. These suggest that BPO can decompose even in lower-than-activation temperature by the solvent to use for its dissolution.

Acetone↗
PubMed1977

Methyl alcohol poisoning III. Ocular toxicity.

The ocular toxicity of methyl alcohol has been investigated in six rhesus monkeys. All the animals developed fundus changes within 43 to 171 hours after its ingestion. The only fundus lesion seen was optic disc edema and associated changes, usually of a marked degree. Fluorescein fundus angiography confirmed the findings. The retinal and choroidal circulations, including the retinal capillary bed, were normal. Ophthalmoscopically and angiographically, optic disc edema in methyl alcohol poisoning was indistinguishable from that seen in raised intracranial pressure, except that no increased intracranial pressure was observed. It is postulated that optic disc edema in methyl alcohol poisoning is due to an axoplasmic flow stasis.

Animals↗
PubMedDate not supplied

[Parkinsonism after methyl alcohol poisoning].

Two cases of parkinsonism due to methyl alcohol poisoning are reported. In the first patient, parkinsonism features were mild and stable, while in the second they progressively developed in the weeks following the poisoning. None of the two patients had significant visual abnormalities during the clinical evolution. Both patients had symmetrical putaminal lesions in CT, and one in NMR imaging. The response to antiparkinsonism drugs was absent in one case and it could not be evaluated in the other because of patient's death. On the basis of theses two cases the clinical and therapeutic features of this type of striatal parkinsonism are compared with those with parkinsonism due to other toxic agents. In view of the topography of the lesions of this poisoning, which is shared by other conditions such as Leber's disease or Leigh's syndrome, and the analogy with the presynaptic action of MPP+ in the parkinsonism due to MPTP, a possible implication of mitochondrial metabolism in the pathogenesis of this syndrome is discussed. The lack of knowledge of the real incidence of this complication in the survivors of methyl alcohol poisoning suggests the need to perform studies with a prolonged and systematic clinical follow up.

Adult↗