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POLYMER FUME FEVER

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Polymer fume fever is an influenza-like syndrome associated with inhalation exposure to certain fluorocarbon thermal decomposition products.

Specific Substances

    1) FUME FEVER, POLYMER
    2) FUME FEVER
    3) PLASTIC FUME FEVER
    4) TEFLON FUME FEVER

Available Forms Sources

    A) FORMS
    1) Polymer fume fever has only been associated with decomposition products of three fluorocarbon-containing polymers: polytetrafluoroethylene (Teflon), fluorinated ethylene-propylene, and perfluoroalkoxyethylene resins (ILO, 1983; Lewis, 1993; HSDB , 1996).
    B) SOURCES
    1) Cases of polymer fume fever have been reported in workers involved with Teflon use or fabrication at high temperatures, and in persons smoking tobacco contaminated with polyfluorocarbon particulates (Albrecht & Bryant, 1987; Brubaker, 1977; Okawa & Polakoff, 1974).
    a) While most cases have been associated with occupational exposure to Teflon decomposition products, one was due to smoking cigarettes contaminated with low-molecular-weight perfluorinated hydrocarbons used in ski wax (Strom & Alexandersen, 1990).
    b) A man developed polymer fume fever after extensive hand contact with Elmer's Slide-All dry lubricant containing micronized polytetrafluoroethylene (PTFE or Teflon) and then hand rolling and smoking a hash-tobacco joint (Patel et al, 2006).
    c) A man developed three episodes of polymer fume fever after it was discovered the patient was using PTFE tape and immediately rolling/smoking his cigarettes without washing his hands prior to handling his cigarettes (Cooper & Gazzi, 1994).
    d) 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, 1989; ILO, 1983). It is inert under ordinary conditions (Budavari, 1989).
    e) Teflon (polytetrafluoroethylene) is available in three types and several resin grades for the production of various products by different processing methods (Grayson, 1985).
    2) 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; Hathaway et al, 1991). There is no evidence that Teflon produces decomposition products at temperatures below 200 degrees C (ILO, 1983).
    3) 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) (Hathaway et al, 1991).
    4) At temperatures above 400 degrees C, the principle toxic decomposition products of Teflon are perfluoroisobutylene and carbonyl fluoride (Okawa & Polakoff, 1974).
    5) 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 (Hathaway et al, 1991).
    6) Particulates, possibly with adsorbed toxic substances, were produced when Teflon was heated to less than 500 degrees C (Clayton & Clayton, 1994). Carbonyl fluoride was the principle decomposition product at temperatures of between 500 and 650 degrees C (Clayton & Clayton, 1994). At temperatures greater than 650 degrees C, carbon tetrafluoride and carbon dioxide were the principal decomposition products (Clayton & Clayton, 1994).
    7) The fumes are more toxic when Teflon is heated to 800 degrees C than when it is heated to 625 degrees C (Clayton & Clayton, 1994). 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, 1994).
    8) 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, 1994; Waritz & Kwon, 1968) .
    9) 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). 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).
    C) USES
    1) Polymer fume fever is an influenza-like syndrome associated with inhalation exposure to certain fluorocarbon thermal decomposition products. Most cases are secondary to exposure to polytetrafluoroethylene (Teflon(R)) at high temperatures. Teflon(R) is used as a non-stick coating for cooking utensils, film or fiber, surgical prosthesis, packings, coaxial spacers and insulators, bearings and gaskets, liners and seals, ablative coatings for space vehicles, piston rings, and as a coating material or tape for chemical vessels, and wirings (ILO, 1983; Lewis, 1993; HSDB , 1996).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) DESCRIPTION: Polymer fume fever is an influenza-like syndrome associated with inhalation exposure to certain fluorocarbon thermal decomposition products. Most cases are secondary to exposure to polytetrafluoroethylene (Teflon(R)) at high temperatures. Teflon(R) is used as a non-stick coating for cooking utensils, film or fiber, surgical prosthesis, packings, coaxial spacers and insulators, bearings and gaskets, liners and seals, ablative coatings for space vehicles, piston rings, and as a coating material or tape for chemical vessels, and wirings.
    B) TOXICOLOGY: Many outbreaks of polymer fume fever involve workers who smoke cigarettes that may be contaminated with Teflon(R) particulate matter. When Teflon was heated in an oven to 450 degrees C and the resultant decomposition products were filtered out, 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. When the temperature is raised, perfluoroisobutylene is present in lethal concentration. At even high temperatures, carbonyl fluoride is the most likely principal toxic decomposition product. Carbonyl fluoride and its hydrolysis product, hydrogen fluoride, are most likely responsible for acute lung injury.
    C) EPIDEMIOLOGY: From 2006 to 2012, regional poison control centers received an average of 9 cases of polymer fume fever per year, with less than half of these cases receiving medical treatment in a healthcare facility. Cases of polymer fume fever have been reported in workers involved with fluorocarbons use or fabrication at high temperatures and in people smoking tobacco contaminated with polyfluorocarbon particulates. Most cases associated with occupational exposure are secondary to Teflon(R) decomposition products.
    D) WITH POISONING/EXPOSURE
    1) Polymer fume fever is similar to metal fume fever. Pulmonary infiltrates are often seen in patients with polymer fume fever; the acute illness is somewhat similar to hypersensitivity pneumonitis. Patients may present with flu-like symptoms, such as chills, fever, profuse sweating, cough, dyspnea, and chest tightness. These symptoms are generally self-limited and last for 12 to 48 hours. A sensation of respiratory discomfort may persist for several weeks after an acute attack. Acute lung injury has been reported in some cases of polymer fume fever, and is more likely to be noted with exposures to fumes evolved from Teflon at temperatures greater than 500 degrees C. Other effects include sinus tachycardia, transient hypertension, metallic smell and taste, headache, weakness, myalgias, malaise, paresthesias, nausea and vomiting. One case of pericarditis has been reported. On the differential cell counts, leukocytosis with a left shift has been reported. Long term sequelae include prolonged decreases in diffusing capacity, reversible obstructive changes, and possible pulmonary fibrosis following multiple episodes of polymer fume fever.

Laboratory Monitoring

    A) Obtain a CBC with differential, pulse oximetry, and chest x-ray for those patients with respiratory symptoms.
    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 concentrations may give an indication of exposure to compounds causing polymer fume fever, but are not well correlated with the degree of exposure or severity of clinical effects. A good indication of exposure to toxic amounts of fluoride compounds is a urinary fluoride concentration of 3 mg/L or greater.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Refer to "INHALATION OVERVIEW" for specific treatment information.
    0.4.3) INHALATION EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Supportive care is the mainstay of treatment for polymer fume fever. Move patients to fresh air and monitor for respiratory distress. If coughing or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with beta2-adrenergic agonists. Consider systemic corticosteroids in patients with significant bronchospasm. Administer antipyretic and anti-inflammatory medications (eg, aspirin, NSAIDs) for symptomatic relief of fever and flu-like symptoms. Monitor pulse oximetry, chest x-rays, arterial blood gases and pulmonary function tests as needed.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Respiratory tract irritation can progress to acute lung injury, which may be delayed in onset up to 24 to 72 hours post-exposure in some cases. 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.
    C) DECONTAMINATION
    1) PREHOSPITAL: As toxicity is through inhalation, there is no need for gastrointestinal decontamination. Removing the patient from the exposure into fresh air is the most important prehospital management. Rescuers should wear self-contained breathing apparatus to avoid to self-contamination in areas with high concentration of fumes. Standard decontamination can be used for skin and eye exposures.
    2) HOSPITAL: There is no role for activated charcoal, gastric lavage, or whole bowel irrigation. 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.
    D) AIRWAY MANAGEMENT
    1) Airway management may be an issue in cases of severe toxicity but there is no reason to intubate early unless the patient's symptoms necessitate immediate intubation.
    E) ANTIDOTE
    1) There is no specific antidote for polymer fume fever.
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: The vast majority of these patients can be managed at home with removal from exposure, symptomatic over-the-counter treatment, and the use of proper protective gear (eg, respirators) in the future.
    2) OBSERVATION CRITERIA: Patients with self-harm exposures or worsening symptoms should be sent to a healthcare facility for observation for 4 to 6 hours. Patients may be discharged home if they are asymptomatic or clearly improving with the caveat that delayed pulmonary edema can occur and should symptoms worsen again, the patient may need to return to a healthcare facility immediately.
    3) ADMISSION CRITERIA: Patients with worsening symptoms that do not improve with initial treatments should be admitted to the hospital for further evaluation. Intubated patients or patients at high risk for intubation should be admitted to the intensive care unit. Patients can be discharged once they are asymptomatic or clearly improving.
    4) CONSULT CRITERIA: Toxicologists and poison centers may be contacted to help facilitate care. Pulmonologists and/or intensivists may be consulted to evaluate the respiratory symptoms of toxic patients, and pulmonary follow-up should be arranged for significant or repeated exposures of polymer fume fever.
    G) PITFALLS
    1) Possible pitfalls include not considering polymer fume fever as the source of a respiratory illness and not realizing that delayed pulmonary edema may occur in these patients.
    H) PREDISPOSING CONDITIONS
    1) Individuals with preexisting pulmonary disease may be at higher risk for toxicity. Smokers are also more likely to develop symptoms of polymer fume fever and have more severe toxicity. Those with repeated episodes of polymer fume fever are also more likely to have more severe sequelae.
    I) DIFFERENTIAL DIAGNOSIS
    1) Metal fume fever can look very similar to polymer fume fever. Other causes of respiratory illness should also be kept on the differential.
    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) TOXICITY: No practical way has been developed to express a safe level of exposure, especially for the prevention of polymer fume fever where the etiologic agent is unknown. Although polymer fume fever is typically a benign, self-limited disease, complications may occur. At least two deaths have been reported in workers who developed acute lung injury from exposure to Teflon decomposition products. Generally, the higher the temperature, the more severe effects are seen.

Clinical Effects

Summary Of Exposure

    A) DESCRIPTION: Polymer fume fever is an influenza-like syndrome associated with inhalation exposure to certain fluorocarbon thermal decomposition products. Most cases are secondary to exposure to polytetrafluoroethylene (Teflon(R)) at high temperatures. Teflon(R) is used as a non-stick coating for cooking utensils, film or fiber, surgical prosthesis, packings, coaxial spacers and insulators, bearings and gaskets, liners and seals, ablative coatings for space vehicles, piston rings, and as a coating material or tape for chemical vessels, and wirings.
    B) TOXICOLOGY: Many outbreaks of polymer fume fever involve workers who smoke cigarettes that may be contaminated with Teflon(R) particulate matter. When Teflon was heated in an oven to 450 degrees C and the resultant decomposition products were filtered out, 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. When the temperature is raised, perfluoroisobutylene is present in lethal concentration. At even high temperatures, carbonyl fluoride is the most likely principal toxic decomposition product. Carbonyl fluoride and its hydrolysis product, hydrogen fluoride, are most likely responsible for acute lung injury.
    C) EPIDEMIOLOGY: From 2006 to 2012, regional poison control centers received an average of 9 cases of polymer fume fever per year, with less than half of these cases receiving medical treatment in a healthcare facility. Cases of polymer fume fever have been reported in workers involved with fluorocarbons use or fabrication at high temperatures and in people smoking tobacco contaminated with polyfluorocarbon particulates. Most cases associated with occupational exposure are secondary to Teflon(R) decomposition products.
    D) WITH POISONING/EXPOSURE
    1) Polymer fume fever is similar to metal fume fever. Pulmonary infiltrates are often seen in patients with polymer fume fever; the acute illness is somewhat similar to hypersensitivity pneumonitis. Patients may present with flu-like symptoms, such as chills, fever, profuse sweating, cough, dyspnea, and chest tightness. These symptoms are generally self-limited and last for 12 to 48 hours. A sensation of respiratory discomfort may persist for several weeks after an acute attack. Acute lung injury has been reported in some cases of polymer fume fever, and is more likely to be noted with exposures to fumes evolved from Teflon at temperatures greater than 500 degrees C. Other effects include sinus tachycardia, transient hypertension, metallic smell and taste, headache, weakness, myalgias, malaise, paresthesias, nausea and vomiting. One case of pericarditis has been reported. On the differential cell counts, leukocytosis with a left shift has been reported. Long term sequelae include prolonged decreases in diffusing capacity, reversible obstructive changes, and possible pulmonary fibrosis following multiple episodes of polymer fume fever.

Vital Signs

    3.3.2) RESPIRATIONS
    A) WITH POISONING/EXPOSURE
    1) TACHYPNEA has been reported in workers with polymer fume fever (Goldstein et al, 1987).
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) HYPERPYREXIA: An elevated temperature is commonly seen in patients with polymer fume fever from exposure to Teflon decomposition products (Greenberg & Vearrier, 2015; Patel et al, 2006; ILO, 1983; Hathaway et al, 1991; Rosenstock & Cullen, 1986).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) HYPERTENSION: Transient hypertension was seen in workers with polymer fume fever (Shusterman & Neal, 1986; Reinl, 1964).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) TACHYCARDIA: Sinus tachycardia has been reported in workers with polymer fume fever (Goldstein et al, 1987; Shusterman & Neal, 1986; Reinl, 1964).

Heent

    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) METALLIC SMELL: A pungent or metallic smell may occur (Goldstein et al, 1987).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) METALLIC TASTE: Workers with polymer fume fever may experience a metallic taste (Goldstein et al, 1987).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYCARDIA
    1) WITH POISONING/EXPOSURE
    a) Sinus tachycardia has been reported (Greenberg & Vearrier, 2015; Goldstein et al, 1987; Shusterman & Neal, 1986; Reinl, 1964).
    B) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Transient hypertension has been seen (Shusterman & Neal, 1986; Reinl, 1964).
    C) PERICARDITIS
    1) WITH POISONING/EXPOSURE
    a) One case of pericarditis occurred, together with acute lung injury, in a worker who inhaled Teflon fumes from grinding (Haugtomt & Haerem, 1989).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Dyspnea, cough, and shortness of breath occur in patients with polymer fume fever (Patel et al, 2006; Rosenstock & Cullen, 1986; Hathaway et al, 1991; Makulova, 1965; Reinl, 1964). Tracheitis and bronchitis may occur (Reinl, 1964).
    B) ACUTE RESPIRATORY FAILURE
    1) WITH POISONING/EXPOSURE
    a) Respiratory failure has been reported in patients with polymer fume fever (Greenberg & Vearrier, 2015).
    C) CHEST PAIN
    1) WITH POISONING/EXPOSURE
    a) Chest discomfort is commonly described in patients with polymer fume fever (Hathaway et al, 1991; Goldstein et al, 1987; Reinl, 1964).
    D) HYPOXIA
    1) WITH POISONING/EXPOSURE
    a) Hypoxia has been reported in patients with polymer fume fever (Greenberg & Vearrier, 2015). Mild hypoxia with pO2s of 64 to 77 mmHg (room air) was noted in a group of workers with polymer fume fever (Goldstein et al, 1987).
    E) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Acute lung injury has been reported in some cases of polymer fume fever; symptoms of chest discomfort and shortness of breath were also present (Hathaway et al, 1991; Sittig, 1985; Ellenhorn & Barceloux, 1988).
    b) Acute lung injury is more likely to be noted with exposure to fumes evolved from Teflon at temperatures of 500 degrees C or greater (ILO, 1983).
    c) At least two deaths have been reported in workers who developed acute lung injury from exposure to Teflon decomposition products (Auclair et al, 1983; Makulova, 1965).
    F) PNEUMONITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 29-year-old man developed evidence of pneumonitis after using a perforated aluminum beverage can as a pipe to ignite marijuana leaves with hairspray-impregnated cotton. After a few inhalations, he developed severe, burning chest discomfort and shortness of breath. The patient was admitted in mild respiratory distress, temperature 38 degrees C, with fine bilateral rales in the lower lobes. Bilateral reticulonodular lung opacities with lower lobe prominence consistent with pneumonitis was found on chest x-ray. Symptoms improved within 24 hours with supplemental oxygen therapy only. The authors concluded that inhalation of pyrolyzed hairspray may cause symptoms consistent with polymer fume fever (Delgado & Waksman, 2004).
    G) SEQUELA
    1) Reversible airways obstruction and reduced diffusing capacity lasted for weeks to months in one individual who developed acute lung injury following inhalation of Teflon decomposition products (Brubaker, 1977).
    H) DISORDER OF LUNG
    1) PREDISPOSING CONDITIONS
    a) Individuals with preexisting pulmonary disease should be precluded from exposure to Teflon decomposition products (Goldstein et al, 1987).
    b) SMOKERS are more likely than nonsmokers to develop symptoms of polymer fume fever when exposed to Teflon decomposition products. Smokers develop a more severe illness than nonsmokers when both become symptomatic (Goldstein et al, 1987).
    c) Workers exposed to Teflon decomposition products, and especially those with a history of one or more episodes of polymer fume fever, should have regular medical surveillance (Goldstein et al, 1987).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache and dizziness may occur with polymer fume fever (Shusterman & Neal, 1986). The headache has lasted up to 4 days in some cases (Shusterman & Neal, 1986).
    B) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) Numbness and tingling in the fingertips have been described (Albrecht & Bryant, 1987).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting have been described in workers with polymer fume fever (Albrecht & Bryant, 1987; Goldstein et al, 1987; Reinl, 1964).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) 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 which is non-specific (Greenberg & Vearrier, 2015; Goldstein et al, 1987; Shusterman & Neal, 1986; Reinl, 1964).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) Myalgias may be part of the flu-like symptoms of polymer fume fever (Greenberg & Vearrier, 2015; Albrecht & Bryant, 1987).
    B) JOINT PAIN
    1) WITH POISONING/EXPOSURE
    a) Arthralgias may occur with polymer fume fever (Greenberg & Vearrier, 2015).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain a CBC with differential, pulse oximetry, and chest x-ray for those patients with respiratory symptoms.
    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 concentrations may give an indication of exposure to compounds causing polymer fume fever, but are not well correlated with the degree of exposure or severity of clinical effects. A good indication of exposure to toxic amounts of fluoride compounds is a urinary fluoride concentration of 3 mg/L or greater.
    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 (Greenberg & Vearrier, 2015; Goldstein et al, 1987; Shusterman & Neal, 1986; Reinl, 1964).
    B) ACID/BASE
    1) Monitor arterial blood gases in patients with severe polymer fume fever. In the majority of other cases, pulse oximetry is sufficient.
    4.1.3) URINE
    A) URINARY CONCENTRATIONS
    1) Monitoring urinary fluoride concentrations might be useful as an indication of exposure to compounds that can cause polymer fume fever. Urinary fluoride concentrations have not been well correlated with the extent of exposure or severity of clinical effects (Clayton & Clayton, 1994; Okawa & Polakoff, 1974).
    a) A good indication of exposure to toxic amounts of fluoride compounds is a urinary fluoride concentration 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 severe polymer fume fever. Diffusing capacity abnormalities and reversible obstructive changes may occur.
    b) Sources have reported both normal and abnormal pulmonary function tests (Greenberg & Vearrier, 2015).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) A chest x-ray can be obtained to evaluate for other causes of fever, chills, and dyspnea such as pneumonia or heart failure in the appropriate clinical context.
    2) Sources have reported both normal and abnormal pulmonary function tests. Chest x-rays are usually normal; however, mild vascular congestion may be observed. Diffuse patchy infiltrates may be observed in severe cases (Greenberg & Vearrier, 2015).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) Patients with worsening symptoms that do not improve with initial treatments should be admitted to the hospital for further evaluation. Intubated patients or patients at high risk for intubation should be admitted to the intensive care unit. Patients can be discharged once they are asymptomatic or clearly improving.
    6.3.3.2) HOME CRITERIA/INHALATION
    A) The vast majority of these patients can be managed at home with removal from exposure, symptomatic over-the-counter treatment, and the use of proper protective gear (eg, respirators) in the future.
    6.3.3.3) CONSULT CRITERIA/INHALATION
    A) Toxicologists and poison centers may be contacted to help facilitate care. Pulmonologists and/or intensivists may be consulted to evaluate the respiratory symptoms of toxic patients, and pulmonary follow-up should be arranged for significant or repeated exposures of polymer fume fever.
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Patients with self-harm exposures or worsening symptoms should be sent to a healthcare facility for observation for 4 to 6 hours. Patients may be discharged home if they are asymptomatic or clearly improving with the caveat that delayed pulmonary edema can occur and should symptoms worsen again, the patient may need to return to a healthcare facility immediately.

Monitoring

    A) Obtain a CBC with differential, pulse oximetry, and chest x-ray for those patients with respiratory symptoms.
    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 concentrations may give an indication of exposure to compounds causing polymer fume fever, but are not well correlated with the degree of exposure or severity of clinical effects. A good indication of exposure to toxic amounts of fluoride compounds is a urinary fluoride concentration of 3 mg/L or greater.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) PREHOSPITAL: As toxicity is through inhalation, there is no need for gastrointestinal decontamination. Removing the patient from the exposure into fresh air is the most important prehospital management. Rescuers should wear self-contained breathing apparatus to avoid to self-contamination in areas with high concentration of fumes. Standard decontamination can be used for skin and eye exposures.

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.
    D) Patients with repeated episodes of polymer fume fever should be referred to a pulmonologist for periodic chest x-rays and pulmonary function tests.
    6.7.2) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Supportive care is the mainstay of treatment for polymer fume fever. Move patients to fresh air and monitor for respiratory distress. If coughing or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with beta2-adrenergic agonists. Consider systemic corticosteroids in patients with significant bronchospasm.
    b) Administer antipyretic and anti-inflammatory medications (eg, aspirin, NSAIDs) for symptomatic relief of fever and flu-like symptoms (Greenberg & Vearrier, 2015).
    c) Monitor pulse oximetry, chest x-rays, arterial blood gases and pulmonary function tests as needed.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Respiratory tract irritation can progress to acute lung injury, which may be delayed in onset up to 24 to 72 hours post-exposure in some cases. 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.
    B) MONITORING OF PATIENT
    1) Obtain a CBC with differential, pulse oximetry, and chest x-ray for those patients with respiratory symptoms.
    2) Monitoring pulmonary function tests may be useful to detect the development of sequelae in patients with one or more episodes of polymer fume fever.
    3) Measuring urinary fluoride concentrations may provide an indication of exposure to compounds causing polymer fume fever, but have not been well correlated with the extent of exposure or severity of clinical effects (Clayton & Clayton, 1994; Okawa & Polakoff, 1974).
    4) A good indication of exposure to toxic amounts of fluoride compounds is a urinary fluoride concentration of 3 mg/L or greater.
    C) 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).
    D) FOLLOW-UP VISIT
    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) 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) ROUTE OF EXPOSURE
    1) INHALATION
    a) 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. All 3 workers were smokers, and 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. 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 (Albrecht & Bryant, 1987).
    b) Brubaker (1977) reported a series of 9 workers exposed to polytetrafluoroethylene 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. One individual had a documented episode of acute lung injury. 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. The mother of one employee developed an illness similar to polymer fume fever after handling possibly contaminated work clothing and then smoking a cigarette (Brubaker, 1977).
    c) One worker had more than 40 episodes of polymer fume fever over a 9 month period, but never developed acute lung injury (HSDB , 1996; 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 , 1996). At autopsy, interstitial pulmonary fibrosis was noted (Goldstein et al, 1987).
    d) 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).
    1) 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).
    2) At the time of the Health Hazard Evaluation, no workers were complaining of symptomatic polymer fume fever, and urinary fluoride concentrations collected from 77 employees ranged from 0.098 to 2.19 mg/L (less than concentrations of 3.0 mg/L or greater indicating potential exposure to toxic concentrations of fluoride compounds) (Okawa & Polakoff, 1974).
    e) 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. 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. Elevated white blood cell counts and mild hypoxia were initially present. Treatment with supplemental oxygen resulted in improvement over 8 hours, and 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 (Goldstein et al, 1987).
    f) 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. Leukocytosis with a left shift was present. The fever persisted for 50 hours after exposure, and headaches lasted for 4 days before clearing (Shusterman & Neal, 1986).

Range Of Toxicity

Summary

    A) TOXICITY: No practical way has been developed to express a safe level of exposure, especially for the prevention of polymer fume fever where the etiologic agent is unknown. Although polymer fume fever is typically a benign, self-limited disease, complications may occur. At least two deaths have been reported in workers who developed acute lung injury from exposure to Teflon decomposition products. Generally, the higher the temperature, the more severe effects are seen.

Minimum Lethal Exposure

    A) Although polymer fume fever is typically a benign, self-limited disease, complications may occur (Greenberg & Vearrier, 2015). At least two deaths have been reported in workers who developed acute lung injury from exposure to Teflon decomposition products (Auclair et al, 1983; Makulova, 1965).

Maximum Tolerated Exposure

    A) Although much has been discovered about the toxicity of various Teflon decomposition products, no practical way has 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).
    B) 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).
    C) No standardized dose-response behavior can be defined, because of the unknown etiologic agent and variable composition of Teflon decomposition products. Nevertheless, symptoms of polymer fume fever have been associated with total airborne fluorine concentrations of 3.5 mg/m(3), expressed as polytetrafluoroethylene, in workers exposed to decomposition products at 350 to 380 degrees C (ACGIH, 1991).

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 that can cause polymer fume fever is a urinary fluoride concentration of 3.0 milligrams per liter or greater (Okawa & Polakoff, 1974).

Pharmacology Toxicology

Toxicologic Mechanism

    A) Polymer fume fever has only been associated with decomposition products of three fluorocarbon-containing polymers: polytetrafluoroethylene (Teflon), fluorinated ethylene-propylene, and perfluoroalkoxyethylene resins produced at high temperatures (Greenberg & Vearrier, 2015; ILO, 1983; Lewis, 1993; HSDB , 1996). Other fluorocarbon breakdown products (eg, octafluoroisobutylene, difluoroethylene, hexafluoroethane, hexafluoropropylene, and octafluorocyclobutane) have also been detected when the decomposition fume of polytetrafluoroethylene was analyzed (Greenberg & Vearrier, 2015).
    B) Many outbreaks of polymer fume fever involve workers who smoke cigarettes that may be contaminated with Teflon particulate matter (polytetrafluoroethylene particles) (Greenberg & Vearrier, 2015; Goldstein et al, 1987; Okawa & Polakoff, 1974; HSDB , 1996). The most common source of exposure is smoking cigarettes contaminated with Teflon dust (HSDB , 1996).
    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).
    C) When Teflon was heated in an oven to 450 degrees C and the resultant decomposition products were filtered out, 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) When the temperature is raised, perfluoroisobutylene is present in lethal concentrations (Waritz & Kwon, 1968).
    2) At even higher temperatures, carbonyl fluoride is most likely the principal toxic decomposition product (Waritz & Kwon, 1968). Carbonyl fluoride and/or its hydrolysis product, hydrogen fluoride, is most likely responsible for acute lung injury (Auclair et al, 1983).

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