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Fluoride Toxicity

  • Author: Richard D Shin, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Feb 17, 2016
 

Background

Fluoride toxicity is characterized by a variety of signs and symptoms. In the United States, poisoning most commonly follows ingestion (accidental or intentional) of fluoride-containing products.

However, in many parts of the world (eg, regions of India and China), elevated levels of fluoride in groundwater result in chronic fluoride toxicity (fluorosis).[1, 2] In southwestern China, fluorosis has also been linked to the burning of coal with high fluoride levels—in particular, indoor burning, including as a cooking fuel.[3] Potentially toxic levels of fluoride have also been found in well water in the US.[4]

Fluoride is found in many common household products, including the following:

  • Toothpaste (eg, sodium monofluorophosphate)
  • Vitamins
  • Dietary supplements (eg, sodium fluoride)
  • Glass-etching or chrome-cleaning agents (eg, ammonium bifluoride)
  • Insecticides and rodenticides (eg, sodium fluoroacetate)

Historically, most cases of serious acute fluoride toxicity have followed accidental ingestion of insecticides or rodenticides.

Symptom onset usually occurs within minutes of exposure, but may be delayed. Manifestations of fluoride toxicity are predominantly gastrointestinal (GI), but neurologic and cardiovascular effects also occur (see Presentation). Long-term exposure to fluoride through elevated levels in drinking water leads to skeletal and dental fluorosis.[1, 4]

Tests for measuring fluoride levels are not available in the emergency department. Assessment of patients with suspected fluoride toxicity is directed toward the consequences of the toxicity, and may include the following:

  • Electrocardiogram
  • Electrolyte levels
  • Fingerstick glucose assay

No antidote for fluoride toxicity exists, and fluoride does not adsorb to activated charcoal. Treatment includes gastric aspiration and lavage, and correction of electrolyte abnormalities. (See Treatment and Medication.)

For patient education information, see the First Aid and Injuries Center, as well as Poisoning and Poison Proofing Your Home.

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Pathophysiology

Fluoride has several mechanisms of toxicity. Upon ingestion, the GI tract is the earliest and most commonly affected organ system. Ingested fluoride can form hydrofluoric acid in the stomach, which leads to GI irritation or corrosive effects.

Once absorbed, fluoride binds calcium ions and may lead to hypocalcemia. Fluoride also has direct cytotoxic effects and interferes with a number of enzyme systems: it disrupts oxidative phosphorylation, glycolysis, coagulation, and neurotransmission (by binding calcium).

Fluoride inhibits Na+/K+ -ATPase, which may lead to hyperkalemia by extracellular release of potassium. Fluoride inhibits acetylcholinesterase, which may be partly responsible for hypersalivation, vomiting, and diarrhea (cholinergic signs). Seizures may result from both hypomagnesemia and hypocalcemia.

Severe fluoride toxicity will result in multiorgan failure. Central vasomotor depression as well as direct cardiotoxicity also may occur. Death usually results from respiratory paralysis, dysrhythmia, or cardiac failure.

Long-term exposure to fluoride in drinking water stimulates osteoblastic bone formation, particularly in cancellous bone, and at low levels (1.00-1.06 ppm), this decreases the risk of overall fractures. At higher levels, however (≥4.32 ppm), fluoride can decrease cortical bone mineral density and increase skeletal fragility, leading to increased fracture risk.[5] In addition to effects on bone, a decrease in insulin sensitivity and insulin signaling has been reported in an animal model of chronic fluoride toxicity.[6]

 

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Etiology

The most common type of exposure is ingestion of products that contain fluoride. To obtain the exact name of the product and how much was ingested is extremely important.

Toothpaste contains 1 mg/g of fluoride as sodium monofluorophosphate. This fluoride formulation has low solubility and is generally nontoxic. The toxic effects following large ingestions of the following products usually are limited to GI discomfort:

  • Toothpaste
  • Oral hygiene products
  • Insecticide
  • Rodenticide
  • Dietary supplements
  • Automobile wheel-cleaning products
  • Glass-etching products

The use of sodium fluoroacetate as a rodenticide was greatly curtailed in the United States by 1990, because of its toxicity to other mammals, and it is currently licensed only for use against coyotes. Its toxicity stems from the similarity of fluoroacetate to acetate; the available evidence suggests that the fluoride component does not contribute.[7]

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Epidemiology

United States statistics

In 2014, the American Association of Poison Control Centers (AAPCC) reported 18,948 exposures involving toothpaste with fluoride, 16,606 of them in children under the age of 6 years.[8] Only 306 cases were actually treated in the emergency department. Moderate effects were seen in 26 cases, and major effects were seen in one case. No deaths were reported.[8]

In 2014, 585 single exposures involving multiple vitamins with fluoride were reported, 91 with adult formulations and 494 with pediatric formulations. No cases resulted in major effects or death.[8]

In 2014, the AAPCC reported four single exposures to sodium monofluoroacetate rodenticides. No moderate or major outcomes occurred, but one death was reported.[8]

Infants and children usually have accidental exposures. Adults usually have intentional exposures.

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Prognosis

Death may result from ingesting as little as 2 g of fluoride in an adult and 16 mg/kg in children. Symptoms may appear with 3-5 mg/kg of fluoride. Estimated toxic dose for fluoride ingestion is 5-10 mg/kg. The estimated lethal dose is 5-10 g (32-64 mg/kg) in adults and 500 mg in small children. The American Association of Poison Control Centers reported no deaths from exposure to fluoride-containing toothpaste in 2014, but one death from sodium monofluoroacetate rodenticide exposure.[8]

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Contributor Information and Disclosures
Author

Richard D Shin, MD Clinical Assistant Instructor, Resident Physician, Department of Emergency Medicine, King's County Hospital, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Mark A Silverberg, MD, MMB, FACEP Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center

Mark A Silverberg, MD, MMB, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Acknowledgements

Michael J Burns, MD Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David C Lee, MD Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School

David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Geofrey Nochimson, MD Consulting Staff, Department of Emergency Medicine, Sentara Careplex Hospital

Geofrey Nochimson, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

References
  1. Jha SK, Singh RK, Damodaran T, Mishra VK, Sharma DK, Rai D. Fluoride in groundwater: toxicological exposure and remedies. J Toxicol Environ Health B Crit Rev. 2013. 16(1):52-66. [Medline].

  2. Samal AC, Bhattacharya P, Mallick A, Ali MM, Pyne J, Santra SC. A study to investigate fluoride contamination and fluoride exposure dose assessment in lateritic zones of West Bengal, India. Environ Sci Pollut Res Int. 2015 Apr. 22 (8):6220-9. [Medline].

  3. Qin X, Wang S, Yu M, Zhang L, Li X, Zuo Z, et al. Child skeletal fluorosis from indoor burning of coal in southwestern China. J Environ Public Health. 2009. 2009:969764. [Medline]. [Full Text].

  4. Felsenfeld AJ, Roberts MA. A report of fluorosis in the United States secondary to drinking well water. JAMA. 1991 Jan 23-30. 265(4):486-8. [Medline].

  5. Li Y, Liang C, Slemenda CW, Ji R, Sun S, Cao J, et al. Effect of long-term exposure to fluoride in drinking water on risks of bone fractures. J Bone Miner Res. 2001 May. 16 (5):932-9. [Medline].

  6. de Cássia Alves Nunes R, Chiba FY, Pereira AG, Pereira RF, de Lima Coutinho Mattera MS, Ervolino E, et al. Effect of Sodium Fluoride on Bone Biomechanical and Histomorphometric Parameters and on Insulin Signaling and Insulin Sensitivity in Ovariectomized Rats. Biol Trace Elem Res. 2016 Feb 15. [Medline].

  7. Proudfoot AT, Bradberry SM, Vale JA. Sodium fluoroacetate poisoning. Toxicol Rev. 2006. 25 (4):213-9. [Medline].

  8. Mowry JB, Spyker DA, Brooks DE, McMillan N, Schauben JL. 2014 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 32nd Annual Report. Clin Toxicol (Phila). 2015 Dec. 53 (10):962-1147. [Medline]. [Full Text].

 
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