Lung - Adverse Effects
Teflon (PTFE: polytetrafluoroethylene)
CAS No. 9002-84-0

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ACTIVITY: US EPA Pesticide List 3 Inert.

Teflon is used in pesticides as an Inert. According to a US EPA Final Rule of April 28, 2004:
Montmorillonite-type clay treated with polytetrafluoroethylene. Carrier. PTFE content not greater than 0.5% of clay (w/w). To be used in pesticide formulations applied to growing crops or to raw agricultural commodities after harvest.

Also, component used in plastic slow release tag.


• Click here to return to the Lung section for fluorine & organofluorine pesticides.

Excerpts of The Toxicology of Perfluoroisobutene by Jiri Patocka and Jiri Bajgar.

Perfluoroisobutene ... is a fluoro-olefin produced by thermal decomposition of polytetrafluoroethylene (PTFE), e.g., Teflon [1].

Overheating of PTFE generates fumes of highly toxic PFIB and poses a serious health hazard to the human respiratory tract. PFIB is approximately ten times as toxic as phosgene [2]. Inhalation of this gas can cause pulmonary edema, which can lead to death. PFIB is included in Schedule 2 of the Chemical Weapons Convention (CWC), as a result of the prompting by one delegation to the Conference on Disarmament [3]. ...

Acute Toxicity. The median lethal concentration (LC50) in single exposures of rats was 0.5 ppm. The intoxicated rats either died with gross pathological signs of pulmonary congestion or recovered with no apparent residual effects. The 15-second LC50 was 361 ppm and the 10-minute LC50 was 17 ppm [9]. Similar high acute toxicity following inhalation was seen in other species with a two hour LC50 in mice reported to be either 1.6 ppm [9] or 0.98 ppm [10], in rabbits either 4.3 ppm [10] or 1.2 ppm [11], in guinea-pigs 1.05 ppm [10] and in cats 3.1 ppm [10]. In experiments in which rats were exposed to a concentration of 12.2 ppm for 10 min, an unusual postexposure latency period of approximately 8 hours was observed prior to the occurrence of pulmonary edema [12].

Human Toxicity ... Five workers accidentally exposed to a gas containing 2 percent PFIB reported irritation of the respiratory tract within 24 h of exposure. The lung irritation was manifested by cough in all cases. The patients developed headache, cough, substernal pain, dyspnoea and fever within the first hour following exposure. The symptoms became worse at six to eight hours after exposure. Also choking or shortness of breath was observed in a majority of the patients. The condition of the patients began to improve on the fifth day and they were discharged from the hospital after two to three weeks. One patient developed a respiratory infection, which required his stay in hospital to be extended to about eight weeks. All the patients were shown to have pulmonary edema and this was confirmed at post mortem on two patients died. One died after 11 days after exposure, the other died after 13 days [16, 17]. According to Kennedy [14], one worker exposed to PFIB for three minutes reported strong subjective symptoms of bad odor, bad taste in the mouth, nausea and weakness. On returning to fresh air, the worker recovered and had no further symptoms. Half an hour later, a concentration of 0.04 ppm of PFIB was measured in the exposure area.
The latency period for PFIB injury is one to four hours until pulmonary edema symptoms appear. In many cases, pulmonary edema clears up in about 72 hours, with little long-term damage [27].

The histopathology of rat lung has been studied after an acute exposure to PFIB at a concentration of 78 ppm for 1.5 min. Within 5 min of exposure, changes to the bronchioles and peribronchial alveoli were observed which took the form of alterations to cilial structure, increased pinocytosis with occasional vesicle formation of type I alveolar epithelial cells. The gradual development of pulmonary edema was visible histologically two to three hours post exposure, with death occurring from seven hours onwards. Animals sacrificed at 24 hours post exposure showed evidence of widespread pulmonary edema and alveolar interstitial infiltration by lympho mononuclear cells and macrophages [19]. In other experiments, PFIB induced pulmonary edema involving a translocation of blood compartment proteins into the lung’s alveolar compartment. By high-performance capillary electrophoresis of proteins from the fluid lining of the lungs of rats exposed to PFIB was estimated that albumin, transferrin and IgG are three major proteins translocated into the alveolar space [20].

1. Zeifman, Y.B., Ter-Gabrielyan, N.P., Knunyants, I.L. The Chemistry of Perfluoroisobutylene. Uspekhi Khimii, 1984; 53: 431-461.
2. Oberdorster, G., Ferin, J., Gelein, J., Finkelstein, R., Baggs, R., Effects of PTFE Fumes in the Respiratory Tract: A Particle Effect? Aerospace Medical Assiciation 65th Annual Scientific Meeting, 1994; 538: A52.
3. CD/CW/WP.239. Verification of the Nonproduction of Chemical Weapons: An Illustrative Example of the Problem of Novel Toxic Chemicals. 12 April 1989.
9. Smith, L.W., Gardner, R.J., Kennedy, G.L., Jr. Short-Term Inhalation Toxicity of Perfluoroisobutylene. Drug Chem Toxicol 1982; 5: 295-303.
14. Kennedy, G.L., Jr., Geisen, R.J. Setting Occupational Exposure Limits for Perfluoroisobutylene, A Highly Toxic Chemical Following Acute Exposure. J Occup Med 1985; 27: 675-.
16. Unpublished data from DuPont Co., cited as Reference 15.
17. Danishevskii, S.L., Kochanov, M.M. Toxicity of Some Fluoroorganic Compounds. Gig Tr Prof Zabol 1961; 5: 3-8.
19. Brown, R.F., Rice, P. Electron Microscopy of Rat Lung Following a Single Acute Exposure to Perfluoroisobutylene (PFIB). A Sequential Study of the First 24 hours Following Exposure. Int J Exp Pathol 1991; 72: 437-450.
20. Gurley, L.R., Buchanan, J.S., London, J.E., Stavert, D.M., Lehnert, B.E. High Performance Capillary Electrophoresis of Proteins from the Fluid Lining of the Lungs of Rats Exposed to Perfluoroisobutylene. J Chromatogr 1991; 559: 411-429.

Ref: Toxicology of Perfluoroisobutene by Jiri Patocka and Jiri Bajgar (Department of Toxicology, Military Medical Academy 500 01 Hradec, Czech Republic). The ASA Newsletter (Applied Science and Analysis, Inc.). 1998.

Oxygen difluoride is a thermal decomposition product of Teflon.
It has many synonyms; it's
primary name is Fluorine monoxide
(CAS No.
7783-41-7). The molecular structure is:

In the US National Institute for Occupational Safety and Health (NIOSH) category of Immediately Dangerous to Life or Health Concentrations (IDLH) - a list of 387 workplace chemicals - the two chemicals that share the rank of most dangerous chemicals for "respirator selection criteria" are:

Oxygen difluoride : IDLH of 0.5 ppm
Lithium hydride : IDLH of 0.5 mg/m3

Human data: Oxygen difluoride is a strong irritant to the entire respiratory tract and causes pulmonary edema and hemorrhage when inhaled for a few hours at 0.5 ppm [Deichmann and Gerarde 1969].

Basis for original (SCP) IDLH: The chosen IDLH is based on the statements by Deichmann and Gerarde [1969] that oxygen difluoride is a strong irritant to the entire respiratory tract and causes pulmonary edema and hemorrhage when inhaled for a few hours at 0.5 ppm. Development of pulmonary signs leading to death may be delayed several hours after the exposure [Deichmann and Gerarde 1969]. In addition, AIHA [1967] reported that the Committee on Toxicology of the National Research Council recommended an Emergency Exposure Limit (EEL) of 0.5 ppm for a 10-minute exposure. This EEL is supposed to be for exposures that are "rare in the lifetime of an individual and permit some degree of reversible injury short of incapacitation" [Smyth 1966].

Lethal concentration data:
Reference LC50 (ppm) Time Adjusted 0.5-hr LC (CF) Derived value
Rat Darmer et al. 1972
1 hr 3.3 ppm (1.25) 0.3 ppm
Mouse Darmer et al. 1972
1 hr 1.9 ppm (1.25) 0.2 ppm
Dog Darmer et al. 1972
1 hr 33 ppm (1.25) 3.3 ppm
Monkey Darmer et al. 1972
1 hr 20 ppm (1.25) 2.0 ppm


AIHA [1967]. Oxygen difluoride. In: Hygienic guide series. Am Ind Hyg Assoc J 28:194-196.

Darmer KI Jr, Haum CC, MacEwen JD [1972]. The acute inhalation toxicology of chlorine pentafluoride. Am Ind Hyg Assoc J 33:661-668.

Deichmann WB, Gerarde HW [1969]. Oxygen difluoride (OF2). In: Toxicology of drugs and chemicals. New York, NY: Academic Press, Inc., p. 444.

Smyth HF Jr [1966]. Military and space short-term inhalation standards. Arch Environ Health 12:488-490.


Abstract: When Teflon is heated the developing fumes produce in exposed humans an influenza-like syndrome (polymer fume fever) or also severe toxic effects like pulmonary edema, pneumonitis and death. The decomposition products and the resulting health effects are temperature-dependent. The toxic effects seem to be related to the ultrafine particulate fraction of the fume. To test the hypothesis that exposure to ultrafine particles results in an increased interstitialization of the particles which is accompanied by an acute pathological inflammation, rats were exposed to titanium dioxide (TiO2) particles by intratracheal instillation and by inhalation. Both acute intratracheal instillation and subchronic inhalation studies on rats show that ultrafine TiO2 particles (~20 nm diameter) access the pulmonary interstitium to a larger extent than fine particles (~250 nm diameter) and that they elicit an inflammatory response as indicated by PMN increase in lavaged cells. The release of ultrafine particles into the air of an enclosed environment from a thermodegradation event or from other sources is a potential hazard for astronauts. Knowing the mechanisms of action is a prerequisite for technical or medical countermeasures.
Ref: Part 2—Biomedical support. Polymer degradation and ultrafine particles: Potential inhalation hazards for astronauts. by J. Ferin and G. Oberdörster (Environmental Health Sciences Center School of Medicine & Dentistry University of Rochester, Rochester, NY 14642, USA). Acta Astronautica Volume 27 , July 1992, Pages 257-259.

Abstract: The effect of exposure to polytetrafluoroethylene (9002-84-0) (PTFE) fumes on the early pulmonary inflammatory response was examined. Male Fischer-344-rats were exposed to PTFE fumes produced at 460 degrees-C. A particle concentration of 5x10(5) particles per cubic centimeter was determined. Controls were sham exposed. Animals were sacrificed 4 hours after exposure and pulmonary lavage was performed. The messenger RNA (mRNA) in lung tissue was analyzed by Northern and slot blot analysis. Membrane hybridization and in-situ hybridization were conducted. The mean percentage of neutrophils (PMNs) in the lavage fluid increased from 0.55% in controls to 55.7% in exposed rats. The mean percentage of lymphocytes increased from 0.5% in controls to 2.64% in exposed rats. The mean percentage of macrophages decreased from 98.9% in controls to 41.6% in exposed rats. Compared to controls, the levels of protein, lactate-dehydrogenase, and beta-glucuronidase in the lavage fluid of rats exposed to PTFE fumes were elevated by 35, 7, and 6.5 fold, respectively. The quantity of mRNAs for various antioxidants and cytokines increased by up to 40 fold, compared to controls, following PTFE exposure. In-situ hybridization revealed that the transcripts of interleukin-6 (IL6), metallothionein (MT), and tumor necrosis factor alpha (TNF-alpha) were not elevated in the cells of control lungs. In lungs exposed to PTFE fumes, the transcripts of MT and IL6 were elevated in lymphatic vessels, large and small airways, inflammatory cells, parenchyma cells, and where pulmonary edema was evident. Following exposure, TNF-alpha transcripts were elevated in the parenchyma and interstitium, whereas the transcripts of surfactant protein-C were increased in type-II cells, the interstitium, and surrounding airways. The authors conclude that exposure to PTFE fumes containing ultrafine particles induces an early pulmonary inflammatory response. This inflammatory process may be mediated by PMNs and the up regulation of cytokines and antioxidants.
Ref: Characterization of the Early Pulmonary Inflammatory Response Associated with PTFE Fume Exposure; by Johnston CJ, Finkelstein JN, Gelein R, Baggs R, Oberdorster G. Toxicology and Applied Pharmacology, Vol. 140, No. 1, pages 154-163, 1996.

Abstract: PTFE (polytetrafluoroethylene) fumes consisting of large numbers of ultrafine (uf) particles and low concentrations of gas-phase compounds can cause severe acute lung injury. Our studies were designed to test three hypotheses:
(i) uf PTFE fume particles are causally involved in the induction of acute lung injury,
(ii) uf PTFE elicit greater pulmonary effects than larger sized PTFE accumulation mode particles, and
(iii) preexposure to the uf PTFE fume particles will induce tolerance. We used uf Teflon (PTFE) fumes (count median particle size ~ 16 nm) generated by heating PTFE in a tube furnace to 486°C to evaluate principles of ultrafine particle toxicity.
Teflon fumes at ultrafine particle concentrations of 50 g/m3 were extremely toxic to rats when inhaled for only 15 min. We found that when generated in argon, the ultrafine Teflon particles alone are not toxic at these exposure conditions; neither were Teflon fume gas-phase constituents when generated in air. Only the combination of both phases when generated in air caused high toxicity, suggesting either the existence of radicals on the surface or a carrier mechanism of the ultrafine particles for adsorbed gas compounds. Aging of the fresh Teflon fumes for 3.5 min led to a predicted coagulation to >100 nm particles which no longer caused toxicity in exposed animals. This result is consistent with a greater toxicity of ultrafine particles compared to accumulation mode particles, although changes in particle surface chemistry during the aging process may have contributed to the diminished toxicity. Furthermore, the pulmonary toxicity of the ultrafine Teflon fumes could be prevented by adapting the animals with short 5-min exposures on 3 days prior to a 15-min exposure. Messages encoding antioxidants and chemokines were increased substantially in nonadapted animals, yet were unaltered in adapted animals. This study shows the importance of preexposure history for the susceptibility to acute ultrafine particle effects.
Ref: Pulmonary Effects Induced by Ultrafine PTFE Particles; Carl J. Johnston, Jacob N. Finkelstein, Pamela Mercer, Nancy Corson, Robert Gelein and Günter Oberdörster. Toxicology and Applied Pharmacology Volume 168, Issue 3 , 1 November 2000, Pages 208-215.

Abstract: The cases of three patients with acute pulmonary oedema caused by inhalation of fumes from heated polytetrafluoroethylene (PTFE) in a plastic factory are described. One patient died from profound hypoxemia and shock shortly after admission, and the other two patients survived after medical treatment. This is the first report of fatal pulmonary oedema in a worker exposed to PTFE heated in a plastic extruding operation. From this observation, it appears that inhalation exposure to pyrolytic products from polytetrafluoroethylene can cause fatal respiratory complications. Special precautions are warranted in this kind of operation to prevent workers from being exposed to these substances.
Ref: Fatal acute pulmonary oedema after inhalation of fumes from polytetrafluoroethylene (PTFE) by LEE CH, GUO YL, TSAI PJ, CHANG HY, CHEN CR, CHEN CW, HSIUE T-R. EUROPEAN RESPIRATORY JOURNAL; 10 (6). 1997. 1408-1411.

Abstract: Information on potential occupational hazards from exposure to carbonyl fluoride (353-50-4) was reviewed. Topics discussed included chemical and physical properties, production, use, manufacturers and distributors, manufacturing processes, occupational exposure, and biological effects. Potential exposure to carbonyl fluoride occurs as a result of the thermal decomposition of polytetrafluoroethylene (PTFE) in air. Effects of acute exposure in animal studies included extreme malaise and weakness which preceded death. Subchronic exposure studies with PTFE pyrolysis products revealed pathologic changes in the respiratory tracts and livers of exposed animals. Protein, glucose, ketones, and occult blood appeared in the urine following exposure. No information was available concerning chronic exposures, carcinogenicity, mutagenicity, teratogenicity, or reproductive effects.
Ref: 1987. Information Profiles on Potential Occupational Hazards: Carbonyl Fluoride. Second Draft. Syracuse Research Corp., NY. Center for Chemical Hazard Assessment. Sponsored by National Inst. for Occupational Safety and Health, Rockville, MD. Report No. NTIS/PB87-174330.

Abstract. Toxic effects following inhalation exposure to polytetrafluoroethylene (9002-84-0) (PTFE) pyrolysis products were determined in rats. Greenacres-Flora-rats were exposed to PTFE pyrolysis products containing hydrolyzable fluoride equal to 50 parts per million of carbonyl fluoride (353-50-4) for 1 hour daily for 5 days. On day 1 and 5 of the exposure period, and 3, 7, and 18 days postexposure urine samples were collected and examined for fluoride excretion and glucose, protein, and ketones. On each of those days, a test animal was killed, and kidney and lung tissues were tested for succinic-dehydrogenase activity. Weight changes and mortality during the course of the experiment were also noted. During the 5 exposure days and shortly afterwards, mortality reached 22 percent, although the total exposure dose was less than half the median lethal dose for one exposure. Daily urinary fluoride excretion jumped to 14 times normal on the first exposure day and remained at 4 times normal by the eighteenth postexposure day. By the fifth exposure day, body weights dropped 30 percent, urine glucose, protein, and ketones were abnormal, and succinic-dehydrogenase activity dropped to near zero in the kidney and had more than doubled in the lung; by the eighteenth post exposure day, these values had returned to normal. The authors conclude that carbonyl fluoride generated during the pyrolysis of PTFE hydrolyzes in body fluids and produces fluoride toxicity. The cumulative effect of repeated exposures is much more toxic than a single equivalent exposure. If death does not result, the metabolic inhibition due to fluoride poisoning is completely reversible.
Ref: Biochemical Changes Associated with Toxic Exposures to Polytetrafluoroethylene Pyrolysis Products by Scheel LD, McMillan L, Phipps FC. American Industrial Hygiene Association Journal, Vol. 29, No. 1, pages 49-53, 1968.

Abstract: 1990 NTIS Report: Perfluoroisobutylene (PFIB) is an extremely toxic organofluoride that can be produced during pyrolysis of tetrafluoroethylene polymers, including Teflon. Inhalation of PFIB at very low concentrations causes acute lung injury, the hallmark of which is pulmonary edema. Several lines of evidence have suggested that hydrolysis of PFIB and resulting production of hydrofluoric acid may be responsible for pulmonary damage. In order to investigate the potential involvement of hydrofluoric acid in producing lung injury and its relationship to the mechanism of fluorocarbon toxicity, we have compared the pulmonary injury produced by PFIB, by dissociated (H(sup +) and F(sup (minus))), and by undissociated (HF) hydrofluoric acid in the deep lung. By delivering hydrofluoric acid by intratracheal instillation in neutral buffer, we demonstrate that F(sup (minus)) produces no significant pulmonary injury as assessed by increased in lung weight and ultrastructural changes. Similarly, instillation of aci [abstract truncated]
Ref: 1990. Preliminary observations of lung injury produced by instillation of HF in acidic and neutral buffer. Brainard JR, Kinkead SA, Kober EM, Sebring RJ, Stavert DM. Los Alamos National Lab., NM. Supporting Agency: Department of Energy, Washington, DC. Report No. NTIS/DE91009941.

Abstract: The pathologic effects of exposure to combustion products of polytetrafluoroethylene (9002-84-0) (PTFE) were studied in rats. Fischer-344-rats received single 30 minute exposures to concentrations from 0.005 to 5.025 milligrams per liter aerosol products of PTFE heated to 595 degrees-C. The median lethal concentration (LC50) was determined. Necropsies were performed at 0, 2, 12, 24, and 36 hours post exposure or between 2 and 17 days. The LC50 for thermal degradation products of PTFE was 0.045 milligrams per liter. Conjunctival erythema and serous occular and nasal discharge were seen in survivors immediately after exposure. Lesions were found in lungs of 84 percent of exposed rats. Focal hemorrhages, edema, and fibrin deposition in the lungs were found. Focal interstitial thickenings developed and increased. Alveolar macrophages became more severe up to 96 hours. Thrombosis or embolism of pulmonary capillaries and veins were found in 38 percent of exposed rats. The degree of pathologic change increased as the dose increased up to the LC50, but fluctuated above that. Disseminated intravascular coagulation occurred in 53 percent of exposed rats and was positively related to the amount of lung damage. Renal infarcts due to disseminated intravascular coagulation were found but no other kidney lesions were seen. The authors conclude that disseminated intravascular coagulation appears to be a consequence of exposure to PTFE combustion products.
Ref: Pathologic Findings In Rats Following Inhalation Of Combustion Products Of Polytetrafluoroethylene (PTFE) by Zook BC, Malek DE, Kenney RA. Toxicology, Vol. 26, No. 1, pages 25-36, 1983.

Abstract: An ultrastructural study was performed on the respiratory system of budgerigars (including 6 controls) which were acutely affected by inhalation of toxic fumes from heated polytetrafluoroethylene (PTFE pyrolysis products) or had survived for 24 h after a sublethal exposure. The controls were exposed to fumes from heated plain Al (not coated with PTFE). The microanatomy of lungs of the controls was described and compared with that of lungs of birds exposed to PTFE pyrolysates. The PTFE pyrolysates caused extensive, severe necrotizing and hemorrhagic pneumonitis. These lesions were associated with amorphous elongate conglomerates of particles which were similar to those isolated on membrane filters from fumes generated from heated PTFE. This supported the hypothesis that the toxic principle in PTFE pyrolysates was related to generated particulates.
Ref: Acute toxicosis of budgerigars (Melopsittacus undulatus) caused by pyrolysis products from heated polytetrafluoroethylene: Microscopic study by WELLS RE, SLOCOMBE RF. Astract: AM J VET RES; 43 (7). 1982. 1243-1248.

Abstract: An incident where five cockatiels (Nymphicus hollandicus) died within 30 minutes following exposure from a frying pan coated with the plastic polytetrafluoroethylene (900-284-0) (PTFE) that had accidentally overheated is reported. Within an hour the owner developed symptoms of polymer fume fever but recovered within 24 hours. A PTFE coated milk pan boiled dry for 15 minutes with the cockatiels in a cage in the next room. The birds were examined by a veterinary surgeon and were found to be normal except for the lungs, which were severely congested and edematous and were considered to be the cause of death. It is concluded that parakeets are unusually susceptable to the pyrolyses products of frying pans coated with plastic polytetrafluoroethylene.
Ref. Case of Polytetrafluoroethylene Poisoning in Cockatiels Accompanied by Polymer Fume Fever in the Owner by Blandford TB, Hughes R, Seamon PJ, Pattison M, Wilderspin MP. Veterinary Record, Vol. 96, pages 175-176, 6 references, 1975.

Abstract: A case of marked progression of chronic obstructive pulmonary disease after several episodes of occupational inhalation fever in a carding machine operator was reported. The patient was a 45 year old male with a history of exertional dyspnea who experienced recurrent episodes of flu like symptoms beginning 2 weeks after starting work at a synthetic textile plant. After approximately 9 months on the job the patient was hospitalized with fever, chills, chest pain, productive cough, and malaise that had not responded to antibiotic treatment. A decreased white cell count was seen along with evidence of moderately severe obstructive disease. The patient returned to work after the acute symptoms resolved; however, he experienced dyspnea with mild exertion at this time. The flu like illnesses continued to recur over the next 18 months at which time the patient stopped working on the advice of his physician. He was hospitalized 1 month later with chest pain and diaphoresis. Severe obstruction with a significant bronchodilator response was seen and he was placed on disability leave. Polymer fume fever due to exposure to polytetrafluoroethylene (9002-84-0) was suspected as the cause of his illness. A subsequent examination of the patient's workplace demonstrated that major renovations had been done since his departure to improve chemical contamination and air quality; however, potential for significant exposures to formaldehyde (50000) were still evident. The authors conclude that polymer fume fever may not always be a benign, self limiting disease and may result in permanent airways damage. Long term follow up is recommended.
Ref: Progression of Chronic Obstructive Pulmonary Disease after Multiple Episodes of an Occupational Inhalation Fever by Kales SN, Christiani DC. Journal of Occupational Medicine, Vol. 36, No. 1, Grant No. T15-OH-07096, pages 75-78, 10 references, 1994.

Abstract: Background: Certain fluorocarbon polymers can produce a clinical syndrome called polymer fume fever when the products of pyrolysis are inhaled. Summary: A previously healthy 21-year-old white man presented with severe chest tightness, difficulty in breathing, pyrexia, nausea, vomiting, and a dry irritating cough. These symptoms occurred suddenly while smoking a cigarette 2 hours after leaving his place of work, where he is a plastics machinist. A chest roentgenogram revealed a bilateral patchy alveolar air space filling pattern involving the mid and lower lung fields. The diagnosis of polymer fume fever was established on the basis of the symptom complex, the association with cigarette smoking, and the occupational exposure to micronized polytetrafluoroethylene. Conclusions: A thorough occupational and smoking history is necessary to recognize polymer fume disease, which may resemble influenza.
Ref: Acute noncardiogenic pulmonary edema due to polymer fume fever. by SILVER MJ, YOUNG DK. CLEVELAND CLINIC JOURNAL OF MEDICINE; 60 (6). 1993. 479-482.

Abstract: Polymer fume fever and other syndromes related to the inhalation of fluoropolymer pyrolysis products were discussed in this review. Polymer fume fever has primarily been seen following the inhalation of thermal decomposition products of materials such as polytetrafluoroethylene (9002-84-0) (PTFE), fluorinated ethylene-propylene (61789002), and perfluoroalkoxyethylene resins. The disease has been identified in plastics, chemical, electronics, textile manufacturing, rubber stamp shop, print shop, and aircraft repair shop workers as well as in several isolated occupational and residential incidents. The pyrolysis and combustion chemistry of PTFE and other fluoropolymers was discussed. Animal studies on fluoropolymer inhalation toxicology and pathology have demonstrated pulmonary hemorrhage, edema, focal emphysema, and interstitial fibrosis and the toxicity varied with the temperature of pyrolysis, the test animal, length of study, and the presence or absence of particles. Early clinical features in humans have included flu like symptoms, chest discomfort, leukocytosis with a left shift, an elevated erythrocyte sedimentation rate, and inconsistent pulmonary function alterations. The disease has generally tended to be acute and self limiting however late sequelae such as pulmonary infiltrates and persistent ventilatory impairment have been documented. A crude dose response relationship for cases with severe pulmonary damage has been suggested. The use of urinary fluoride levels for biological monitoring of fluoride exposure was discussed. Exposure standards established by the OSHA were presented.
Ref: Polymer Fume Fever and Other Fluorocarbon Pyrolysis-Related Syndromes. by Shusterman DJ. Occupational Medicine: State of the Art Reviews, Vol. 8, No. 3, pages 519-531, 66 references, 1993.

Abstract: Perfluoroisobutene (PFIB) is produced by the pyrolysis, and as a by-product during the manufacture, of polytetrafluoroethylene. When inhaled it produces a fulminating and sometimes fatal pulmonary oedema similar to that of phosgene after a latent peroid of 6-8 h. As part of a study to determine the retained dose and the factors that control the amount retained, this study has investigated the retention in rats of inhaled PFIB at concentrations of 10, 50 and 250 mugl/-1 in a flow-through system combining head-only exposure and plethysmography. Uptake of PFIB was measured by gas chromatography during elevated and reduced inspired volume and respiratory rate induced by exposure to increased CO2 and injection of pentobartione, respectively. The percentage of PFIB retained in the upper airways and lungs was found to be 27.5, 28.1 and 23.7% of the amount inspired at the three concentrations tested. The rate of uptake (nmol min-1 kg-1) of PFIB was a power law of the amount inha [astract truncated]
Ref: Retention of inhaled perfluoroisobutene in the rat. by MAIDMENT MP, UPSHALL DG. J APPL TOXICOL; 12 (6). 1992. 393-400.

Abstract: Fluoropolymers, especially polytetrafluoroethylene (PTFE), have good fire-resistance properties, but their application is limited by concerns over the toxicity of their thermal decomposition products. In experiments using a tube furnace system similar to the DIN 53 436 method, the 30-minute (+ 14 days observation) LC50 im mass loss terms was found to be 2.9 mg l-1 (Standard Error 0.04) under non-flaming conditions, approximately ten times as toxic as wood and most other materials. Toxicity was due to upper respiratory tract and airway irritation, and was consistent with the known effects of carbonyl fluoride and hydrogen fluoride. When decomposed in the NBS cup furnace test under non-flaming conditions, PTFE evolved extreme-toxicity products with an LC50 of approximately 0.05 mg l-1 (mass loss), approximately 1000 times as toxic as wood and most other materials. Toxicity was due to deep lung irritation and oedema. Investigations of the range of conditions under which the [abstract truncated]
Ref: Recent developments in understanding the toxicity of PTFE thermal decomposition products. by PURSER DA. FIRE MATER; 16 (2). 1992. 67-75.

Abstract: The toxic effects of thermal degradation products of polytetrafluoroethylene (9002-84-0) (PTFE) and tetrafluoroethylene (116-14-3) / hexafluoropropylene (116-15-4) copolymer (FEP) were studied in rats. Twenty two male Crl:CD-BR-rats were exposed to FEP pyrolysis products in a National Bureau of Standards (NBS) exposure chamber for 30 minutes; 4 rats were killed 1 to 4 hours after for microscopic examination of lung and nasal sections and the remaining 18 were observed for 24 hours post exposure. Four rats exposed to air only were used as controls. Further experimentation involved exposure of 14 rats to PTFE pyrolysis products in a low temperature decomposition exposure system for 4 hours; again, some rats were killed 1 to 4 hours thereafter for microscopic evaluations and the remaining rats were observed for 24 hours. Determinations were made regarding the presence of gaseous hydrogen fluoride and particle size. An intratracheal instillation experiment was also conducted in which rats were exposed to 0.05 milligrams aged PTFE particulate agglomerates and their lungs were examined microscopically. In the NBS chamber, the approximate lethal concentration (ALC) of particulate generated was 0.3mg/m3 of FEP pyrolysis products; in the second chamber, the ALC of fume evolved from PTFE was 0.1mg/m3. Fresh particles, 0.02 to 0.15 micrometers, were thought to be the toxic agents. In the inhalation studies, exposed rats died from pulmonary congestion and edema but only minimal respiratory epithelial damage was seen in the nasal cavity or airways. Pulmonary lesions were characterized by alveolar and interstitial edema and intraalveolar hemorrhage due to damaged Type-I pneumocytes and were associated with alveolar capillary neutrophilia. The authors recommended investigation of the mode of action of PTFE particulates on Type-I pneumocytes.
Ref: Pulmonary Response of Rats Exposed to Polytetrafluoroethylene and Tetrafluoroethylene Hexafluoropropylene Copolymer Fume and Isolated Particles. by Lee KP, Seidel WC. Inhalation Toxicology, Vol. 3, No. 3, pages 237-264, 53 references, 1991.


Abstract: The effects of flame retarded plastics on toxicity were investigated in male albino Sprague-Dawley-rats. The substances used in the investigation were: polytetrafluoroethylene (9002-84-0) (PTFE), a copolymer of vinylidene fluoride and hexafluoropropene (116-15-4) (VF), a copolymer of VF/HFP with unidentified additives, and a polymer of VF/HFP and tetrafluoroethylene (116-14-3). The fluoropolymer samples consisted of 16 millimeter (mm) plugs with a 6mm hole in the middle, shaved until the desired weight was obtained. When ambient system pressure was reached, animals were dropped in an exposure chamber. Exposures were conducted for 30 minutes and the rats were removed for observation. Animals were necropsied for examination. Supplemental pyrolysis exposures were conducted at the calculated maximum sublethal dose of each fluoropolymer. The three VF/HFP substances were similar in that complete degradation took place at 525 to 550 degrees-C. The comparable temperature required for PTFE was 625 degrees. Rats exposed to lethal doses of the pyrolysates showed lesions with initial capillary damage leading to pulmonary edema, cell hypertrophy, and desquamation. After 1 week post exposure, lungs returned to normal. Exposures to doses of the pyrolysates at sublethal values were similar but differed in that the degree of damage was more restricted. The authors conclude that the three hydrogen containing elastomers produced a less toxic pyrolysate than PTFE. Identification of the compounds responsible for the pulmonary damage is presently being carried out.
Ref: Toxicity Associated With Flame-Retarded Plastics . by Carter VL Jr. Bafus DA, Warrington HP, Harris ES. Physiological and Toxicological Aspects of Combustion Products: International Symposium, National Academy of Sciences, Washington, D.C., pages 96-104, 4 references, 1976.

Abstract: The relative toxicities of thermal degradation products from four fluoropolymers were determined in rats. The polymers were polytetrafluoroethylene (9002-84-0) (PTFE), copolymers of vinylidene fluoride (75387) and hexafluoropropene (116-15-4) with and without additives (VF2-A and VF2/HFP), and the terpolymers of PTFE, VF2, and HFP (VF2/HFP/TFE). Male Sprague-Dawley-rats were exposed for 30 minutes to the pyrolysis products of VF2/HFP, VF2/HFP-A, and VF2/HFP/TFE at 550 and 800 degrees-C, and to the pyrolysis products of PTFE at 625 and 800 degrees-C. Survivors were killed at 1, 2, 4, 8, 16, and 32 days postexposure and examined for pathological changes in organs and tissues. Hydrolyzable fluoride concentrations were determined for pyrolysis products of all polymers at both temperatures. At 550 degrees-C, the median lethal dose ranged from 1.06 grams (g) VF2/HFP-A to 2.36g VF2/HFP. The median lethal dose of PTFE at 625 degrees-C was 0.5g. At 800 degrees-C, the median lethal dose ranged from 0.38g PTFE (for a 5 minute exposure) to 0.59g VF2/HFP (for a 30 minute exposure). Initial pathological response to pyrolysates included capillary damage leading to pulmonary edema, and alveolar hypertrophy and desquamation. For survivors, edema was resolved and a proliferative phase began after 48 hours. Lungs returned to normal after 1 week. No other organ system was involved. No relationship was found between hydrolyzable fluoride concentrations of pyrolysates and toxicities. The authors conclude that the pyrolysis products of PTFE are more toxic than those of polymers containing VF2 and HFP.
Ref: The Acute Inhalation Toxicity in Rats from the Pyrolysis Products of Four Fluoropolymers. by Carter VL Jr, Bafus DA, Warrington HP, Harris ES. Toxicology and Applied Pharmacology, Vol. 30, No. 3, pages 369-376, 9 references, 1974.

Abstract: Studies by the du Pont Company investigating the toxicity of pyrolysis products of two tetrafluoroethylene (TFE) resins, Teflon-1 and Teflon-6 (9002-84-0) are reviewed. TFE resins are physiologically inert, but when subjected to temperatures of 300 degrees-C and above, toxic effects in rats are observed. In addition to causing death of experimental animals, toxic symptoms include pulmonary congestion and edema, bronchitis, bronchopneumonia, chronic pneumonia, and emphysema. As temperature increases above 300 degrees-C, the rate of thermal decomposition increases and the pyrolysis products change. Small quantities of carbon dioxide and fluorides that do not appear to be important toxicologically are evolved when TFE resins are exposed to temperatures from 300 to 350 degrees-C. However, a fine particulate material evolving during pyrolysis is toxic to rats. The observed toxicity of pyrolysis products heated to 380 degrees-C and above may be due chiefly to octafluoroisobutylene [also known as Perfluoroisobutylene] (382-21-8). The relative toxicity of pyrolysis products of Teflon-1 and Teflon-6 corresponds to the amount of matter evolved. Filtration of the pyrolysis stream significantly reduces the toxicity of the products evolved at temperatures of 325 and 350 degrees-C. New manufacturing techniques for TFE resins have resulted in products with improved thermal stability and corresponding lower toxicity of pyrolysis products. The authors conclude that experimental work is still needed to allow exact characterization of the toxic pyrolysis products of TFE resins.
Ref: The Toxicity of the Pyrolysis Products of "Teflon" TFE-Fluorocarbon Resins. Clayton JW Jr, Hood DB, Raynsford GE. Haskell Laboratory for Toxicology and Industrial Medicine, E. I. du Pont de Nemours and Co., Inc., Wilmington, Delaware, Presented at the American Industrial Hygiene Association Annual Meeting, 9 pages, 1959.

Abstract: Teflon (9002-84-0) vapor toxicity under various thermal conditions is reviewed. It is noted that under normal usage conditions Teflon is among the most inert, nontoxic, and nonflammable substances tested. The primary uses of Teflon are described. Its nontoxic nature has been proven by animals tests. At 200 degrees-C or higher Teflon decomposes to release toxic fumes which cause polymer fume fever in humans. The incidence of this reaction among Teflon workers is discussed and the symptoms described. It is noted that the effects last for 1 to 2 hours but rarely longer, and recovery is complete within 24 to 36 hours. The rate of decomposition of Teflon resins at various temperatures ranging from 200 to 500 degrees is described and the products of pyrolysis at these temperatures are specified. The major component of pyrolysis at 400 degrees is the monomer tetrafluoroethylene (116-14-3) a relatively innocuous gas which comprises at least 95 to 97 percent of the gaseous output and hexafluoropropylene (116-15-4) (2 to 3 percent). Trace amounts of hydrogen fluoride (7664393) have also been detected especially in the presence of moisture during Teflon pyrolysis, as well as perfluoroisobutylene (382-21-8). The toxicity of the latter two compounds in animals is discussed. The toxic response in animals is reviewed in terms of human maximal allowable concentrations. Other features of the pyrolytic decomposition of Teflon such as weight loss at various temperatures is tabulated. Control measures for storage of Teflon and other fluorocarbon plastics, fabrication, installation and maintenance of components utilizing Teflon and disposal of scrap Teflon are discussed as well as personal hygiene, ventilation during heating of Teflon, use of emergency personal protective equipment, and maintenance of adequate medical records. Ref: Environmental And Occupational Health Information Letter Number 13A. Toxicity Of Products Of Thermal Decomposition Of Teflon. Anonymous. Office of the Surgeon, Air Material Command, Wright-Patterson Air Force Base, Ohio, 7 pages, 9 references, 1958.

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