Hangovers occur commonly.

- A study in college students found that 25% had experienced a hangover in the previous week and 29% reported losing school time for hangover recovery.

- 15% of men and women who have consumed alcohol experience hangovers at least monthly and ten percent of British men reported hangover-related problems at work at least monthly.

- An estimated 9.23% (11.6 million workers) of the U.S. labor force work with a hangover.

- About 23% of drinkers do not report any hangover after drinking to intoxication.

Several factors which do not in themselves cause alcohol hangover are known to influence its severity. These factors include personality, genetics, health status, age, sex, associated activities during drinking such as smoking, the use of other drugs, physical activity such as dancing, as well as sleep quality and duration.

- Genetics: alleles associated with aldehyde dehydrogenase (ALDH) and flushing phenotypes (alcohol flush reaction) in Asians are known genetic factors that influence alcohol tolerance and the development of hangover effects. Existing data shows that drinkers with genotypes known to lead to acetaldehyde accumulation are more susceptible to hangover effects. The fact that about 25% of heavy drinkers claim that they have never had a hangover is also an indication that genetic variation plays a role in individual differences of hangover severity.

- Age: some people experience hangovers as getting worse as one ages. This is thought to be caused by declining supplies of alcohol dehydrogenase, the enzyme involved in metabolizing alcohol. Although it is actually unknown whether hangover symptoms and severity change with age, research shows that drinking patterns change across ages, and heavy drinking episodes that may result in hangover are much less often experienced as age increases.

- Sex: at the same number of drinks, women are more prone to hangover than men, and this is likely explained by sex differences in the pharmacokinetics of alcohol. Women attain a higher blood alcohol concentration (BAC) than men at the same number of drinks. At equivalent BACs, men and women appear to be indistinguishable with respect to most hangover effects.

- Cigarette smoking: acetaldehyde which is absorbed from cigarette smoking during alcohol consumption is regarded as a contributor to alcohol hangover symptoms.

Once kidney failure has developed in dogs and cats, the outcome is poor.

Cows and horses as well as pet animals are also susceptible to the effects of lead toxicity. Sources of lead exposure in pets can be the same as those that present health threats to humans sharing the environment, such as paint and blinds, and there is sometimes lead in toys made for pets. Lead poisoning in a pet dog may indicate that children in the same household are at increased risk for elevated lead levels.

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.

"Argemone mexicana" (family Papaveraceae), a native of West Indies and naturalized in India, is known as “Shailkanta” in Bengal and “Bharbhanda” in Uttar Pradesh. It is also popularly known as “Pivladhatura” or “Satyanashi”, meaning devastating. The plant grows wildly in mustard and other fields. Its seeds are black in colour and are similar to the dark coloured mustards seeds ("Brassica juncea") in shape and size. Adulteration of argemone seeds in light yellow colored mustard seeds ("Brassica compestris") can easily be detected, but these seeds are rather difficult to visualize when mixed with dark coloured mustard seeds.

Argemone seeds yield approximately 35% oil. Alkaloid content in argemone oil varies from 0.44% to 0.50%. Argemone seeds find use as a substitute because of the easy availability, low cost and their complete miscibility of their oil with mustard oil.

Narcosis is potentially one of the most dangerous conditions to affect the scuba diver below about . Except for occasional amnesia of events at depth, the effects of narcosis are entirely removed on ascent and therefore pose no problem in themselves, even for repeated, chronic or acute exposure. Nevertheless, the severity of narcosis is unpredictable and it can be fatal while diving, as the result of illogical behavior in a dangerous environment.

Tests have shown that all divers are affected by nitrogen narcosis, though some experience lesser effects than others. Even though it is possible that some divers can manage better than others because of learning to cope with the subjective impairment, the underlying behavioral effects remain. These effects are particularly dangerous because a diver may feel they are not experiencing narcosis, yet still be affected by it.

Auto-brewery syndrome, also known as gut fermentation syndrome, is a rare medical condition in which intoxicating quantities of ethanol are produced through endogenous fermentation within the digestive system. One gastrointestinal organism, "Saccharomyces cerevisiae", a type of yeast, has been identified as a pathogen for this condition.

Claims of endogenous fermentation of this type have been used as a defense against drunk driving charges.

One case went undetected for 20 years.

It has also been investigated, but eliminated, as a possible cause of sudden infant death syndrome.

A variant occurs in persons with liver abnormalities that prevent them from excreting or breaking down alcohol normally. Patients with this condition can develop symptoms of auto-brewery syndrome even when the gut yeast produces a quantity of alcohol that is too small to intoxicate a healthy individual.

During the latter part of the 20th century, the number of poisonings from salicylates declined, mainly because of the increased popularity of other over-the-counter analgesics such as paracetamol (acetaminophen). Fifty-two deaths involving single-ingredient aspirin were reported in the United States in 2000; however, in all but three of these cases, the reason for the ingestion of lethal doses was intentional—predominantly suicidal.

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.

Ethylene glycol involved in aircraft de-icing and anti-icing operations is released onto land and eventually to waterways. A report prepared for the World Health Organization in 2000 stated that laboratory tests exposing aquatic organisms to stream water receiving runoff from airports have shown toxic effects and death (p. 12). Field studies in the vicinity of an airport have reported toxic signs consistent with ethylene glycol poisoning, fish kills, and reduced biodiversity, although those effects could not definitively be ascribed to ethylene glycol (p. 12). The process of biodegrading of glycols also increases the risk to organisms, as oxygen levels become depleted in surface waters (p. 13). Another study found the toxicity to aquatic and other organisms was relatively low, but the oxygen-depletion effect of biodegradation was more serious (p. 245). Further, "Anaerobic biodegradation may also release relatively toxic byproducts such as acetaldehyde, ethanol, acetate, and methane (p. 245)."

In Canada, Environment Canada reports that "in recent years, management practices at Canada’s major airports have improved with the installation of new ethylene glycol application and mitigation facilities or improvements to existing ones." Since 1994, federal airports must comply with the Glycol Guidelines of the Canadian Environmental Protection Act, monitoring and reporting on concentrations of glycols in surface water. Detailed mitigation plans include storage and handling issues (p. 27), spill response procedures, and measures taken to reduce volumes of fluid (p. 28). Considering factors such as the "seasonal nature of releases, ambient temperatures, metabolic rates and duration of exposure", Environment Canada stated in 2014 that "it is proposed that ethylene glycol is not entering the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity".

In the U.S., airports are required to obtain stormwater discharge permits and ensure that wastes from deicing operations are properly collected and treated. Large new airports may be required to collect 60 percent of aircraft deicing fluid after deicing. Airports that discharge the collected aircraft deicing fluid directly to waters of the U.S. must also meet numeric discharge requirements for chemical oxygen demand. A report in 2000 stated that ethylene glycol was becoming less popular for aircraft deicing in the U.S., due to its reporting requirements and adverse environmental impacts (p. 213), and noted a shift to the use of propylene glycol (p. I-3).

Those routes include contaminated air, water, soil, and food, and also, for birds ingestion of grit (lead shots, lead bullets).ingestion of paints,materials that are left out from the factories like batteries etc.

Aspirin poisoning has controversially been cited as a possible cause of the high mortality rate during the 1918 flu pandemic, which killed 50 to 100 million people.

In dairy cattle, ketosis is a common ailment that usually occurs during the first weeks after giving birth to a calf. Ketosis is in these cases sometimes referred to as "acetonemia". A study from 2011 revealed that whether ketosis is developed or not depends on the lipids a cow uses to create butterfat. Animals prone to ketosis mobilize fatty acids from adipose tissue, while robust animals create fatty acids from blood phosphatidylcholine (lecithin). Healthy animals can be recognized by high levels of milk glycerophosphocholine and low levels of milk phosphocholine. Point of care diagnostic tests are available and are reasonably useful.

In sheep, ketosis, evidenced by hyperketonemia with beta-hydroxybutyrate in blood over 0.7 mmol/L, occurs in pregnancy toxemia. This may develop in late pregnancy in ewes bearing multiple fetuses, and is associated with the considerable glucose demands of the conceptuses. In ruminants, because most glucose in the digestive tract is metabolized by rumen organisms, glucose must be supplied by gluconeogenesis, for which propionate (produced by rumen bacteria and absorbed across the rumen wall) is normally the principal substrate in sheep, with other gluconeogenic substrates increasing in importance when glucose demand is high or propionate is limited. Pregnancy toxemia is most likely to occur in late pregnancy because most fetal growth (and hence most glucose demand) occurs in the final weeks of gestation; it may be triggered by insufficient feed energy intake (anorexia due to weather conditions, stress or other causes), necessitating reliance on hydrolysis of stored triglyceride, with the glycerol moiety being used in gluconeogenesis and the fatty acid moieties being subject to oxidation, producing ketone bodies. Among ewes with pregnancy toxemia, beta-hydroxybutyrate in blood tends to be higher in those that die than in survivors. Prompt recovery may occur with natural parturition, Caesarean section or induced abortion. Prevention (through appropriate feeding and other management) is more effective than treatment of advanced stages of ovine ketosis.

The cause of narcosis is related to the increased solubility of gases in body tissues, as a result of the elevated pressures at depth (Henry's law). Modern theories have suggested that inert gases dissolving in the lipid bilayer of cell membranes cause narcosis. More recently, researchers have been looking at neurotransmitter receptor protein mechanisms as a possible cause of narcosis. The breathing gas mix entering the diver's lungs will have the same pressure as the surrounding water, known as the ambient pressure. After any change of depth, the pressure of gases in the blood passing through the brain catches up with ambient pressure within a minute or two, which results in a delayed narcotic effect after descending to a new depth. Rapid compression potentiates narcosis owing to carbon dioxide retention.

A divers' cognition may be affected on dives as shallow as , but the changes are not usually noticeable. There is no reliable method to predict the depth at which narcosis becomes noticeable, or the severity of the effect on an individual diver, as it may vary from dive to dive even on the same day.

Significant impairment due to narcosis is an increasing risk below depths of about , corresponding to an ambient pressure of about . Most sport scuba training organizations recommend depths of no more than because of the risk of narcosis. When breathing air at depths of – an ambient pressure of about – narcosis in most divers leads to hallucinations, loss of memory, and unconsciousness. A number of divers have died in attempts to set air depth records below . Because of these incidents, "Guinness World Records" no longer reports on this figure.

Narcosis has been compared with altitude sickness regarding its variability of onset (though not its symptoms); its effects depend on many factors, with variations between individuals. Thermal cold, stress, heavy work, fatigue, and carbon dioxide retention all increase the risk and severity of narcosis. Carbon dioxide has a high narcotic potential and also causes increased blood flow to the brain, increasing the effects of other gases. Increased risk of narcosis results from increasing the amount of carbon dioxide retained through heavy exercise, shallow or skip breathing, or because of poor gas exchange in the lungs.

Narcosis is known to be additive to even minimal alcohol intoxication, and also to the effects of other drugs such as cannabis (which is more likely than alcohol to have effects that last into a day of abstinence from use). Other sedative and analgesic drugs, such as opiate narcotics and benzodiazepines, add to narcosis.

Some clinicians regard eliminating carbohydrates as unhealthy and dangerous. However, it is not necessary to eliminate carbohydrates from the diet completely to achieve ketosis. Other clinicians regard ketosis as a safe biochemical process that occurs during the fat-burning state. Ketosis, which is accompanied by gluconeogenesis (the creation of glucose de novo from pyruvate), is the specific state that concerns some clinicians. However, it is unlikely for a normally functioning person to reach life-threatening levels of ketosis, defined as serum beta-hydroxybutyrate (B-OHB) levels above 15 millimolar (mM) compared to ketogenic diets among non diabetics, which "rarely run serum B-OHB levels above 3 mM." This is avoided with proper basal secretion of pancreatic insulin. People who are unable to secrete basal insulin, such as type 1 diabetics and long-term type II diabetics, are liable to enter an unsafe level of ketosis, eventually resulting in a coma that requires emergency medical treatment. The anti-ketosis conclusions have been challenged by a number of doctors and advocates of low-carbohydrate diets, who dispute assertions that the body has a preference for glucose and that there are dangers associated with ketosis.

Hereditary fructose intolerance (HFI) is an inborn error of fructose metabolism caused by a deficiency of the enzyme aldolase B. Individuals affected with HFI are asymptomatic until they ingest fructose, sucrose, or sorbitol. If fructose is ingested, the enzymatic block at aldolase B causes an accumulation of fructose-1-phosphate. This accumulation has downstream effects on gluconeogenesis and regeneration of adenosine triphosphate (ATP). Symptoms of HFI include vomiting, hypoglycemia, jaundice, hemorrhage, hepatomegaly, hyperuricemia and potentially kidney failure. While HFI is not clinically a devastating condition, there are reported deaths in infants and children as a result of the metabolic consequences of HFI. Death in HFI is always associated with problems in diagnosis.

HFI is an autosomal recessive condition caused by mutations in the "ALDOB" gene, located at 9q22.3. HFI is typically suspected based on dietary history, especially in infants who become symptomatic after breast feeding. This suspicion is typically confirmed by molecular analysis. Treatment of HFI involves strict avoidance of fructose in the diet. Older patients with HFI typically self-select a diet low in fructose, even before being diagnosed.

Treatment of HFI depends on the stage of the disease, and the severity of the symptoms. Stable patients without acute intoxication events are treated by careful dietary planning that avoids fructose and its metabolic precursors. Fructose is replaced in the diet by glucose, maltose or other sugars. Management of patients with HFI often involves dietitians who have a thorough knowledge of what foods are acceptable.

The normal human kidney, through suppression of anti-diuretic hormone, is normally able to excrete vast amounts of dilute urine. Thus a normal adult can drink up to 20 liters per day of water without becoming hyponatremic. However, the intake of solutes is also necessary to excrete free water. Under normal circumstances, this is clinically irrelevant. In the lack of proper solute intake, the amount of free water excretion can be severely limited. Without adequate solute intake, the normal functioning electrolyte gradient that pulls water into urine will be effectively destroyed.

Briefly, to excrete free water from urine, the urine flow (which is solute clearance + free water clearance) will equal the rate of solute excretion divided by the urine osmolality. With a diet of only solute poor beer, only about 200-300 mOSM (normal 750 mOSM to greater than 900 mOSM) of solute will be excreted per day, capping the amount of free water excretion at four liters. Any intake above 4 liters would lead to a dilution of the serum sodium concentration and thus hyponatremia.

Any vomiting or GI absorptive problems due to alcohol intoxication can also compound the effect of potomania due to additional electrolyte and acid-base disturbances.

Having a particular genetic variant (A-allele of ADH1B rs1229984) is associated with non-drinking and lower alcohol consumption. This variant is also associated with favorable cardiovascular profile and a reduced risk of coronary heart disease compared to those without the genetic variant, but it is unknown whether this may be caused by differences in alcohol consumption or by additional confounding effects of the genetic variant itself.

As with all cases of hyponatremia, extreme caution must be taken to avoid the fatal consequences of rapidly correcting electrolytes (e.g. Central pontine myelinolysis, edema). Special considerations with the treatment of potomania are needed. Because this could be a chronic condition, low sodium may be normal for the patient, so an especially careful correction is warranted. It is also very important to note that due to the normal kidney function, and lack of other intrinsic or toxic cause of the electrolyte disturbance, restoration of dietary solutes will correct the electrolytes to normal serum levels. This again must be done with caution.

While little detailed genetic research has been done, it has been shown that alcoholism tends to run in families with possible involvement of differences in alcohol metabolism and the genotype of alcohol-metabolizing enzymes.

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.

Acrodynia is a condition of pain and dusky pink discoloration in the hands and feet most often seen in children chronically exposed to heavy metals, especially mercury.

The word "acrodynia" is derived from the Greek, where ακρος means "end" or "" and οδυνη means pain. As such, it might be (erroneously) used to indicate that a patient has pain in the hands or feet. However, acrodynia is a disease rather than a symptom. The condition is known by a large number of other names including pink disease, hydrargyria, mercurialism, erythredema, erythredema polyneuropathy, Bilderbeck's, Selter's, Swift's and Swift-Feer disease.

Causes of increased anion gap include:

- Lactic acidosis

- Ketoacidosis

- Chronic renal failure (accumulation of sulfates, phosphates, urea)

- Intoxication:

- Organic acids, salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, isoniazid

- Sulfates, metformin

- Massive rhabdomyolysis

A mnemonic can also be used - MUDPILES

- M-Methanol

- U-Uremia (chronic kidney failure)

- D-Diabetic ketoacidosis

- P-Paraldehyde

- I-Infection, Iron, Isoniazid, Inborn errors of metabolism

- L-Lactic acidosis

- E-Ethylene glycol (Note: Ethanol is sometimes included in this mnemonic, as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication.)

- S-Salicylates