en.wikipedia.org/wiki/Chelation_therapy

This statement is incorrect because calcium disodium EDTA is specifically used in children for severe lead poisoning.

• CDC says that when a child’s blood lead level is 45 µg/dL or higher, clinicians should consult specialists to initiate chelation therapy.
• ATSDR’s lead management guideline says children with blood lead levels above 70 µg/dL or with encephalopathy should receive parenteral therapy with BAL and EDTA.
• The FDA/DailyMed label for edetate calcium disodium states that it is indicated for lead poisoning and lead encephalopathy “in both pediatric populations and adults.”

The important distinction is between edetate calcium disodium (used for lead poisoning) and disodium EDTA / edetate disodium (a different formulation that can cause fatal hypocalcemia if used incorrectly). So the article’s blanket claim that “EDTA should not be used in the treatment of children” is wrong; what should not be used for pediatric chelation is disodium EDTA, not all EDTA formulations.

This sentence inaccurately describes the comparator arm in the NIH-funded TACT trial.

According to NIH/NCCIH and NHLBI’s BioLINCC study record, TACT was a double-blind, placebo-controlled, 2×2 factorial trial. Patients were randomized to receive intravenous disodium EDTA chelation therapy or a placebo infusion, and separately to receive high-dose vitamins/minerals or placebo pills.

That means the trial was not “chelation therapy versus normal recommended therapy including statins and aspirin.” Standard medical care after myocardial infarction continued in the background for participants; the randomized comparison was EDTA vs placebo, not chelation vs standard therapy.

Misdescribing the study this way could make readers think the control group did not receive placebo infusions or that chelation replaced ordinary cardiac care in the treatment arm, which is not how TACT was designed.

This statement is incorrect because succimer (DMSA) did not replace BAL and EDTA across lead, arsenic, and mercury poisoning in U.S. practice.

Key evidence:

1. FDA labeling for succimer (CHEMET) says it is indicated for lead poisoning in pediatric patients with blood lead levels above 45 mcg/dL. It is not FDA-labeled as the primary U.S. treatment for arsenic or mercury poisoning.
2. Edetate calcium disodium (calcium EDTA) remains FDA-labeled for lead poisoning and lead encephalopathy in both pediatric patients and adults.
3. ATSDR’s lead guideline says children with severe lead poisoning or encephalopathy should receive parenteral therapy with BAL and EDTA, showing those drugs remain in use for serious cases rather than having been “replaced.”
4. For arsenic poisoning, ATSDR states that chelating agents such as dimercaprol can prevent effects if given within a few hours of exposure.
5. For mercury poisoning, CDC notes that succimer is used off-label for mercury toxicity, while NCBI’s LiverTox says dimercaprol’s current indications include mercury and arsenic poisoning.

So while DMSA/succimer became an important and often preferred oral chelator for some situations, the article’s claim that it “quickly replaced both BAL and EDTA as the primary treatment” for all three poisonings in the United States is too broad and factually wrong.

This sentence conflates two different parts of chelation history.

• The Oxford wartime research on Lewisite led to the development of dimercaprol (British anti-Lewisite, BAL).
• NIH’s historical summary of EDTA says that the initial medical uses were BAL for arsenical poisoning and citrate for lead intoxication, and that EDTA was later used for lead poisoning, with FDA approval in 1953.

So the Oxford chemists searching for a Lewisite antidote did not “learn that EDTA was particularly effective in treating lead poisoning” as part of that wartime discovery. The relevant wartime antidote was BAL, while EDTA entered medical use later for lead and other indications.

This statement gets the timing wrong.

NIH/NCCIH’s summary of the TACT study says the trial was conducted between 2003 and 2011 and that its results were reported in 2013. NHLBI’s BioLINCC study record likewise identifies the primary publication as the JAMA paper "Effect of disodium EDTA chelation regimen on cardiovascular events in patients with previous myocardial infarction: The TACT Randomized Trial" (2013;309(12):1241-1250).

November 2012 was when TACT results were publicly presented, but the main trial paper was published in 2013, so saying the "final results ... were published in November 2012" is inaccurate.

This table entry is inaccurate because it assigns acute iron poisoning to deferoxamine, deferasirox, and deferiprone as if all three share that indication.

According to current FDA/DailyMed labeling:

• Deferoxamine is indicated both as an adjunct to standard measures for the treatment of acute iron intoxication and for chronic/transfusional iron overload.
• Deferasirox is indicated for chronic iron overload due to blood transfusions, not acute iron poisoning.
• Deferiprone is indicated for transfusional iron overload in thalassemia (and related labeled uses depending on product), not acute iron poisoning.

So the table is wrong to list all three together as treatments for both acute iron poisoning and iron overload. Only deferoxamine has the acute-intoxication indication.