FLUORIDE

Sodium fluoride, sodium duosilicate (NA2SiF6) and cryolite (Na3AIF6) are used as insecticides, rodenticides and delousing powders (Baselt, 2000).
Fluoride promotes the resistance of tooth decay in children (Baselt, 2000).
Fluoride can increase the density and calcification of bone, its use has been recommended for individuals with osteoporosis at a daily dose of 33-220 mg as the sodium salt (Baselt, 2000).

In a multicenter prospective study, long term exposure (20 years) to fluoridated drinking water in older women did not increase the risk of fracture and may have had a protective effect (Phipps et al, 2000).

EPIDEMIOLOGY

Dermal exposures are common. Systemic fluoride poisoning is uncommon, but deaths are reported to poison centers each year, primarily from exposure to hydrofluoric acid. Toxicity is very rare following exposure to household dental products (toothpaste and dental rinses), but is theoretically possible following ingestion of fluoride supplements. Fluorosis is common in some areas of Asia due to high fluoride content of water (Hussain et al, 2010; Augenstein et al, 1991).

FORMS

Dietary fluoride supplements come in both tablet and liquid form. The fluoride ion F is responsible for producing toxicity in poisonings.
TOOTHPASTE

The fluoride in toothpaste is usually sodium or stannous fluoride or sodium monofluorophosphate. Fluoride toothpaste commonly contains a maximum of 1 milligram of fluoride per gram of toothpaste.
If an entire 6.4 oz tube of toothpaste containing 1 mg/g of fluoride were ingested and retained, this would represent over 200 mg of fluoride.
The maximum allowable amount of fluoride in a tube of toothpaste is 260 mg. Serious symptoms might occur, if a large portion of the tube's contents were ingested by a child.
Fluoride ion amounts should be calculated with all toothpaste ingestions. If the fluoride content is not available, an estimate using 1 mg/g is conservative.

SOURCES

SUMMARY - Fluoride is found in insecticides, rodenticides, the petroleum industry, glass etching, and timber preservation industries, dietary supplements, swine anthelmintics. Fluoride is often added to city water supplies.

For information on HYDROFLUORIC ACID, please see that management.

Manifestations of ammonium fluorosilicate toxicity are similar to sodium fluoride.

Ammonium fluosilicate, silicofluoride, hexaflurosilicate, diammonium hexafluoro silicate and other fluosilicate salts are hydrolyzed by alkali to the fluoride ion.

TABLE 2: FLUORIDE PRODUCT CONVERSIONS

PROFESSIONAL STRENGTH PRODUCTS

Superdent(R) topical fluoride gel contains 1.23% fluoride (Fisher et al, 1991).
Common professionally applied dental treatments include 2% NaF (equivalent to 0.91% F); 8% SnF2 (equivalent to 1.95% F); 10% SnF2 (equivalent to 2.4% F) or Acidulated Phosphate Fluoride Gel (equivalent to 1.23% F).

FLUORIDE VARNISHES

Fluoride varnishes are available in the United States and were created to prolong contact of the fluoride with tooth enamel. The USFDA has approved these products as medical devices to be used as cavity liners and for the treatment of hypersensitive teeth. Two commercially available fluoride varnishes in the US have concentrations of fluoride of 22,600 ppm F. These products are intended for application by dental professionals (Beltran-Aguilar et al, 2000).
Plasma fluoride concentrations were analyzed in four children (ages 4, 5, 12 and 14 years) after application of a fluoride varnish (Duraphat(R)). The amount of varnish applied ranged from 2.3 to 5.0 milligrams. Peak plasma fluoride concentrations of 3.2 to 6.3 micromolar were observed within two hours of treatment, which was followed by a rapid two-hour decrease. Levels were comparable to brushing with a fluoridated toothpaste or after ingesting a 1 milligram fluoride tablet. The authors concluded that acute toxicity with these products is minimal, and the risk of dental fluorosis is low due to the infrequent application of these varnishes (Beltran-Aguilar et al, 2000).

DENTAL FLUOROSIS SECONDARY TO INCREASED SOURCES OF FLUORIDE

Sources of substantial amounts of ingested fluoride that may contribute to dental fluorosis in young children, other than drinking water, may include bottled water, fruit juices, ready-to- feed infant formulas, soft drinks processed in fluorinated areas, and tea (Levi & Zarei-M, 1991; (Nowak & Nowak, 1989; Flaitz et al, 1989; Stannard et al, 1990; Wiatrowski et al, 1975; Singer & Ophaug, 1979; Johnson & Bawden, 1987; McKnight-Hanes et al, 1988; Clovis & Hargreaves, 1988; Smid & Kruger, 1985).
FOODS: One cup of tea contains 1 to 4 mg of fluoride (Richmond, 1986).
WELL WATER: Fluorosis may occur in some areas as a result of the natural occurrence of fluoride in the groundwater (Felsenfeld & Roberts, 1991).
MINERAL WATER: Some mineral waters contain 8.5 mg/L of fluoride, and have been associated with the development of skeletal fluorosis (Lantz et al, 1987).
BOTTLED WATER: Some bottled water may be lacking in fluoride (McGire, 1989).
META-ANALYSIS - In a review of 214 studies on water fluoridation, a dose-dependent increase in dental fluorosis was found. At a fluoride level of 1 ppm an estimated 12.5% of exposed individuals would develop fluorosis that would produce an aesthetic concern. Of note, the authors did report that the quality of the studies reviewed was low to moderate (McDonagh et al, 2000).
MUNCIPAL WATER SUPPLIES

Fluoride may be added to city or geographic water supplies at the recommended level of 1 ppm to promote the resistance to tooth decay in children (Baselt, 2000).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

USES: Several fluoride salts are used in dental products. Chronic fluoride poisoning (fluorosis) may occur in areas where the water has very high fluoride concentrations. Fluoride-liberating chemicals (such as ammonium fluoride, ammonium bifluoride, and sodium fluorosilicate) are used in some automobile wheel cleaners and rust removers. Sodium fluoride was used as a rodenticide. Hydrofluoric acid (HF) is used in etching glass and cleaning silicon chip products. Ammonium bifluoride and hydrofluoric acid are covered in separate managements.

PHARMACOLOGY: Fluoride promotes remineralization of decalcified dental enamel and may interfere with the growth of bacteria in dental plaque.

TOXICOLOGY: Sodium fluoride reacts with the gastric acid to form hydrofluoric acid. The major toxic effects of fluoride are due to the chelation of calcium and magnesium. In tissue, the local hypocalcemia causes pain and cellular death. Systemic hypocalcemia and hypomagnesemia may cause cardiac dysrhythmias and cardiovascular collapse. Fluoride opens the calcium-dependent potassium channels on erythrocytes resulting in hyperkalemia. Fluoride also impairs oxidative phosphorylation. Long-term ingestion of water with high fluoride concentrations results in weak and brittle bones (fluorosis).

EPIDEMIOLOGY: Dermal exposures are common. Systemic fluoride poisoning is uncommon, but deaths are reported to poison centers each year, primarily from exposure to hydrofluoric acid. Toxicity is very rare following exposure to household dental products (toothpaste and dental rinses), but is theoretically possible following ingestion of fluoride supplements. Fluorosis is common in some areas of Asia due to high fluoride content of water.

WITH POISONING/EXPOSURE

MILD TO MODERATE TOXICITY: Acute ingestion of dental products containing sodium fluoride generally causes minor gastrointestinal upset. Skin exposure to household products with higher concentrations of fluoride ion results in pain that develops slowly. The tissue may appear normal but the patient can have severe pain. Over time the skin may become hyperemic with subsequent blanching and cogitative necrosis. Eye exposure can cause irritation and corneal edema; if fluoride concentration is higher, conjunctival ischemia and chemosis may develop. Inhalation causes minor upper respiratory tract irritation. Nausea and vomiting frequently occurs within 30 to 60 minutes of ingestion.
SEVERE TOXICITY: Severe toxicity generally only develops after exposure to industrial products containing fairly high concentrations of sodium fluoride or sodium bifluoride. Severe burns (ocular and dermal) may occur following exposure to higher concentration products. Burns involving more than 5% body surface area (BSA) from low concentration products or more than 1% BSA from high concentration products may produce systemic fluoride poisoning. Systemic toxicity most commonly occurs following ingestion, but may occur following dermal or inhalational exposure. Inhalation may cause acute lung injury from direct tissue injury. Symptoms of serious toxicity include skeletal muscle weakness and spasm, respiratory muscle weakness, and respiratory arrest. Ventricular dysrhythmias and fibrillation are thought to be the main cause of death. Patients may have severe toxicity without significant oral or gastrointestinal symptoms.

Editor's Note: An ERG guide with information appropriate to this material does not exist.

ACUTE CLINICAL EFFECTS

SUMMARY

PHARMACOLOGY: Fluoride promotes remineralization of decalcified dental enamel and may interfere with the growth of bacteria in dental plaque.
TOXICOLOGY: Sodium fluoride reacts with the gastric acid to form hydrofluoric acid. The major toxic effects of fluoride are due to the chelation of calcium and magnesium. In tissue, the local hypocalcemia causes pain and cellular death. Systemic hypocalcemia and hypomagnesemia may cause cardiac dysrhythmias and cardiovascular collapse. Fluoride opens the calcium-dependent potassium channels on erythrocytes resulting in hyperkalemia. Fluoride also impairs oxidative phosphorylation. Long-term ingestion of water with high fluoride concentrations results in weak and brittle bones (fluorosis).
EPIDEMIOLOGY: Dermal exposures are common. Systemic fluoride poisoning is uncommon, but deaths are reported to poison centers each year, primarily from exposure to hydrofluoric acid. Toxicity is very rare following exposure to household dental products (toothpaste and dental rinses), but is theoretically possible following ingestion of fluoride supplements. Fluorosis is common in some areas of Asia due to high fluoride content of water.
MILD TO MODERATE TOXICITY: Acute ingestion of dental products containing sodium fluoride generally causes minor gastrointestinal upset. Skin exposure to household products with higher concentrations of fluoride ion results in pain that develops slowly. The tissue may appear normal but the patient can have severe pain. Over time the skin may become hyperemic with subsequent blanching and cogitative necrosis. Eye exposure can cause irritation and corneal edema; if fluoride concentration is higher, conjunctival ischemia and chemosis may develop. Inhalation causes minor upper respiratory tract irritation. Nausea and vomiting frequently occurs within 30 to 60 minutes of ingestion.
SEVERE TOXICITY: Severe toxicity generally only develops after exposure to industrial products containing fairly high concentrations of sodium fluoride or sodium bifluoride. Severe burns (ocular and dermal) may occur following exposure to higher concentration products. Burns involving more than 5% body surface area (BSA) from low concentration products or more than 1% BSA from high concentration products may produce systemic fluoride poisoning. Systemic toxicity most commonly occurs following ingestion, but may occur following dermal or inhalational exposure. Inhalation may cause acute lung injury from direct tissue injury. Symptoms of serious toxicity include skeletal muscle weakness and spasm, respiratory muscle weakness, and respiratory arrest. Ventricular dysrhythmias and fibrillation are thought to be the main cause of death. Patients may have severe toxicity without significant oral or gastrointestinal symptoms.

CARDIOVASCULAR

CARDIAC ARREST: Cardiac arrest was reported in several cases of fluoride exposure (Lech, 2011; Arnow et al, 1994).
DYSRHYTHMIA: Cardiac dysrhythmias secondary to hypocalcemia or hyperkalemia can occur following fluoride toxicity (Clancy, 2002).

DERMATOLOGIC

BURN: Severe burns (ocular and dermal) may occur following exposure to higher concentration products. Burns involving more than 5% body surface area (BSA) from low concentration products or more than 1% BSA from high concentration products may produce systemic fluoride poisoning (Greco et al, 1988).
PAIN: Skin exposure to household products with higher concentrations of fluoride ion results in pain that develops slowly. The tissue may appear normal but the patient can have severe pain. Over time the skin may become hyperemic with subsequent blanching and cogitative necrosis (Hojer et al, 2002).
DERMATITIS: Skin eruptions may occur. Sodium fluoride, ammonium fluoride, and sodium hexafluorosilicate have all been reported to produce contact pustular reactions on previously damaged or inflamed skin (Fisher et al, 1959; Becker & O'Brien, 1959; Dooms-Goossens et al, 1985).

FLUID ELECTROLYTE

Severe hypocalcemia may occur (Harchelroad & Gowtz, 1993; Swanson et al, 1993).

GASTROINTESTINAL

VOMITING: Acute ingestion can result in the following: epigastric pain, dysphagia, salivation, nausea, vomiting, and hematemesis (Augenstein et al, 1991; Gessner et al, 1994; Swanson et al, 1993).
EPIGASTRIC PAIN: Epigastric pain, anorexia and nausea were common complaints in patients taking therapeutic doses (30 mg/day) of sodium fluoride (Das et al, 1994).
GASTRITIS: In one study all 10 patients taking 30 mg/day of sodium fluoride for at least 3 months demonstrated petechiae, erosions and erythema on upper gastrointestinal endoscopy, compared with 0 of 10 control subjects (Das et al, 1994).
DIARRHEA: Diarrhea has been reported with therapeutic use of sodium fluoride (Das et al, 1994).

HEENT

EYES

EYE IRRITATION: Eye exposure can cause irritation and corneal edema; if fluoride concentration is higher, conjunctival ischemia and chemosis may develop (McCulley et al, 1983).

NOSE

RHINITIS: With the use of a potassium aluminum tetrafluoride flux, rhinitis has been reported (Hjortsberg et al, 1994).

THROAT

DENTAL FLUOROSIS: Exposure of children to excessive fluoride results in defective dental enamel formation, causing pits to form in teeth (Ishu & Suckling, 1991).

MUSCULOSKELETAL

SKELETAL FLUOROSIS: A In a survey of aluminum workers exposed to fluoride, 20% had possible or definite fluorosis after 1 to 32 years. Symptoms included joint pain, limited joint mobility, ossifications on x-ray, osteosclerosis, and thickening of long bone cortices (Czerwinski et al, 1988).

Prolonged exposure to water contaminated with high levels of fluoride (0.86 to 1.33 mcg/mL) and fluoride contaminated soil may cause fluorosis. Effects of fluorosis may include brittle bones, calcification of ligaments, and joint pain (Abdennebi et al, 1995). Histological changes such as osteomalacia may occur.

MUSCLE PAIN AND SPASM: Skeletal muscle weakness and spasm may occur with serious toxicity (Klasner et al, 1996). Myalgia and arthralgia of leg muscles and joints was reported with topically applied fluoride gel (Eichmiller et al, 2005).

NEUROLOGIC

HYPERREFLEXIA: Hypocalcemia secondary to fluoride toxicity can result in an increase in skeletal muscle excitability, hyperactive reflexes, painful muscular spasms (particularly in the extremities), weakness, and tetanic contractures approximately 3 to 5 hours after exposure (Arena, 1979).

RESPIRATORY

RESPIRATORY PARALYSIS: Respirations are first stimulated, then depressed with toxicity. Death usually is from muscle respiratory paralysis (Heifetz & Horowitz, 1986). Symptoms of serious toxicity include respiratory muscle weakness and respiratory arrest (Klasner et al, 1996).
REACTIVE AIRWAY: Cough, chest tightness and a decrease in FEV1 after methacholine challenge were reported in workers exposed to potassium aluminum tetrafluoride via inhalation during the soldering of aluminum (Hjortsberg et al, 1994).

CHRONIC CLINICAL EFFECTS

Chronic fluoride exposure can produce cumulative toxicity. Systemic absorption of more than 6 mg per day can produce FLUOROSIS, a condition characterized by nausea, vomiting, loss of appetite, diarrhea or constipation, anemia, weakness, and joint stiffness. Daily absorption of 20 to 80 mg of fluoride will lead to fluorosis in 10 to 20 years (Hathaway et al, 1991).

The major hazard of chronic fluoride exposure is to the bone (Clayton & Clayton, 1994). Chronic exposure can produce OSTEOSCLEROSIS, sometimes with a latent period as long as 20 years (ACGIH, 1992). Osteosclerosis is an increased bone density in characteristic patterns (Hodge & Smith, 1977). Calcification of ligaments can also be involved, making movement stiff and painful. About 10% of subjects developed osteosclerosis when fluoride was present at 8 ppm in the drinking water.

Dental fluorosis (mottled teeth) occurs from exposure during development of tooth enamel (from before birth to approximately age 8 years) and is therefore not a factor in workers with occupational exposures.

Other effects noted with chronic fluoride exposure are allergic contact dermatitis and asthma (Saric, 1986), and an increase in respiratory infections (Hodge & Smith, 1977). Ingestion of sodium fluoride over a period of 3 to 12 months for treatment of otosclerosis produced gastrointestinal disturbances, petechiae, erosions, and erythema of the upper gastrointestinal tract (Das et al, 1994).

Asthma in aluminum potroom workers was associated with exposure to total airborne fluorides in excess of 0.5 mg/m(3) (Soyseth & Kongerud, 1992). These workers were also exposed to SULFUR DIOXIDE which is known to induce asthma, and a possible contribution by the latter cannot be ruled out.

One study of 41 aluminum workers exposed to an average airborne fluoride concentration of 0.91 mg/m(3) (34% gaseous at a concentration of 0.31 mg/m(3)) found that the area under the plasma concentration versus time curve and the total amount of fluoride excreted were good measures of gaseous fluoride exposure, and that wearing gas masks decreased the total exposure to 30 to 40% (Ehrnebo & Ekstrand, 1986). Another study related urinary fluoride levels with clinical effects (Memi, 1985).

Increased deaths from chronic obstructive lung disease were linked with exposure to pot emissions 20 to 39 years previously in a cohort of Norwegian aluminum smelter workers. Fluorides comprised of the most prevalent exposures in these workers (Ronneberg, 1995a; Ronneberg, 1995b). These excess deaths could not be attributed to fluorides alone because of mixed exposures to COAL TAR PITCH VOLATILES, SULFUR DIOXIDE, and CARBON MONOXIDE (Ronneberg, 1995a).

Because the daily environmental intake of fluoride can be significant, especially in vegetarians and persons living in areas where high fluoride content in the drinking water is endemic, the concentration of fluoride in the plasma increases with age (Hanhijarvi, 1975). It decreases during pregnancy, and is increased in hemodialysis patients (Hanhijarvi, 1975). In one epidemiological study, there was a correlation between fluoride content in the water and heart disease (Jansen & Thomson, 1974).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

PREHOSPITAL: Decontamination generally is not required after inadvertent ingestion of a dental product. Administer a calcium-containing antacid.

DILUTION

Administer milk (preferred) or water (1 or 2 glassfuls) to dilute the corrosive fluoride salt in the oropharynx, esophagus, and stomach.
Milk provides calcium ions which may bind to fluoride ions and decrease their penetrability and systemic absorption.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

ACUTE

GENERAL/SUMMARY

Industrial exposure to fluoride is generally due to inhalation of dust that is produced during the processing of fluoride-containing minerals in various industries. The threshold limit value for fluoride in air is 2.5 mg/m(3) (expressed as F) (Baselt, 2004).
Thirty-two to 64 mg/kg of fluoride should be considered fatal if untreated (Heifetz & Horowitz, 1986).

CASE REPORTS

PEDIATRICS

Death has been reported following ingestion of 200 mg (16 mg/kg) of fluoride in a 3-year-old boy (Eichler et al, 1982).
Lethargy and vomiting was described in a 13-month-old 30 minutes after ingesting an unknown amount of insecticide powder (65% sodium fluoride/35% talc); within 1 hour the patient was limp, comatose, and in respiratory failure. The patient went into cardiac arrest and died 5 hours after ingestion (Augenstein et al, 1991).

ADULTS

A 38-year-old man died of intractable ventricular fibrillation associated with severe hypocalcemia (serum level near 0) approximately 3 hours after inadvertently ingesting approximately 100 mL of liquid containing 70% zinc hexafluorosilicate (Lech, 2011).
A 56-year-old man died of intractable ventricular fibrillation associated with hypomagnesemia and hypocalcemia after ingesting a spoonful of etching cream containing 20% ammonium bifluoride and 13% sodium bifluoride (Swanson et al, 1993).
Fatal cardiac arrest was reported in three patients on chronic hemodialysis after exposure to fluoride used in the water purification system during dialysis (Arnow et al, 1994).

MAXIMUM TOLERATED EXPOSURE

ROUTE OF EXPOSURE

INGESTION

Mild fluorosis has been seen after 0.1 mg/kg/day, indicating a narrow therapeutic range (AAP, 1986).

Accidental ingestion of sodium fluoride by children usually does not present serious risk if the amount of fluoride ingested is less than 5 mg/kg (Spoerke et al, 1980).
Most gastrointestinal symptoms occur within the first hour following ingestion (Spoerke et al, 1980). The recommended limit of sodium fluoride stored in the home is 264 mg.

Though some radiological evidence of fluoride effects on bone can be detected at intake of 5 to 8 parts per million fluoride, these are said not to be clinically significant. Pathological skeletal fluorosis requires intake of 10 to 25 mg F-/day for 10 to 20 years (Heifetz & Horowitz, 1986).
As the fluoride supplementation is removed, the symptoms, except for mottling, will disappear (Grandjean & Thomsen, 1983).

DENTAL ENAMEL FLUOROSIS

It has been estimated, based on studies in rats, that single ingestions of 3 grams of a 0.1% fluoride-containing dentifrice may produce fluoride levels capable of causing tooth mottling. This amount is 2 to 3 times greater than that used for normal tooth brushing. Dental fluorosis is a potential concern in very small children who brush several times a day with these products, and who do not expectorate (Trautner & Einwag, 1988).
Enamel fluorosis was reported in a 12-year-old girl who received daily tooth brushing from the age of 5 months with a fluoridated product. Mottling was evident at 6 years of age (Stephen, 1984).
Teeth are only susceptible to dental fluorosis during the period of mineralization, until about 5 to 6 years of age (Heifetz & Horowitz, 1986).

ACUTE

The toxic range is approximately 5 to 10 mg/kg of fluoride (11 to 22 mg/kg of NaF) with GI symptoms usually developing at 3 to 5 mg/kg of fluoride or more (6.6 to 11 mg/kg of NaF) (Spoerke et al, 1980).
The amount of sodium fluoride ingested by children has been correlated with the risk of developing symptoms (Augenstein et al, 1991). Ingested doses of ELEMENTAL FLUORIDE were associated with clinical signs in children in this study (ingested dose of elemental fluoride was calculated using the ratio of 1 mg fluoride per 2.2 mg sodium fluoride) -
INGESTEDDOSE F ION (mg/kg) TOTAL N NUMBER WITH SYMPTOMS % WITH SYMPTOMS
Less than 1 36 3 8%
1 to less than 2 6 1 17%
2 to less than 3 15 4 27%
3 to less than 4 10 5 50%
4-8.4 3 3 100%
TOTAL 70 16
Nausea alone was associated with ingestion of 47 to 94 mg in contaminated drinking water (Vogt et al, 1982).
Vomiting was associated with ingestion of 94 to 188 mg in drinking water in individuals aged 9 to 70 years (Vogt et al, 1982).
Serious toxicity including GI hemorrhage, hypocalcemia, hypomagnesemia, ventricular tachycardia and ventricular fibrillation occurred in a 43-year-old following an ingestion of up to 25 ounces of Superdent(R) topical fluoride gel (1.23% fluoride) (Fisher et al, 1991). The patient survived with treatment consisting of cardioversion and aggressive calcium and magnesium replacement.

CHRONIC

Low level exposure to airborne fluoride initially results in mucous membrane irritation of the eyes, nose and throat. Ongoing exposure may produce symptoms of early fluoride toxicity that can include respiratory distress, neurological abnormalities, gastrointestinal pain and muscular fibrillation(Baselt, 2004) .
Daily absorption of 10 to 80 mg of fluoride over years can result in crippling skeletal fluorosis due to excessive calcification of bone resulting in stiffening of ligaments and fusion of joints (Baselt, 2004).
CASE REPORT: A 48-year old woman who chronically ingested 1 to 2 gallons of brewed black tea containing an estimated 14.6 mg of fluoride ion/gallon daily from the age of 12 years developed symptoms consistent with phase 3 (crippling) skeletal fluorosis. After 6 months of ergocalciferol therapy and cessation from drinking tea, she reported nearly complete resolution of pain. She was lost to follow up after 6 months (Izuora et al, 2011).

Carcinogenicity Ratings for CAS16984-48-8 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Fluorides, as F

A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

EPA (U.S. Environmental Protection Agency, 2011): Not Listed
IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Fluorides (inorganic, used in drinking-water)

3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.

NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
MAK (DFG, 2002): Not Listed
NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS16984-48-8 (U.S. Environmental Protection Agency, 2011):

Not Listed

TOXICITY VALUES

LD50- (INTRAVENOUS)MOUSE:
- 22, 800 mcg/kg (RTECS , 2000)

CALCULATIONS

AMBIENT CONVERSIONS

WATER

A liter of water with 1 part per million of fluoride will provide a total of 1 milligram of fluoride. Thirty-four students became ill after drinking water with concentrated sodium fluoride (375 parts per million). Symptoms were mild and two-thirds of the patients reported complete resolution within 24 hours (Hoffman et al, 1980). Drinking water with greater than 2 ppm of fluoride increases the risk of fluorosis in children less than 8 years of age(Centers for Disease Control and Prevention, 2001).

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS16984-48-8 (American Conference of Governmental Industrial Hygienists, 2010):

Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

Adopted Value

Fluorides, as F

TLV:

TLV-TWA: 2.5 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A4
Codes: BEI
Definitions:

A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.

TLV Basis - Critical Effect(s): Bone dam; fluorosis
Molecular Weight: Varies

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

AIHA WEEL Values for CAS16984-48-8 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS16984-48-8 (National Institute for Occupational Safety and Health, 2007):

Not Listed

OSHA PEL Values for CAS16984-48-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Fluorides (as F)
Table Z-1 for Fluorides (as F):

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3: 2.5

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: No
Notation(s): Not Listed

Table Z-2 for Fluoride as dust (Z37.28-1969):

8-hour TWA:25 mg/m(3)
Acceptable Ceiling Concentration:
Acceptable Maximum Peak above the Ceiling Concentration for an 8-hour Shift:

Concentration:
Maximum Duration:

Notation(s): Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS16984-48-8 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS16984-48-8 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS16984-48-8 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS16984-48-8 (U.S. Environmental Protection Agency, 2010b):

Not Listed
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS16984-48-8 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS16984-48-8 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Not Listed

DOT List of Marine Pollutants for CAS16984-48-8 (49 CFR 172.101 - App. B, 2005):

Not Listed

EPA TSCA Inventory for CAS16984-48-8 (EPA, 2005):

Not Listed

LABELS

NFPA

NFPA Hazard Ratings for CAS16984-48-8 (NFPA, 2002):

Not Listed

-PERSONAL PROTECTION

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 16984-48-8.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS16984-48-8 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

Editor's Note: An ERG guide with information appropriate to this material does not exist.

NFPA Extinguishing Methods for CAS16984-48-8 (NFPA, 2002):

Not Listed

EVACUATION PROCEDURES

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

AIHA ERPG Values for CAS16984-48-8 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS16984-48-8 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Fluorides (as F)
TEEL-0 (units = mg/m3): 2.5
TEEL-1 (units = mg/m3): 7.5
TEEL-2 (units = mg/m3): 12.5
TEEL-3 (units = mg/m3): 250
Definitions:

TEEL-0: The threshold concentration below which most people will experience no adverse health effects.
TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure.
TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape.
TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.

AEGL Values for CAS16984-48-8 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS16984-48-8 (National Institute for Occupational Safety and Health, 2007):

Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

SMALL LEAK/SPILL

Editor's Note: An ERG guide with information appropriate to this material does not exist.

LARGE LEAK/SPILL

Editor's Note: An ERG guide with information appropriate to this material does not exist.

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

18.99

-REFERENCES

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.

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National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.

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FLUORIDE

Classification | Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents