Chelation therapy for acute inorganic mercury poisoning can be done with DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), -penicillamine (DPCN), or dimercaprol (BAL). Only DMSA is FDA-approved for use in children for treating mercury poisoning. However, several studies found no clear clinical benefit from DMSA treatment for poisoning due to mercury vapor. No chelator for methylmercury or ethylmercury is approved by the FDA; DMSA is the most frequently used for severe methylmercury poisoning, as it is given orally, has fewer side-effects, and has been found to be superior to BAL, DPCN, and DMPS. α-Lipoic acid (ALA) has been shown to be protective against acute mercury poisoning in several mammalian species when it is given soon after exposure; correct dosage is required, as inappropriate dosages increase toxicity. Although it has been hypothesized that frequent low dosages of ALA may have potential as a mercury chelator, studies in rats have been contradictory. Glutathione and "N"-acetylcysteine (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain.

Chelation therapy can be hazardous if administered incorrectly. In August 2005, an incorrect form of EDTA (edetate disodium) used for chelation therapy resulted in hypocalcemia, causing cardiac arrest that killed a five-year-old autistic boy.

Experimental findings have demonstrated an interaction between selenium and methylmercury, but epidemiological studies have found little evidence that selenium helps to protect against the adverse effects of methylmercury.

Chelation therapy is a medical procedure that involves the administration of chelating agents to remove heavy metals from the body. Chelating agents are molecules that have multiple electron-donating groups, which can form stable coordination complexes with metal ions. Complexation prevents the metal ions from reacting with molecules in the body, and enable them to be dissolved in blood and eliminated in urine. It should only be used in people who have a diagnosis of metal intoxication. That diagnosis should be validated with tests done in appropriate biological samples.

Chelation therapy is administered under very careful medical supervision due to various inherent risks. When the therapy is administered properly, the chelation drugs have significant side effects. Chelation administered inappropriately can cause neurodevelopmental toxicity, increase risk of developing cancer, and cause death; chelation also removes essential metal elements and requires measures to prevent their loss.

Treatment of mild metal fume fever consists of bedrest, keeping the patient well hydrated, and symptomatic therapy (e.g. aspirin for headaches) as indicated. In the case of non-allergic acute lung injury, standard or recommended approaches to treatment have not been defined.

The consumption of large quantities of cow's milk, either before or immediately after exposure is a traditional remedy. However, the United Kingdom Health and Safety Executive challenges this advice, warning, "Don’t believe the stories about drinking milk before welding. It does not prevent you getting metal fume fever."

Therapy is supportive and includes removal from further beryllium exposure. For very severe cases mechanical ventilation may be required.

The mainstays of treatment are removal from the source of lead and, for people who have significantly high blood lead levels or who have symptoms of poisoning, chelation therapy. Treatment of iron, calcium, and zinc deficiencies, which are associated with increased lead absorption, is another part of treatment for lead poisoning. When lead-containing materials are present in the gastrointestinal tract (as evidenced by abdominal X-rays), whole bowel irrigation, cathartics, endoscopy, or even surgical removal may be used to eliminate it from the gut and prevent further exposure. Lead-containing bullets and shrapnel may also present a threat of further exposure and may need to be surgically removed if they are in or near fluid-filled or synovial spaces. If lead encephalopathy is present, anticonvulsants may be given to control seizures, and treatments to control swelling of the brain include corticosteroids and mannitol. Treatment of organic lead poisoning involves removing the lead compound from the skin, preventing further exposure, treating seizures, and possibly chelation therapy for people with high blood lead concentrations.

A chelating agent is a molecule with at least two negatively charged groups that allow it to form complexes with metal ions with multiple positive charges, such as lead. The chelate that is thus formed is nontoxic and can be excreted in the urine, initially at up to 50 times the normal rate. The chelating agents used for treatment of lead poisoning are edetate disodium calcium (CaNaEDTA), dimercaprol (BAL), which are injected, and succimer and d-penicillamine, which are administered orally.

Chelation therapy is used in cases of acute lead poisoning, severe poisoning, and encephalopathy, and is considered for people with blood lead levels above 25 µg/dL. While the use of chelation for people with symptoms of lead poisoning is widely supported, use in asymptomatic people with high blood lead levels is more controversial. Chelation therapy is of limited value for cases of chronic exposure to low levels of lead. Chelation therapy is usually stopped when symptoms resolve or when blood lead levels return to premorbid levels. When lead exposure has taken place over a long period, blood lead levels may rise after chelation is stopped because lead is leached into blood from stores in the bone; thus repeated treatments are often necessary.

People receiving dimercaprol need to be assessed for peanut allergies since the commercial formulation contains peanut oil. Calcium EDTA is also effective if administered four hours after the administration of dimercaprol. Administering dimercaprol, DMSA (Succimer), or DMPS prior to calcium EDTA is necessary to prevent the redistribution of lead into the central nervous system. Dimercaprol used alone may also redistribute lead to the brain and testes. An adverse side effect of calcium EDTA is renal toxicity. Succimer (DMSA) is the preferred agent in mild to moderate lead poisoning cases. This may be the case in instances where children have a blood lead level >25μg/dL. The most reported adverse side effect for succimer is gastrointestinal disturbances. It is also important to note that chelation therapy only lowers blood lead levels and may not prevent the lead-induced cognitive problems associated with lower lead levels in tissue. This may be because of the inability of these agents to remove sufficient amounts of lead from tissue or inability to reverse preexisting damage.

Chelating agents can have adverse effects; for example, chelation therapy can lower the body's levels of necessary nutrients like zinc. Chelating agents taken orally can increase the body's absorption of lead through the intestine.

Chelation challenge, also known as provocation testing, is used to indicate an elevated and mobilizable body burden of heavy metals including lead. This testing involves collecting urine before and after administering a one-off dose of chelating agent to mobilize heavy metals into the urine. Then urine is analyzed by a laboratory for levels of heavy metals; from this analysis overall body burden is inferred. Chelation challenge mainly measures the burden of lead in soft tissues, though whether it accurately reflects long-term exposure or the amount of lead stored in bone remains controversial. Although the technique has been used to determine whether chelation therapy is indicated and to diagnose heavy metal exposure, some evidence does not support these uses as blood levels after chelation are not comparable to the reference range typically used to diagnose heavy metal poisoning. The single chelation dose could also redistribute the heavy metals to more sensitive areas such as central nervous system tissue.

Prevention of metal fume fever in workers who are at risk (such as welders) involves avoidance of direct contact with potentially toxic fumes, improved engineering controls (exhaust ventilation systems), personal protective equipment (respirators), and education of workers regarding the features of the syndrome itself and proactive measures to prevent its development.

In some cases, the product's design may be changed so as to eliminate the use of risky metals. NiCd rechargeable batteries are being replaced by NiMH. These contain other toxic metals, such as chromium, vanadium and cerium. Cadmium is often replaced by other metals. Zinc or nickel plating can be used instead of cadmium plating, and brazing filler alloys now rarely contain cadmium.

Dimercaprol and dimercaptosuccinic acid are chelating agents that sequester the arsenic away from blood proteins and are used in treating acute arsenic poisoning. The most important side effect is hypertension. Dimercaprol is considerably more toxic than succimer.

DMSA monoesters, e.g. MiADMSA, are promising antidotes for arsenic poisoning. Calcium sodium edetate is also used.

Supplemental potassium decreases the risk of experiencing a life-threatening heart rhythm problem from arsenic trioxide.

It is difficult to differentiate the effects of low level metal poisoning from the environment with other kinds of environmental harms, including nonmetal pollution. Generally, increased exposure to heavy metals in the environment increases risk of developing cancer.

Without a diagnosis of metal toxicity and outside of evidence-based medicine, but perhaps because of worry about metal toxicity, some people seek chelation therapy to treat autism, cardiovascular disease, Alzheimer's disease, or any sort of neurodegeneration. Chelation therapy does not improve outcomes for those diseases.

Some medications that can be used for erethism are Traid and Ritalin. Methylphenidate (Ritalin) is a stimulant drug approved for therapy of attention-deficit hyperactivity disorder, postural orthostatic tachycardia syndrome and narcolepsy. It may also be prescribed for off-label use in treatment-resistant cases of lethargy, depression (mood), or neural insult.

One treatment of mercury poisoning was to admit fresh air to the patient by having him go outside daily as much as possible. Stimulants such as ammonia have also been documented to help restore pulse to a normal rhythm. For a more comprehensive reading of treatment, see Mercury poisoning, 'Treatment' section.

Acute beryllium poisoning is an occupational disease. Relevant occupations are those where beryllium is mined, processed or converted into metal alloys, or where machining of metals containing beryllium or recycling of scrap alloys occurs.

Beryllium is regarded extraordinarily hazardous to health upon enough amounts of dust, mists, or fumes consisting fragments little enough to inhale (typically 10µm or less). Metallographic preparation equipment and laboratory work surfaces must be damp wiped occasionally to inhibit buildup of particles. Cutting, grinding, and polishing procedures which manufacture dusts or fumes must be handled within sufficiently vented coverings supplied with particular filters.

The effect of mercury took some time – the latent period between ingestion and the first symptoms (typically paresthesia – numbness in the extremities) was between 16 and 38 days. Paresthesia was the predominant symptom in less serious cases. Worse cases included ataxia (typically loss of balance), blindness or reduced vision, and death resulting from central nervous system failure. Anywhere between 20 and 40 mg of mercury has been suggested as sufficient for paresthesia (between 0.5 and 0.8 mg/kg of body weight). On average, individuals affected consumed 20 kg or so of bread; the 73,000 tonnes provided would have been sufficient for over 3 million cases.

The hospital in Kirkuk received large numbers of patients with symptoms that doctors recognised from the 1960 outbreak. The first case of alkylmercury poisoning was admitted to hospital on 21 December. By 26 December, the hospital had issued a specific warning to the government. By January 1972, the government had started to strongly warn the populace about eating the grain, although dispatches did not mention the large numbers already ill. The Iraqi Army soon ordered disposal of the grain and eventually declared the death penalty for anyone found selling it. Farmers dumped their supplies wherever possible, and it soon got into the water supply (particularly the River Tigris), causing further problems. The government issued a news blackout and released little information about the outbreak.

The World Health Organization assisted the Iraqi government through the supply of drugs, analytical equipment and expertise. Many new treatments were tried, since existing methods for heavy metal poisoning were not particularly effective. Dimercaprol was administered to several patients, but caused rapid deterioration of their condition. It was ruled out as a treatment for this sort of poisoning following the outbreak. Polythiol resins, penicillamine and dimercaprol sulfonate all helped, but are believed to have been largely insignificant in overall recovery and outcomes. Dialysis was tested on a few patients late in the treatment period, but they showed no clinical improvement. The result of all treatments was varied, with some patients' blood mercury level being dramatically reduced, but a negligible effect in others. All patients received periods of treatment interspersed with lay periods; continuous treatment was suggested in future cases. Later treatment was less effective in reducing blood toxicity.

In cases of suspected copper poisoning, penicillamine is the drug of choice, and dimercaprol, a heavy metal chelating agent, is often administered. Vinegar is not recommended to be given, as it assists in solubilizing insoluble copper salts. The inflammatory symptoms are to be treated on general principles, as are the nervous ones.

There is some evidence that alpha-lipoic acid (ALA) may work as a milder chelator of tissue-bound copper. Alpha lipoic acid is also being researched for chelating other heavy metals, such as mercury.

There is no cure for berylliosis; the goals of treatment are to reduce symptoms and slow the progression of disease.

Although the evidence that stopping exposure to beryllium decreases progression of the disease, it is still considered to be an accepted approach to treatment in any stage of disease.

People with early stages of disease, without lung function abnormalities or clinical symptoms, are periodically monitored with physical exams, pulmonary function testing and radiography.

Once clinical symptoms or significant abnormalities in pulmonary function testing appear, treatments include oxygen and oral corticosteroids and whatever supportive therapy is required.

In most cases, lead poisoning is preventable by avoiding exposure to lead. Prevention strategies can be divided into individual (measures taken by a family), preventive medicine (identifying and intervening with high-risk individuals), and public health (reducing risk on a population level).

Recommended steps by individuals to reduce the blood lead levels of children include increasing their frequency of hand washing and their intake of calcium and iron, discouraging them from putting their hands to their mouths, vacuuming frequently, and eliminating the presence of lead-containing objects such as blinds and jewellery in the house. In houses with lead pipes or plumbing solder, these can be replaced. Less permanent but cheaper methods include running water in the morning to flush out the most contaminated water, or adjusting the water's chemistry to prevent corrosion of pipes. Lead testing kits are commercially available for detecting the presence of lead in the household. As hot water is more likely than cold water to contain higher amounts of lead, use only cold water from the tap for drinking, cooking, and for making baby formula. Since most of the lead in household water usually comes from plumbing in the house and not from the local water supply, using cold water can avoid lead exposure. Measures such as dust control and household education do not appear to be effective in changing children's blood levels.

Screening is an important method in preventive medicine strategies. Screening programs exist to test the blood of children at high risk for lead exposure, such as those who live near lead-related industries.

Prevention measures also exist on national and municipal levels. Recommendations by health professionals for lowering childhood exposures include banning the use of lead where it is not essential and strengthening regulations that limit the amount of lead in soil, water, air, household dust, and products. Regulations exist to limit the amount of lead in paint; for example, a 1978 law in the US restricted the lead in paint for residences, furniture, and toys to 0.06% or less. In October 2008, the US Environmental Protection Agency reduced the allowable lead level by a factor of ten to 0.15 micrograms per cubic meter of air, giving states five years to comply with the standards. The European Union's Restriction of Hazardous Substances Directive limits amounts of lead and other toxic substances in electronics and electrical equipment. In some places, remediation programs exist to reduce the presence of lead when it is found to be high, for example in drinking water. As a more radical solution, entire towns located near former lead mines have been "closed" by the government, and the population resettled elsewhere, as was the case with Picher, Oklahoma in 2009.

In humans, heavy metal poisoning is generally treated by the administration of chelating agents.

These are chemical compounds, such as (calcium disodium ethylenediaminetetraacetate) that convert heavy metals to chemically inert forms that can be excreted without further interaction with the body. Chelates are not without side effects and can also remove beneficial metals from the body. Vitamin and mineral supplements are sometimes co-administered for this reason.

Soils contaminated by heavy metals can be remediated by one or more of the following technologies: isolation; immobilization; toxicity reduction; physical separation; or extraction. "Isolation" involves the use of caps, membranes or below-ground barriers in an attempt to quarantine the contaminated soil. "Immobilization" aims to alter the properties of the soil so as to hinder the mobility of the heavy contaminants. "Toxicity reduction" attempts to oxidise or reduce the toxic heavy metal ions, via chemical or biological means into less toxic or mobile forms. "Physical separation" involves the removal of the contaminated soil and the separation of the metal contaminants by mechanical means. "Extraction" is an on or off-site process that uses chemicals, high-temperature volatization, or electrolysis to extract contaminants from soils. The process or processes used will vary according to contaminant and the characteristics of the site.

Cadmium is a naturally occurring toxic heavy metal with common exposure in industrial workplaces, plant soils, and from smoking. Due to its low permissible exposure to humans, overexposure may occur even in situations where trace quantities of cadmium are found. Cadmium is used extensively in electroplating, although the nature of the operation does not generally lead to overexposure. Cadmium is also found in some industrial paints and may represent a hazard when sprayed. Operations involving removal of cadmium paints by scraping or blasting may pose a significant hazard. Cadmium is also present in the manufacturing of some types of batteries. Exposures to cadmium are addressed in specific standards for the general industry, shipyard employment, construction industry, and the agricultural industry.

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.

Beryllium poisoning is poisoning by the toxic effects of beryllium, or more usually its compounds. It takes two forms:

- Acute beryllium poisoning, usually as a result of exposure to soluble beryllium salts

- Chronic beryllium disease (CBD) or berylliosis, usually as a result of long-term exposure to beryllium oxide usually caused by inhalation.

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.

Cookware in which copper is the main structural element (as opposed to copper clad, copper sandwiched or copper colored) is sometimes manufactured without a lining when intended to be used for any of a number of specific culinary tasks, such as preparing preserves or meringues. Otherwise, copper cookware is lined with a non-reactive metal to prevent contact between acidic foods and the structural copper element of the cookware.

Excepting for acute or chronic conditions, exposure to copper in cooking is generally considered harmless. Following Paracelsus, dosage makes the poison; as this pertains to copper "a defense mechanism has apparently evolved as a consequence of which toxicity in man is very unusual."

Acute exposure and attendant copper toxicity is possible when cooking or storing highly acidic foods in unlined copper vessels for extended periods, or by exposing foodstuffs to reactive copper salts (copper corrosion, or verdigris). Continuous, small ("chronic") exposures of acidic foods to copper may also result in toxicity in cases where either surface area interaction potentials are significant, pH is exceptionally low and concentrated (in the case of cooking with, for example, vinegar or wine), or both, and insufficient time elapses between exposures for normal homeostatic elimination of excess copper.

Exceptions to the above may be observed in the case of jam, jelly and preserve -making, wherein unlined copper vessels are used to cook (not to store) acidic preparations, in this case of fruit. Methods of jamming and preserving specify sugar as chemically necessary to the preserving (antibacterial) action, which has the additional effect of mediating (buffering) the interaction of fruit acid with copper, permitting the use of the metal for its efficient thermal transfer properties.

Pharmaceutical injuries can occur when a person is injured by a dangerous, defective or contaminated medication. Many pharmaceutical toxic injury cases are mass tort cases, as most medications are consumed by thousands of people. The cases are often litigated against drug manufacturers and distributors, and potentially against prescribing physicians. When prosecuted against drug manufacturers and distributors, pharmaceutical toxic tort cases differ from medical malpractice suits in that pharmaceutical toxic tort cases are essentially product liability cases, the defective product being the drug.

Several health authorities have issued related guidance documents, which need to be considered for drug development:

- ICH (International Conference on Harmonisation of Technical Requirements for Registration of Pharmaceuticals for Human Use)

- M3(R2) "Guidance on Nonclinical Safety Studies for the Conduct of Human Clinical Trials and Marketing Authorization for Pharmaceuticals"

- S9 "Nonclinical Evaluation for Anticancer Pharmaceuticals"

- S10 "Photosafety Evaluation"

- EMA (European Medicines Agency)

- "Note for Guidance on Photosafety Testing" (revision on-hold)

- "Question & Answers on the Note for Guidance on Photosafety Testing"

- FDA (U.S. Food and Drug Administration)

- MHLW/PMDA (Japanese Ministry of Health, Labour and Welfare / Pharmaceuticals and Medical Devices Agency)

People may be exposed to toxic chemicals or similar dangerous substances from pharmaceutical products, consumer products, the environment, or in the home or at work. Many toxic tort cases arise either from the use of medications, or through exposure at work.