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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:
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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