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

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Index
Lung
Polymer Fume Fever
Thermal Decomposition Products
Abstracts
NTIS Reports

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.

Structure:

Due to length these adverse effects are presented separately:

Lung

Polymer Fume Fever

Thermal Decomposition Products

Effects below are:
Birds
Blood
Body Weight Decrease
Brain
Chemical Weapons
Cholinesterase activity
Liver
Urinary fluoride level


Birds

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: The intoxication and toxicity in small pet birds after exposure to accidentally overheated cooking pans coated with polytetrafluoroethylene (9002840) (PTFE) coating is reported. In analogy to the accidental death of pet birds exposed to the gaseous pyrolysis products of pans coated with PTFE, the disease pattern was reproduced experimentally be heating dry PTFE lined pans to temperatures slightly above 500 degrees C. In contrast to guinea-pigs and mice which remained healthy after 90 minute sealed chamber exposures, the parakeets died from the toxic volatile products after 20 to 30 minutes, showing signs of acute pulmonary edema. The cause of death was determined to be acute myodegeneration cordis and acute nuclear liver dystrophy. There was found to be a distinct relationship between bodyweight and the time to onset of death in regards to the sensitivity among the birds. It is concluded that the tolerance discrepancy between birds and small mammals can be attributed to the fact that the birds' air sacks provide a much enlarged resorption surface of the respiratory tract. (German: English translation available)
Ref: Intoxications with Lethal Outcomes in Small Pet Birds after Accidental Overheating of Cooking Pans Coated with Polytetrafluoroethylene Coating. by Ehrsam H. Schweizer Archiv fuer Tierheilkunde, Vol. 111, pages 181-186, 3 references, 1969.

PTFE toxicity in birds by Woodhall S, Stamford M. Letter. Vet Rec. 2004 Dec 11;155(24):784.

Suspected PTFE toxicity in wild birds. Pennycott TW, Middleton JD. Letter. Vet Rec. 1997 Sep 6;141(10):255.

PTFE toxicity in birds. Forbes NA, Jones D. Letter. Vet Rec. 1997 Jul 26;141(4):107.

RISKS TO PET BIRDS FROM EXPOSURE TO PYROLYSIS PRODUCTS OF PTFE-COATED PANS AND COOKING OILS. LUMEIJ JT. TIJDSCHRIFT VOOR DIERGENEESKUNDE; 122 (24). 1997. 720.

Exposure of Japanese quail and parakeets to the pyrolysis products of fry pans coated with Teflon and common cooking oils. Griffith FD, Stephens SS, Tayfun FO. Am Ind Hyg Assoc J. 1973 Apr;34(4):176-8.

Blood (click on for all fluorinated pesticides)

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.

Definition of hypoxemia: low blood oxygen: inadequate oxygen in the blood

Abstract. Workers at a polytetrafluoroethylene (9002-84-0) (PTFE) plastic production plant were investigated to ascertain whether chronic exposure to this chemical was correlated with changes in biochemical indicators of toxicity. The exposed group comprised 129 workers (47 male and 82 female), of mean age 33.5 years (yr) and mean exposure period 8 months. A group removed from exposure was comprised of 32 workers (mean age 32.1yr) who had been exposed for a mean duration of 2.2yr, but had left the workplace and had been unexposed for more than 1yr (mean duration 1.8yr). A control group of 74 subjects had been employed in nonproduction work at the factory for more than 1yr and had never been exposed to the chemical. Urine and blood samples were collected at the start of the workday. Inorganic fluorides in urine were detected using an ion selective electrode method, and blood cholinesterase (ChE) levels were determined by colorimetry, using acetylthiocholine-iodide as substrate. Results showed that the urinary inorganic fluorides in the exposed group were significantly higher than in the controls. The group removed from exposure was not tested. ChE activities of whole blood, erythrocytes and plasma in the exposed group were higher than those of the group removed from exposure group, and both were significantly higher than those of the control group (23.2%, 17.5%, and 33.7% above control levels, respectively, in the exposed group and 11.2%, 11.2% and 8.7% above control levels, respectively, in the formerly exposed group). ChE activities in males of the exposed group were much higher than in females; whole blood, erythrocyte and plasma activities were enhanced by 22%, 22.5%, and 47.9%, respectively, in males, as opposed to 21.1%, 17.5% and 35.2%, respectively, in females. The authors conclude that exposure to organic fluorides during PTFE production results in a reversible increase in ChE activity in whole blood, erythrocytes, and plasma, which may indicate a protective response in the exposed worker. An increase in urinary inorganic fluoride may be used as an indicator of exposure.
Ref: ELEVATED CHOLINESTERASE ACTIVITY AND INCREASED URINARY EXCRETION OF INORGANIC FLUORIDES IN THE WORKERS PRODUCING FLUORINE-CONTAINING PLASTIC POLYTETRAFLUOROETHYLENE by XU B, ZHANG J, MAO G, YANG G, CHEN A, AOYAMA K, MATSUSHITA T, UEDA A. BULL ENVIRON CONTAM TOXICOL; 49 (1). 1992. 44-50.

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.

Body Weight Decrease (click on for all fluorinated pesticides)

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.

Brain (click on for all fluorinated pesticides)

Note: tetrafluoroethylene is a major thermal breakdown product of Teflon.

Abstract: The toxic properties of the tetrafluoroethylene (9002-84-0) monomer and of products of the thermal treatment of the tetrafluoroethylene polymer in acute experiments on cats, rabbits, albino rats and albino mice are reported. In rats and rabbits the inhalation of monomer induced hyperemia of organs, especially the brain, hemorrhage in the spleen and lungs, and dystrophic changes in the kidneys. Emphysema and atelectasis was observed in the lungs, desquamation of the epithelium in the bronchi also was observed. The threshold mortality for the monomer was 2.5 volume percent for albino rats and 4.0 volume percent for rabbits. The pyrolytic decomposition of tetrafluoroethylene polymer was lethal to cats, rabbits, mice, and rats. Death was caused by acute pulmonary edema, sometimes accompanied by pneumonia. Renal dystrophy was observed in the cats. There was acute irritation of the upper respiratory tract mucosa in all test animals. It is concluded that the pathology observed upon inhalation of the products of thermal decomposition of the polymer is apparently explained by the presence in the pyrolyses gas of difluorophosgene, perfluoroisobutylene (382-21-8), and other highly toxic hydrocarbons. (Russian: English translation available)
Ref: Toxicity of Tetrafluoroethylene by Zhemerdi A. Trudy Leningradskogo Sanitarno-gigienicheskogo Meditsinskogo Instituta, Vol. 44, pages 164-176, 1958. Document Number: NIOSH/00080478.

Chemical Weapons (click on for all fluorinated 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]. The aim of the inclusion of chemicals, such as PFIB was to cover those chemicals, which would pose a high risk to the CWC. Subsequently PFIB, specifically, was included in the final text of the CWC.
[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.
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.
http://www.asanltr.com/ASANews-98/pfib.html

Cholinesterase activity

Abstract. Workers at a polytetrafluoroethylene (9002-84-0) (PTFE) plastic production plant were investigated to ascertain whether chronic exposure to this chemical was correlated with changes in biochemical indicators of toxicity. The exposed group comprised 129 workers (47 male and 82 female), of mean age 33.5 years (yr) and mean exposure period 8 months. A group removed from exposure was comprised of 32 workers (mean age 32.1yr) who had been exposed for a mean duration of 2.2yr, but had left the workplace and had been unexposed for more than 1yr (mean duration 1.8yr). A control group of 74 subjects had been employed in nonproduction work at the factory for more than 1yr and had never been exposed to the chemical. Urine and blood samples were collected at the start of the workday. Inorganic fluorides in urine were detected using an ion selective electrode method, and blood cholinesterase (ChE) levels were determined by colorimetry, using acetylthiocholine-iodide as substrate. Results showed that the urinary inorganic fluorides in the exposed group were significantly higher than in the controls. The group removed from exposure was not tested. ChE activities of whole blood, erythrocytes and plasma in the exposed group were higher than those of the group removed from exposure group, and both were significantly higher than those of the control group (23.2%, 17.5%, and 33.7% above control levels, respectively, in the exposed group and 11.2%, 11.2% and 8.7% above control levels, respectively, in the formerly exposed group). ChE activities in males of the exposed group were much higher than in females; whole blood, erythrocyte and plasma activities were enhanced by 22%, 22.5%, and 47.9%, respectively, in males, as opposed to 21.1%, 17.5% and 35.2%, respectively, in females. The authors conclude that exposure to organic fluorides during PTFE production results in a reversible increase in ChE activity in whole blood, erythrocytes, and plasma, which may indicate a protective response in the exposed worker. An increase in urinary inorganic fluoride may be used as an indicator of exposure.
Ref: ELEVATED CHOLINESTERASE ACTIVITY AND INCREASED URINARY EXCRETION OF INORGANIC FLUORIDES IN THE WORKERS PRODUCING FLUORINE-CONTAINING PLASTIC POLYTETRAFLUOROETHYLENE by XU B, ZHANG J, MAO G, YANG G, CHEN A, AOYAMA K, MATSUSHITA T, UEDA A. BULL ENVIRON CONTAM TOXICOL; 49 (1). 1992. 44-50.

Liver (click on for all fluorinated pesticides)

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.

Urinary fluoride level

Abstract: Urinary fluoride levels were investigated as an index of polytetrafluoroethylene (PTFE) exposure, since carbonyl fluoride, a pyrolysis product of PTFE, is metabolized and excreted as inorganic fluoride ion. Spot urine samples and occupational histories relating to polyment fume fever were obtained from 77 workers at a small PTFE fabricating plant. Environmental air samples for PTFE were taken. Air levels of PTFE ranging from 0-5.48 mg/m-3 were found. All urine values fell below the level at which systemic effects are reported to occur. Analysis of variance demonstrated that the mean urinary fluoride level among workers who had 1 or more years of exposure to PFTE who also had experienced 1 or more reported episodes of polymer fume fever was significantly higher (P< 0.01) than that among employees with less than 1 yr or more of exposure and no history of polymer fume fever. Additional exposure beyond 1 yr and additional polymer fume fever episodes did not result in the further elevation of urine fluoride levels.
Ref: Urinary fluoride levels in polytetrafluoroethylene fabricators; POLAKOFF PL, BUSCH KA , OKAWA MT. AM IND HYG ASSOC J; 35 (2). 1974 99-106.

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. Workers at a polytetrafluoroethylene (9002-84-0) (PTFE) plastic production plant were investigated to ascertain whether chronic exposure to this chemical was correlated with changes in biochemical indicators of toxicity. The exposed group comprised 129 workers (47 male and 82 female), of mean age 33.5 years (yr) and mean exposure period 8 months. A group removed from exposure was comprised of 32 workers (mean age 32.1yr) who had been exposed for a mean duration of 2.2yr, but had left the workplace and had been unexposed for more than 1yr (mean duration 1.8yr). A control group of 74 subjects had been employed in nonproduction work at the factory for more than 1yr and had never been exposed to the chemical. Urine and blood samples were collected at the start of the workday. Inorganic fluorides in urine were detected using an ion selective electrode method, and blood cholinesterase (ChE) levels were determined by colorimetry, using acetylthiocholine-iodide as substrate. Results showed that the urinary inorganic fluorides in the exposed group were significantly higher than in the controls. The group removed from exposure was not tested. ChE activities of whole blood, erythrocytes and plasma in the exposed group were higher than those of the group removed from exposure group, and both were significantly higher than those of the control group (23.2%, 17.5%, and 33.7% above control levels, respectively, in the exposed group and 11.2%, 11.2% and 8.7% above control levels, respectively, in the formerly exposed group). ChE activities in males of the exposed group were much higher than in females; whole blood, erythrocyte and plasma activities were enhanced by 22%, 22.5%, and 47.9%, respectively, in males, as opposed to 21.1%, 17.5% and 35.2%, respectively, in females. The authors conclude that exposure to organic fluorides during PTFE production results in a reversible increase in ChE activity in whole blood, erythrocytes, and plasma, which may indicate a protective response in the exposed worker. An increase in urinary inorganic fluoride may be used as an indicator of exposure.
Ref: ELEVATED CHOLINESTERASE ACTIVITY AND INCREASED URINARY EXCRETION OF INORGANIC FLUORIDES IN THE WORKERS PRODUCING FLUORINE-CONTAINING PLASTIC POLYTETRAFLUOROETHYLENE by XU B, ZHANG J, MAO G, YANG G, CHEN A, AOYAMA K, MATSUSHITA T, UEDA A. BULL ENVIRON CONTAM TOXICOL; 49 (1). 1992. 44-50.

 
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