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.

Paracetamol poisoning, also known as acetaminophen poisoning, is caused by excessive use of the medication paracetamol (acetaminophen). Most people have few or non-specific symptoms in the first 24 hours following overdose. This may include feeling tired, abdominal pain, or nausea. This is typically followed by a couple of days without any symptoms after which yellowish skin, blood clotting problems, and confusion occurs. Additional complications may include kidney failure, pancreatitis, low blood sugar, and lactic acidosis. If death does not occur, people tend to recover fully over a couple of weeks. Without treatment some cases will resolve while others will result in death.

Paracetamol poisoning can occur accidentally or as an attempt to end one's life. Risk factors for toxicity include alcoholism, malnutrition, and the taking of certain other medications. Liver damage results not from paracetamol itself, but from one of its metabolites, "N"-acetyl-"p"-benzoquinone imine (NAPQI). NAPQI decreases the liver's glutathione and directly damages cells in the liver. Diagnosis is based on the blood level of paracetamol at specific times after the medication was taken. These values are often plotted on the Rumack-Matthew nomogram to determine level of concern.

Treatment may include activated charcoal if the person presents soon after the overdose. Attempting to force the person to vomit is not recommended. If there is a potential for toxicity, the antidote acetylcysteine is recommended. The medication is generally given for at least 24 hours. Psychiatric care may be required following recovery. A liver transplant may be required if damage to the liver becomes severe. The need for transplant is often based on low blood pH, high blood lactate, poor blood clotting, or significant hepatic encephalopathy. With early treatment liver failure is rare. Death occurs in about 0.1% of cases.

Paracetamol poisoning was first described in the 1960s. Rates of poisoning vary significantly between regions of the world. In the United States more than 100,000 cases occur a year. In the United Kingdom it is the medication responsible for the greatest number of overdoses. Young children are most commonly affected. In the United States and the United Kingdom paracetamol is the most common cause of acute liver failure.

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.

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.

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.

After ingestion, toxic features usually develop within a few minutes. The major lethal consequence of aluminium phosphide ingestion is profound circulatory collapse, and is reportedly secondary to these toxins generated, which lead due to direct effects on cardiomyocytes, fluid loss, and adrenal gland damage. The signs and symptoms are non-specific, dose dependent and evolve with time passing. The dominant clinical feature is severe hypotension refractory to dopamine therapy. Other features may include dizziness, fatigue, tightness in the chest, headache, nausea, vomiting, diarrhoea, ataxia, numbness, paraesthesia, tremor, muscle weakness, diplopia and jaundice. If severe inhalation occurs, the patient may develop acute respiratory distress syndrome (ARDS), heart failure, arrhythmias, convulsion and coma. Late manifestation include liver and kidney toxicities.

The diagnosis of AAlP usually depends on the clinical suspicion or history (self-report or by attendants). In some nations, tablets of AlP are also referred to as "rice tablets" and, if there is a history of rice tablet ingestion, then it should be treated differently from other types of rice tablets that are made up of herbal products. For a silver nitrate test on gastric aspirate, diluted gastric content can be positive.

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.

In acute poisoning, typical neurological signs are pain, muscle weakness, numbness and tingling, and, rarely, symptoms associated with inflammation of the brain. Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms. Lead's effects on the mouth include astringency and a metallic taste. Gastrointestinal problems, such as constipation, diarrhea, poor appetite, or weight loss, are common in acute poisoning. Absorption of large amounts of lead over a short time can cause shock (insufficient fluid in the circulatory system) due to loss of water from the gastrointestinal tract. Hemolysis (the rupture of red blood cells) due to acute poisoning can cause anemia and hemoglobin in the urine. Damage to kidneys can cause changes in urination such as decreased urine output. People who survive acute poisoning often go on to display symptoms of chronic poisoning.

Chronic poisoning usually presents with symptoms affecting multiple systems, but is associated with three main types of symptoms: gastrointestinal, neuromuscular, and neurological. Central nervous system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal symptoms usually result from exposure over longer periods. Signs of chronic exposure include loss of short-term memory or concentration, depression, nausea, abdominal pain, loss of coordination, and numbness and tingling in the extremities. Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning. A "lead hue" of the skin with pallor and/or lividity is another feature. A blue line along the gum with bluish black edging to the teeth, known as a Burton line, is another indication of chronic lead poisoning. Children with chronic poisoning may refuse to play or may have hyperkinetic or aggressive behavior disorders. Visual disturbance may present with gradually progressing blurred vision as a result of central scotoma, caused by toxic optic neuritis.

The symptoms of organophosphate poisoning include muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis. Other symptoms include hypertension, and hypoglycemia.

Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur.

The effects of organophosphate poisoning on muscarinic receptors are recalled using the mnemonic SLUDGEM (salivation, lacrimation, urination, defecation, gastrointestinal motility, emesis, miosis) An additional mnemonic is MUDDLES: miosis, urination, diarrhea, diaphoresis, lacrimation, excitation, and salivation.

The onset and severity of symptoms, whether acute or chronic, depends upon the specific chemical, the route of exposure (skin, lungs, or GI tract), the dose, and the individuals ability to degrade the compound, which the PON1 enzyme level will affect.

Acute aluminium phosphide poisoning (AAlPP) is a large, though under-reported, problem throughout the world, particularly in the Indian subcontinent. Aluminium phosphide (AlP), which is readily available as a fumigant for stored cereal grains, sold under various brand names such as "QuickPhos" and "Celphos", is highly toxic, especially when consumed from a freshly opened container. Death results from profound shock, myocarditis and multi-organ failure. Aluminium phosphide has a fatal dose of between . It has been reported to be the most common cause of suicidal death in North India. Deaths have also been reported in Iran. In January 2017, four children died at a trailer park in Amarillo, Texas, after the pesticide was used under the home to kill rats. Several incidents of death in travelers in Thailand and other parts of Southeast Asia may have been caused by aluminum phosphide or chlorpyrifos, an organophosphate insecticide, used in an attempt to kill bedbugs in hotels. Wired magazine reported on the problem in March 2014. A short film in Arabic on Youtube that focused on the problem in Saudi Arabia had over 3.5 million hits in 2014. The CDC has classified phosphine as immediately dangerous to life at 50 parts per million.

Nicotine poisoning describes the symptoms of the toxic effects of nicotine following ingestion, inhalation, or skin contact. Nicotine poisoning can potentially be deadly, though serious or fatal overdoses are rare. Historically, most cases of nicotine poisoning have been the result of use of nicotine as an insecticide. More recent cases of poisoning typically appear to be in the form of Green Tobacco Sickness, or due to unintended ingestion of tobacco or tobacco products or consumption of nicotine-containing plants.

The estimated lower limit of a lethal dose of nicotine has been reported as between 500 and 1000 mg. Children may become ill following ingestion of one cigarette; ingestion of more than this may cause a child to become severely ill. The nicotine in the e-liquid of an electronic cigarette can be hazardous to infants and children, through accidental ingestion or skin contact. In some cases children have become poisoned by topical medicinal creams which contain nicotine.

People who harvest or cultivate tobacco may experience Green Tobacco Sickness (GTS), a type of nicotine poisoning caused by skin contact with wet tobacco leaves. This occurs most commonly in young, inexperienced tobacco harvesters who do not consume tobacco.

Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

Cholinergic syndrome occurs in acute poisonings with OP pesticides and is directly related to levels of AChE activity. Symptoms include miosis, sweating, lacrimation, gastrointestinal symptoms, respiratory difficulties, shortness of breath, slowed heart rate, cyanosis, vomiting, diarrhea, trouble sleeping, as well as other symptoms. Along with these central effects can be seen and finally seizures, convulsions, coma, respiratory failure. If the person survives the first day of poisoning personality changes can occur, aggressive events, psychotic episodes, disturbances and deficits in memory and attention, as well as other delayed effects. When death occurs, it is most commonly due to respiratory failure from the combination of central and peripheral effects, paralysis of respiratory muscles and depression of the brain respiratory center. For people afflicted with cholinergic syndrome, atropine sulfate combined with an oxime is used to combat the effects of the acute OP poisoning. Diazepam is sometimes also administered in combination with the atropine and oximes.

The intermediate syndrome (IMS) appears in the interval between the end of the cholinergic crisis and the onset of OPIDP. Symptoms associated with IMS manifest within 24–96 hours after exposure. The exact etiology, incidence, and risk factors associated with IMS are not clearly understood, but IMS is recognized as a disorder of neuromuscular junctions. IMS occurs when a person has a prolonged and severe inhibition of AChE and has been linked to specific OP pesticides such as methylparathion, dichlorvos, and parathion. Patients present with increasing weakness of facial, neck flexor and respiratory muscles.

OPIDP occurs in a small percentage of cases, roughly two weeks after exposure, where temporary paralysis occurs. This loss of function and ataxia of peripheral nerves and spinal cord is the phenomenon of OPIDP. Once the symptoms begin with shooting pains in both legs, the symptoms continue to worsen for 3–6 months. In the most severe cases quadriplegia has been observed. Treatment only affects sensory nerves, not motor neurons which may permanently lose function. The aging and phosphorylation of more than 70% of functional NTE in peripheral nerves is one of the processes involved in OPIDP. Standard treatments for OP poisoning are ineffective for OPIDP.

COPIND occurs without cholinergic symptoms and is not dependent on AChE inhibition. COPIND appears with a delay and is long lasting. Symptoms associated with COPIND include cognitive deficit, mood change, autonomic dysfunction, peripheral neuropathy, and extrapyramidal symptoms. The underlying mechanisms of COPIND have not been determined, but it is hypothesized that withdrawal of OP pesticides after chronic exposure or acute exposure could be a factor.

The above symptoms can advance to:

- facial rash (intense itching may accompany the rash.)

- torso or body rash: The rash associated with scombroid poisoning is a form of urticaria, but most commonly does not include wheals (patchy areas of skin-swelling also known as hives) that may be seen in true allergies.

- edema (this is generalized if it occurs at all)

- short-term diarrhea

- abdominal cramps

Nicotine poisoning tends to produce symptoms that follow a biphasic pattern. The initial symptoms are mainly due to stimulatory effects and include nausea and vomiting, excessive salivation, abdominal pain, pallor, sweating, hypertension, tachycardia, ataxia, tremor, headache, dizziness, muscle fasciculations, and seizures. After the initial stimulatory phase, a later period of depressor effects can occur and may include symptoms of hypotension and bradycardia, central nervous system depression, coma, muscular weakness and/or paralysis, with difficulty breathing or respiratory failure.

From September 1, 2010 to December 31, 2014, there were at least 21,106 traditional cigarette calls to US poison control centers. During the same period, the ten most frequent adverse effects to traditional cigarettes reported to US poison control centers were vomiting (80.0%), nausea (9.2%), drowsiness (7.8%), cough (7.2%), agitation (6.6%), pallor (3.0%), tachycardia (2.5%), diaphoresis (1.5%), dizziness (1.5%), and diarrhea (1.4%). 95% of traditional cigarette calls were related to children 5 years old or less. Most of the traditional cigarette calls were a minor effect.

Calls to US poison control centers related to e-cigarette exposures involved inhalations, eye exposures, skin exposures, and ingestion, in both adults and young children. Minor, moderate, and serious adverse effects involved adults and young children. Minor effects correlated with e-cigarette liquid poisoning were tachycardia, tremor, chest pain and hypertension. More serious effects were bradycardia, hypotension, nausea, respiratory paralysis, atrial fibrillation and dyspnea. The exact correlation is not fully known between these effects and e-cigarettes. 58% of e-cigarette calls to US poison control centers were related to children 5 years old or less. E-cigarette calls had a greater chance to report an adverse effect and a greater chance to report a moderate or major adverse effect than traditional cigarette calls. Most of the e-cigarette calls were a minor effect.

From September 1, 2010 to December 31, 2014, there were at least 5,970 e-cigarette calls to US poison control centers. During the same period, the ten most frequent adverse effects to e-cigarettes and e-liquid reported to US poison control centers were vomiting (40.4%), eye irritation or pain (20.3%), nausea (16.8%), red eye or conjunctivitis (10.5%), dizziness (7.5%), tachycardia (7.1%), drowsiness (7.1%), agitation (6.3%), headache (4.8%), and cough (4.5%).

In the worst cases, the poisoning may cause:

- blurred vision

- respiratory distress

- swelling of the tongue

In rare cases, the poisoning may result in death. The coroner's report on Noelene and Yvana Bischoff, mother and daughter tourists from Australia who died suddenly in Bali in January 2014, concluded their deaths were caused by scombroid food poisoning.

Symptoms of arsenic poisoning begin with headaches, confusion, severe diarrhea, and drowsiness. As the poisoning develops, convulsions and changes in fingernail pigmentation called leukonychia striata (Mees's lines, or Aldrich-Mees's lines) may occur. When the poisoning becomes acute, symptoms may include diarrhea, vomiting, vomiting blood, blood in the urine, cramping muscles, hair loss, stomach pain, and more convulsions. The organs of the body that are usually affected by arsenic poisoning are the lungs, skin, kidneys, and liver. The final result of arsenic poisoning is coma and death.

Arsenic is related to heart disease (hypertension-related cardiovascular disease), cancer, stroke (cerebrovascular diseases), chronic lower respiratory diseases, and diabetes.

Chronic exposure to arsenic is related to vitamin A deficiency, which is related to heart disease and night blindness.

Inorganic arsenites (arsenic(III)) in drinking water have a much higher acute toxicity than organic arsenates (arsenic(V)). The acute minimal lethal dose of arsenic in adults is estimated to be 70 to 200 mg or 1 mg/kg/day.

The peripheral autonomic nervous system, central nervous system and the heart are the main systems that are affected following overdose. Initial or mild symptoms typically develop within 2 hours and include tachycardia, drowsiness, a dry mouth, nausea and vomiting, urinary retention, confusion, agitation, and headache. More severe complications include hypotension, cardiac rhythm disturbances, hallucinations, and seizures. Electrocardiogram (ECG) abnormalities are frequent and a wide variety of cardiac dysrhythmias can occur, the most common being sinus tachycardia and intraventricular conduction delay resulting in prolongation of the QRS complex and the PR/QT intervals. Seizures, cardiac dysrhythmias, and apnea are the most important life-threatening complications.

If cyanide is inhaled it can cause a coma with seizures, apnea, and cardiac arrest, with death following in a matter of seconds. At lower doses, loss of consciousness may be preceded by general weakness, giddiness, headaches, vertigo, confusion, and perceived difficulty in breathing. At the first stages of unconsciousness, breathing is often sufficient or even rapid, although the state of the person progresses towards a deep coma, sometimes accompanied by pulmonary edema, and finally cardiac arrest. A cherry red skin color that changes to dark may be present as the result of increased venous hemoglobin oxygen saturation. Cyanide does not directly cause cyanosis. A fatal dose for humans can be as low as 1.5 mg/kg body weight.

Exposure to lower levels of cyanide over a long period (e.g., after use of improperly processed cassava roots as a primary food source in tropical Africa) results in increased blood cyanide levels, which can result in weakness and a variety of symptoms, including permanent paralysis, nervous lesions, hypothyroidism, and miscarriages. Other effects include mild liver and kidney damage.

Diarrhetic shellfish poisoning (DSP) is one of the four recognized symptom types of shellfish poisoning, the others being paralytic shellfish poisoning, neurotoxic shellfish poisoning and amnesic shellfish poisoning.

As the name suggests, this syndrome manifests itself as intense diarrhea and severe abdominal pains. Nausea and vomiting may sometimes occur too.

DSP and its symptoms usually set in within about half an hour of ingesting infected shellfish, and last for about one day. A recent case in France, though, with 20 people consuming oysters manifested itself after 36 hours. The causative poison is okadaic acid, which inhibits intestinal cellular de-phosphorylation. This causes the cells to become very permeable to water and causes profuse, intense diarrhea with a high risk of dehydration. As no life-threatening symptoms generally emerge from this, no fatalities from DSP have ever been recorded.

Arsenic poisoning is a medical condition that occurs due to elevated levels of arsenic in the body. If exposure occurs over a brief period of time symptoms may include vomiting, abdominal pain, encephalopathy, and watery diarrhea that contains blood. Long-term exposure can result in thickening of the skin, darker skin, abdominal pain, diarrhea, heart disease, numbness, and cancer.

The most common reason for long-term exposure is contaminated drinking water. Groundwater most often becomes contaminated naturally; however, contamination may also occur from mining or agriculture. Recommended levels in water are less than 10–50 µg/l (10–50 parts per billion). Other routes of exposure include toxic waste sites and traditional medicines. Most cases of poisoning are accidental. Arsenic acts by changing the functioning of around 200 enzymes. Diagnosis is by testing the urine, blood, or hair.

Prevention is by using water that does not contain high levels of arsenic. This may be achieved by the use of special filters or using rainwater. There is not good evidence to support specific treatments for long-term poisoning. For acute poisonings treating dehydration is important. Dimercaptosuccinic acid (DMSA) or dimercaptopropane sulfonate (DMPS) may be used while dimercaprol (BAL) is not recommended. Hemodialysis may also be used.

Through drinking water, more than 200 million people globally are exposed to higher than safe levels of arsenic. The areas most affected are Bangladesh and West Bengal. Acute poisoning is uncommon. The toxicity of arsenic has been described as far back as 1500 BC in the Ebers papyrus.

Hepatotoxicity (from "hepatic toxicity") implies chemical-driven liver damage. Drug-induced liver injury is a cause of acute and chronic liver disease.

The liver plays a central role in transforming and clearing chemicals and is susceptible to the toxicity from these agents. Certain medicinal agents, when taken in overdoses and sometimes even when introduced within therapeutic ranges, may injure the organ. Other chemical agents, such as those used in laboratories and industries, natural chemicals (e.g., microcystins) and herbal remedies can also induce hepatotoxicity. Chemicals that cause liver injury are called hepatotoxins.

More than 900 drugs have been implicated in causing liver injury (see LiverTox, external link, below) and it is the most common reason for a drug to be withdrawn from the market. Hepatotoxicity and drug-induced liver injury also account for a substantial number of compound failures, highlighting the need for drug screening assays, such as stem cell-derived hepatocyte-like cells, that are capable of detecting toxicity early in the drug development process. Chemicals often cause subclinical injury to the liver, which manifests only as abnormal liver enzyme tests.

Drug-induced liver injury is responsible for 5% of all hospital admissions and 50% of all acute liver failures.

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.

There are also cases where other hydrazine derivative drugs, such as the MAOI antidepressant iproniazid, are associated with liver damage. Phenelzine has been associated with abnormal liver tests. Toxic effects can develop from antibiotics.