What Makes You Go Blind In Moonshine?

What is Moonshine Blindness? – Moonshine blindness has two ugly sides. First of all, there is the propaganda that was spread around the 1920s when governments attempted to stop people from producing their own moonshine. A lot of effort went into prohibiting the production of moonshine.

• Many cases of poisoning and blindness were spread to discourage moonshine brewers despite that many of these cases were not related or were false.
• And then there is the real cause of moonshine blindness.
• Moonshine blindness can occur when someone consumes too much methanol.
• When methanol is consumed, it is changed into formaldehyde and is known as methanol poisoning.

Methanol poisoning can cause damage to your eyes and can even result in blindness in severe cases.

What causes alcohol blindness?

Alcohol Addiction Increases the Risk of Blindness The type of alcohol that has the potential to cause blindness is methanol. These substances can immediately damage the nervous system, including the eye nerves. Initially, it causes inflammation, followed by the death of nervous system tissue, which can cause blindness and lead to death.

The alcohol content of alcoholic beverages varies. Most types of alcoholic beverages that are drunk are types of ethanol compounds with the molecular formula C2H5OH. This type of alcohol can affect the central nervous system, so when it is drunk, it will certainly cause the person consuming it to lose consciousness, and in severe conditions, it can cause death.

In the manufacture of adulterated alcohol (self-mixed), it is often mixed with methanol (CH3OH) or benzene (C6H6). These materials can also cause poisoning and cause permanent nerve damage (blindness or death). The mixed material has been fused with alcohol and cannot be separated or decomposed.

1. Methanol is a type of chemical substance that can cause blindness and paralysis when it enters the body.
2. In mild cases, benzene causes a deficiency of erythrocytes (a condition when the level of red blood cells in the body falls below the normal range) and leukocytes (a condition when the number of white blood cells in the body falls below normal).

Meanwhile, in severe cases, benzene will cause nausea and even death due to heart and respiratory system failure. For cases of sudden blurry vision, an ophthalmologist will provide maximum therapy in the form of high-dose drug injections. The therapy given aims to reduce swelling of the optic nerve due to methanol or alcohol intoxication.

• Individual responses vary from therapy given; if it is not too late, sometimes visual acuity can improve, but if there has been total tissue damage, it will be difficult to return to normal so that blindness occurs.
• We cannot predict the occurrence of death.
• However, alcohol that has been mixed with methanol is very dangerous when consumed.

Consumption of 70% alcohol that has been mixed with methanol can cause blindness and paralysis. In severe cases, it can cause cardiac arrest and death, and the cases are quite common in our society. Of course, many types of cancer are also triggered by alcohol consumption.

• Alcohol consumption can trigger cancer in several areas of the body, including the mouth, esophagus, throat, larynx (part of the respiratory system), and liver.
• In the human body, alcohol will activate several types of enzymes that trigger the development of cancer cells.
• Alcohol will also damage the DNA in the body so that some parts of the cells will grow and multiply uncontrollably.

Given the dangers that can cause everything from blindness to death, it is appropriate for all of us to stay away from alcohol and start living a healthy life without it. : Alcohol Addiction Increases the Risk of Blindness

How long does methanol take to blind you?

From Wikipedia, the free encyclopedia

Methanol toxicity
Other names	Methanol poisoning, methanol overdose
Molecular structure of methanol
Specialty	Emergency medicine
Symptoms	Decreased level of consciousness, poor coordination, vomiting, abdominal pain, specific smell on the breath
Complications	Blindness, kidney failure
Causes	Methanol (such as found in windshield washer fluid )
Diagnostic method	Blood acidosis, increased osmol gap, methanol blood level
Differential diagnosis	Infections, exposure to other toxic alcohols, serotonin syndrome, diabetic ketoacidosis
Prevention	Consuming safe alcoholic beverages
Treatment	Antidote, hemodialysis
Medication	Fomepizole, ethanol
Prognosis	Good with early treatment
Frequency	1,700 cases per year (US)

Methanol toxicity (also methanol poisoning ) is poisoning from methanol, characteristically via ingestion. Symptoms may include a decreased level of consciousness, poor or no coordination, vomiting, abdominal pain, and a specific smell on the breath.

• Decreased vision may start as early as twelve hours after exposure.
• Long-term outcomes may include blindness and kidney failure,
• Blindness may occur after drinking as little as 10 mL; death may occur after drinking quantities over 15 mL (median 100 mL, varies depending on body weight).
• Methanol poisoning most commonly occurs following the drinking of windshield washer fluid,

This may be accidental or as part of an attempted suicide, Toxicity may also rarely occur through extensive skin exposure or breathing in fumes. When methanol is broken down by the body it results in formaldehyde, formic acid, and formate which cause much of the toxicity.

The diagnosis may be suspected when there is acidosis or an increased osmol gap and confirmed by directly measuring blood levels. Other conditions that can produce similar symptoms include infections, exposure to other toxic alcohols, serotonin syndrome, and diabetic ketoacidosis, Early treatment increases the chance of a good outcome.

Treatment consists of stabilizing the person, followed by the use of an antidote, The preferred antidote is fomepizole, with ethanol used if this is not available. Hemodialysis may also be used in those where there is organ damage or a high degree of acidosis,

• Other treatments may include sodium bicarbonate, folate, and thiamine,
• Outbreaks of methanol ingestion have occurred due to contamination of drinking alcohol,
• This is more common in the developing world,
• In 2013 more than 1700 cases occurred in the United States.
• Those affected are usually adult and male.

Toxicity to methanol has been described as early as 1856.

Is it ethanol or methanol that makes you blind?

Is it true that 10 ml of pure methanol can cause blindness? Methanol is definitely something to avoid ingesting -in any quantity. Methanol (wood alcohol) is a simple alcohol very closely related to ethanol, the intoxicating chemical in whiskey, beer, and wine.

But methanol is extremely poisonous and toxic specifically to the nervous system. It is so toxic to the optic nerve that even small quantities can cause permanent blindness. But why would anybody drink it in the first place? During the era of prohibition in the U.S., some people would distill their own “moonshine” illegally.

Methanol was an occasional accidental distillation contaminant. There were several episodes of endemic blindness when the contaminated booze was distributed and consumed. Even today, “denatured” alcohol is sold in hardware and drugstores. This product is actually ethanol made unfit for human consumption by the addition of some methanol.

How much methanol causes blindness?

Conclusion – From the reported data from methanol exposure in human beings, the dose response is related to methanol exposure dose and urinary methanol concentration. The relationship between the level of oral/respiration exposure and clinical symptoms was reviewed in previous reports.

• The lethal dose of pure methanol in humans is estimated at 15.8–474 g/person as the range and 56.2 g/person as the median.
• Oral intake of 3.16–11.85 g/person of pure methanol could cause blindness.
• Even at low dose levels, pure methanol (oral and respiration exposure) might result in a lethal dose or result in blindness as a clinical symptom.

Careful attention is necessary.

Is a shot of moonshine safe?

Methanol Risks – While the flammability of the moonshine distillation process is dangerous in and of itself, the health effects of moonshine-methanol consumption pose an even bigger threat. More people have died from drinking moonshine than by any explosions at stills, despite the few old and handmade stills that are left.

1. A major risk of drinking moonshine is methanol blindness.
2. Detecting methanol upon the first step is impossible, and consuming more of it will simply get the person drunker.
3. However, it’s eventually metabolized as its toxic metabolite, formic acid, in the body, which can have an extremely harmful effect.

Just 10 milliliters (ml) of methanol is all it takes to cause permanent optic and partial nerve damage, if not complete blindness. As little as 30 ml of methanol is lethal, and, for reference, a standard shot glass in the U.S. holds 40 ml. Old stills use car radiators during the distilling process, which often contain lead soldering and remnants of antifreeze glycol products that could contaminate and add toxins to the moonshine.

• Larger batches of moonshine are more likely to contain methanol.
• Because methanol is vaporized or evaporated at a lower temperature than alcohol, the first liquid produced by the distillation process usually contains methanol.
• While moonshiners have adopted new ways to discard methanol, some moonshiners will actually add it back into the batch to make the drink more potent.

However, because these processes aren’t regulated, there’s no way of knowing whether the illicit alcohol actually contains any methanol.

Is methanol blindness reversible?

Abstract. Methanol-induced optic neuropathy (Me-ION) is a serious condition that may result in long-term or irreversible visual impairment or even blindness secondary to damage and loss of function of the optic nerve and retina.

Can you recover from methanol blindness?

Reversal of Methanol-Induced Blindness in Adults by Autologous Bone Marrow-Derived Stem Cells: A Case Series – PubMed Introduction: Methanol ingestion leads to severe damage to visual pathways and permanent loss of vision. Current treatment is aimed at removal of methanol from system and prevention of generation of toxic metabolites along with symptomatic management of patient.

Autologous bone marrow mononuclear stem cells (MNC) can be used to rejuvenate the damaged retinal cells and restoration of vision. Methods: Five patients suffering from methanol induced complete blindness within three months of insult and no known comorbidities during the past 6 months were enrolled to receive autologous bone marrow derived mononuclear cell fraction on compassionate grounds.

The visual acuity and visual evoked responses (VER) were done at the time of enrollment and during follow-up visits. Observations and results: Visual acuity of these patients at the time of enrollment: no perception of light. Improvement in visual acuity was recorded by 7 days which reached maximum at 3 weeks after treatment in three patients and three months in two patients.

The patients had acuity of 6/9, finger counting and reading with magnifying glasses with no subsequent improvement till 2 years of follow-up. Visual Evoked Responses demonstrated improvements following treatment. No adverse reactions were noticed during follow-up. Conclusion: Treatment with Autologous Bone marrow derived MNC offers a new line of management in patients with loss of vision following methanol ingestion.

The efficacy and safety of this line of management needs to be evaluated in controlled clinical trials. : Reversal of Methanol-Induced Blindness in Adults by Autologous Bone Marrow-Derived Stem Cells: A Case Series – PubMed

What will happen if someone drank 100% methanol?

Outlook (Prognosis) – Methanol is extremely poisonous. As little as 2 tablespoons (30 milliliters) can be deadly to a child. About 2 to 8 ounces (60 to 240 milliliters) can be deadly for an adult. Blindness is common and often permanent despite medical care.

How do you know if moonshine is safe?

One way to test the purity of a moonshine liquor is to pour some in a metal spoon and set it on fire. If it burns with a blue flame, it is more likely safe to drink. If it produces a yellow or red flame, it is an indication of the presence of lead.

Does all moonshine have methanol?

Typically, about 10% of the alcohol created can be methanol. If your fermentation creates 10% alcohol in total, you are looking at 1% of your total mash to be methanol. Fortunately, methanol can be removed from moonshine during the distillation process.

Can you recover from methanol poisoning?

Methanol poisoning can be treated successfully if diagnosed within 10-30 hours of ingestion. If you suspect someone might have methanol poisoning, get them to a hospital which has dialysis equipment as soon as possible.

How fast does methanol poisoning occur?

Methanol: Systemic Agent

CAS #: 67-56-1 RTECS #: PC1400000 UN #: 1230 (Guide 131)

Common Names:

Carbinol Methyl alcohol Wood alcohol

APPEARANCE : Colorless watery liquid. DESCRIPTION : Methanol is a toxic alcohol that is used industrially as a solvent, pesticide, and alternative fuel source. It also occurs naturally in humans, animals, and plants. Foods such as fresh fruits and vegetables, fruit juices, fermented beverages, and diet soft drinks containing aspartame are the primary sources of methanol in the human body. Most methanol poisonings occur as a result of drinking beverages contaminated with methanol or from drinking methanol-containing products. In the industrial setting, inhalation of high concentrations of methanol vapor and absorption of methanol through the skin are as effective as the oral route in producing toxic effects. The characteristic pungent (alcohol) odor of methanol does not provide sufficient warning of low levels of exposure. METHODS OF DISSEMINATION :

Indoor Air: Methanol can be released into indoor air as a liquid spray (aerosol). Water: Methanol can be used to contaminate water. Food: Methanol may be used to contaminate food. Outdoor Air: Methanol can be released into outdoor air as a liquid spray (aerosol). Agricultural: If methanol is released into the air as a liquid spray (aerosol), it has the potential to contaminate agricultural products.

ROUTES OF EXPOSURE : Methanol can be absorbed into the body by inhalation, ingestion, skin contact, or eye contact. Ingestion is an important route of exposure.

GENERAL INFORMATION : First Responders should use a NIOSH-certified Chemical, Biological, Radiological, Nuclear (CBRN) Self Contained Breathing Apparatus (SCBA) with a Level A protective suit when entering an area with an unknown contaminant or when entering an area where the concentration of the contaminant is unknown. Level A protection should be used until monitoring results confirm the contaminant and the concentration of the contaminant. NOTE: Safe use of protective clothing and equipment requires specific skills developed through training and experience. LEVEL A: (RED ZONE) : Select when the greatest level of skin, respiratory, and eye protection is required. This is the maximum protection for workers in danger of exposure to unknown chemical hazards or levels above the IDLH or greater than the AEGL-2.

A NIOSH-certified CBRN full-face-piece SCBA operated in a pressure-demand mode or a pressure-demand supplied air hose respirator with an auxiliary escape bottle. A Totally-Encapsulating Chemical Protective (TECP) suit that provides protection against CBRN agents. Chemical-resistant gloves (outer). Chemical-resistant gloves (inner). Chemical-resistant boots with a steel toe and shank. Coveralls, long underwear, and a hard hat worn under the TECP suit are optional items.

LEVEL B: (RED ZONE) : Select when the highest level of respiratory protection is necessary but a lesser level of skin protection is required. This is the minimum protection for workers in danger of exposure to unknown chemical hazards or levels above the IDLH or greater than AEGL-2.

A NIOSH-certified CBRN full-face-piece SCBA operated in a pressure-demand mode or a pressure-demand supplied air hose respirator with an auxiliary escape bottle. A hooded chemical-resistant suit that provides protection against CBRN agents. Chemical-resistant gloves (outer). Chemical-resistant gloves (inner). Chemical-resistant boots with a steel toe and shank. Coveralls, long underwear, a hard hat worn under the chemical-resistant suit, and chemical-resistant disposable boot-covers worn over the chemical-resistant suit are optional items.

LEVEL C: (YELLOW ZONE) : Select when the contaminant and concentration of the contaminant are known and the respiratory protection criteria factors for using Air Purifying Respirators (APR) or Powered Air Purifying Respirators (PAPR) are met. This level is appropriate when decontaminating patient/victims.

A NIOSH-certified CBRN tight-fitting APR with a canister-type gas mask or CBRN PAPR for air levels greater than AEGL-2. A NIOSH-certified CBRN PAPR with a loose-fitting face-piece, hood, or helmet and a filter or a combination organic vapor, acid gas, and particulate cartridge/filter combination or a continuous flow respirator for air levels greater than AEGL-1. A hooded chemical-resistant suit that provides protection against CBRN agents. Chemical-resistant gloves (outer). Chemical-resistant gloves (inner). Chemical-resistant boots with a steel toe and shank. Escape mask, face shield, coveralls, long underwear, a hard hat worn under the chemical-resistant suit, and chemical-resistant disposable boot-covers worn over the chemical-resistant suit are optional items.

LEVEL D: (GREEN ZONE) : Select when the contaminant and concentration of the contaminant are known and the concentration is below the appropriate occupational exposure limit or less than AEGL-1 for the stated duration times.

Limited to coveralls or other work clothes, boots, and gloves.

CHEMICAL DANGERS :

Methanol reacts violently with strong oxidants, causing a fire and explosion hazard.

EXPLOSION HAZARDS :

Mixtures of methanol vapor and air are explosive. Lower explosive (flammable) limit in air (LEL), 6.0%; upper explosive (flammable) limit in air (UEL), 36%. Agent presents a vapor explosion and poison (toxic) hazard indoors, outdoors, or in sewers. Run-off to sewers may create an explosion hazard. Containers may explode when heated.

FIRE FIGHTING INFORMATION :

Methanol is highly flammable. The agent will be easily ignited by heat, sparks, or flames. Fire will produce irritating, corrosive, and/or toxic gases. Vapors may travel to the source of ignition and flash back. Run-off to sewers may create a fire hazard. Caution: The agent has a very low flash point. Use of water spray when fighting fires may be inefficient. For small fires, use dry chemical, carbon dioxide, water spray, or alcohol-resistant foam. For large fires, use water spray, fog, or alcohol-resistant foam. Move containers from the fire area if it is possible to do so without risk to personnel. Dike fire control water for later disposal; do not scatter the agent. Use water spray or fog; do not use straight streams. For fire involving tanks or car/trailer loads, fight the fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after the fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tanks. Always stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from the area and let the fire burn. Run-off from fire control or dilution water may cause pollution. If the situation allows, control and properly dispose of run-off (effluent).

INITIAL ISOLATION AND PROTECTIVE ACTION DISTANCES :

If a tank, rail car, or tank truck is involved in a fire, isolate it for 0.5 mi (800 m) in all directions; also consider initial evacuation for 0.5 mi (800 m) in all directions. This agent is not included in the DOT ERG 2004 Table of Initial Isolation and Protective Action Distances. In the DOT ERG 2004 orange-bordered section of the guidebook, there are public safety recommendations to isolate a methanol (Guide 131) spill or leak area immediately for at least 150 ft (50 m) in all directions.

PHYSICAL DANGERS :

Methanol vapors may be heavier than air. They will spread along the ground and collect and stay in poorly-ventilated, low-lying, or confined areas (e.g., sewers, basements, and tanks). Hazardous concentrations may develop quickly in enclosed, poorly-ventilated, or low-lying areas. Keep out of these areas. Stay upwind. Liquid agent is lighter than water.

NFPA 704 Signal :

Health: 1 Flammability: 3 Reactivity: 0 Special:

SAMPLING AND ANALYSIS :

OSHA: 91 NIOSH: 2000, 3800

ADDITIONAL SAMPLING AND ANALYSIS INFORMATION : References are provided for the convenience of the reader and do not imply endorsement by NIOSH.

AIR MATRIX Allen TM, Falconer TM, Cisper ME, Borgerding AJ, Wilkerson CW Jr., Real-time analysis of methanol in air and water by membrane introduction mass spectrometry. Anal Chem 73(20):4830-4835.De Paula PP, Santos E, De Freitas FT, De Andrade JB, Determination of methanol and ethanol by gas chromatography following air sampling onto florisil cartridges and their concentrations at urban sites in the three largest cities in Brazil. Talanta 49(2):245-252. Leibrock E, Slemr J, Method for measurement of volatile oxygenated hydrocarbons in ambient air. Atmos Environ 31(20):3329-3339. Marley NA, Gaffney JS, A comparison of flame ionization and ozone chemiluminescence for the determination of atmospheric hydrocarbons. Atmos Environ 32(8):1435-1444. NIOSH, NMAM Method 2000 Methanol. In: NIOSH Manual of analytical methods.4th ed. Cincinnati, OH: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, DHHS (NIOSH) Publication 94-113. OSHA, Methyl Alcohol Method 91. Salt Lake City, UT.U.S. Department of Labor, Organic Methods Evaluation Branch, OSHA Salt Lake Technical Center. Qin T, Xu X, Polak T, Pacakova V, Stulik K, Jech L, A simple method for the trace determination of methanol, ethanol, acetone, and pentane in human breath and in the ambient air by preconcentration on solid sorbents followed by gas chromatography. Talanta 44(9):1683-1690. Reichert J, Coerdt W, Ache HJ, Development of a surface acoustic wave sensor array for the detection of methanol in fuel vapours. Sens Actuators B: Chem 13(1-3):293-296. Tyras H, Spectrophotometric determination of methyl alcohol in the atmosphere. Z Gesamte Hyg 35(2):96-97. OTHER No references were identified for this sampling matrix for this agent. SOIL MATRIX Poole SK, Poole CF, Chromatographic models for the sorption of neutral organic compounds by soil from water and air. J Chromatogr A 845(1-2):381-400. SURFACES Almuzara C, Cos O, Baeza M, Gabriel D, Valero F, Methanol determination in Pichia pastoris cultures by flow injection analysis. Biotechnol Lett 24(5):413-417. WATER Blanco M, Coello J, Iturriaga H, Maspoch S, Porcel M, Simultaneous enzymatic spectrophotometric determination of ethanol and methanol by use of artificial neural networks for calibration. Anal Chim Acta 398(1):83-92.Martinezsegura G, Rivera MI, Garcia LA, Methanol analysis by gas-chromatography–comparative-study using 3 different columns. J Agric Univ Puerto Rico 69(2):135-144. Pettersson J, Roeraade J, Quantitative accuracy in the gas chromatographic analysis of solvent mixtures. J Chromatogr A 985(1-2):21-27. Wilson LA, Ding JH, Woods AE, Gas-chromatographic determination and pattern-recognition analysis of methanol and fusel oil concentrations in whiskeys. J Assoc Off Anal Chem 74(2):248-256.

TIME COURSE : Adverse health effects from methanol poisoning may not become apparent until after an asymptomatic period of 1 to 72 hours. EFFECTS OF SHORT-TERM (LESS THAN 8-HOURS) EXPOSURE : Methanol’s toxicity is due to its metabolic products. The by-products of methanol metabolism cause an accumulation of acid in the blood (metabolic acidosis), blindness, and death. Initial adverse health effects due to methanol poisoning include drowsiness, a reduced level of consciousness (CNS depression), confusion, headache, dizziness, and the inability to coordinate muscle movement (ataxia). Other adverse health effects may include nausea, vomiting (emesis), and heart and respiratory (cardiopulmonary) failure. Prognosis is poor in patient/victims with coma or seizure and severe metabolic acidosis (pH <7). Early on after methanol exposure, there may be a relative absence of adverse health effects. This does not imply insignificant toxicity. Methanol toxicity worsens as the degree of metabolic acidosis increases, and thus, becomes more severe as the time between exposure and treatment increases. EYE EXPOSURE :

Irritation, redness, and pain.

INGESTION EXPOSURE :

Ingestion of methanol may cause a wide range of adverse health effects:

Neurological: headache, dizziness, agitation, acute mania, amnesia, decreased level of consciousness including coma, and seizure. Gastrointestinal: Nausea, vomiting, lack of an appetite (anorexia), severe abdominal pain, gastrointestinal bleeding (hemorrhage), diarrhea, liver function abnormalities, and inflammation of the pancreas (pancreatitis). Ophthalmologic: visual disturbances, blurred vision, sensitivity to light (photophobia), visual hallucinations (misty vision, skin over the eyes, snowstorm, dancing spots, flashes), partial to total loss of vision, and rarely eye pain. Visual examination may reveal abnormal findings. Fixed dilated pupils are a sign of severe exposure to methanol. Other: Electrolyte imbalances. Kidney failure, blood in the urine (hematuria), and muscle death at the cellular level (rhabdomyolysis) have been reported in severe poisonings. Fatal cases often present with fast heart rate (tachycardia) or slow heart rate (bradycardia) and an increased rate of respiration. Low blood pressure (hypotension) and respiratory arrest occur when death is imminent.

INHALATION EXPOSURE : SKIN EXPOSURE :

Irritation. See Ingestion Exposure.

INTRODUCTION : The purpose of decontamination is to make an individual and/or their equipment safe by physically removing toxic substances quickly and effectively. Care should be taken during decontamination, because absorbed agent can be released from clothing and skin as a gas. Your Incident Commander will provide you with decontaminants specific for the agent released or the agent believed to have been released. DECONTAMINATION CORRIDOR : The following are recommendations to protect the first responders from the release area:

Position the decontamination corridor upwind and uphill of the hot zone. The warm zone should include two decontamination corridors. One decontamination corridor is used to enter the warm zone and the other for exiting the warm zone into the cold zone. The decontamination zone for exiting should be upwind and uphill from the zone used to enter. Decontamination area workers should wear appropriate PPE. See the PPE section of this card for detailed information. A solution of detergent and water (which should have a pH value of at least 8 but should not exceed a pH value of 10.5) should be available for use in decontamination procedures. Soft brushes should be available to remove contamination from the PPE. Labeled, durable 6-mil polyethylene bags should be available for disposal of contaminated PPE.

INDIVIDUAL DECONTAMINATION : The following methods can be used to decontaminate an individual:

Decontamination of First Responder:

Begin washing PPE of the first responder using soap and water solution and a soft brush. Always move in a downward motion (from head to toe). Make sure to get into all areas, especially folds in the clothing. Wash and rinse (using cold or warm water) until the contaminant is thoroughly removed. Remove PPE by rolling downward (from head to toe) and avoid pulling PPE off over the head. Remove the SCBA after other PPE has been removed. Place all PPE in labeled durable 6-mil polyethylene bags.

Decontamination of Patient/Victim:

Remove the patient/victim from the contaminated area and into the decontamination corridor. Remove all clothing (at least down to their undergarments) and place the clothing in a labeled durable 6-mil polyethylene bag. Thoroughly wash and rinse (using cold or warm water) the contaminated skin of the patient/victim using a soap and water solution. Be careful not to break the patient/victim’s skin during the decontamination process, and cover all open wounds. Cover the patient/victim to prevent shock and loss of body heat. Move the patient/victim to an area where emergency medical treatment can be provided.

GENERAL INFORMATION : Initial treatment is primarily supportive of respiratory and cardiovascular function. The goal of treatment is to either prevent the conversion of methanol to toxic metabolites or to rapidly remove the toxic metabolites and correct metabolic and fluid abnormalities. ANTIDOTE : Fomepizole and ethanol are effective antidotes against methanol toxicity. Fomepizole or ethanol should be administered as soon as possible once the patient/victim has been admitted to a medical care facility. See Long Term Implications: Medical Treatment for further instruction. EYE :

Immediately remove the patient/victim from the source of exposure. Immediately wash eyes with large amounts of tepid water for at least 15 minutes. Seek medical attention immediately.

INGESTION :

Immediately remove the patient/victim from the source of exposure. Ensure that the patient/victim has an unobstructed airway. Do not induce vomiting (emesis). Seek medical attention immediately.

INHALATION :

Immediately remove the patient/victim from the source of exposure. Evaluate respiratory function and pulse. Ensure that the patient/victim has an unobstructed airway. If shortness of breath occurs or breathing is difficult (dyspnea), administer oxygen. Assist ventilation as required. Always use a barrier or bag-valve-mask device. If breathing has ceased (apnea), provide artificial respiration. Seek medical attention immediately.

SKIN :

Immediately remove the patient/victim from the source of exposure. See the Decontamination section for patient/victim decontamination procedures. Seek medical attention immediately.

MEDICAL TREATMENT : Antidotes fomepizole or ethanol should be administered intravenously as soon as possible to block the conversion of methanol to formic acid and prevent acidosis. Fomepizole is preferred as its efficacy and safety have been demonstrated, and its therapeutic dose is more easily maintained. Once the patient/victim has become acidotic, administration of fomepizole or ethanol may not provide much benefit, but they may be administered at the discretion of the physician in charge. Hemodialysis is the most effective form of treatment for an acidotic patient/victim. Folinic acid (leucovorin) should also be administered intravenously to increase the rate at which formate is metabolized into less toxic chemicals. DELAYED EFFECTS OF EXPOSURE : The most common permanent adverse health effects following severe methanol poisoning are damage to or death of the nerve leading from the eye to the brain (optic neuropathy or atrophy), resulting in blindness; disease caused by damage to a particular region of the brain, resulting in difficulty walking and moving properly (Parkinsonism); damage to the brain caused by exposure to toxins, resulting in abnormal thought (encephalopathy); and damage to the peripheral nervous system. EFFECTS OF CHRONIC OR REPEATED EXPOSURE : Methanol is not suspected to be a carcinogen. Chronic or repeated exposure to methanol is suspected to be a developmental toxicity risk. It is unknown whether chronic or repeated exposure to methanol is a reproductive toxicity risk. Methanol may cause birth defects of the central nervous system in humans. Chronic poisoning from repeated exposure to methanol vapor may produce inflammation of the eye (conjunctivitis), recurrent headaches, giddiness, insomnia, stomach disturbances, and visual failure. The most noted health consequences of longer-term exposure to lower levels of methanol are a broad range of effects on the eye. Inflammatory changes and irritation of the skin (dermatitis), occurs with chronic or repeated exposure to methanol.

INCIDENT SITE :

Consult with the Incident Commander regarding the agent dispersed, dissemination method, level of PPE required, location, geographic complications (if any), and the approximate number of remains. Coordinate responsibilities and prepare to enter the scene as part of the evaluation team along with the FBI HazMat Technician, local law enforcement evidence technician, and other relevant personnel. Begin tracking remains using waterproof tags.

RECOVERY AND ON-SITE MORGUE :

Wear PPE until all remains are deemed free of contamination. Establish a preliminary (holding) morgue. Gather evidence, and place it in a clearly labeled impervious container. Hand any evidence over to the FBI. Remove and tag personal effects. Perform a thorough external evaluation and a preliminary identification check. See the Decontamination section for decontamination procedures. Decontaminate remains before they are removed from the incident site.

See Guidelines for Mass Fatality Management During Terrorist Incidents Involving Chemical Agents, U.S. Army Soldier and Biological Chemical Command (SBCCOM), November, 2001 for detailed recommendations.

NIOSH REL :

STEL (skin): 250 ppm (325 mg/m 3 ) TWA (skin): 200 ppm (260 mg/m 3 )

OSHA PEL :

TWA (8-hour): 200 ppm (260 mg/m 3 )

ACGIH TLV :

STEL (skin): 250 ppm TLV (skin): 200 ppm

NIOSH IDLH : 6,000 ppm DOE TEEL :

TEEL-0: 250 mg/m 3 TEEL-1: 694 mg/m 3 TEEL-2: 2,750 mg/m 3 TEEL-3: 9,300 mg/m 3

AIHA ERPG :

ERPG-1: 200 ppm ERPG-2: 1,000 ppm ERPG-3: 5,000 ppm

Acute Exposure Guidelines

	10 min	30 min	60 min	4 hr	8 hr
AEGL 1 (discomfort, non-disabling) – ppm	670 ppm	670 ppm	530 ppm	340 ppm	270 ppm
AEGL 2 (irreversible or other serious, long-lasting effects or impaired ability to escape) – ppm	11,000 ppm*	4,000 ppm	2,100 ppm	730 ppm	520 ppm
AEGL 3 (life-threatening effects or death) – ppm	**	14,000 ppm*	7,200 ppm*	2,400 ppm	1,600 ppm

Lower Explosion Limit (LEL) = 55,000 ppm * = > 10% LEL; ** = > 50% LEL AEGL 3 – 10 min = ** 40,000 ppm For values denoted as * safety consideration against the hazard(s) of explosion(s) must be taken into account For values denoted as ** extreme safey considerations against the hazard(s) of explosion(s) must be taken into account Level of Distinct Order Awareness (LOA) = 8.9 ppm IMPORTANT NOTE: Interim AEGLs are established following review and consideration by the National Advisory Committee for AEGLs (NAC/AEGL) of public comments on Proposed AEGLs. Interim AEGLs are available for use by organizations while awaiting NRC/NAS peer review and publication of Final AEGLs. Changes to Interim values and Technical Support Documents may occur prior to publication of Final AEGL values. In some cases, revised Interim values may be posted on this Web site, but the revised Interim Technical Support Document for the chemical may be subject to change. (Further information is available through ).

What is the antidote for methanol?

Abstract – Epidemiology: Almost all cases of acute methanol toxicity result from ingestion, though rarely cases of poisoning have followed inhalation or dermal absorption. The absorption of methanol following oral administration is rapid and peak methanol concentrations occur within 30-60minutes.

Mechanisms of toxicity: Methanol has a relatively low toxicity and metabolism is responsible for the transformation of methanol to its toxic metabolites. Methanol is oxidized by alcohol dehydrogenase to formaldehyde. The oxidation of formaldehyde to formic acid is facilitated by formaldehyde dehydrogenase.

Formic acid is converted by 10-formyl tetrahydrofolate synthetase to carbon dioxide and water. In cases of methanol poisoning, formic acid accumulates and there is a direct correlation between the formic acid concentration and increased morbidity and mortality.

• The acidosis observed in methanol poisoning appears to be caused directly or indirectly by formic acid production.
• Formic acid has also been shown to inhibit cytochrome oxidase and is the prime cause of ocular toxicity, though acidosis can increase toxicity further by enabling greater diffusion of formic acid into cells.

Features: Methanol poisoning typically induces nausea, vomiting, abdominal pain, and mild central nervous system depression. There is then a latent period lasting approximately 12-24 hours, depending, in part, on the methanol dose ingested, following which an uncompensated metabolic acidosis develops and visualfunction becomes impaired, ranging from blurred vision and altered visual fields to complete blindness.

Management: For the patient presenting with ophthalmologic abnormalities or significant acidosis, the acidosis should be corrected with intravenous sodium bicarbonate, the further generation of toxic metabolite should be blocked by the administration of fomepizole or ethanol and formic acid metabolism should be enhanced by the administration of intravenous folinic acid.

Hemodialysis may also be required to correct severe metabolic abnormalities and to enhance methanol and formate elimination. For the methanol poisoned patient without evidence of clinical toxicity, the first priority is to inhibit methanol metabolism with intravenous ethanol orfomepizole.

1. Although there are no clinical outcome data confirming the superiority of either of these antidotes over the other, there are significant disadvantages associated with ethanol.
2. These include complex dosing, difficulties with maintaining therapeutic concentrations, the need for more comprehensive clinical and laboratory monitoring, and more adverse effects.

Thus fomepizole is very attractive, however, it has a relatively high acquisition cost. Conclusion: The management of methanol poisoning includes standard supportive care, the correction of metabolic acidosis, the administration of folinic acid, the provision of an antidote to inhibit the metabolism of methanol to formate, and selective hemodialysis to correct severe metabolic abnormalities and to enhance methanol and formate elimination.

Can you get methanol poisoning from moonshine?

Moonshine is related to southern culture, heritage, and tradition, but its origin can be traced back to Pennsylvania. Around 1791, when the distilled-spirits tax was implemented, farmers grew frustrated and were determined to do something about the matter.

Does homemade moonshine have methanol?

A Tale of Chemistry and Poison Photo by Sam Johnson from Pexels During the American Prohibition, moonshine was responsible for over 750 deaths and more than a hundred thousand cases of blindness or paralysis in New York City alone. Over eighty years later, in early 2019, several outbreaks of toxic alcohol poisoning lead to hundreds of deaths and injuries in northeast India.

The culprit in both these cases was methanol contamination. Chemically, the only difference between methanol and ethanol is the number of carbons (two in ethanol and one in methanol). Methanol and ethanol taste about the same and produce about the same initial intoxicating effect. The only difference is that methanol, once ingested, is metabolized by the liver into formaldehyde and formic acid, chemicals that can damage the optic nerve, leading to blindness, and eventually resulting in death.

Methanol is a common contaminant of moonshine, which is typically made from fermenting a “mash” of corn, sugar, and yeast for a few days and then distilling the mixture. During the fermentation process, the enzymes in the yeast convert the sugar into energy for the cell.

• A byproduct of this reaction is ethanol, the main ingredient of alcohol.
• Methanol is not a direct byproduct of fermentation, but instead forms from the breakdown of pectin in corn.
• After fermentation, the slurry is distilled by boiling it and running the gas through a still.
• The first element of the still is a long upward shaft through which the gas rises.

The length of this shaft prevents anything that is not gas from escaping to the next stage. Next, the gas travels downwards through another shaft that’s kept ice cold. On the other side of this shaft, the gas is cool enough to condense into liquid again. Photo by Davide Baraldi from Pexels Methanol is easily removed in regulated alcohol production, and extensive testing is required by the U.S. Food and Drug Administration (FDA) to ensure that very little methanol makes it into the final batch. In the case of alcohol that is used for industrial or scientific purposes, methanol is often added back into the batch after distillation to make it toxic and thus not subject to alcoholic beverage tax.

Bootleggers can use this cheaper methanol-tainted alcohol to turn a considerable profit. During Prohibition, the government doubled the amount of methanol in industrial alcohol to make it more toxic and discourage bootleggers from stealing and redistributing it. Bootleggers put significant effort into overcoming these measures, hiring chemists to distill the toxic chemicals out of their alcohol.

But the government only doubled down their efforts, adding up to 10% methanol and a whole slew of other poisons including chloroform, gasoline, and mercury salts. The only thing these measures accomplished, however, was to poison and kill an estimated 10,000 Americans by the time the Prohibition ended.

1. These days, epidemics of toxic alcohol poisoning still occur around the world in poor areas, like the tea plantations in India, where unscrupulous bootleggers sell cheap alcohol laced with methanol or lead.
2. Lead can be leached from truck radiators, which are frequently used in crude distillation setups.

Drinkers discern very little difference between clean alcohol and alcohol laced with methanol, and the body’s immediate reaction to the alcohol is the same. It’s only hours later, once the methanol has been digested and converted to formic acid, that the poison presents itself with convulsions, blindness, and death.

How do distilleries avoid methanol?

2.1.3. Inhibition of Pectin Methylesterase by Sterilization of Mash – A significant reduction of methanol by 40–90% can be achieved by thermal deactivation of pectin methylesterase (often referred to as “mash heating”). There are various suggestions for temperature/time combinations to achieve the enzyme’s denaturation.

Sterilization at temperatures higher than 70 °C was generally suggested to effectively prevent the production of methanol by inactivation of pectin methylesterase, Methanol can be reduced by targeted thermal deactivation of pectin methylesterase by heating the mash to 80 °C up to 85 °C for a holding time of 30 min or to 60 °C for 45 min,

Pasteurization at 72 °C for 15 s prevented the production of methanol in fermented plant beverages containing Morinda citrifolia (noni fruit), In cider spirit, the pasteurization (30 min at 50 °C, then heated to about 85 °C) of the apple juice prior to fermentation reduced the methanol content by 34–46%,

Lower methanol levels were obtained in Williams and plums by heating the mash to 65 °C for 5 min, followed by re-cooling for fermentation, Xia et al. confirmed that autoclaving by steam injection of the mash of jujube reduced the methanol content in the spirit significantly by a factor of about eight.

The authors also determined pectin methylesterase activity confirming that their treatment method reduced the activity to one-fifth to half of that without treatment. Further technological approaches for inactivation of methylesterase are thermosonication (ultrasound plus temperature at 70° led to 30% methanol reduction in plum wine) or use of microwaves (70 °C for 1 min led to 70% methanol reduction in plum wine).

What are 3 ways alcohol affects vision?

Unhealthy amounts of alcohol consumption can lead to a decrease in peripheral vision, weakened eye muscles, a thinning of the cornea, and loss of color vision —all things that can lead to permanent vision loss.

Which alcohol causes blindness even death?

Vision loss after accidental methanol intoxication: a case report 1 1st Department of Ophthalmology, University of Athens Medical School, ‘G. Genimmatas’ General Hospital Athens, 154 Mesogion Avenue, Holargos 11527, Athens, Greece Find articles by 1 1st Department of Ophthalmology, University of Athens Medical School, ‘G.

Genimmatas’ General Hospital Athens, 154 Mesogion Avenue, Holargos 11527, Athens, Greece Find articles by 2 2nd Department of Ophthalmology, University of Athens Medical School, ‘Attikon’ Hospital, 1 Rimini Street, Haidari 12462, Athens, Greece Find articles by 1 1st Department of Ophthalmology, University of Athens Medical School, ‘G.

Genimmatas’ General Hospital Athens, 154 Mesogion Avenue, Holargos 11527, Athens, Greece Find articles by

1 1st Department of Ophthalmology, University of Athens Medical School, ‘G. Genimmatas’ General Hospital Athens, 154 Mesogion Avenue, Holargos 11527, Athens, Greece 2 2nd Department of Ophthalmology, University of Athens Medical School, ‘Attikon’ Hospital, 1 Rimini Street, Haidari 12462, Athens, Greece Corresponding author. Marilita M Moschos: ; Nikolaos S Gouliopoulos: ; Alexandros Rouvas: ; Ioannis Ladas:

Received 2013 Jun 18; Accepted 2013 Nov 18. © 2013 Moschos et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Methanol intoxication is a dangerous situation because it often results in permanent problems such as visual deterioration, metabolic disturbances, neurological dysfunction, and even death.
2. We present, to the best of our knowledge, the first case of irreversible bilateral blindness due to methanol intoxication caused by accidental ingestion of rubbing liquid.

A 49-year-old Greek man developed bilateral irreversible blindness after accidental methanol intoxication. He underwent complete ophthalmological examination, including electroretinogram, visual evoked potentials, multifocal-visual evoked potentials, and optical coherence tomography scan of the optic nerve.

Complete laboratory evaluation, urine drug testing, neurological examination, and computed tomography scans were also performed. Visual acuity demonstrated no light perception bilaterally, pupils were semi-dilated and unreactive to light, while the retina was normal in both eyes. Electroretinogram was normal, while visual evoked potentials, multifocal-visual evoked potentials recording, and optical coherence tomography scanning of both optic nerve heads were pathological in both eyes.

The neurological examination and the computed tomography scans did not reveal any abnormalities. The laboratory evaluation was normal and the urine drug test was negative for benzodiazepines, opiates, cocaine, amphetamines, salicylates, barbiturates, and phencyclidine.

This is the first case report of methanol intoxication which documents both anatomical and functional abnormalities by means of optical coherence tomography and electrophysiological tests correspondingly. The ocular findings and the reported electrophysiological changes support the hypothesis that methanol affects photoreceptors, Müller cells, and the retrolaminar portion of the optic nerve.

Keywords: Methanol Intoxication, Bilateral Blindness, ERG, VEPs, Multifocal VEPs, OCT Methanol is a clear, colourless and volatile fluid which smells and tastes like ethanol and therefore it is difficult to differentiate methanol from alcohol. Its main uses are as a raw material for industrial solvents, antifreeze production and in bootleg whiskey.

Accidental ingestion of methanol is common (more than half of the methanol intoxication cases), preventable and causes serious side effects. Methanol intoxication (even in small amounts) is very dangerous because it can cause severe visual dysfunction (including irreversible bilateral blindness), metabolic disturbances, permanent neurological dysfunction and even death,

We present, to the best of our knowledge, the first case of methanol intoxication caused by accidental ingestion of rubbing liquid. A 49-year-old healthy Greek man without any prior significant medical history, working as a cook on a merchant ship, drank accidentally a glass of 70% methanol rubbing solution, while he was on board.

One day later he complained for blurred vision and painful eye movement in both eyes. The second day he woke up blind. He remained on board since the ship was heading to Australia and so treatment was impossible. When the ship reached Australia, he was hospitalized for a week. On arrival his vital signs were within normal limits and his examination tests revealed normal muscle tone.

His initial laboratory evaluation included a complete blood count, electrolytes, blood urea nitrogen, creatinine, and serum glucose. All test results were within the normal range for the patient’s age. A urine drug test was negative for benzodiazepines, opiates, cocaine, amphetamines, phencyclidine, salicylates, and barbiturates.

• The blood methyl alcohol and formic acid values could not be determined.
• No treatment was given due to patient’s late arrival.
• He then was transferred to the University Eye Clinic of Athens.
• At presentation he underwent a complete ophthalmological examination.
• Visual acuity was no light perception in both eyes.

The pupils were semi-dilated and unreactive to light. Fundus examination revealed an unremarkable retina in both eyes with the exception of pronounced pale, atrophic optic discs with “pseudoglaucomatous” thinning of the neuroretinal rim area. Electroretinogram (ERG) was normal in both eyes (Figure ).

Visual evoked potentials (VEPs) were nearly extinguished (Figure ). Multifocal-visual evoked potential (mf-VEP) recording was also pathological in area 0 (right eye: 169 nV/deg2 and left eye: 186 nV/deg2) (Figure ). Optical coherence tomography (OCT) of the optic nerve head demonstrated abnormally low values of the retinal nerve fiber layer (RNFL) thickness equal to 128 μm in the superior, 39 in the nasal, 108 in the inferior, and 72 in the temporal quadrant of the right eye (OD), and 134, 99, 92, and 58 correspondingly of the left eye (OS) (Figure ).

Multifocal visual evoked potential recording; Multifocal Visual evoked potential 3D plot and corresponding traces of the right eye (3a) and the left eye (3b) respectively. Area 0 is very diminished bilaterally (right eye: 169 nV/deg 2, left eye: 186 nv/deg 2 ).

Optical coherence tomography recording around the optic nerve head; retinal nerve fiber layer thickness in the right eye (OD) in μm (128 in the superior, 39 in the nasal, 108 in the inferior, and 72 in the temporal quadrant) and retinal nerve fiber layer thickness in the left eye (OS) (134, 99, 92, and 58 correspondingly).

Neurological examination with the patient awake revealed no extrapyramidal motor disturbances and computed tomography (CT) scans showed no abnormalities. Anion gap was less than 30 mg/dL and no treatment was deemed necessary to initiate. The patient was discharged on the fourth day.

He was reexamined one month later. The situation remained unchanged. Methanol intoxication is followed by a 12–24 hour latency period, after which appear its symptoms and signs which are related to the gastrointestinal, to the ocular, and to the nervous system. Early ocular findings include photophobia, blurred vision, painful eye movements, disturbances of pupil reactions and colour vision, decreased visual acuity, visual field defects and optic disc oedema with tortuous retinal vessels.

Their absence on the initial examination is a good prognostic sign and there is not any case reported with permanent visual loss after an initial normal examination, Myelin damage at the retrolaminar optic nerve has been shown in histopathological examination.

1. In our case, VEPs were almost extinguished and OCT scan of the optic nerve revealed highly decreased values.
2. These findings are in accordance with the literature and are probably a result of the fact that methanol affects photoreceptors, Müller cells, and the retrolaminar portion of the optic nerve,

Methanol intoxication should be early recognised and treated in order to prevent permanent health problems and patient’s death. The treatment includes the treatment of the metabolic acidosis by oral or intravenous bicarbonate administration, the prevention of further oxidation of methanol to toxic metabolites (formaldehyde and formic acid) by competitive inhibition of the enzyme alcohol dehydrogenase (by ethyl alcohol or fomepizole), and the elimination of methanol and its metabolites by haemodialysis.

Our patient developed irreversible blindness bilaterally because he was not treated in the maximum time of two days since the methanol ingestion. This is the first case report of methanol intoxication which documents both anatomical and functional ocular abnormalities by means of OCT and electrophysiological tests correspondingly.

The ocular findings and the reported electrophysiological changes support the hypothesis that methanol affects photoreceptors, Müller cells, and the retrolaminar portion of the optic nerve. It describes a case which has a broader clinical impact across medicine.

1. Our case also underlines the importance of the early recognition and treatment initiation in cases of methanol ingestion.
2. Written informed consent was obtained from the patient for publication of this case report and any accompanying images.
3. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

The authors declare that they have no competing interests. MMM participated in writing the case report and examined the patient. NSG participated in writing the case report. AR initially examined the patient. IL performed the OCT examination. All authors read and approved the final manuscript.

Shusterman D, Osterloh JD, Ambre J. Methanol Toxicity. Am Fam Physician.1993; 47 :163–171. Benton CD, Calhoun FP. The ocular effects of methyl alcohol poisoning: report of a catastrophe involving 320 persons. Am J Opthalmol.1952; 36 :1677–1685. McKellar MJ, Hidajat RR, Elder MJ. Acute ocular methanol toxicity: clinical and electrophysiological features. Aust NZ J Opthalmol.1997; 25 :225–230.

Articles from BMC Research Notes are provided here courtesy of BioMed Central : Vision loss after accidental methanol intoxication: a case report

Can alcohol affect eyesight permanently?

Long-term effects of alcohol on your vision – Long-term effects of alcohol abuse can have detrimental consequences on your vision and eye health. In extreme cases, toxic amblyopia, the result of a toxic reaction in the optic nerve which causes permanent vision loss.

Excessive alcohol may increase your risk of age-related macular degeneration ; WHO’s report revealed that the average person’s daily consumption is 33g of pure alcohol, which is the equivalent of 2 glasses of wine. A study in Australia revealed that drinking more than 20g of alcohol a day results in a 20% increased chance of developing early AMD compared to those who consume no alcohol.

Poor diet and over-consumption of alcohol may also be related to developing cataracts, Prolonged alcohol abuse will eventually affect your vision through vitamin deficiency. The liver can only process so much alcohol at a time and heavy drinking can affect the absorption of vitamins in the liver which are needed to maintain healthy eyes and good vision.

Will my eyesight improve if I stop drinking?

Within 24 hours – Drinking alcohol increases blood-sugar levels which can lead to blurred vision, as it causes the eye lens to swell, reducing your ability to see. After 24 hours of no alcohol, your blood-sugar levels will normalise and any vision impairment will return to normal. In other words, banishing your beer goggles.