Fluoride toxicity is a condition in which there are elevated levels of the fluoride ion in the body. Although fluoride is safe for dental health at low concentrations, sustained consumption of large amounts of soluble fluoride salts is dangerous. Referring to a common salt of fluoride, sodium fluoride (NaF), the lethal dose for most adult humans is estimated at 5 to 10 g (which is equivalent to 32 to 64 mg/kg elemental fluoride/kg body weight). Ingestion of fluoride can produce gastrointestinal discomfort at doses at least 15 to 20 times lower (0.2–0.3 mg/kg or 10 to 15 mg for a 50 kg person) than lethal doses. Although it is helpful for dental health in low dosage, chronic exposure to fluoride in large amounts interferes with bone formation. In this way, the most widespread examples of fluoride poisoning arise from consumption of ground water that is abnormally fluoride-rich.

Signs of ethylene glycol poisoning depend upon the time after ingestion. Symptoms usually follow a three-step progression, although poisoned individuals will not always develop each stage.

- Stage 1 (30 minutes to 12 hours) consists of neurological and gastrointestinal symptoms and looks similar to alcohol poisoning. Poisoned individuals may appear to be intoxicated, dizzy, lacking coordination of muscle movements, drooling, depressed, and have slurred speech, seizuring, abnormal eye movements, headaches, and confusion. Irritation to the stomach may cause nausea and vomiting. Also seen are excessive thirst and urination. Over time, the body metabolizes ethylene glycol into other toxins.

- Stage 2 (12 to 36 hours) where signs of "alcohol" poisoning appear to resolve, underlying severe internal damage is still occurring. An elevated heart rate, hyperventilation or increased breathing effort, and dehydration may start to develop, along with high blood pressure and metabolic acidosis. These symptoms are a result of accumulation of organic acids formed by the metabolism of ethylene glycol. Additionally low calcium concentrations in the blood, overactive muscle reflexes, muscle spasms, QT interval prolongation, and congestive heart failure may occur. If untreated, death most commonly occurs during this period.

- Stage 3 (24 to 72 hours) kidney failure is the result of ethylene glycol poisoning. In cats, this stage occurs 12–24 hours after getting into antifreeze; in dogs, at 36–72 hours after getting into antifreeze. During this stage, severe kidney failure is developing secondary to calcium oxalate crystals forming in the kidneys. Severe lethargy, coma, depression, vomiting, seizures, drooling, and inappetance may be seen. Other symptoms include acute tubular necrosis, red blood cells in the urine, excess proteins in the urine, lower back pain, decreased or absent production of urine, elevated blood concentration of potassium, and acute kidney failure. If kidney failure occurs it is typically reversible, although weeks or months of supportive care including hemodialysis may be required before kidney function returns.

Following an oral intake of extremely high doses of zinc (where 300 mg Zn/d – 20 times the US RDA – is a "low intake" overdose), nausea, vomiting, pain, cramps and diarrhea may occur. There is evidence of induced copper deficiency, alterations of blood lipoprotein levels, increased levels of LDL, and decreased levels of HDL at long-term intakes of 100 mg Zn/d. The USDA RDA is 15 mg Zn/d.

There is also a condition called the "zinc shakes" or "zinc chills" or metal fume fever that can be induced by the inhalation of freshly formed zinc oxide formed during the welding of galvanized materials.

Whilst fluoridated water is associated with decreased levels of fractures in a population, toxic levels of fluoride have been associated with a weakening of bones and an increase in hip and wrist fractures. The U.S. National Research Council concludes that fractures with fluoride levels 1–4 mg/L, suggesting a dose-response relationship, but states that there is "suggestive but inadequate for drawing firm conclusions about the risk or safety of exposures at [2 mg/L]".

Consumption of fluoride at levels beyond those used in fluoridated water for a long period of time causes skeletal fluorosis. In some areas, particularly the Asian subcontinent, skeletal fluorosis is endemic. It is known to cause irritable-bowel symptoms and joint pain. Early stages are not clinically obvious, and may be misdiagnosed as (seronegative) rheumatoid arthritis or ankylosing spondylitis.

Tin poisoning refers to the toxic effects of tin and its compounds. Cases of poisoning from tin metal, its oxides, and its salts are "almost unknown"; on the other hand certain organotin compounds are almost as toxic as cyanide.

Ethylene glycol poisoning is poisoning caused by drinking ethylene glycol. Early symptoms include intoxication, vomiting and abdominal pain. Later symptoms may include a decreased level of consciousness, headache, and seizures. Long term outcomes may include kidney failure and brain damage. Toxicity and death may occur even after drinking a small amount.

Ethylene glycol is a colorless, odorless, sweet liquid, commonly found in antifreeze. It may be drunk accidentally or purposefully in an attempt to cause death. When broken down by the body it results in glycolic acid and oxalic acid which cause most of the toxicity. The diagnosis may be suspected when calcium oxalate crystals are seen in the urine or when acidosis or an increased osmol gap is present in the blood. Diagnosis may be confirmed by measuring ethylene glycol levels in the blood; however, many hospitals do not have the ability to perform this test.

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, thiamine, and magnesium.

More than 5000 cases of poisoning occur in the United States each year. Those affected are often adults and male. Deaths from ethylene glycol have been reported as early as 1930. An outbreak of deaths in 1937 due to a medication mixed in a similar compound, diethylene glycol, resulted in the Food, Drug, and Cosmetic Act of 1938 in the United States which mandated evidence of safety before new medications could be sold. Antifreeze products sometimes have a substance to make it bitter added to discourage drinking by children and other animals but this has not been found to be effective.

Zinc toxicity is a medical condition involving an overdose on, or toxic overexposure to, zinc. Such toxicity levels have been seen to occur at ingestion of greater than 225 mg of zinc. Excessive absorption of zinc can suppress copper and iron absorption. The free zinc ion in solution is highly toxic to bacteria, plants, invertebrates, and even vertebrate fish. Zinc is an essential trace metal with very low toxicity in humans.

Metal toxicity or metal poisoning is the toxic effect of certain metals in certain forms and doses on life. Some metals are toxic when they form poisonous soluble compounds. Certain metals have no biological role, i.e. are not essential minerals, or are toxic when in a certain form. In the case of lead, any measurable amount may have negative health effects. Often heavy metals are thought as synonymous, but lighter metals may also be toxic in certain circumstances, such as beryllium and lithium. Not all heavy metals are particularly toxic, and some are essential, such as iron. The definition may also include trace elements when in abnormally high doses may be toxic. An option for treatment of metal poisoning may be chelation therapy, which is a technique which involves the administration of chelation agents to remove metals from the body.

Toxic metals sometimes imitate the action of an essential element in the body, interfering with the metabolic process resulting in illness. Many metals, particularly heavy metals are toxic, but some heavy metals are essential, and some, such as bismuth, have a low toxicity. Most often the definition of toxic metals includes at least cadmium, manganese, lead, mercury and the radioactive metals. Metalloids (arsenic, polonium) may be included in the definition. Radioactive metals have both radiological toxicity and chemical toxicity. Metals in an oxidation state abnormal to the body may also become toxic: chromium(III) is an essential trace element, but chromium(VI) is a carcinogen.

Toxicity is a function of solubility. Insoluble compounds as well as the metallic forms often exhibit negligible toxicity. The toxicity of any metal depends on its ligands. In some cases, organometallic forms, such as methylmercury and tetraethyl lead, can be extremely toxic. In other cases, organometallic derivatives are less toxic such as the cobaltocenium cation.

Decontamination for toxic metals is different from organic toxins: because toxic metals are elements, they cannot be destroyed. Toxic metals may be made insoluble or collected, possibly by the aid of chelating agents, or through bioremediation. Alternatively, they can be diluted into a sufficiently large reservoir, such as the sea, because immediate toxicity is a function of concentration rather than amount.

Toxic metals can bioaccumulate in the body and in the food chain. Therefore, a common characteristic of toxic metals is the chronic nature of their toxicity. This is particularly notable with radioactive heavy metals such as radium, which imitates calcium to the point of being incorporated into human bone, although similar health implications are found in lead or mercury poisoning. The exceptions to this are barium and aluminium, which can be removed efficiently by the kidneys.

ICD-9-CM code 985.8 "Toxic effect of other specified metals" includes acute & chronic copper poisoning (or other toxic effect) whether intentional, accidental, industrial etc.

- In addition, it includes poisoning and toxic effects of other metals including tin, selenium nickel, iron, heavy metals, thallium, silver, lithium, cobalt, aluminum and bismuth. Some poisonings, e.g. zinc phosphide, would/could also be included as well as under 989.4 Poisoning due to other pesticides, etc.

- Excluded are toxic effects of mercury, arsenic, manganese, beryllium, antimony, cadmium, and chromium.

Animal lead poisoning (also known as avian plumbism, or avian saturnism for birds) is a veterinary condition and pathology caused by increased levels of the heavy metal lead in animal's body.

Lead interferes with a variety of body and natural processes.

It is toxic to many organs and tissues including the heart, bones, intestines, kidneys, and reproductive and nervous systems. It mainly affects the haematopoietic system. It also affects the sulfhydryl group containing enzymes and also thiol content of erythrocyte. It inhibits the enzyme delta amino levaminic acid dehydrogenase enzyme(ALA) which is present in the rbc.

It is therefore particularly toxic to young animals, mainly dogs and cattle.

As in humans, "animal lead poisoning" may be acute (from intense exposure of short duration) or chronic (from repeat low-level exposure over a prolonged period). Acute intoxication can quickly lead to death.

Acute symptoms of copper poisoning by ingestion include vomiting, hematemesis (vomiting of blood), hypotension (low blood pressure), melena (black "tarry" feces), coma, jaundice (yellowish pigmentation of the skin), and gastrointestinal distress. Individuals with glucose-6-phosphate deficiency may be at increased risk of hematologic effects of copper. Hemolytic anemia resulting from the treatment of burns with copper compounds is infrequent.

Chronic (long-term) effects of copper exposure can damage the liver and kidneys. Mammals have efficient mechanisms to regulate copper stores such that they are generally protected from excess dietary copper levels.

Those same protection mechanisms can cause milder symptoms, which are often misdiagnosed as psychiatric disorders. There is a lot of research going on regarding the function of the Cu/Zn ratio in many conditions, neurological, endocrinological and psychological. The diagnostic difficulties arise from the fact that many of the substances that protect us from excess copper perform important functions in our neurological and endocrine systems. When they are used to bind copper in the plasma, to prevent it from being absorbed in the tissues, their own function may go unfulfilled. Such symptoms often include mood swings, irritability, depression, fatigue, excitation, difficulty focusing, feeling out of control, etc. To further complicate diagnosis, some symptoms of excess copper are similar to those of a copper deficit.

The U.S. Environmental Protection Agency's Maximum Contaminant Level (MCL) in drinking water is 1.3 milligrams per liter. The MCL for copper is based on the expectation that a lifetime of consuming copper in water at this level is without adverse effect (gastrointestinal). The US EPA lists copper as a micronutrient and a toxin. Toxicity in mammals includes a wide range of animals and effects such as liver cirrhosis, necrosis in kidneys and the brain, gastrointestinal distress, lesions, low blood pressure, and fetal mortality. The Occupational Safety and Health Administration (OSHA) has set a limit of 0.1 mg/m for copper fumes (vapor generated from heating copper) and 1 mg/m for copper dusts (fine metallic copper particles) and mists (aerosol of soluble copper) in workroom air during an eight-hour work shift, 40-hour work week. Toxicity to other species of plants and animals is noted to varying levels.

Tin has no known natural biological role in living organisms. It is not easily absorbed by animals and humans. The low toxicity is relevant to the widespread use of tin in dinnerware and canned food. Nausea, vomiting and diarrhea have been reported after ingesting canned food containing 200 mg/kg of tin. This observation led, for example, the Food Standards Agency in the UK to propose upper limits of 200 mg/kg. A study showed that 99.5% of the controlled food cans contain tin in an amount below that level. However un-lacquered tin cans with food of a low pH for example fruits and pickled vegetables can contain elevated concentrations of tin.

The toxic effects of tin compounds is based on the interference with the iron and copper metabolism. For example, it affects heme and cytochrome P450, and decreases their effectiveness.

Organotin compounds can be very toxic. "Tri-"n"-alkyltins" are phytotoxic and, depending on the organic groups, can be powerful bactericides and fungicides. Other triorganotins are used as miticides and acaricides.

Tributyltin (TBT) was extensively used in marine antifouling paints, until discontinued for leisure craft due to concerns over longer term marine toxicity in high traffic areas such as marinas with large numbers of static boats.

Aspirin overdose has potentially serious consequences, sometimes leading to significant morbidity and death. Patients with mild intoxication frequently have nausea and vomiting, abdominal pain, lethargy, ringing in the ears, and dizziness. More significant signs and symptoms occur in more severe poisonings and include high body temperature, fast breathing rate, respiratory alkalosis, metabolic acidosis, low blood potassium, low blood glucose, hallucinations, confusion, seizure, cerebral edema, and coma. The most common cause of death following an aspirin overdose is cardiopulmonary arrest usually due to pulmonary edema.

Poisoning is a condition or a process in which an organism becomes chemically harmed (poisoned) by a toxic substance or venom of an animal.

Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the degree of exposure. Absorption of a poison is necessary for systemic poisoning (that is, in the blood throughout the body). In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons. Furthermore, many common household medications are not labeled with skull and crossbones, although they can cause severe illness or even death. In the medical sense, toxicity and poisoning can be caused by less dangerous substances than those legally classified as a poison. Toxicology is the study and practice of the symptoms, mechanisms, diagnosis, and treatment of poisoning.

Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not occur immediately or after each exposure. The patient gradually becomes ill, or becomes ill after a long latent period. Chronic poisoning most commonly occurs following exposure to poisons that bioaccumulate, or are biomagnified, such as mercury, gadolinium, and lead.

Contact or absorption of poisons can cause rapid death or impairment. Agents that act on the nervous system can paralyze in seconds or less, and include both biologically derived neurotoxins and so-called nerve gases, which may be synthesized for warfare or industry.

Inhaled or ingested cyanide, used as a method of execution in gas chambers, almost instantly starves the body of energy by inhibiting the enzymes in mitochondria that make ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction.

Most biocides, including pesticides, are created to act as poisons to target organisms, although acute or less observable chronic poisoning can also occur in non-target organisms (secondary poisoning), including the humans who apply the biocides and other beneficial organisms. For example, the herbicide 2,4-D imitates the action of a plant hormone, which makes its lethal toxicity specific to plants. Indeed, 2,4-D is not a poison, but classified as "harmful" (EU).

Many substances regarded as poisons are toxic only indirectly, by toxication. An example is "wood alcohol" or methanol, which is not poisonous itself, but is chemically converted to toxic formaldehyde and formic acid in the liver. Many drug molecules are made toxic in the liver, and the genetic variability of certain liver enzymes makes the toxicity of many compounds differ between individuals.

Exposure to radioactive substances can produce radiation poisoning, an unrelated phenomenon.

A toxic heavy metal is any relatively dense metal or metalloid that is noted for its potential toxicity, especially in environmental contexts. The term has particular application to cadmium, mercury, lead and arsenic, all of which appear in the World Health Organisation's list of 10 chemicals of major public concern. Other examples include manganese, chromium, cobalt, nickel, copper, zinc, selenium, silver, antimony and thallium.

Heavy metals are found naturally in the earth. They become concentrated as a result of human caused activities and can enter plant, animal, and human tissues via inhalation, diet, and manual handling. Then, they can bind to and interfere with the functioning of vital cellular components. The toxic effects of arsenic, mercury, and lead were known to the ancients, but methodical studies of the toxicity of some heavy metals appear to date from only 1868. In humans, heavy metal poisoning is generally treated by the administration of chelating agents. Some elements otherwise regarded as toxic heavy metals are essential, in small quantities, for human health.

Salicylate poisoning, also known as aspirin poisoning, is the acute or chronic poisoning with a salicylate such as aspirin. The classic symptoms are ringing in the ears, nausea, abdominal pain, and a fast breathing rate. Early on these may be subtle while larger doses may result in fever. Complications can include swelling of the brain or lungs, seizures, low blood sugar, or cardiac arrest.

While usually due to aspirin, other possible causes include oil of wintergreen and bismuth subsalicylate. Excess doses can be either on purpose or accidental. Small amounts of oil of wintergreen can be toxic. Diagnosis is generally based on repeated blood tests measuring aspirin levels and blood gases. While a type of graph has been created to try to assist with diagnosis, its general use is not recommended. In overdose maximum blood levels may not occur for more than 12 hours.

Efforts to prevent poisoning include child-resistant packaging and a lower number of pills per package. Treatment may include activated charcoal, intravenous sodium bicarbonate with dextrose and potassium chloride, and dialysis. Giving dextrose may be useful even if the blood sugar is normal. Dialysis is recommended in those with kidney failure, decreased level of consciousness, blood pH less than 7.2, or high blood salicylate levels. If a person requires intubation a fast respiratory rate may be required.

The toxic effects of salicylates have been described since at least 1877. In 2004 more than 20,000 cases with 43 deaths were reported in the United States. About 1% of those with an acute overdose die while chronic overdoses may have worse outcomes. Older people are at higher risks of toxicity for any given dose.

Argyria or argyrosis is a condition caused by inappropriate exposure to chemical compounds of the element silver, or to silver dust. The most dramatic symptom of argyria is that the skin turns blue or bluish-grey. It may take the form of "generalized argyria" or "local argyria". Generalized argyria affects large areas over much of the visible surface of the body. Local argyria shows in limited regions of the body, such as patches of skin, parts of the mucous membrane or the conjunctiva.

The first indication of iron poisoning by ingestion is stomach pain, as iron is corrosive to the lining of the gastrointestinal tract, including the stomach. Nausea and vomiting are also common symptoms and bloody vomiting may occur. The pain then abates for 24 hours as the iron passes deeper into the body, resulting in metabolic acidosis, which in turn damages internal organs, particularly the brain and the liver. Iron poisoning can cause hypovolemic shock due to iron's potent ability to dilate the blood vessels. Death may occur from liver failure.

If intake of iron is for a prolonged period of time, symptoms are likely to be similar to other causes of iron overload.

Symptoms may include:

- Abnormal softening of the skull bone (craniotabes—infants and children)

- Blurred vision

- Bone pain or swelling

- Bulging fontanelle (infants)

- Changes in consciousness

- Decreased appetite

- Dizziness

- Double vision (young children)

- Drowsiness

- Headache

- Gastric mucosal calcinosis

- Heart valve calcification

- Hypercalcemia

- Increased intracranial pressure manifesting as cerebral edema, papilledema, and headache (may be referred to as Idiopathic intracranial hypertension)

- Irritability

- Liver damage

- Nausea

- Poor weight gain (infants and children)

- Skin and hair changes

- Cracking at corners of the mouth

- Hair loss

- Higher sensitivity to sunlight

- Oily skin and hair (seborrhea)

- Premature epiphyseal closure

- Skin peeling, itching

- Spontaneous fracture

- Yellow discoloration of the skin (aurantiasis cutis)

- Uremic pruritus

- Vision changes

- Vomiting

Fluoride or fluorine deficiency is a disorder which may cause increased dental caries (or tooth decay, is the breakdown of dental tissues by the acidic products released by the "bacterial fermentation of dietary carbohydrates.") and possibly osteoporosis (a bone disorder which leads to a decrease in bone mass, and an increase in bone fragility), due to a lack of fluoride in the diet; however, there are anti-osteoporotic functional food ingredients that can help decrease the risk of osteoporosis fractures. In terms of dietary sources, fish and tea are considered natural sources of fluoride, as well as tap water that has been fluoridated. The extent to which the condition truly exists, and its relationship to fluoride poisoning has given rise to some controversy. Fluorine is not considered to be an essential nutrient, but the importance of fluorides for preventing tooth decay is well-recognized, although the effect is predominantly topical. Prior to 1981, the effect of fluorides was thought to be largely systemic and preeruptive, requiring ingestion. Fluoride is considered essential in the development and maintenance of teeth by the American Dental Hygienists' Association. Fluoride is also essential as it incorporates into the teeth to form and harden teeth enamels so that the teeth are more acid resistant as well as more resistant to cavity forming bacteria. Caries-inhibiting effects of fluoride were first seen in 1902 when fluoride in high concentrations was found to stain teeth and prevent tooth decay.

Fluoride salts, particularly sodium fluoride (NaF), are used in the treatment and prevention of osteoporosis. Symptoms such as fractured hips in the elderly or brittle and weak bones are caused due to fluorine deficiency in the body. Fluoride stimulates bone formation and increases bone density, however bone with excess fluoride content has an abnormal structure resulting in increased fragility. Thus fluoride therapy results in large increases in bone mineral density but the effect on fracture rates, while positive, is small.

Disputes over the essentiality of fluorine date back to the 19th century, when fluorine was observed in teeth and bones. In 1973 a trial found reduced reproduction in mice fed fluorine-deficient diets, but a subsequent investigation determined that this was due to reduced iron absorption.

Chromium toxicity refers to the fact that chromium is toxic.

Water-insoluble chromium(III) compounds and chromium metal are not considered a health hazard, while the toxicity and carcinogenic properties of chromium(VI) have been known for a long time. An investigation into hexavalent chromium release into drinking water was the basis of the true story of Erin Brockovich, dramatised as Erin Brockovich (film).

Because of the specific transport mechanisms, only limited amounts of chromium(III) enter the cells. Several "in vitro" studies indicated that high concentrations of chromium(III) in the cell can lead to DNA damage. Acute oral toxicity ranges between 1900 and 3300 µg/kg. The proposed beneficial effects of chromium(III) and its use in dietary supplements yielded some controversial results, but recent reviews suggest that moderate uptake of chromium(III) through dietary supplements poses no risk.

The World Health Organization-recommended maximum allowable concentration in drinking water for chromium (VI) is 0.05 milligrams per litre.

The LD50 for chromium(VI) ranges between 50 and 150 mg/kg. In the body, chromium(VI) is reduced by several mechanisms to chromium(III) already in the blood before it enters the cells. The chromium(III) is excreted from the body, whereas the chromate ion is transferred into the cell by a transport mechanism, one by which sulfate and phosphate ions also enter the cell. The acute toxicity of chromium(VI) is due to its strong oxidative properties. After it reaches the bloodstream, it damages blood cells by oxidation reactions. Hemolysis, and subsequently kidney and liver failure, are the results of this damage. Aggressive dialysis can improve the situation.

The carcinogenity of chromate dust has been known for a long time, and in 1890 the first publication described the elevated cancer risk of workers in a chromate dye company.

Three mechanisms have been proposed to describe the genotoxicity of chromium(VI). The first mechanism includes highly reactive hydroxyl radicals and other reactive radicals which are byproducts of the reduction of chromium(VI) to chromium(III). The second process includes the direct binding of chromium(V), produced by reduction in the cell, and chromium(IV) compounds, to the DNA. The last mechanism attributes the genotoxicity to the binding to the DNA of the end product of the chromium(III) reduction.

Chromium salts (chromates) are also the cause of allergic reactions in some people. Chromates are often used to manufacture, among other things, leather products, paints, cement, mortar, and anti-corrosives. Contact with products containing chromates can lead to allergic contact dermatitis and irritant dermatitis, resulting in ulceration of the skin, sometimes referred to as "chrome ulcers". This condition is often found in workers that have been exposed to strong chromate solutions in electroplating, tanning and chrome-producing manufacturers.

In some parts of Russia, pentavalent chromium was reported as one of the causes of premature dementia.

Various pesticides such as rodenticides may cause secondary poisoning. Some pesticides require multiple feedings spanning several days; this increases the time a target organism continues to move after ingestion, raising the risk of secondary poisoning of a predator.

The signs and symptoms of paracetamol toxicity occur in three phases. The first phase begins within hours of overdose, and consists of nausea, vomiting, a pale appearance, and sweating. However, patients often have no specific symptoms or only mild symptoms in the first 24 hours of poisoning. Rarely, after massive overdoses, patients may develop symptoms of metabolic acidosis and coma early in the course of poisoning.

The second phase occurs between 24 h and 72 h following overdose and consists of signs of increasing liver damage. In general, damage occurs in liver cells as they metabolize the paracetamol. The individual may experience right upper quadrant abdominal pain. The increasing liver damage also changes biochemical markers of liver function; International normalized ratio (INR) and the liver transaminases ALT and AST rise to abnormal levels. Acute kidney failure may also occur during this phase, typically caused by either hepatorenal syndrome or multiple organ dysfunction syndrome. In some cases, acute kidney failure may be the primary clinical manifestation of toxicity. In these cases, it has been suggested that the toxic metabolite is produced more in the kidneys than in the liver.

The third phase follows at 3 to 5 days, and is marked by complications of massive liver necrosis leading to fulminant liver failure with complications of coagulation defects, low blood sugar, kidney failure, hepatic encephalopathy, brain swelling, sepsis, multiple organ failure, and death. If the third phase is survived, the liver necrosis runs its course, and liver and kidney function typically return to normal in a few weeks. The severity of paracetamol toxicity varies depending on the dose and whether appropriate treatment is received.

Hypervitaminosis is a condition of abnormally high storage levels of vitamins, which can lead to toxic symptoms. Specific medical names of the different conditions are derived from the vitamin involved: an excess of vitamin A, for example, is called hypervitaminosis A.

Hypervitaminoses are primarily caused by fat-soluble vitamins (D, E, K and A), as these are stored by the body for longer period than the water-soluble vitamins.

Generally, toxic levels of vitamins stem from high supplement intake and not from natural food. Toxicities of fat-soluble vitamins can also be caused by a large intake of highly fortified foods, but natural food rarely deliver dangerous levels of fat-soluble vitamins. The Dietary Reference Intake recommendations from the United States Department of Agriculture define a "tolerable upper intake level" for most vitamins.

Thallium and its compounds are often highly toxic. Contact with skin is dangerous, and adequate ventilation should be provided when melting this metal. Many thallium(I) compounds are highly soluble in water and are readily absorbed through the skin. Exposure to them should not exceed 0.1 mg per m of skin in an 8-hour time-weighted average (40-hour work week). Thallium is a suspected human carcinogen.

Part of the reason for thallium's high toxicity is that, when present in aqueous solution as the univalent thallium(I) ion (Tl), it exhibits some similarities with essential alkali metal cations, particularly potassium (due to similar ionic radii). It can thus enter the body via potassium uptake pathways. Other aspects of thallium's chemistry differ strongly from that of the alkali metals, such as its high affinity for sulfur ligands. Thus, this substitution disrupts many cellular processes (for instance, thallium may attack sulfur-containing proteins such as cysteine residues and ferredoxins). Thallium's toxicity has led to its use (now discontinued in many countries) as a rat and ant poison.

Among the distinctive effects of thallium poisoning are hair loss (which led to its initial use as a depilatory before its toxicity was properly appreciated) and damage to peripheral nerves (victims may experience a sensation of walking on hot coals), although the loss of hair only generally occurs in low doses; in high doses the thallium kills before this can take effect. Thallium was once an effective murder weapon before its effects became understood and an antidote (Prussian blue) discovered. Indeed, thallium poisoning has been called the "poisoner's poison" since thallium is colorless, odorless and tasteless; its slow-acting, painful and wide-ranging symptoms are often suggestive of a host of other illnesses and conditions.