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FLUORINE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Fluorine is a diatomic halogen gas. Elemental fluorine is not found free in nature. Fluorine is the most reactive nonmetal, the most electronegative element, and has a higher oxidation potential than ozone (Budavari, 1996). It is a very corrosive and toxic gas (Stokinger, 1982).

Specific Substances

    1) Bifluoriden (Dutch)
    2) Fluor (Dutch, French, German, Polish)
    3) Fluoro (Italian)
    4) Fluorures acide (French)
    5) Fluoruri acidi (Italian)
    6) Saeure fluoride (German)
    7) CAS 7782-41-4
    1.2.1) MOLECULAR FORMULA
    1) F2

Available Forms Sources

    A) SOURCES
    1) Fluorine is available in both gas and liquid form.
    2) Important sources of fluorine are cryolite, fluorite, and florapatite.
    B) USES
    1) Conversion of uranium tetrafluoride to uranium hexafluoride; oxidizer in rocket fuel systems; manufacture of various fluorides and fluorocarbons (Proctor et al, 1988; Clayton & Clayton, 1994); insecticidal sprays for fruits and vegetables; mining of phosphate rock to superphosphate to be used as fertilizer (Finkel, 1983)
    2) Fluorine is used as one component of liquid rocket fuel and in chemical lasers. It is also used in the production of metallic and other fluorides; the production of fluorocarbons; and as an active constituent of fluoridating compounds used in drinking water, toothpastes, etc (Sax & Lewis, 1989; HSDB , 2000). It is also used as a gaseous surface treatment agent for polyethylene bottles (HSDB , 2000).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Fluorine is an extremely strong tissue irritant, causing caustic irritation of eyes, skin, and mucous membranes. Thermal burns or frostbite may occur. Chronic absorption can cause mottled tooth enamel, osteosclerosis, and ligament calcification.
    0.2.3) VITAL SIGNS
    A) Both fever and chills have been reported.
    0.2.4) HEENT
    A) Human volunteers exposed to up to 25 ppm have shown little irritation.
    B) Eyelid eczema may occur and attenuation of retinal arteries may result from prolonged exposure.
    C) Fluorine is irritating to nasal mucosa.
    0.2.6) RESPIRATORY
    A) Respiratory tract irritation may progress to pulmonary edema.
    0.2.7) NEUROLOGIC
    A) Lethargy with delayed-onset dyspnea was reported in mice.
    0.2.9) HEPATIC
    A) Focal liver necrosis was reported in exposed mice.
    0.2.14) DERMATOLOGIC
    A) Thermal burns or frostbite may occur.
    0.2.15) MUSCULOSKELETAL
    A) Osteosclerosis has been reported with prolonged exposure.
    0.2.20) REPRODUCTIVE
    A) In one animal study, no malformations were found following injection of fluorine-ion containing dust extracts.
    B) At the time of this review, no studies of the possible reproductive effects of fluorine in humans or experimental animals were found.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the potential

Laboratory Monitoring

    A) The fatal plasma level of fluorine is 3 mg/L. Urinary fluorine output of less than 5 mg/L is used as an index of safe working level for long-term exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    2) Direct contact with fluorine liquid may produce frostbite injury.

Range Of Toxicity

    A) Toxic by inhalation; strong irritant to tissue. Fatal plasma level of fluorine is 3 milligrams/liter.
    B) Irritation of the eyes and nose occurred at 100 ppm for 1 minute.
    C) No ill effects were seen from intermittent exposures of up to 20 mg/m(3) for 9 years.

Clinical Effects

Summary Of Exposure

    A) Fluorine is an extremely strong tissue irritant, causing caustic irritation of eyes, skin, and mucous membranes. Thermal burns or frostbite may occur. Chronic absorption can cause mottled tooth enamel, osteosclerosis, and ligament calcification.

Vital Signs

    3.3.1) SUMMARY
    A) Both fever and chills have been reported.
    3.3.3) TEMPERATURE
    A) CHILLS were noted 1 to 2 hours after exposure (Dreisbach, 1987).
    B) FEVER may progress for 1 to 2 days and regress over 10 to 30 days (Dreisbach, 1987).

Heent

    3.4.1) SUMMARY
    A) Human volunteers exposed to up to 25 ppm have shown little irritation.
    B) Eyelid eczema may occur and attenuation of retinal arteries may result from prolonged exposure.
    C) Fluorine is irritating to nasal mucosa.
    3.4.3) EYES
    A) Little irritation was reported in human volunteers exposed to up to 25 ppm. Moderate to severe irritation occurred with exposure to 100 ppm with no after effects reported for up to 1 minute of exposure. Contact with high concentrations is presumed to be highly destructive (Grant & Schuman, 1993).
    1) Fluorine was found to be an eye irritant in humans, and experimental animals (Hathaway et al, 1996; RTECS , 2000).
    B) Eyelid eczema may occur (Finkel, 1983).
    C) ATTENUATION OF THE RETINAL ARTERIES was demonstrated in 75 men who had fluorine exposure for 6 to 15 years (Karczewicz et al, 1989).
    3.4.5) NOSE
    A) Fluorine is very irritating to the nose at 100 ppm (Hathaway et al, 1996).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CHEST PAIN
    1) Sore throat and chest pain persisted for 6 hours after two human volunteers briefly tolerated 25 ppm of fluorine (Hathaway et al, 1996).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory tract irritation may progress to pulmonary edema.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Fluorine is toxic by inhalation and is an extremely strong irritant to tissue (HSDB , 2000). Respiratory tract injuries and irritation have occurred from fluorine; cough and hemoptysis have been reported.
    B) ACUTE LUNG INJURY
    1) INHALATION - Pulmonary edema follows laryngospasm and bronchospasm induced by exposure to high concentrations of fluorine; usually delayed in onset and progress over 1 to 2 days (Ricca, 1970; Dreisbach, 1987); may regress over 10 to 30 days (Dreisbach, 1987). Other symptoms may include choking and chills lasting 1 to 2 hours after exposure; pulmonary edema is often preceded by fever, cough, tightness in the chest, rales, and cyanosis (HSDB , 2000).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PULMONARY HEMORRHAGE
    a) MICE - Pulmonary congestion and hemorrhage were among the autopsy findings in mice with delayed onset of labored breathing following exposure to 150 ppm for 60 minutes (Keplinger & Suissa, 1968).

Neurologic

    3.7.1) SUMMARY
    A) Lethargy with delayed-onset dyspnea was reported in mice.
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SOMNOLENCE
    a) MICE - Lethargy occurred with delayed-onset dyspnea following exposure of mice to 25 ppm (Hygienic Guide Series, 1965).

Hepatic

    3.9.1) SUMMARY
    A) Focal liver necrosis was reported in exposed mice.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATIC NECROSIS
    a) MICE - Focal liver necrosis was observed to be of delayed onset in exposed mice (Keplinger & Suissa, 1968).

Dermatologic

    3.14.1) SUMMARY
    A) Thermal burns or frostbite may occur.
    3.14.2) CLINICAL EFFECTS
    A) THERMAL BURN
    1) Thermal burns are produced by fluorine gas as a result of the violent reaction between the skin and fluorine (Stokinger, 1982; Hathaway et al, 1996).
    B) FROSTBITE
    1) Direct contact with liquid fluorine may cause frostbite injury (CHRIS , 2000).

Musculoskeletal

    3.15.1) SUMMARY
    A) Osteosclerosis has been reported with prolonged exposure.
    3.15.2) CLINICAL EFFECTS
    A) OSTEOSCLEROSIS
    1) CHRONIC TOXICITY
    a) Osteosclerosis, especially of the spine and pelvic bones, has been reported after 20 to 30 years occupational and/or environmental exposure to fluorine (Nemeth & Zsogon, 1989).
    b) Calcification of the spinal ligaments was reported after prolonged exposure to fluorine (Nemeth & Zsogon, 1989). Cervical compression has also been reported due to fluorosis and is considered a common site of compressive myelopathy, which can present as weakness of all limbs (Raman et al, 1980).
    c) Fractures and periarticular pain were reported in women under treatment with fluorine for 12 months (Marcelli et al, 1989).
    d) CASE REPORT - A 35-year-old with leg pain had severe osteomalacia, with a serum fluorine concentration of 1040 ppm (normal = 440 ppm) after 5 years of ingesting 4 liters of mineral water daily which contained 9 mg of fluorine/liter (Thivolle et al, 1986). Repeat bone imaging one year later after the cessation of mineral water revealed no abnormalities.
    e) CASE REPORT (NIFLUMIC ACID) - Several cases of skeletal-induced fluorosis have been reported following the long-term use of niflumic acid (a nonsteroidal antiinflammatory agent that contains fluorine) (Meunier et al, 1980).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) DISORDER OF ENDOCRINE SYSTEM
    1) Calcitonin elevation and moderate functional changes of the hypophysis-thyroid gland system, not accompanied by clinical manifestations, were observed among workers in fluorine production (Tokar et al, 1989).

Reproductive

    3.20.1) SUMMARY
    A) In one animal study, no malformations were found following injection of fluorine-ion containing dust extracts.
    B) At the time of this review, no studies of the possible reproductive effects of fluorine in humans or experimental animals were found.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) LACK OF EFFECT
    a) No malformations or chromosomal aberrations were observed when pregnant mice and rats were given subcutaneous injections of fluorine-ion-containing dust extracts from aluminum factory stacks (Cavagna et al, 1969; HSDB , 2000).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7782-41-4 (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):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the potential

Genotoxicity

    A) At the time of this review, no data were available to assess the mutagenic or genotoxic potential of fluorine.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) The fatal plasma level of fluorine is 3 mg/L. Urinary fluorine output of less than 5 mg/L is used as an index of safe working level for long-term exposure.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) The fatal plasma level of fluorine is 3 milligrams/liter (Dreisbach, 1987).
    4.1.3) URINE
    A) URINARY LEVELS
    1) Urinary fluorine excretion of less than 5 milligrams/liter is used as an index of safe working level for long-term exposure (Finkel, 1983).

Methods

    A) OTHER
    1) The fluorine content of human hair was measured using x-ray fluorescence analysis. Fluorine was significantly higher in male subjects, and the fluorine content of female hair increased with age (Watanabe et al, 1992).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Monitor symptomatic patients until symptom-free.

Monitoring

    A) The fatal plasma level of fluorine is 3 mg/L. Urinary fluorine output of less than 5 mg/L is used as an index of safe working level for long-term exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    6.5.2) PREVENTION OF ABSORPTION
    A) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Fluorine is normally a gas, but may cause irritation on ingestion.
    2) Fluorine liquid will cause frostbite.
    3) Monitor patients for burn development and treat appropriately.
    4) Monitor for electrolyte abnormalities.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN
    1) Treat burn as any thermal burn (Finkel, 1983).
    B) FROSTBITE
    1) PREHOSPITAL
    a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
    2) REWARMING
    a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
    b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
    c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
    d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
    3) WOUND CARE
    a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
    b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
    c) The injured extremities should be elevated and should not be allowed to bear weight.
    d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
    e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
    f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
    g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
    h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
    i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
    j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
    k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
    l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
    m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
    n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) Toxic by inhalation; strong irritant to tissue. Fatal plasma level of fluorine is 3 milligrams/liter.
    B) Irritation of the eyes and nose occurred at 100 ppm for 1 minute.
    C) No ill effects were seen from intermittent exposures of up to 20 mg/m(3) for 9 years.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) INHALATION -
    a) The lowest published toxic concentration in man for fluorine inhalation was 25 ppm/5 minutes (HSDB , 2000).
    b) Toxic by inhalation; strong irritant to tissue (HSDB , 2000). Fatal plasma level of fluorine is 3 milligrams/liter.
    2) ANIMAL DATA
    a) Uniform fatality occurred in guinea pigs, mice, rabbits, and rats in exposures ranging from 10,000 parts per million for 5 minutes to 200 parts per million for 3 hours. Cause of death was respiratory damage with pulmonary edema (Stokinger, 1982).
    b) Seizures occurred at exposures of lesser concentrations for up to 35 days in dogs, many of which were fatal (Stokinger, 1982).

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) INHALATION, OCULAR, AND DERMAL -
    a) Repeated short-term exposures of 15 mg/m(3) were well-tolerated (Belles, 1965).
    b) Human volunteers tolerated concentrations of 10 ppm fluorine for 15 minutes with a minimum of irritation. However, a few intermittent exposures at this same concentration were repeated at 3 to 5 minute intervals every 15 minutes for two to three hours with some slight irritation to the eyes and skin reported (ACGIH, 1986).
    c) Intermittent exposures up to 20 mg/m(3) (approximately 10 ppm) for periods of 5 to 30 minutes in fluorine workers during a 9 year time period showed no ill effects (Lyon, 1962).
    d) Slight eye irritation occurred at 23 ppm but could be inhaled without respiratory irritation. At 50 ppm for 5 minutes, eye and nasal irritation occurred (Clayton & Clayton, 1994).
    e) 25 to 40 mg/m(m) - nasal and eye irritation (Belles, 1965).
    f) Severe dyspnea was reported at 75 mg/m(3) (Rickey RP, 1959).
    g) Marked irritation of eyes and nose occurred at levels between 67 to 100 ppm and became very uncomfortable after only a few seconds (Clayton & Clayton, 1994).
    h) Dermal irritation occurred from skin exposure between 150 and 300 mg/m(3) (Belles, 1965).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) ACUTE
    a) The fatal plasma level of elemental fluorine is 3 milligrams per liter (Dreisbach, 1987; HSDB , 2000).

Workplace Standards

    A) ACGIH TLV Values for CAS7782-41-4 (American Conference of Governmental Industrial Hygienists, 2010):
    1) 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.
    a) Adopted Value
    1) Fluorine
    a) TLV:
    1) TLV-TWA: 1 ppm
    2) TLV-STEL: 2 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): URT, eye, and skin irr
    d) Molecular Weight: 38.0
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS7782-41-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Fluorine
    2) REL:
    a) TWA: 0.1 ppm (0.2 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 25 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7782-41-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Fluorine
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Fluorine (soluble fluoride)
    3) 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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Fluorine
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7782-41-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Fluorine
    2) Table Z-1 for Fluorine:
    a) 8-hour TWA:
    1) ppm: 0.1
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.2
    a) 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.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) RTECS, 2000 Budavari, 1996 Sax & Lewis, 1989:)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Free fluorine (F1) is a highly reactive element, and rarely found in nature; elemental fluorine is produced by the electrolysis of anhydrous hydrogen fluoride in a molten solution of potassium fluoride. It is formed at the anode and hydrogen at the cathode with the major impurity being hydrogen fluoride (Clayton & Clayton, 1994).

Toxicologic Mechanism

    A) Fluorine and fluorides act as direct cellular poisons by interfering with calcium metabolism and enzyme mechanisms (Dreisbach, 1987).
    B) Fluorine is an irritant. Dermal cutaneous burns are caused by the violent reaction between the skin and fluorine producing a thermal burn (Hathaway et al, 1996).

Physicochemical

Physical Characteristics

    A) This compound exists as a pale yellow to light green, strong, pungent, irritating smelling gas (ITI, 1988) Fire Protection Guide, 1978; (HSDB , 2000).
    B) It is a reactive diatomic gas (Budavari, 1996).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) F1 = 18.998; atomic weight for elemental state is F2 = 37.99 (CHRIS , 2000; HSDB , 2000)

Other

    A) ODOR THRESHOLD
    1) 0.035 ppm (CHRIS , 2002)

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