Antifreeze products for automotive use containing propylene glycol in place of ethylene glycol are available, and are generally considered safer to use, as it possesses an unpleasant taste in contrast to the perceived "sweet" taste of toxic ethylene glycol-based coolants, and only produces lactic acid in an animal's body, as their muscles do when exercised.

When using antifreeze products containing ethylene glycol, recommended safety measures include:

- Cleaning up any spill immediately and thoroughly. Spills may be cleaned by sprinkling cat litter, sand or other absorbent material directly on the spill. Once fully absorbed, while wearing protective gloves, the material may be scooped into a plastic bag, sealed and disposed. The spill area may be scrubbed with a stiff brush and warm, soapy water. The soapy water is not recommended to be drained in a storm drain.

- Checking vehicles regularly for leaks.

- Storing antifreeze in clearly marked original sealed containers, in areas that are inaccessible to pets or small children.

- Keeping pets and small children away from the area when draining the car radiator.

- Disposing of used antifreeze only by taking to a service station.

- If antifreeze is placed in toilets, ensuring the lid is down and the door closed.

Following decontamination and the institution of supportive measures, the next priority is inhibition of further ethylene glycol metabolism using antidotes. The antidotes for ethylene glycol poisoning are ethanol and fomepizole. This antidotal treatment forms the mainstay of management of ethylene glycol poisoning. The toxicity of ethylene glycol comes from its metabolism to glycolic acid and oxalic acid. The goal of pharmacotherapy is to prevent the formation of these metabolites. Ethanol acts by competing with ethylene glycol for alcohol dehydrogenase, the first enzyme in the degradation pathway. Because ethanol has a much higher affinity for alcohol dehydrogenase, about a 100-times greater affinity, it successfully blocks the breakdown of ethylene glycol into glycolaldehyde, which prevents the further degradation. Without oxalic acid formation, the nephrotoxic effects can be avoided, but the ethylene glycol is still present in the body. It is eventually excreted in the urine, but supportive therapy for the CNS depression and metabolic acidosis will be required until the ethylene glycol concentrations fall below toxic limits. Pharmaceutical grade ethanol is usually given intravenously as a 5 or 10% solution in 5% dextrose, but it is also sometimes given orally in the form of a strong spirit such as whisky, vodka, or gin.

Fomepizole is a potent inhibitor of alcohol dehydrogenase; similar to ethanol, it acts to block the formation of the toxic metabolites. Fomepizole has been shown to be highly effective as an antidote for ethylene glycol poisoning. It is the only antidote approved by the U.S. Food and Drug Administration for the treatment of ethylene glycol poisoning. Both antidotes have advantages and disadvantages. Ethanol is readily available in most hospitals, is inexpensive, and can be administered orally as well as intravenously. Its adverse effects include intoxication, hypoglycemia in children, and possible liver toxicity. Patients receiving ethanol therapy also require frequent blood ethanol concentration measurements and dosage adjustments to maintain a therapeutic ethanol concentration. Patients therefore must be monitored in an intensive care unit. Alternatively, the adverse side effects of fomepizole are minimal and the approved dosing regimen maintains therapeutic concentrations without the need to monitor blood concentrations of the drug. The disadvantage of fomepizole is that it is expensive. Costing US$1,000 per gram, an average course used in an adult poisoning would cost approximately $3,500 to $4,000. Despite the cost, fomepizole is gradually replacing ethanol as the antidote of choice in ethylene glycol poisoning. Adjunct agents including thiamine and pyridoxine are often given, because they may help prevent the formation of oxalic acid. The use of these agents is based on theoretical observations and there is limited evidence to support their use in treatment; they may be of particular benefit in people who could be deficient in these vitamins such as malnourished or alcoholic patients.

In general, the simultaneous use of multiple drugs should be carefully monitored by a qualified individual such as board certified and licensed medical doctor, either an MD or DO Close association between prescribing physicians and pharmacies, along with the computerization of prescriptions and patients' medical histories, aim to avoid the occurrence of dangerous drug interactions. Lists of contraindications for a drug are usually provided with it, either in monographs, package inserts (accompanying prescribed medications), or in warning labels (for OTC drugs). CDI/MDI might also be avoided by physicians requiring their patients to return any unused prescriptions. Patients should ask their doctors and pharmacists if there are any interactions between the drugs they are taking.

On June 30, 2009, an FDA advisory panel recommended that Vicodin and another painkiller, Percocet, be removed from the market because they have allegedly caused over 400 deaths a year. The problem is with paracetamol (acetaminophen/Tylenol for example ) overdose and liver damage. These two drugs, in combination with other drugs like Nyquil and Theraflu, can cause death by multiple drug intake and/or drug overdose. Another solution would be to not include paracetamol with Vicodin or Percocet.

Research is being done by organizations such as NINDS (National Institute of Neurological Disorders and Stroke) on what substances can cause encephalopathy, why they do this, and eventually how to protect, treat, and cure the brain from this condition.

Substance intoxication is a type of substance use disorder which is potentially maladaptive and impairing, but reversible, and associated with recent use.

If the symptoms are severe, the term "substance intoxication delirium" may be used.

Generic slang terms include: getting high or being stoned or blazed (all usually in reference to cannabis), with many more specific slang terms for each particular type of intoxicant. Alcohol intoxication is even graded in intensity, from buzzed, to tipsy, all the way up to hammered, smashed, wasted, destroyed, and a number of other similar terms.

Examples (and ICD-10 code) include:

- F10.0 alcohol intoxication

- F11.0 opioid intoxication

- F12.0 cannabinoid intoxication

- F13.0 sedative and hypnotic intoxication (see benzodiazepine overdose and barbiturate overdose)

- F14.0 cocaine intoxication

- F15.0 caffeine intoxication

- F16.0 hallucinogen intoxication (See for example Lysergic acid diethylamide effects)

- F17.0 tobacco intoxication

The term contact high is sometimes used to describe intoxication without direct administration, either by second-hand smoke as with cannabis, or by placebo in the presence of others who are high.

Toxic encephalopathy is a neurologic disorder caused by exposure to neurotoxic organic solvents such as toluene, following exposure to heavy metals such as manganese; or exposure to extreme concentrations of any natural toxin such as cyanotoxins found in shellfish or freshwater cyanobacteria crusts. Toxic encephalopathy can occur following acute or chronic exposure to neurotoxicants, which includes all natural toxins. Exposure to toxic substances can lead to a variety of symptoms, characterized by an altered mental status, memory loss, and visual problems. Toxic encephalopathy can be caused by various chemicals, some of which are commonly used in everyday life, or cyanotoxins which are bio-accumulated from Harmful algal blooms (HAB's) which have settled on the benthic layer of a waterbody. Toxic encephalopathy can permanently damage the brain and currently treatment is mainly just for the symptoms.

Sun avoidance, avoidance of tanning booths, and usage of broad spectrum sunscreen that blocks both UVA and UVB.

Identification and avoidance of the offending drug.

The values of soluble cobalt salts has been estimated to be between 150 and 500 mg/kg. Thus, for a 100 kg person the LD would be about 20 grams.

Exposure to cobalt metal dust is most common in the fabrication of tungsten carbide. Another potential source is wear and tear of metal-on-metal hip prostheses; however, this is a relatively uncommon phenomenon with 18 reported cases being documented in the medical literature.

The treatment for auto-brewery syndrome is a change in diet requiring low carbohydrates and high protein. Sugar is fermented into alcohol, and a diet that effectively lowers sugars also lowers the alcohol that can be fermented from it. Anything that causes an imbalance between the beneficial and harmful bacteria in the gut can help increase the chance that fermentation in the gut will develop. This can include not only antibiotics, but also overindulgence in sugars and carbohydrates. Watching what you eat could lower the risk of gut fermentation syndrome, and taking probiotics could further protect you by increasing the number of good bacteria in your system.

Withdrawal of the contaminated cooking oil is the most important initial step. Bed rest with leg elevation and a protein-rich diet are useful. Supplements of calcium, antioxidants (vitamin C and E), and thiamine and other B vitamins are commonly used. Corticosteroids and antihistaminics such as promethazine have been advocated by some investigators, but demonstrated efficacy is lacking. Diuretics are used universally but caution must be exercised not to deplete the intravascular volume unless features of frank congestive cardiac failure are present, as oedema is mainly due to increased capillary permeability. Cardiac failure is managed by bed rest, salt restriction, digitalis and diuretics. Pneumonia is treated with appropriate antibiotics. Renal failure may need dialysis therapy and complete clinical recovery is seen. Glaucoma may need operative intervention, but generally responds to medical management.

An alcohol enema, also known colloquially as butt-chugging, is the act of introducing alcohol into the rectum and colon via the anus. This method of alcohol consumption can be dangerous and even deadly because it leads to faster intoxication since the alcohol is absorbed directly into the bloodstream and neutralizes the body's ability to reject the toxin by vomiting.

An alcohol enema is a faster method of alcohol intoxication since the alcohol is absorbed directly into the bloodstream. The lower gastrointestinal tract lacks the alcohol dehydrogenase enzyme present in the stomach and liver that breaks down ethanol into acetylaldehyde, which is actually more toxic than ethanol (drinking alcohol) and is responsible for most chronic effects of ethanol. When rectally absorbed, ethanol will still eventually arrive at the liver, but the high alcohol content could overwhelm the organ. Additionally, consuming the alcohol rectally neutralizes the body's ability to reject the toxin by vomiting.

The standard of care is discontinuation of the environmental exposure, and chelation therapy (with EDTA or maybe better, DMSA).

Pseudoporphyria can be induced by a wide range of medications, excessive UV-A exposure, and hemodialysis. One frequently reported drug is naproxen. A frequent source of UV-A exposure is tanning booths.

As recognition of pseudoporphyria increases and the number of new medications expands, the list of etiologic agents associated with pseudoporphyria will most likely continue to grow. Agents associated with pseudoporphyria are as follows:

- Propionic acid derivatives (NSAIDs) - naproxen, diflunisal, ketoprofen, oxaprozin, mefenamic acid, rofecoxib

- Ketone NSAID-nabumetone

- Antibiotics - nalidixic acid, tetracycline, oxytetracycline, ampicillin-sulbactam, cefepime, fluoroquinolones (M Poh, personal communication, June 1999)

- Antifungals - voriconazole

- Diuretics - furosemide, chlorthalidone, butamide, triamterene/hydrochlorothiazide

- Antiarrhythmics - amiodarone

- Chemotherapy - 5-fluorouracil

- Immunosuppressants - cyclosporine

- Sulfones - dapsone

- Vitamins - brewers' yeast, pyridoxine

- Vitamin A derivatives - etretinate, isotretinoin

- Muscle relaxants - carisoprodol/aspirin

- Nonsteroidal antiandrogens - flutamide

- Other - hemodialysis, excessive UV-A, cola, oral contraceptive pills (levonorgestrel and ethinylestradiol), narrowband UV-B phototherapy (rarely)

The short-term effects of alcohol (also known formally as ethanol) consumption–due to drinking beer, wine, distilled spirits or other alcoholic beverages–range from a decrease in anxiety and motor skills and euphoria at lower doses to intoxication (drunkenness), stupor, unconsciousness, anterograde amnesia (memory "blackouts"), and central nervous system depression at higher doses. Cell membranes are highly permeable to alcohol, so once alcohol is in the bloodstream it can diffuse into nearly every cell in the body.

The concentration of alcohol in blood is measured via blood alcohol content (BAC). The amount and circumstances of consumption play a large part in determining the extent of intoxication; for example, eating a heavy meal before alcohol consumption causes alcohol to absorb more slowly. The amount of alcohol consumed largely determines the extent of hangovers, although hydration also plays a role. After excessive drinking, stupor and unconsciousness can occur. Extreme levels of consumption can lead to alcohol poisoning and death (a concentration in the blood stream of 0.40% will kill half of those affected). Alcohol may also cause death indirectly, by asphyxiation from vomit.

Alcohol can greatly exacerbate sleep problems. During abstinence, residual disruptions in sleep regularity and sleep patterns are the greatest predictors of relapse.

Besides India, widespread epidemics have been reported from Mauritius, Fiji Islands, Northwest Cape districts of South Africa, Madagascar and also from Nepal. Apart from a South African study, where the epidemic occurred through contamination in wheat flour, all the epidemics occurred through the consumption of mustard oil contaminated with argemone oil.

In these populations mustard oil is the prime edible oil by culture.

The earliest reference to argemone oil poisoning was made by Lyon, who reported four cases of poisoning in Calcutta in 1877 from the use of this oil in food.

Since then, epidemic dropsy has been reported from Bengal, Bihar, Orissa, Madhya Pradesh, Haryana, Assam, J&K, Uttar Pradesh, Gujarat, Delhi and Maharashtra, mainly due to consumption of food cooked in argemone oil mixed with mustard oil or occasionally by body massage with contaminated oil.

The epidemic in 1998 at New Delhi, India is the largest so far, in which over 60 persons lost their lives and more than 3000 victims were hospitalized. Few studies reported the findings in patients affected with this condition.

Even after that the epidemics occurred at alarming frequency in Gwalior (2000), Kannauj (2002) and Lucknow (2005) cities of India.

Mercury compounds like calomel were historically used for various medical purposes: as laxatives, diuretics, antiseptics or antimicrobial drugs for syphilis, typhus and yellow fever

. Teething powders were a widespread source of mercury poisoning until the recognition of mercury toxicity in the 1940s.

However, mercury poisoning and acrodynia still exist today. Modern sources of mercury intoxication include broken thermometers.

Acute alcohol poisoning is a medical emergency due to the risk of death from respiratory depression and/or inhalation of vomit if emesis occurs while the patient is unconscious and unresponsive. Emergency treatment for acute alcohol poisoning strives to stabilize the patient and maintain a patent airway and respiration, while waiting for the alcohol to metabolize. This can be done by removal of any vomitus or, if patient is unconscious or has impaired gag reflex, intubation of the trachea using an endotracheal tube to maintain adequate airway:

Also:

- Treat hypoglycaemia (low blood sugar) with 50 ml of 50% dextrose solution and saline flush, as ethanol induced hypoglycaemia is unresponsive to glucagon.

- Administer the vitamin thiamine to prevent Wernicke-Korsakoff syndrome, which can cause a seizure (more usually a treatment for chronic alcoholism, but in the acute context usually co-administered to ensure maximal benefit).

- Apply hemodialysis if the blood concentration is dangerously high (>400 mg/dL), and especially if there is metabolic acidosis.

- Provide oxygen therapy as needed via nasal cannula or non-rebreather mask.

- Provide parenteral Metadoxine.

Additional medication may be indicated for treatment of nausea, tremor, and anxiety.

A normal liver detoxifies the blood of alcohol over a period of time that depends on the initial level and the patient's overall physical condition. An abnormal liver will take longer but still succeeds, provided the alcohol does not cause liver failure.

People having drunk heavily for several days or weeks may have withdrawal symptoms after the acute intoxication has subsided.

A person consuming a dangerous amount of alcohol persistently can develop memory blackouts and idiosyncratic intoxication or pathological drunkenness symptoms.

Long-term persistent consumption of excessive amounts of alcohol can cause liver damage and have other deleterious health effects.

Sunscreen is effective and thus recommended to prevent melanoma and squamous-cell carcinoma. There is little evidence that it is effective in preventing basal-cell carcinoma. Other advice to reduce rates of skin cancer includes avoiding sunburning, wearing protective clothing, sunglasses and hats, and attempting to avoid sun exposure or periods of peak exposure. The U.S. Preventive Services Task Force recommends that people between 9 and 25 years of age be advised to avoid ultraviolet light.

The risk of developing skin cancer can be reduced through a number of measures including decreasing indoor tanning and mid day sun exposure, increasing the use of sunscreen, and avoiding the use of tobacco products.

There is insufficient evidence either for or against screening for skin cancers. Vitamin supplements and antioxidant supplements have not been found to have an effect in prevention. Evidence for a benefit from dietary measures is tentative.

Zinc oxide and titanium oxide are often used in sun screen to provide broad protection from UVA and UVB ranges.

Eating certain foods may decrease the risk of sunburns but this is much less than the protection provided by sunscreen.

Treatment initially may include ketamine or midazolam and haloperidol injected into a muscle to sedate the person. Rapid cooling may be required in those with high body temperature. Other supportive measures such as intravenous fluids and sodium bicarbonate may be useful.

Erythema ab igne was once commonly seen in the elderly who stood or sat closely to open fires or electric heaters; however, erythema ab igne has been reported in both young and elderly individuals. Women have a higher incidence of erythema ab igne than men. Although wide use of central heating has reduced the overall incidence of erythema ab igne, it is still sometimes found in people exposed to heat from other sources such as heating pads, space heaters, hot water bottles, and electronic devices.