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TEFLON DECOMPOSITION

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Teflon is a highly stable thermoplastic homopolymer of tetrafluoroethylene composed of at least 20,000 C2F4 monomer units linked into quite long, unbranched chains, with a molecular weight that may be in the millions (Budavari, 1996; ILO, 1983).

Specific Substances

    1) Teflon
    2) Aflon
    3) Algoflon
    4) Fluon
    5) Polyflon
    6) Tetrafluoroethene polymer
    7) Tetrafluoroethylene polymer
    8) CAS 9002-84-0
    9) DECOMPOSITION PRODUCTS, POLYTETRAFLUOROETHYLENE
    10) DECOMPOSITION PRODUCTS, TEFLON
    11) POLYTETRAFLUOROETHYLENE DECOMPOSITION PRODUCTS
    12) POLYTETRAFLUOROETHYLENE PYROLYSIS PRODUCTS
    13) PYROLYSIS PRODUCTS, POLYTETRAFLUOROETHYLENE
    14) PYROLYSIS PRODUCTS, TEFLON
    15) TEFLON PYROLYSIS PRODUCTS
    1.2.1) MOLECULAR FORMULA
    1) (C2-F4)n

Available Forms Sources

    A) FORMS
    1) Teflon (polytetrafluoroethylene) is available in three types and several resin grades for the production of various products by different processing methods (Grayson, 1985).
    a) The GRANULAR type is available in resin grades of agglomerates, coarse, finely divided, and presintered.
    b) GRANULAR types may be processed by molding, preforming, sintering, and ram extrusion, and are used for the production of gaskets, packing, seals, wrappings, electronic components, bearings, molded sheets, rods, heavy-walled and other tubing, tapes, and molded shapes for a variety of applications including chemical, electrical, mechanical, and nonadhesive (adherent) products.
    c) FINE POWDER types are used for the production of wire coating, thin-walled and other tubing, pipe, overbraided hose, spaghetti tubing, thread-sealant tape, pipeliners, and porous structures.
    d) DISPERSION types are used in the production of impregnation materials, coatings, packing, film, and bearings.
    B) SOURCES
    1) Teflon is prepared by controlled polymerization of tetrafluoroethylene in emulsion under pressure. Peroxides or persulfates are used as free radical catalysts (Budavari, 1996; ILO, 1983).
    a) Teflon is inert under ordinary conditions (Budavari, 1996).
    2) DECOMPOSITION PRODUCTS
    a) Depending on the temperature of thermal decomposition, a variety of oxidized products containing fluorine, carbon, and oxygen -- including carbonyl fluoride and hydrogen fluoride -- may be released from Teflon (Sittig, 1985; Proctor et al, 1988). There is no evidence that Teflon produces decomposition products at temperatures below 200 degrees C (ILO, 1983).
    b) At temperatures of 315 to 375 degrees C and up to 500 degrees C, Teflon decomposition products are primarily the monomer tetrafluoroethylene, perfluoroisopropylene, other C4-C5 perfluoro-compounds, and an unidentified waxy particulate fume (which may be the etiologic agent for polymer fume fever) (Proctor et al, 1988).
    c) At temperatures above 400 degrees C, the principle toxic decomposition products of Teflon are PERFLUOROISOBUTYLENE and CARBONYL FLUORIDE (Okawa & Polakoff, 1974).
    d) At decomposition temperatures of 500 to 800 degrees C, the principal decomposition product is CARBONYL FLUORIDE, which is hydrolyzable to CARBON DIOXIDE and HYDROGEN FLUORIDE (Proctor et al, 1988).
    e) Particulates, possibly with adsorbed toxic substances, were produced when Teflon was heated to less than 500 degrees C (Clayton & Clayton, 1982). Carbonyl fluoride was the principle decomposition product at temperatures of between 500 and 650 degrees C (Clayton & Clayton, 1982). At temperatures greater than 650 degrees C, carbon tetrafluoride and carbon dioxide were the principal decomposition products (Clayton & Clayton, 1982).
    3) COOKING
    a) Normal cooking use of Teflon-coated pans does not present a danger to either pet birds or humans, but gross overheating can poison birds, which are more susceptible to the toxicity of the decomposition products (Griffith et al, 1973; Wells et al, 1982). Self-cleaning oven operation has also been fatal to pet birds caged near the oven (Stoltz et al, 1992).
    b) Accidental overheating has resulted in polymer fume fever which cleared in 24 hours in one human case (Blandford et al, 1975).
    C) USES
    1) Teflon (polytetrafluoroethylene) is used as a non-stick coating for cooking utensils, as a film or fiber, in surgical prostheses, in packings, in coaxial spacers and insulators, in bearings and gaskets, in liners and seals, ablative coatings for space vehicles, in piston rings, and as a coating material or tape for chemical vessels, wiring, etc. (ILO, 1983; Sax & Lewis, 1987; HSDB , 2002).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Although polytetrafluoroethylene (Teflon) is inert under ordinary circumstances, when the polymer is heated under conditions of inadequate ventilation, polymer fume fever may result.
    1) Polymer fume fever is an influenza-like syndrome. When Teflon is heated to between 315 and 375 degrees C, inhalation exposure to the fumes can cause chills, fever, profuse sweating, cough, dyspnea, flu-like symptoms, and chest tightness, which are generally self-limited and last for 24 to 48 hours. Respiratory discomfort and pulmonary function abnormalities may persist for several weeks after an acute attack.
    B) Pulmonary edema has been reported in some cases, with symptoms of chest discomfort and shortness of breath. Pulmonary edema is more likely to be noted with exposure to fumes evolved from Teflon at temperatures up to 500 degrees C or greater.
    C) Polymer fume fever is similar to metal fume fever, and occurs after inhalation exposure to the pyrolysis products of fluorocarbon polymers, especially polytetrafluoroethylene (Teflon). Pulmonary infiltrates often occur in patients with polymer fume fever.
    0.2.3) VITAL SIGNS
    A) Hyperpyrexia, mild sinus tachycardia, and reversible mild hypertension have been reported in patients with polymer fume fever.
    0.2.4) HEENT
    A) Some Teflon decomposition products are irritants of the eyes and mucous membranes. A pungent or metallic smell and a metallic taste may occur in patients with polymer fume fever.
    0.2.5) CARDIOVASCULAR
    A) Mild sinus tachycardia and reversible mild hypertension may occur in patients with polymer fume fever.
    0.2.6) RESPIRATORY
    A) Respiratory tract irritation, pneumonitis, and noncardiogenic pulmonary edema may occur. Mild hypoxia has been reported in patients with polymer fume fever. Sequelae have included prolonged decreases in diffusing capacity, reversible obstructive changes, and possibly pulmonary fibrosis following multiple episodes of polymer fume fever.
    0.2.7) NEUROLOGIC
    A) Headache, weakness, malaise, and paresthesias have been reported in patients with polymer fume fever.
    0.2.8) GASTROINTESTINAL
    A) Nausea and vomiting may occur with polymer fume fever.
    0.2.10) GENITOURINARY
    A) Workers exposed to Teflon decomposition products may have increased levels of urinary fluoride.
    0.2.13) HEMATOLOGIC
    A) Leukocytosis with a left shift in the differential count has been reported in patients with polymer fume fever.
    B) Disseminated intravascular coagulopathy was noted in one animal experiment. This effect has not been reported in exposed humans.
    0.2.14) DERMATOLOGIC
    A) Some Teflon decomposition products are skin irritants.
    0.2.15) MUSCULOSKELETAL
    A) Myalgias may occur in patients with polymer fume fever.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) Experimental animals implanted subcutaneously with Teflon have developed local sarcomas, and one human with a Teflon surgical implant has been reported who developed a local sarcoma.

Laboratory Monitoring

    A) Monitor CBC with differential count, arterial blood gases, and chest x-ray in patients with polymer fume fever, significant respiratory tract irritation, or pulmonary edema.
    B) Monitoring pulmonary function tests may be useful to detect the development of sequelae in patients with one or more episodes of polymer fume fever.
    C) Measuring urinary fluoride levels may give an indication of exposure, but are not well correlated with the degree of exposure or severity of clinical effects in polymer fume fever.

Treatment Overview

    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) Respiratory tract irritation, if severe, can progress to pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    C) Administer 100 percent humidified supplemental oxygen with assisted ventilation, if required, to patients with chest discomfort, cough, or dyspnea. Rescuers should wear Self-Contained Breathing Apparatus (SCBA) to avoid self-contamination in areas with high concentrations of fumes.
    D) Administration of antipyretic medications (aspirin, acetaminophen, etc.) may be useful for symptomatic relief of fever and flu-like symptoms. A history of possible allergy or intolerance should be obtained before these medications are prescribed.
    E) 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.
    F) Short-term administration of corticosteroids has been suggested for use in the treatment of polymer fume fever, but their actual utility in this setting is unknown.
    G) Patients with multiple episodes of polymer fume fever might be at risk for the development of chronic pulmonary complications and should have periodic surveillance with chest x-rays and pulmonary function tests.
    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).

Range Of Toxicity

    A) Specific dose-response relationships for human exposures are difficult to determine due to the differences in Teflon decomposition products generated under various workplace conditions. Range of toxicity and causative agents are principally determined through animal studies.
    1) Different Teflon decomposition products vary widely in toxicity in experimental animals.

Clinical Effects

Summary Of Exposure

    A) Although polytetrafluoroethylene (Teflon) is inert under ordinary circumstances, when the polymer is heated under conditions of inadequate ventilation, polymer fume fever may result.
    1) Polymer fume fever is an influenza-like syndrome. When Teflon is heated to between 315 and 375 degrees C, inhalation exposure to the fumes can cause chills, fever, profuse sweating, cough, dyspnea, flu-like symptoms, and chest tightness, which are generally self-limited and last for 24 to 48 hours. Respiratory discomfort and pulmonary function abnormalities may persist for several weeks after an acute attack.
    B) Pulmonary edema has been reported in some cases, with symptoms of chest discomfort and shortness of breath. Pulmonary edema is more likely to be noted with exposure to fumes evolved from Teflon at temperatures up to 500 degrees C or greater.
    C) Polymer fume fever is similar to metal fume fever, and occurs after inhalation exposure to the pyrolysis products of fluorocarbon polymers, especially polytetrafluoroethylene (Teflon). Pulmonary infiltrates often occur in patients with polymer fume fever.

Vital Signs

    3.3.1) SUMMARY
    A) Hyperpyrexia, mild sinus tachycardia, and reversible mild hypertension have been reported in patients with polymer fume fever.
    3.3.2) RESPIRATIONS
    A) Tachypnea has been reported in workers with polymer fume fever (Goldstein et al, 1987) and following acute exposure to fumes of Teflon decomposition (Zanen & Rietveld, 1993).
    3.3.3) TEMPERATURE
    A) An elevated temperature commonly occurs in patients with polymer fume fever from exposure to Teflon decomposition products (ILO, 1983; Proctor et al, 1988; Rosenstock & Cullen, 1986).
    1) The fever usually clears within 24 hours (ILO, 1983; Proctor et al, 1988; Reinl, 1964), but has lasted as long as 50 hours in some cases (Shusterman & Neal, 1986).
    3.3.4) BLOOD PRESSURE
    A) Mild reversible hypertension was reported in workers with polymer fume fever (Shusterman & Neal, 1986; Reinl, 1964).
    3.3.5) PULSE
    A) Mild sinus tachycardia has been reported in workers with polymer fume fever (Goldstein et al, 1987; Shusterman & Neal, 1986; Reinl, 1964) and following acute exposure to fumes of Teflon decomposition (Zanen & Rietveld, 1993).

Heent

    3.4.1) SUMMARY
    A) Some Teflon decomposition products are irritants of the eyes and mucous membranes. A pungent or metallic smell and a metallic taste may occur in patients with polymer fume fever.
    3.4.3) EYES
    A) Eye irritation may be noted (Sax & Lewis, 1989; Reinl, 1964).
    B) RATS exposed to Teflon decomposition products from Teflon heated at 595 degrees C developed conjunctival irritation and serous discharges from the eyes (Proctor et al, 1988) Zook et al, 1983).
    3.4.5) NOSE
    A) Inhalation of fumes can cause irritation of the mucosa of the nose and throat (Sax & Lewis, 1989; HSDB , 2002).
    B) A pungent or metallic smell may occur in polymer fume fever (Goldstein et al, 1987).
    3.4.6) THROAT
    A) Inhalation of fumes can cause irritation of the mucosa of the nose and throat (Sax & Lewis, 1989; HSDB , 2002).
    B) Workers with polymer fume fever may experience a metallic taste (Goldstein et al, 1987).

Cardiovascular

    3.5.1) SUMMARY
    A) Mild sinus tachycardia and reversible mild hypertension may occur in patients with polymer fume fever.
    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) Mild sinus tachycardia has been reported in workers with polymer fume fever (Goldstein et al, 1987; Shusterman & Neal, 1986; Reinl, 1964).
    2) CASE REPORT - Tachycardia, with a pulse rate of 124 beats/minute, was reported in a 26-year-old female following exposure to fumes from Teflon decomposition from a faulty microwave oven (Zanen & Rietveld, 1993).
    B) HYPERTENSIVE EPISODE
    1) Mild reversible hypertension has been reported in workers with polymer fume fever (Shusterman & Neal, 1986; Reinl, 1964).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory tract irritation, pneumonitis, and noncardiogenic pulmonary edema may occur. Mild hypoxia has been reported in patients with polymer fume fever. Sequelae have included prolonged decreases in diffusing capacity, reversible obstructive changes, and possibly pulmonary fibrosis following multiple episodes of polymer fume fever.
    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) Dyspnea, hyperventilation, cough, and shortness of breath usually occur in patients with polymer fume fever (Rosenstock & Cullen, 1986; Proctor et al, 1988; Makulova, 1965; Reinl, 1964; Zanen & Rietveld, 1993). Tracheitis and bronchitis may occur (Reinl, 1964).
    2) Polymer fume fever is quite similar to metal fume fever, and occurs after inhalation exposure to the pyrolysis products of fluorocarbon polymers, especially polytetrafluoroethylene (Teflon) (Finkel, 1983). Pulmonary infiltrates are often seen in patients with polymer fume fever, and the acute illness is somewhat similar to hypersensitivity pneumonitis (Rosenstock & Cullen, 1986).
    3) CASE REPORT - A 26-year-old female was reported to experience dyspnea with hypoxia (O2 saturation of 89% and O2 tension (P02) of 54.2 mmHg) following exposure to Teflon decomposition from a faulty microwave oven. Restrictive ventilatory capacity with decreased diffusion capacity was demonstrated from pulmonary function tests. Exertional dyspnea and abnormal pulmonary function tests were still present one month following exposure (Zanen & Rietveld, 1993).
    B) CHEST PAIN
    1) Chest discomfort or tightness is commonly described in patients with polymer fume fever (Proctor et al, 1988; Goldstein et al, 1987; Reinl, 1964; Zanen & Rietveld, 1993).
    C) ACUTE LUNG INJURY
    1) Acute lung injury (noncardiogenic pulmonary edema) and rales may occur in patients inhaling Teflon decomposition products (Ellenhorn & Barceloux, 1988; Proctor et al, 1988; Brubaker, 1977; HSDB , 2002).
    a) At least two deaths have been reported in workers who developed pulmonary edema from exposure to Teflon decomposition products (Auclair et al, 1983; Makulova, 1965).
    D) HYPOXEMIA
    1) Mild hypoxia with pO2's of 64 to 77 mmHg (room air) was noted in a group of workers with polymer fume fever (Goldstein et al, 1987).
    E) IRRITATION SYMPTOM
    1) Inhalation of Teflon pyrolysis products causes irritation of the mucous membranes (HSDB , 2002).
    F) SEQUELA
    1) Reversible airways obstruction and reduced diffusing capacity lasted for weeks to months in one individual who developed pulmonary edema following inhalation of Teflon decomposition products (Brubaker, 1977).
    a) CASE REPORT - Another worker had more than 40 episodes of polymer fume fever over a 9 month period, but never developed pulmonary edema (HSDB , 2002; Goldstein et al, 1987). Eighteen months later, this worker developed shortness of breath on exertion and had an alveolar-capillary block on pulmonary function testing (HSDB , 2002). At autopsy, interstitial pulmonary fibrosis was noted (Goldstein et al, 1987).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ACUTE LUNG INJURY
    a) RATS - At necropsy, rats exposed to Teflon decomposition products from Teflon heated at 595 degrees C had fibrin deposits, focal hemorrhages, and edema in the lungs (Proctor et al, 1988).
    2) ATELECTASIS
    a) PARAKEETS - Almost total atelectasis was reported following microscopic examination of the lung parenchyma during necropsy of 2 parakeets exposed to fumes from Teflon decomposition. There was also evidence of multiple bronchial hemorrhages (Zanen & Rietveld, 1993).

Neurologic

    3.7.1) SUMMARY
    A) Headache, weakness, malaise, and paresthesias have been reported in patients with polymer fume fever.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) Headache and dizziness may occur with polymer fume fever. The headache has lasted up to 4 days in some cases (Shusterman & Neal, 1986).
    B) PARESTHESIA
    1) Numbness and tingling in the fingertips have been described in patients with polymer fume fever (Albrecht & Bryant, 1987).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SOMNOLENCE
    a) RATS exposed to Teflon decomposition products from Teflon heated at 595 degrees C developed lethargy (Proctor et al, 1988) Zook et al, 1983).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and vomiting may occur with polymer fume fever.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea and vomiting have been described in workers with polymer fume fever (Albrecht & Bryant, 1987; Goldstein et al, 1987; Reinl, 1964).

Genitourinary

    3.10.1) SUMMARY
    A) Workers exposed to Teflon decomposition products may have increased levels of urinary fluoride.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL URINE
    1) Elevated levels of urinary fluoride have been seen in experimental animals and humans exposed to Teflon decomposition products (Clayton & Clayton, 1982; HSDB , 2002).
    a) One worker who was sintering granular Teflon had urinary fluoride levels of 5 milligrams per liter (Clayton & Clayton, 1982).
    b) A group of workers with a high incidence of prior episodes of polymer fume fever from inhalation of Teflon decomposition products did not have elevated urinary fluoride levels (Okawa & Polakoff, 1974).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) URINE ABNORMAL
    a) RATS developed a urinary fluoride excretion of 4 times normal when exposed to Teflon decomposition products for 1 hour (Clayton & Clayton, 1982; Scheel et al, 1968a).

Hematologic

    3.13.1) SUMMARY
    A) Leukocytosis with a left shift in the differential count has been reported in patients with polymer fume fever.
    B) Disseminated intravascular coagulopathy was noted in one animal experiment. This effect has not been reported in exposed humans.
    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) White blood cell counts of 12,700 to 20,000 per cubic millimeter with left-shifted differential counts have been observed in workers with polymer fume fever (Goldstein et al, 1987; Shusterman & Neal, 1986; Reinl, 1964).
    2) CASE REPORT - Leukocytosis, with white blood cell count of 41,700 per cubic millimeter, was reported in a 26-year-old female after exposure to Teflon decomposition from a faulty microwave oven. Differential blood count consisted of 1% metamyelocytes, 7% rod shaped white cells, 88% neutrophils, 3% lymphocytes, and 1% monocytes (Zanen & Rietveld, 1993).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DISSEMINATED INTRAVASCULAR COAGULATION
    a) RATS - Disseminated intravascular coagulopathy (DIC) has been reported in rats fatally poisoned with pyrolysis products of Teflon evolved during a 30-minute exposure at 595 degrees C (Zook et al, 1983). This effect has not been reported in exposed humans.

Dermatologic

    3.14.1) SUMMARY
    A) Some Teflon decomposition products are skin irritants.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Some Teflon decomposition products are skin irritants (Sax & Lewis, 1989).

Musculoskeletal

    3.15.1) SUMMARY
    A) Myalgias may occur in patients with polymer fume fever.
    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) Myalgias may be part of the flu-like symptoms of polymer fume fever (Albrecht & Bryant, 1987).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS9002-84-0 (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) IARC Classification
    a) Listed as: Polytetrafluoroethylene
    b) Carcinogen Rating: 3
    1) 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.
    3.21.2) SUMMARY/HUMAN
    A) Experimental animals implanted subcutaneously with Teflon have developed local sarcomas, and one human with a Teflon surgical implant has been reported who developed a local sarcoma.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) TEFLON DECOMPOSITION PRODUCTS - No data were available on the possible carcinogenicity of Teflon decomposition products at the time of this review.
    B) SARCOMA
    1) TEFLON - Experimental animals implanted subcutaneously with Teflon have developed local sarcomas (Proctor et al, 1988), and one human with a Teflon surgical implant has been reported who developed a local sarcoma (HSDB , 2002).

Genotoxicity

    A) At the time of this review, no data were available on the potential genotoxicity of Teflon decomposition products.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor CBC with differential count, arterial blood gases, and chest x-ray in patients with polymer fume fever, significant respiratory tract irritation, or pulmonary edema.
    B) Monitoring pulmonary function tests may be useful to detect the development of sequelae in patients with one or more episodes of polymer fume fever.
    C) Measuring urinary fluoride levels may give an indication of exposure, but are not well correlated with the degree of exposure or severity of clinical effects in polymer fume fever.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) Monitor the white blood cell count in patients with polymer fume fever, as leukocytosis with a left shift may occur (Goldstein et al, 1987; Shusterman & Neal, 1986; Reinl, 1964).
    B) ACID/BASE
    1) Monitor arterial blood gases in patients with more severe polymer fume fever, pulmonary edema, or respiratory tract irritation.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Monitoring urinary fluoride levels might be useful as an indication of exposure, but have not been well correlated with the extent of exposure or severity of clinical effects in polymer fume fever (Clayton & Clayton, 1982; Okawa & Polakoff, 1974).
    a) Elevated levels of fluoride have been found in the urine of experimental animals and humans exposed to fluoride-containing thermal decomposition products of Teflon (Clayton & Clayton, 1982; Scheel et al, 1968a; HSDB , 1989).
    2) One worker who was sintering granular Teflon had urinary fluoride levels of 5 milligrams per liter (Clayton & Clayton, 1982).
    3) A good indication of exposure to toxic amounts of fluoride compounds is a urinary fluoride level of 3.0 milligrams per liter or greater (Okawa & Polakoff, 1974).
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) Monitor pulmonary function tests in patients with more severe polymer fume fever or pulmonary edema. Diffusing capacity abnormalities and reversible obstructive changes may occur (Brubaker, 1977; HSDB , 1989; Goldstein et al, 1987).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If respiratory tract irritation is present, monitor chest x-ray.

Methods

    A) OTHER
    1) Teflon decomposition products are decomposed in part by hydrolysis in alkaline solutions, and can thus be determined in the air as fluoride to provide some index of exposure (Sittig, 1985) ACGIH, 1989).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Monitoring

    A) Monitor CBC with differential count, arterial blood gases, and chest x-ray in patients with polymer fume fever, significant respiratory tract irritation, or pulmonary edema.
    B) Monitoring pulmonary function tests may be useful to detect the development of sequelae in patients with one or more episodes of polymer fume fever.
    C) Measuring urinary fluoride levels may give an indication of exposure, but are not well correlated with the degree of exposure or severity of clinical effects in polymer fume fever.

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) IRRITATION SYMPTOM
    1) Respiratory tract irritation, if severe, can progress to noncardiogenic pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) There are no controlled studies indicating that early administration of corticosteroids can prevent the development of noncardiogenic pulmonary edema in patients with inhalation exposure to respiratory irritant substances, and long-term use may cause adverse effects (Boysen & Modell, 1989).
    a) However, based on anecdotal experience, some clinicians do recommend early administration of corticosteroids (such as methylprednisolone 1 gram intravenously as a single dose) in an attempt to prevent the later development of pulmonary edema.
    1) Anecdotal experience with dimethyl sulfate inhalation showed possible benefit of methylprednisolone in the TREATMENT of noncardiogenic pulmonary edema (Ip et al, 1989).
    3) Anecdotal experience also indicated that systemic corticosteroids may have possible efficacy in the TREATMENT of drug-induced noncardiogenic pulmonary edema (Zitnik & Cooper, 1990; Stentoft, 1990; Chudnofsky & Otten, 1989) or noncardiogenic pulmonary edema developing after cardiopulmonary bypass (Maggart & Stewart, 1987).
    4) It is not clear from the published literature that administration of systemic corticosteroids early following inhalation exposure to respiratory irritant substances can PREVENT the development of noncardiogenic pulmonary edema. The decision to administer or withhold corticosteroids in this setting must currently be made on clinical grounds.
    B) OXYGEN
    1) Administer 100 percent humidified supplemental oxygen with assisted ventilation, if required, to patients with chest discomfort, cough, or dyspnea. Rescuers should wear Self-Contained Breathing Apparatus (SCBA) to avoid self-contamination in areas with high concentrations of fumes.
    C) SUPPORT
    1) Administration of antipyretic medications (aspirin, acetaminophen, etc.) may be useful for symptomatic relief of fever and flu-like symptoms. The history of possible allergy or intolerance should be obtained before these medications are prescribed.
    D) MONITORING OF PATIENT
    1) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    2) Measuring urinary fluoride levels may provide an indication of exposure, but have not been well correlated with the extent of exposure or severity of clinical effects in polymer fume fever (Clayton & Clayton, 1982; Okawa & Polakoff, 1974).
    3) Elevated white blood cell counts may occur. Monitor CBC in patients with significant exposure.
    E) 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).
    F) CORTICOSTEROID
    1) Short-term administration of corticosteroids has been suggested for use in the treatment of polymer fume fever (Brubaker, 1977), but their actual utility in this setting is unknown.
    G) CHRONIC DISEASE OF RESPIRATORY SYSTEM
    1) Patients with multiple episodes of polymer fume fever might be at risk for the development of chronic pulmonary complications and should have periodic surveillance with chest x-rays and pulmonary function tests.

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).

Abstracts

Case Reports

    A) ADVERSE EFFECTS
    1) Albrecht & Bryant (1987) reported the cases of 3 workers in a rubber and metal stamp company who each developed multiple episodes of polymer fume fever over a 9-month period following the introduction of a polytetrafluoroethylene-based mold release compound into the process. This mold compound contained less than 1 percent Teflon. All symptoms disappeared when use of the mold release compound was discontinued.
    a) All 3 workers were smokers and all 3 developed multiple episodes of malaise, myalgias, fever, shaking chills, weakness, nausea, numbness and tingling of the fingertips, and dry cough. Temperatures were as high as 103 degrees F in some cases.
    b) Poor industrial hygiene practices contributed to the development of these episodes of polymer fume fever: smoking was allowed in the workplace, hand washing was not routinely done before smoking or eating, and local exhaust ventilation was inadequate. When these deficiencies were corrected, no further symptoms occurred.
    2) Brubaker (1977) reported a series of 9 workers exposed to polytetrafluoroethylene (Teflon) heated to no more than 250 degrees F in a mold spraying and cleaning operation. All 9 workers were smokers, and had one or more episodes of polymer fume fever with symptoms of chills, fever, chest pain, shortness of breath, and cough.
    a) One individual had a documented episode of pulmonary edema. Recurrent chest pain and cough sufficient to prevent a return to work were still present at 3 weeks after the acute episode. A moderately severe reversible airway obstructive pattern was seen on pulmonary function testing at 3 weeks, although the chest x-ray had returned to normal. At 2 months, the patient was asymptomatic and the reversible airway obstruction had cleared, although pulmonary function testing showed a reduced diffusing capacity.
    b) The mother of one employee developed an illness similar to polymer fume fever after handling possibly contaminated work clothing and then smoking a cigarette.
    B) CHRONIC EFFECTS
    1) One worker had more than 40 episodes of polymer fume fever over a 9 month period, but never developed pulmonary edema (HSDB , 1989; Goldstein et al, 1987). Eighteen months later, this worker developed shortness of breath on exertion and had an alveolar-capillary block on pulmonary function testing (HSDB , 1989). At autopsy, interstitial pulmonary fibrosis was noted (Goldstein et al, 1987).
    2) In a NIOSH Health Hazard Evaluation of a Teflon product manufacturing facility, 80 percent of workers (60/70) stated on a questionnaire that they had experienced polymer fume fever sometime in the past, and 50 percent had at least one episode in the preceding year (Okawa & Polakoff, 1974).
    a) Fourteen percent of these workers had experienced more than 3 episodes of polymer fume fever in the preceding year, and one-third of the workers had stayed home from work at some time because of polymer fume fever symptoms. Only 10 percent of individuals experiencing symptoms of polymer fume fever had ever consulted a physician for the condition (Okawa & Polakoff, 1974).
    b) At the time of the Health Hazard Evaluation, no workers were complaining of symptomatic polymer fume fever. Urinary fluoride levels collected from 77 employees ranged from 0.098 to 2.19 mg/L (less than levels of 3.0 mg/L or greater indicating potential exposure to toxic levels of fluoride compounds) (Okawa & Polakoff, 1974).
    C) ACUTE EFFECTS
    1) Goldstein et al (1987) reported a series of 6 workers in an electronics laboratory where Teflon contamination occurred during a cable heating test for electrical conductivity. The onset of symptoms began about 15 minutes after initial exposure, and progressed over the following hour.
    a) Initial complaints were a dry throat, cough, and a metallic smell and taste. Dramatic improvement followed symptomatic treatment in an emergency department, but three of these individuals had subsequent worsening of symptoms over the following 4 hours, with cough, dyspnea, weakness, chills, and fever to 38.3 to 39.7 degrees C. Two patients also had nausea and vomiting. Mild tachycardia and tachypnea were noted.
    b) Elevated white blood cell counts and mild hypoxia were initially present. Treatment with supplemental oxygen resulted in improvement over 8 hours. Laboratory abnormalities returned to normal over 2 days. Pulmonary function tests done 3 weeks after exposure showed mild obstructive disease, but the patients were all heavy smokers.
    2) A mechanical engineer developed shaking chills, fever to 38.9 degrees C, headache, dizziness, mild sinus tachycardia (104/minute), and mild hypertension (150/74 mmHg) after being exposed to smoke from Teflon tape inadvertently left in a reaction chamber (Shusterman & Neal, 1986). Leukocytosis with a left shift was present. The fever persisted for 50 hours after exposure, and headaches lasted for 4 days before clearing.

Range Of Toxicity

Summary

    A) Specific dose-response relationships for human exposures are difficult to determine due to the differences in Teflon decomposition products generated under various workplace conditions. Range of toxicity and causative agents are principally determined through animal studies.
    1) Different Teflon decomposition products vary widely in toxicity in experimental animals.

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) SUMMARY - The various Teflon decomposition products vary widely in toxicity in experimental animals (ILO, 1983).
    a) RATS - The LC50 in rats for a 4-hour inhalation exposure varies from 40,000 ppm for the tetrafluoroethylene monomer to 0.76 ppm for perfluoroisobutylene (ILO, 1983).
    b) BIRDS - Birds are more susceptible to the toxic effects of Teflon decomposition products than humans (Griffith et al, 1973).
    2) SPECIFIC SUBSTANCE
    a) The Teflon decomposition product perfluoroisobutylene is the most toxic of the known fluoroalkene compounds, and has a toxicity 10 times greater than that of phosgene in experimental animals (Ellenhorn & Barceloux, 1988; Waritz & Kwon, 1968), with a 6-hour inhalation exposure to 0.5 ppm being lethal (Waritz & Kwon, 1968).
    b) In inhalation experiments with perfluoroisobutylene, rats were given nose-only exposure to various concentrations for between 0.25 and 10 minutes (Smith et al, 1982). LC50's were calculated for a 0.25-minute exposure (361 ppm) and a 10-minute exposure (17 ppm).
    c) The development of weight loss and pulmonary impairment was seen up to 48 hours after the exposure. Affected animals either died with pulmonary congestion or recovered completely without apparent sequelae (Smith et al, 1982).
    d) Rats and mice were killed by a 2-hour inhalation exposure to 0.018 or 0.015 mg/L of perfluoroisobutylene (Karpov, 1963).
    e) It has been proposed that peroxyl radicals generated during combustion of perfluoro polymers (e.g., polytetrafluoroethylene) may play a role in pulmonary toxicity (Pryor et al, 1990).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Although much has been discovered about the toxicity of the various Teflon decomposition products, no practical way has ever been developed to express a safe level for exposure, especially for the prevention of polymer fume fever where the etiologic agent is unknown (Okawa & Polakoff, 1974).
    2) Safe use of Teflon products without special engineering controls can generally be done at process temperatures of 275 degrees C (527 degrees F) or lower (Okawa & Polakoff, 1974).
    3) It has been concluded that 300 degrees C is the highest safe temperature at which polytetrafluoroethylene can be used (Ushakov et al, 1985). When the worker is exposed to polymer temperatures between 300 to 500 degrees C, polymer-fume fever often occurs (HSDB , 2002).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) A good indication of exposure to toxic amounts of fluoride compounds is a urinary fluoride level of 3.0 milligrams per liter or greater (Okawa & Polakoff, 1974).
    2) OCCUPATIONAL
    a) One worker who was sintering granular Teflon had urinary fluoride levels of 5 milligrams per liter (Clayton & Clayton, 1982).
    3) ANIMAL DATA
    a) Rats developed a urinary fluoride excretion of 4 times normal when exposed to Teflon decomposition products for 1 hour (Clayton & Clayton, 1982).

Workplace Standards

    A) ACGIH TLV Values for CAS9002-84-0 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS9002-84-0 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS9002-84-0 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    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): 3 ; Listed as: Polytetrafluoroethylene
    a) 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.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    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 CAS9002-84-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES

Pharmacology Toxicology

Toxicologic Mechanism

    A) Many incidences of polymer fume fever involve workers who smoke cigarettes that may be contaminated with Teflon particulate matter (Goldstein et al, 1987; Okawa & Polakoff, 1974; HSDB , 1989). A common source of exposure is smoking cigarettes contaminated with Teflon dust (HSDB , 1989).
    1) It has been postulated that smokers may be more susceptible to polymer fume fever than nonsmokers, as after an exposure, a higher percentage of smokers become symptomatic than nonsmokers (Goldstein et al, 1987). In one outbreak, all 6 exposed individuals became ill, but the 3 smokers in the group had more serious clinical courses (Goldstein et al, 1987).
    B) The factor involved in the production of polymer fume fever on exposure to heated Teflon has not been identified, but the illness usually occurs when the fumes are evolved at temperatures between 300 and 500 degrees C (HSDB , 1989).
    1) Pyrolysis of polytetrafluoroethylene at atmospheric pressure yielded 33 percent perfluoroisobutylene at 750 degrees C (Fokin & Kosyrev, 1960).
    a) Perfluoroisobutylene intoxication in experimental animals characteristically causes pulmonary edema with hyperemia and hemorrhages (Danishevskii & Kochanov, 1961).
    b) Visible effects in experimental animals exposed to Teflon decomposition products include acute upper respiratory tract mucosal irritation followed by death from pneumonitis and pulmonary edema (Zhemerdey, 1958). Observed hyperemia and irritation may be caused by the presence of various fluorocarbon pyrolysis byproducts (Zhemerdey, 1958).
    2) In guinea pigs, mice, rabbits, cats, and rats, the toxicity of the evolved Teflon decomposition products was greater at temperatures above 500 degrees C than below 400 degrees C (Treon et al, 1954; Ushakov et al, 1985). In these studies, no animals died with exposure to pyrolysis products evolved at 300 degrees C (Treon et al, 1954; Ushakov et al, 1985).
    a) Observed symptoms in the animals were oral and nasal discharges, respiratory distress, dyspnea, gasping respirations, corneal injury, and premorbid seizures (Treon et al, 1954).
    3) In rats exposed to Teflon decomposition products evolved at 595 degrees C, respiratory distress was followed by death (Zook et al, 1983). Necropsy findings were focal hemorrhages, fibrin deposition, and edema in the lungs, thrombosis of pulmonary capillaries with hypertrophy and hyperplasia of alveolar cells, accumulated macrophages in the alveoli, and disseminated intravascular coagulopathy (Zook et al, 1983).
    4) The inhalation toxicity of Teflon decomposition products is related to both the decomposition temperature and a time-dependent atmospheric reaction, with those pyrolysis products produced at 700 degrees C above a methane flame being 850 times more toxic than those produced at a similar temperature in a cup furnace (Williams et al, 1987).
    C) Chronic daily poisoning of experimental animals with Teflon pyrolysis products evolved at just above 500 degrees C caused a toxic syndrome consistent with chronic fluoride poisoning (Scheel et al, 1968a). Urinary excretion of fluoride was 4 times normal in these animals after a single inhalation exposure (Scheel et al, 1968a).
    1) In these experiments, the lung and kidney were the target organs (Scheel et al, 1968a). Inhibition of succinic dehydrogenase was also noted (Scheel et al, 1968a). The observed fluoride toxicity was reversible by about 18 days after cessation of exposure (Scheel et al, 1968a)
    D) When Teflon is pyrolyzed in an electric furnace at 550 degrees C, the principle toxic effects in a variety of experimental animal species were due to the hydrolyzable fluoride-containing products produced (Scheel et al, 1968b). Exposure to the particulate matter resulting from Teflon decomposition under these conditions was irritating to the lungs for at least 7 to 10 days following exposure (Scheel et al, 1968b).
    1) The reversible portion of the pulmonary injuries observed in these studies were pulmonary edema and hemorrhage (Scheel et al, 1968b). Irreversible focal emphysema and interstitial fibrosis were also observed in some animals (Scheel et al, 1968b).
    E) When Teflon was heated in an oven to 450 degrees C and the resultant decomposition products were filtered such that the particulate fraction, but not the hydrolyzable fluorocarbons, were removed, the toxicity to experimental animals was essentially prevented. This finding suggests that toxicity is due to a particulate-adsorbed toxic agent (Waritz & Kwon, 1968).
    1) However, when the temperature is raised, perfluoroisobutylene is present in lethal concentrations (Waritz & Kwon, 1968). At even higher temperatures, carbonyl fluoride is most likely the principal toxic decomposition product (Waritz & Kwon, 1968).
    F) Perfluoroisobutylene, a Teflon decomposition product, is the most toxic of the known fluoroalkene compounds, and has a toxicity 10 times greater than that of phosgene in experimental animals. It is a potent irritant of the eyes, skin, and mucous membranes.
    1) The fumes are more toxic when Teflon is heated to 800 degrees C than when it is heated to 625 degrees C (Clayton & Clayton, 1982). In one occupational setting, cases of polymer fume fever were noted in either smokers or employees who worked in areas where the temperature of thermal processing was 480 degrees C instead of the prescribed 360 degrees C (Clayton & Clayton, 1982).
    2) Animal studies show that fresh fumes are more toxic, with toxicity decreasing within minutes of fume formation, apparently due to aggregation of the particulates (Williams et al, 1987; Seidel et al, 1991). Enhanced toxicity is restored if the aggregated particulates are reheated (Lee & Seidel, 1991).
    3) Filtering the particulate material produced at temperatures of 450 degrees C prevented the development of clinical signs in subsequently exposed experimental animals, indicating that the particulates themselves contain the toxic agent (Clayton & Clayton, 1982; Waritz & Kwon, 1968).
    4) The syndromes that result from exposure to Teflon decomposition products occur at temperatures much higher than those achieved when Teflon-coated cooking utensils are used for food preparation (Sittig, 1985; Dodson, 1988; Griffith et al, 1973).

Physicochemical

Physical Characteristics

    A) Teflon (polytetrafluoroethylene) is a greyish-white or opaque milk-whitish plastic material that is inert, temperature-resistant, and has a waxy, slippery feel (Proctor et al, 1988; ILO, 1983; Sax & Lewis, 1987; HSDB , 2002).
    1) Teflon can be greyish-white transparent thin sheets, a soft and waxy milk-white solid, or a white powder (HSDB , 2002).
    B) Teflon decomposition products are mostly colorless gases.

Molecular Weight

    A) >1,000,000 (Budavari, 1996; ILO, 1983)

Animal Toxicology

Clinical Effects

    11.1.1) AVIAN/BIRD
    A) Polymer fume fever is not generally associated with normal temperatures generated during cooking with Teflon-coated utensils (ILO, 1983; Griffith et al, 1973). However, accidental overheating has resulted in deaths in pet birds (which are more susceptible) (Blandford et al, 1975; Griffith et al, 1973).

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