Information about Fluoride Poisoning
| DiseasesDB | 29228 |
|---|---|
| eMedicine | emerg/181 |
| MeSH | D005458 |
| Part of a series on |
| Toxicology and poison |
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Poisoning most commonly occurs following ingestion (accidental or intentional) of products that contain fluoride.
When ingested directly, fluoride compounds are readily absorbed by the intestines; over time, the compound is excreted through the urine, and the half-life for concentration of fluorine compounds is on an order of hours. Fluoride is taken out of circulation by the body and trace amounts bound in bone. Urine tests are a good indication of high exposure to fluoride compounds in the recent past.
Skin or eye contact with many fluoride compounds (in high concentrations) is dangerous.
The only generally accepted adverse effect of low concentration water fluoridation at this time is dental fluorosis. It is a condition caused by 'excessive' intake of fluorine compounds over an extended period of time during tooth development (before teeth erupt into the mouth), and can cause yellowing of teeth, hypothyroidism, or brittling of bones and teeth. The definition of 'excessive' in the context of fluorosis falls on the order of parts per million (ppm) and is generally accepted to mean significantly higher than the 0.7 to 1.2 ppm amounts recommended for fluoridated water. Fluoride in small amount is beneficial to teeth see Fluoride therapy.
One of the side effects of fluoride poisoning is gastro-intestinal inflammation as fluoride toxicity has a corrosive effect on the mucous membrane which line the gut[1]. Among the potential metabolic disturbances reported caused by fluoride toxicity is the increased impact of the natural plant toxin, salicylate[2],which may have particular significance in subgroups who already have high incidence of salicylate intolerance such as the ADHD and autism populations (see Autism therapies).
Possible sources
The following is a list of possible sources of poisoning. Some of them have not been proven scientifically as the causes of poisoning, but they are still of interest because some people state they are. As such, the accuracy of the following list is doubtful at best. Historically, most cases of fluoride poisoning have been caused by accidental ingestion of insecticides or rodenticides.- Air pollution
- Anesthetics
- Antibiotics
- Automobile wheel-cleaning products
- Contaminated beverages and food products
- Dietary supplements that contain sodium fluoride
- Fluoridated milk
- Fluoridated salt
- Fluoridation of public water supplies
- Fluoride tablets
- Glass-etching or Chrome-cleaning agents like ammonium bifluoride
- Groundwater pollution
- Household products
- Industrial exposure to fluxes used to lower melting points of metals.
- Insecticides containing sodium fluoride
- Mattresses emitting fluoride gases
- Scotchgard
- Soy products
- Rodenticides containing sodium fluoride
- Tea
- Teflon
- Toothpaste or other oral dental products containing sodium monofluorophosphate
- Vaccine contamination
Chronic Toxicity
This article is focused on acute toxicity: the results of ingesting a large amount of fluoride in a short period of time. Chronic toxicity, the result of ingesting small amounts of fluoride over a long period of time, results in dental fluorosis and skeletal fluorosis. These conditions are seen in areas where there is natural fluoride in the drinking water at levels above that added in public water supplies in the United States.Symptoms of Acute Toxicity
Fluoride toxicity is characterized by a variety of signs and symptoms. Symptom onset usually occurs within minutes of exposure. Severity of symptoms can depend on the amount of fluoride compounds ingested.Symptoms of fluoride poisoning point towards some kind of profound metabolic dysfunction, very similar to the symptoms of hypothyroidism.
Gastrointestinal
When poisoned by fluoride, gastrointestinal signs predominate.- Abdominal pain
- Diarrhea
- Dysphagia
- Hypersalivation
- Mucosal injury
- Nausea
- Vomiting
Electrolyte abnormalities
Neurologic effects
- Headache
- Hyperactive reflexes
- Muscle weakness
- Muscular spasm
- Paresthesia
- Seizures
- Tetanic contractions
- Tremor
Cardiovascular
Method of action
Ingested fluoride initially acts locally on the intestinal mucosa. It can form hydrofluoric acid in the stomach, which leads to gastrointestinal irritation or corrosion. After ingestion, the gastrointestinal tract is the earliest and most commonly affected organ system.Treatment
In case of accidental swallowing, give milk, calcium carbonate or milk of magnesia to slow absorption. Eye or skin contact should be treated by removing any contaminated clothing and flushing with water.References
External links
- "287" The Body Burden Movie for Theatrical Release 2008 will cover fluoride poisoning
- The "287" Body Burden blog
- Fluoride Action Network An international coalition seeking to broaden public awareness about the toxicity of fluoride compounds and the health impacts of current fluoride exposures.
- eMedicine article about Fluoride Toxicity by Geoffrey Nochimson, MD
- Acute fluoride poisoning from a public water system. Gessner BD, Beller M, Middaugh JP, Whitford GM.
- Re-Examination of Acute Toxicity of Fluoride, by Kenji Akiniwa, Tokyo, Japan
- Website of the "Parents of Fluoride poisoned children" foundation
- http://www.slweb.org/galletti.html fluoride may be used reliably to reduce thyroid function. This is therapeutic with hyperthyroidism.
- http://www.bruha.com/pfpc/html/symptoms.html Since fluorides reduce thyroid function, the full list of conditions associated with hypothyroidism(177 conditions) is also present in fluoride poisoning.
- impact of fluoride toxicity on salicylate levels and gut inflamation
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history of poisons[1] stretches over a period from before 4500 BC to the present day. Poisons have been used for many purposes across the span of human existence as weapons, anti-venoms and medicines.
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poisons are substances that can cause damage, illness, or death to organisms, usually by chemical reaction or other activity on the molecular scale, when a sufficient quantity is absorbed by an organism.
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Acceptable Daily Intake or ADI is a measure of the amount of a specific substance (usually a food additive, or a residue of a veterinary drug or pesticide) in food or drinking water that can be ingested (orally) over a lifetime without an appreciable health risk.
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Acute toxicity describes the adverse effects of a substance which result either from a single exposure[1] or from multiple exposures in a short space of time (usually less than 24 hours).
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Bioaccumulation occurs when an organism absorbs a toxic substance at a rate greater than that at which the substance is lost. Thus, the longer the biological half-life of the substance the greater the risk of chronic poisoning, even if environmental levels of the toxin are very
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The fixed-dose procedure (FDP) was proposed in 1984 to assess a substance's acute oral toxicity using fewer animals with less suffering than the older LD50 test developed in 1927.
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Mycotoxin (from the Greek μύκης (mykes, mukos) "fungus") is a toxin produced by an organism of the fungus kingdom, which includes mushrooms, molds and yeasts. Most fungi are aerobic (use oxygen).
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Fictional chemical weapons
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The Bradford sweets poisoning was the accidental arsenic poisoning of more than 200 people in Bradford, England in 1858; an estimated 20 people died when sweets accidentally made with arsenic were sold from a market stall.
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Minamata disease
Classification & external resources
The crippled hand of a Minamata disease victim (W. E. Smith)
ICD-10 T56.1
ICD-9 985.0
MedlinePlus 001651
Minamata disease
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Classification & external resources
The crippled hand of a Minamata disease victim (W. E. Smith)
ICD-10 T56.1
ICD-9 985.0
MedlinePlus 001651
Minamata disease
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Niigata Minamata disease
Classification & external resources
The crippled hand of a Minamata disease victim
ICD-10 T56.1
ICD-9 985.0
MedlinePlus 001651
Niigata Minamata disease
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Classification & external resources
The crippled hand of a Minamata disease victim
ICD-10 T56.1
ICD-9 985.0
MedlinePlus 001651
Niigata Minamata disease
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Alexander Litvinenko suddenly fell ill and was hospitalised. He died three weeks later, becoming the first known victim of lethal polonium-210-induced acute radiation syndrome.
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