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.

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.

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

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

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.

The most important initial treatment for ethylene glycol poisoning is stabilizing the patient. As ethylene glycol is rapidly absorbed, gastric decontamination is unlikely to be of benefit unless it is performed within 60 minutes of ingestion. Traditionally, gastric lavage or nasogastric aspiration of gastric contents are the most common methods employed in ethylene glycol poisoning. The usefulness of gastric lavage has, however, been questioned, and it is now no longer used routinely in poisoning situations. Ipecac-induced vomiting is not recommended. As activated charcoal does not adsorb glycols, it is not recommended as it will not be effective at preventing absorption. It is only used in the presence of a toxic dose of another poison or drug. Patients with significant poisoning often present in a critical condition. In this situation stabilization of the patient including airway management with intubation should be performed in preference to gastrointestinal decontamination. Patients presenting with metabolic acidosis or seizures require treatment with sodium bicarbonate and anticonvulsives such as a benzodiazepine respectively. Sodium bicarbonate should be used cautiously as it can worsen hypocalcemia by increasing the plasma protein binding of calcium. If hypocalcemia occurs it can be treated with calcium replacement although calcium supplementation can increase the precipitation of calcium oxalate crystals leading to tissue damage. Intubation and respiratory support may be required in severely intoxicated patients; patients with hypotension require treatment with intravenous fluids and possibly vasopressors.

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.

There is no effective treatment or antidote for ciguatera poisoning. The mainstay of treatment is supportive care. There is some evidence that calcium channel blockers like nifedipine and verapamil are effective in treating some of the symptoms that remain after the initial sickness passes, such as poor circulation and shooting pains through the chest. These symptoms are due to the cramping of arterial walls caused by maitotoxin Ciguatoxin lowers the threshold for opening voltage-gated sodium channels in synapses of the nervous system. Opening a sodium channel causes depolarization, which could sequentially cause paralysis, heart contraction, and changing the senses of hot and cold. Some medications such as amitriptyline may reduce some symptoms, such as fatigue and paresthesia, although benefit does not occur in every case.

Mannitol was once used for poisoning after one study reported symptom reversal. Follow-up studies in animals and case reports in humans also found benefit from mannitol. However, a randomized, double-blind clinical trial found no difference between mannitol and normal saline, and based on this result, mannitol is no longer recommended.

Long term management of chronic Ciguatera includes avoiding trigger food and environmental triggers, and managing symptoms with medications and or lifestyle.

Caution may be needed with anesthesia and should be discussed with your healthcare providers.

Treatment is in the form of supportive care. If there is light-headedness, the victim should lie with feet partly elevated. If there is severe wheezing, then intramuscular epinephrine should be given, 0.5–1 ml at dilution of 1/1000 (standard medical emergency kit). An intravenous antihistamine like diphenhydramine should be given if needed.

Hyperbaric oxygen is also used in the treatment of carbon monoxide poisoning, as it may hasten dissociation of CO from carboxyhemoglobin and cytochrome oxidase to a greater extent than normal oxygen. Hyperbaric oxygen at three times atmospheric pressure reduces the half life of carbon monoxide to 23 (~80/3 minutes) minutes, compared to 80 minutes for oxygen at regular atmospheric pressure. It may also enhance oxygen transport to the tissues by plasma, partially bypassing the normal transfer through hemoglobin. However, it is controversial whether hyperbaric oxygen actually offers any extra benefits over normal high flow oxygen, in terms of increased survival or improved long-term outcomes. There have been randomized controlled trials in which the two treatment options have been compared; of the six performed, four found hyperbaric oxygen improved outcome and two found no benefit for hyperbaric oxygen. Some of these trials have been criticized for apparent flaws in their implementation. A review of all the literature on carbon monoxide poisoning treatment concluded that the role of hyperbaric oxygen is unclear and the available evidence neither confirms nor denies a medically meaningful benefit. The authors suggested a large, well designed, externally audited, multicentre trial to compare normal oxygen with hyperbaric oxygen.

Specific treatments for acute pesticide poisoning are often dependent on the pesticide or class of pesticide responsible for the poisoning. However, there are basic management techniques that are applicable to most acute poisonings, including skin decontamination, airway protection, gastrointestinal decontamination, and seizure treatment.

Decontamination of the skin is performed while other life-saving measures are taking place. Clothing is removed, the patient is showered with soap and water, and the hair is shampooed to remove chemicals from the skin and hair. The eyes are flushed with water for 10–15 minutes. The patient is intubated and oxygen administered, if necessary. In more severe cases, pulmonary ventilation must sometimes be supported mechanically. Seizures are typically managed with lorazepam, phenytoin and phenobarbitol, or diazepam (particularly for organochlorine poisonings).

Gastric lavage is not recommended to be used routinely in pesticide poisoning management, as clinical benefit has not been confirmed in controlled studies; it is indicated only when the patient has ingested a potentially life-threatening amount of poison and presents within 60 minutes of ingestion. An orogastric tube is inserted and the stomach is flushed with saline to try to remove the poison. If the patient is neurologically impaired, a cuffed endotracheal tube inserted beforehand for airway protection. Studies of poison recovery at 60 minutes have shown recovery of 8%–32%. However, there is also evidence that lavage may flush the material into the small intestine, increasing absorption. Lavage is contra-indicated in cases of hydrocarbon ingestion.

Activated charcoal is sometimes administered as it has been shown to be successful with some pesticides. Studies have shown that it can reduce the amount absorbed if given within 60 minutes, though there is not enough data to determine if it is effective if time from ingestion is prolonged. Syrup of ipecac is not recommended for most pesticide poisonings because of potential interference with other antidotes and regurgitation increasing exposure of the esophagus and oral area to the pesticide.

Urinary alkalinisation has been used in acute poisonings from chlorophenoxy herbicides (such as 2,4-D, MCPA, 2,4,5-T and mecoprop); however, evidence to support its use is poor.

Further treatment for other complications such as seizure, hypotension, cardiac abnormalities, pulmonary edema, and acidosis may be required. Increased muscle activity and seizures should be treated with dantrolene or diazepam; diazepam should only be given with appropriate respiratory support. Hypotension requires treatment with intravenous fluids; vasopressors may be required to treat myocardial depression. Cardiac dysrhythmias are treated with standard advanced cardiac life support protocols. If severe, metabolic acidosis is treated with sodium bicarbonate. Treatment with sodium bicarbonate is controversial as acidosis may increase tissue oxygen availability. Treatment of acidosis may only need to consist of oxygen therapy. The delayed development of neuropsychiatric impairment is one of the most serious complications of carbon monoxide poisoning. Brain damage is confirmed following MRI or CAT scans. Extensive follow up and supportive treatment is often required for delayed neurological damage. Outcomes are often difficult to predict following poisoning, especially people who have symptoms of cardiac arrest, coma, metabolic acidosis, or have high carboxyhemoglobin levels. One study reported that approximately 30% of people with severe carbon monoxide poisoning will have a fatal outcome. It has been reported that electroconvulsive therapy (ECT) may increase the likelihood of delayed neuropsychiatric sequelae (DNS) after carbon monoxide (CO) poisoning.

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.

Various Caribbean folk and ritualistic treatments originated in Cuba and nearby islands. The most common old-time remedy involves bed rest subsequent to a guanabana juice enema. Other folk treatments range from directly porting and bleeding the gastrointestinal tract to "cleansing" the diseased with a dove during a Santería ritual. In Puerto Rico, natives drink a tea made from mangrove buttons, purportedly high in B vitamins, to flush the toxic symptoms from the system. There has never been a funded study of these treatments.

An account of ciguatera poisoning from a linguistics researcher living on Malakula island, Vanuatu, indicates the local treatment: "We had to go with what local people told us: avoid salt and any seafood. Eat sugary foods. And they gave us a tea made from the roots of ferns growing on tree trunks. I don't know if any of that helped, but after a few weeks, the symptoms faded away."

Senescent leaves of "Heliotropium foertherianum" (Boraginaceae), also known as octopus bush, a plant used in many Pacific islands as a traditional medicine to treat ciguatera fish poisoning, contain rosmarinic acid and derivatives, which are known for their antiviral, antibacterial, antioxidant and anti-inflammatory properties. Rosmarinic acid may remove the ciguatoxins from their sites of action, as well as being an anti-inflammatory.

Lithium is used in some medications, specifically to treat bipolar disorder. The level of "sufficient" medication is thought by many physicians to be close to toxic tolerance for kidney function. Therefore, the patient is often monitored for this purpose.

The initial treatment of nicotine poisoning may include the administration of activated charcoal to try to reduce gastrointestinal absorption. Treatment is mainly supportive and further care can include control of seizures with the administration of a benzodiazepine, intravenous fluids for hypotension, and administration of atropine for bradycardia. Respiratory failure may necessitate respiratory support with rapid sequence induction and mechanical ventilation. Hemodialysis, hemoperfusion or other extracorporeal techniques do not remove nicotine from the blood and are therefore not useful in enhancing elimination. Acidifying the urine could theoretically enhance nicotine excretion, although this is not recommended as it may cause complications of metabolic acidosis.

Current antidotes for OP poisoning consist of a pretreatment with carbamates to protect AChE from inhibition by OP compounds and post-exposure treatments with anti-cholinergic drugs. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of "-oximes" has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally. These antidotes are effective at preventing lethality from OP poisoning, but current treatment lack the ability to prevent post-exposure incapacitation, performance deficits, or permanent brain damage. While the efficacy of atropine has been well-established, clinical experience with pralidoxime has led to widespread doubt about its efficacy in treatment of OP poisoning.

Enzyme bioscavengers are being developed as a pretreatment to sequester highly toxic OPs before they can reach their physiological targets and prevent the toxic effects from occurring. Significant advances with cholinesterases (ChEs), specifically human serum BChE (HuBChE) have been made. HuBChe can offer a broad range of protection for nerve agents including soman, sarin, tabun, and VX. HuBChE also possess a very long retention time in the human circulation system and because it is from a human source it will not produce any antagonistic immunological responses. HuBChE is currently being assessed for inclusion into the protective regimen against OP nerve agent poisoning. Currently there is potential for PON1 to be used to treat sarin exposure, but recombinant PON1 variants would need to first be generated to increase its catalytic efficiency.

One other agent that is being researched is the Class III anti-arrhythmic agents. Hyperkalemia of the tissue is one of the symptoms associated with OP poisoning. While the cellular processes leading to cardiac toxicity are not well understood, the potassium current channels are believed to be involved. Class III anti-arrhythmic agents block the potassium membrane currents in cardiac cells, which makes them a candidate for become a therapeutic of OP poisoning.

Later stage treatment consists of cleaning the iron from the blood, using a chelating agent such as deferoxamine. If this fails then dialysis is the next step.

For precious animals ;

- Repeat screening, case management to abate sources

- Medical and environmental evaluation,

- veterinary evaluation, chelation, case management

- If necessary, veterinary hospitalization, immediate chelation, case management.

The mainstays of treatment are removal from the source of lead and, for precious animals who have significantly high blood lead levels or who have symptoms of poisoning, chelation therapy with a chelating agent.

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.

The amount of iron ingested may give a clue to potential toxicity. The therapeutic dose for iron deficiency anemia is 3–6 mg/kg/day. Toxic effects begin to occur at doses above 10–20 mg/kg of elemental iron. Ingestions of more than 50 mg/kg of elemental iron are associated with severe toxicity.

- A 325-mg tablet of ferrous sulfate heptahydrate has 65 mg (20%) of elemental iron

- A 325-mg tablet of ferrous gluconate has 39 mg (12%) of elemental iron

- A 325-mg tablet of ferrous fumarate has 107.25 mg (33%) of elemental iron

- 200 mg ferrous sulfate, dried, has 65 mg (33%) of elemental iron

In terms of blood values, iron levels above 350–500 µg/dL are considered toxic, and levels over 1000 µg/dL indicate severe iron poisoning.

Prevention is mainly the role of the state, through the definition of strict rules of hygiene and a public services of veterinary surveying of animal products in the food chain, from farming to the transformation industry and delivery (shops and restaurants). This regulation includes:

- traceability: in a final product, it must be possible to know the origin of the ingredients (originating farm, identification of the harvesting or of the animal) and where and when it was processed; the origin of the illness can thus be tracked and solved (and possibly penalized), and the final products can be removed from the sale if a problem is detected;

- enforcement of hygiene procedures such as HACCP and the "cold chain";

- power of control and of law enforcement of veterinarians.

In August 2006, the United States Food and Drug Administration approved Phage therapy which involves spraying meat with viruses that infect bacteria, and thus preventing infection. This has raised concerns, because without mandatory labelling consumers would not be aware that meat and poultry products have been treated with the spray.

At home, prevention mainly consists of good food safety practices. Many forms of bacterial poisoning can be prevented by cooking it sufficiently, and either eating it quickly or refrigerating it effectively. Many toxins, however, are not destroyed by heat treatment.

Techniques that help prevent food borne illness in the kitchen are hand washing, rinsing produce, preventing cross-contamination, proper storage, and maintaining cooking temperatures. In general, freezing or refrigerating prevents virtually all bacteria from growing, and heating food sufficiently kills parasites, viruses, and most bacteria. Bacteria grow most rapidly at the range of temperatures between , called the "danger zone". Storing food below or above the "danger zone" can effectively limit the production of toxins. For storing leftovers, the food must be put in shallow containers

for quick cooling and must be refrigerated within two hours. When food is reheated, it must reach an internal temperature of or until hot or steaming to kill bacteria.

Accidental poisonings can be avoided by proper labeling and storage of containers. When handling or applying pesticides, exposure can be significantly reduced by protecting certain parts of the body where the skin shows increased absorption, such as the scrotal region, underarms, face, scalp, and hands. Safety protocols to reduce exposure include the use of personal protective equipment, washing hands and exposed skin during as well as after work, changing clothes between work shifts, and having first aid trainings and protocols in place for workers.

Personal protective equipment for preventing pesticide exposure includes the use of a respirator, goggles, and protective clothing, which have all have been shown to reduce risk of developing pesticide-induced diseases when handling pesticides. A study found the risk of acute pesticide poisoning was reduced by 55% in farmers who adopted extra personal protective measures and were educated about both protective equiment and pesticide exposure risk. Exposure can be significantly reduced when handling or applying pesticides by protecting certain parts of the body where the skin shows increased absorption, such as the scrotal region, underarms, face, scalp, and hands. Using chemical-resistant gloves has been shown to reduce contamination by 33–86%.

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.