# CRITERIA DOCUMENT: RECOMMENDATIONS FOR AN OCCUPATIONAL EXPOSURE STANDARD FOR THE DECOMPOSITION PRODUCTS OF FLUOROCARBON POLYMERS
recommends that exposure to the decomposition products of fluorocarbon polymers in the workplace be controlled by adherence to the following sections. The standard is designed to protect the health and provide for the safety of employees for up to a 10-hour work shift, 40-hour workweek, over a working lifetime. The recommended standard for the decomposition products of fluorocarbon polymers emphasizes good work practices and engineering controls and medical management. Since no measurable environmental level of any single decomposition product of fluorocarbon polymers can ensure complete protection of worker health, no occupational exposure limit is recommended in this document. The criteria and standard will be subject to review and revision as necessary.
Fluorocarbon polymers include polymers of substituted polyethylene monomers of the general formula (XCX-XCF)n, where X can be F, H, Cl, CF3, or CF3-CF2-CF2-0. The decomposition products of fluorocarbon polymers are defined as substances which are thermally generated from fluorocarbon polymers.
The greatest danger to workers exposed to the decomposition products of fluorocarbon polymers is from inhalation. Adverse effects could result from exposure to dusts of undecomposed fluorocarbon polymers, from exposure to the decomposition products, or from exposure to a single or several 1 decomposition products. The major concern in occupational exposure to the decomposition products of fluorocarbon polymers is their potential for causing polymer fume fever and damage to the respiratory tract. Polymer fume fever is characterized by headache, aching joints, general malaise, cough, shivering, chills, fever, tachycardia, and possible chest discomfort. The temperature may rise as high as 39.6 C (103.3 F ) .
Adherence to all provisions of the recommended standard is required in work areas in which fluorocarbon polymers are used, regardless of the concentration of airborne decomposition products of fluorocarbon polymers.
Occupational exposure is defined as any exposure to fluorocarbon polymers that may involve the production of decomposition products.
The products liberated from fluorocarbon polymers by the application of heat vary with the polymer, the temperature to which it is exposed, and the humidity of the ambient air. Because there is insufficient information on which to establish a safe workplace environmental concentration, none is recommended.
Both employers and employees should take all steps possible to keep occupational exposure to the decomposition products of fluorocarbon polymers as near to zero as possible. Careful adherence to all sections of this recommended standard will facilitate accomplishment of this aim. Controls which may be appropriate include isolation of a process within a controlled ventilation area, installation of safeguards to prevent thermal excursions, and installation of redundant temperature monitoring systems and associated alarms.
(a) Coveralls, or equivalent clothing, and gloves should be worn by the employee in areas where bulk fluorocarbon polymer dust is handled or where contact of powdered polymer with the skin is likely.

# (b)
Respiratory protective equipment to be used, if necessary, during emergencies or during the performance of nonroutine maintenance or repair activities in which exposure to the decomposition products of fluorocarbon polymers is likely should be provided in accordance with Table 1-1. Applicable regulations for the use of respirators are found in 29 CFR 1910.134.

# (c)
When a respirator is required by paragraph (b) of this section, it shall be selected and used in accordance with Administration (previously by the Bureau of Mines) as specified under the provisions of 30 CFR 11. The employer shall ensure that respirators are adequately cleaned and maintained, and that employees are instructed in the proper use and testing for leakage of respirators assigned to them.
Respirators shall be easily accessible, and employees shall be informed of their locations. (1) Half-mask respirator equipped with combination acid-gas/organic-vapor sorbent and high-efficiency filter cartridge (2) Full-facepiece gas mask equipped with acidgas/organic-vapor sorbent and high-efficiency filter canister, changed every 4 hours Maintenance (Equipment breakdown or cleaning of distillation vessels, etc; no time limit) Type C supplied-air respirator operated in demand, pressure-demand, or continuous-flow mode and equipped with full facepiece, hood, helmet, or suit where there is occupational exposure to the decomposition products of fluorocarbon polymers. As a further precaution, the carrying of smoking materials into such areas shall be prohibited.
Employees shall be instructed to wash their hands before smoking.

# (b)
In sintering or molding operations where fluorocarbon polymer is heated above its melting point, temperatures in excess of the manufacturers' recommended range should be avoided whenever possible. To prevent overheating, ovens shall be fitted with an automatic temperature cutout set at the manufacturers' recommended temperature for the fluorocarbon polymer.
(c) If necessary to prevent accumulation or recirculation of the decomposition products of fluorocarbon polymers in the workplace, ovens shall be fitted with a local exhaust ventilation system. An appropriate alarm shall be incorporated into any exhaust system in case of its failure.
(d) Local exhaust ventilation, located as close as possible to the operation, shall be used whenever welding, cutting, or related hightemperature operations are performed.
(e) Exhaust systems and ductwork shall be kept in good repair so that design airflows and pressures are maintained. Airflow and pressure should be measured at least twice a year. Continuous airflow indicators (oil or water manometers) are recommended. A log shall be kept showing design airflow or pressure and the results of periodic inspection.
(f) Ventilation systems discharging to outside air must be designed to conform to applicable local, state, and federal air pollution regulations and must not constitute a hazard to employees or to the general population.
(g)
General Housekeeping
(1) Spills of fluorocarbon polymers shall be cleaned up, preferably by vacuuming. Care shall be taken that polymer dust is not blown onto steampipes or other heated equipment.
(2) Emphasis shall be placed on prompt and frequent cleanup of dust to prevent accumulation of fluorocarbon polymers.
(3) Equipment shall be maintained regularly, and necessary repairs shall be made promptly.
(4) Fluorocarbon polymer scrap and waste shall be collected in special containers and, if not reused, shall be disposed of by high temperature incineration or by burying. Where excessive contamination of clothing with fluorocarbon polymer dust is likely, employers shall provide employees with launderable clothing for repeated use or disposable outer garments for one-time use.
(e) Laundry personnel should be informed of the hazards and of safe procedures if they are likely to encounter clothing contaminated with fluorocarbon polymers.

# II. INTRODUCTION
This report presents the criteria and the recommended standard that were prepared to meet the need for preventing occupational disease or injury arising from exposure to the decomposition products of fluorocarbon polymers.
The criteria document fulfills the responsibility of the

# III. BIOLOGIC EFFECTS OF EXPOSURE

# Extent of Exposure
Fluorocarbon polymers are made from substituted polyethylene monomers of the general formula (XCF-XCF)n, where X can be H, F, Cl, CF3, or CF3-CF2-CF2-0 , Copolymers, made from two monomers with as little as 10% of the comonomer, and terpolymers, made from three monomers, are additional forms of fluorocarbon polymers . Fluorocarbon telomers are fluorocarbon polymers of low-molecular-weight produced by chemical reactions that limit the degree of polymerization .
Some important commercial fluorocarbon polymers are listed, along with the monomers used in their preparation, in Table III-l .
The preparation of unsaturated fluorocarbon monomers from saturated fluorinated hydrocarbons is normally carried out in closed systems. These processes present a potential hazard because such toxic byproducts as perfluoroisobutylene (PFIB) may be formed . Fluorocarbon polymers are prepared from the monomers by conventional free-radical polymerization techniques, but the preparation of each polymer requires different formulation procedures involving a variety of redox catalyst systems ,  Because of its high viscosity at temperatures greater than its crystalline melting point (327 C), PTFE must be processed by techniques similar to those used for processing powdered metals or ceramics (eg, compression molding or ram extrusion) . The heat treatments necessary for processing fluorocarbon polymers may result in the generation of toxic decomposition products .
Total estimated production of fluorocarbon polymers in 1974 was approximately 27 million pounds, 67% of which was PTFE. Other fluorocarbon polymers, including fluorocarbon elastomers, accounted for the remaining 9 million pounds . NIOSH estimates that 5,000 workers are exposed to the decomposition products of fluorocarbon polymers.

# Identification of Decomposition Products
The decomposition products of fluorocarbon polymers depend not only on the chemical composition of the intact polymers but also on the conditions under which they are decomposed. The temperature to which the polymer is subjected, the atmosphere in which decomposition occurs, and the material of the vessel used can alter the kinds and quantities of the decomposition products formed.
The studies that discuss the identities of the products of pyrolysis of fluorocarbon polymers that have been found [A,  give the following general picture of the pyrolysis products: at temperatures that produce just softening or melting of the polymer, the monomer tends to be the principal pyrolysis product. This is true for PTFE up to a temperature of about 500 C. At the same time, however, perfluoropropene, other perfluoro compounds containing four or five carbon atoms, and a particulate, waxy fume are generated. For PTFE, the principal pyrolysis product within the range of temperatures from 500 to 800 C becomes carbonyl fluoride. This compound hydrolyzes readily to hydrogen fluoride and carbon dioxide, so that, in the presence of moist air, these may appear to be the principal pyrolysis products in this temperature range. At temperatures above 800 C, the principal pyrolysis products of PTFE are tetrafluoromethane, hydrofluoric acid, and carbon dioxide. If pyrolysis occurs in the presence of glass, silicon tetrafluoride may be formed by reaction between the silicon in the glass and hydrofluoric acid.
Pyrolysis of PTFE in a vacuum at 360-700 C has yielded almost 100% of its monomer, tetrafluoroethylene . Zapp et al  reported that a fine dust or sublimate was produced at temperatures above 200 C. Harris  reported the evolution of a mineral acid when PTFE was pyrolyzed at 140-325 C. Adams  found that hydrogen fluoride was released when PTFE was heated above 300 C. Waritz and Kwon  found that hydrolyzable fluoride was evolved from PTFE heated at 400 C and suggested that this was carbonyl fluoride or hydrogen fluoride. Zapp et al  reported that carbonyl fluoride was not detected by the method of analysis used when PTFE was decomposed at 300-550 C.
Other pyrolysis products of PTFE that have been identified include: octafluorocyclobutane (0FCB) at 300-360 C and at 500-550 C , perfluoroisobutylene (PFIB) at 380-400 C , at 475-480 C , and at 500-550 C , tetrafluoroethylene (TFE) at 450-480 C  and at 500-550 C , hexafluoropropylene (HFP) at 450-480 C  and at 500-550 C , hexafluoroethane (HFE) at 300-360 C , an unidentified five-carbon olefin at 500-550 C , and a higher-boiling residue consisting of a complex mixture of perfluoroolefins at 500-550 C .
Silicon tetrafluoride has been formed from the pyrolysis of PTFE at temperatures ranging from 300 to 650 C  and was probably produced by the reaction of hydrogen fluoride with silicon dioxide from the glass vessel. Table X-2 summarizes these results.
Several investigators  have indicated that particulate material or sublimate, with particle size ranging from 0.2 urn to .0.5 /um, was evolved when PTFE was decomposed. Some authors speculated that this particulate material contained absorbed hydrogen fluoride , acidic carboxyl groups , or oxygen difluoride . The short chain represents the primary particle. Difluorocarbene (DFC) would tend to form preferentially. Combination of two DFC moieties would form TFE, and one TFE could combine with one DFC moiety to form HFP.
Although theoretical, Errede*s hypothesis  does account for the formation of the pyrolysis products of PTFE that have been identified.
Further evidence of the multiplicity of the pyrolysis products was obtained by mass spectrometric analysis . Typical mass spectra of the products of PTFE pyrolysis in air  and of the particles so obtained were reported by Coleman et al  and are shown in Tables X-3 and X-4.
The decomposition products of other fluorocarbon polymers have not been so intensively studied as those of PTFE. Polychlorotrifluoroethylene (PCTFE) heated at 347-418 C in a vacuum yielded 27% of the monomer, chlorotrifluoroethylene . Birnbaum et al  found that pyrolysis of PCTFE in air at 375 C and at 400 C produced hydrolyzable fluoride, which they thought was carbonyl fluoride. No carbonyl chloride (phosgene) was found.
The authors speculated that fluorocarbonylchloride (C0FC1) and chlorodifluoroacetylchloride (CF2C1C0C1) had been evolved and presented evidence for the formation of a variety of fluorinated, chlorinated compounds with up to three carbon atoms.
The authors also found a particulate with a mean particle size of 0.5 /im.
When a copolymer of vinylidene fluoride (VF2) and hexafluoropropylene (HFP) and a terpolymer of VF2, HFP, and TFE decomposed at 550 C and 800 C, carbon monoxide and carbon dioxide were produced . Clayton  has suggested that decomposition of VF2-HFP, VF2-HFP-TFE, and polyvinyl fluoride would produce hydrogen fluoride, but he gave no experimental data to support this theory. Clayton  also suggested that the decomposition of fluorinated ethylene propylene (FEP), a copolymer of TFE and HFP, would produce HFP; again, no experimental data were given. Madorsky et al  reported that pyrolysis of polyvinyl fluoride and polyvinylidene fluoride in a vacuum at 372-500 C produced hydrogen fluoride and a waxlike material consisting of chain fragments of low volatility.

# Effects on Humans
As early as 1951, Harris  described two cases of an influenza like syndrome in workers who had been experimenting with PTFE for an unspecified period. The first worker, 29 years old, was exposed to fumes emitted from PTFE heated in an extruder with a malfunctioning thermostat.
Although the extrusion process was normally carried out at 350 C, the machine in this instance overheated to about 450-500 C. had asthma attacks for many years, although he had been symptom-free for 18 months prior to this incident. Harris noted that the exhaust ventilation system on the oven was subsequently found to be inadequate and that, once that situation was remedied, no further attacks occurred. He called the illness of these workers polymer fume fever, which he proposed was caused by inhalation of fume from heated PTFE, and noted the similarity of this syndrome to metal fume fever.
Harris  also noted that the two cases he had diagnosed as polymer fume fever were similar to two cases of illness in PTFE workers described to him by HF Gilbert in a personal communication. Because the symptoms so closely resembled those seen in metal fume fever, Harris  analyzed PTFE ash and the sublimate evolved from PTFE heated at 400 C for various metals. The sensitivity of the method of analysis was not reported. From these studies, Harris concluded that the concentrations of metals in the ash and the sublimate could not explain their findings, so that a toxic fume from heated PTFE seemed to be the responsible agent in polymer fume fever from PTFE.
In 1967, Bruton  described two cases of illness in aviation employees whose work involved contact with a neoprene door seal that had been sprayed with an aerosol of an unspecified fluorocarbon telomer.
Smoking was not permitted in the hangar; however, toward the end of his shift, the first worker had smoked a cigarette in an office where smoking was allowed. Approximately 30 minutes later, he experienced shivering and chills, which lasted for about 6 hours, but no other effects. The second worker had been handling the polymer spray for approximately 1 year and had become ill once before when he failed to wash his hands before smoking after working with the aerosol. On this occasion, he started to smoke a cigarette during his break and realized by the taste that it was contaminated. He extinguished the cigarette immediately, but, within 30 minutes, he began to shiver and developed a headache and muscular aches, but no respiratory effects. Recovery was complete within 24 hours.
Bruton  believed that the polymer-treated surface had contaminated the cigarettes.
To demonstrate the possibility of hand contamination, he conducted an informal experiment in which the aerosol was sprayed onto a clean aluminum surface according to the manufacturer's instructions. When he wiped the surface with his finger, a line across the sprayed surface and a faint white dust on his finger were visible. The author suggested that handling of objects treated with aerosols of fluorocarbon telomers represented a hazard to smokers because of the possibility of contamination of smoking materials. He noted that workers should be required to wash their hands before smoking to avoid contaminating smoking materials. Although Bruton diagnosed this syndrome as polymer fume fever, he did not disprove the possibility that the respiratory symptoms were due to other causes. He was correct in assuming that the temperature of the cigarette was sufficient to cause pyrolysis of the fluorocarbon telomer, however, since the temperature of the burning zone of cigarettes has been shown to range from 854 to 913 C .
In 1964, Nuttall et al  reported an incident of in-flight illness that affected 35 passengers, including 2 flight surgeons and 4 of 5 crew members, on a C54 aircraft. The total flight time was 165 minutes, and the authors mentioned a flight altitude of 9,500 feet. The auxiliary power unit (APU) of the aircraft was located in the rear compartment, which "freely communicated" with the main passenger cabin. The crew compartment door was closed. After the passengers and crew members boarded the plane, the APU was started; fume and odor levels within the main cabin were reported to have been "normal." Takeoff was delayed because of magneto trouble, and the passengers debarked after the APU had run for approximately an hour. A few had mild symptoms of respiratory Irritation, and some became nauseated when they smoked. About 1.5 hours later, the passengers reboarded the aircraft and the APU was restarted. The plane took off 45 minutes later and the APU was turned off. Within 1 hour of takeoff, most of the passengers and two of the crew members had chest discomfort and general malaise, including chills, nausea, and respiratory distress in some. One passenger vomited and collapsed and was found 5-10 minutes later in a cyanotic state with a weak and rapid pulse.
A second passenger had severe respiratory distress and moderate collapse. Six passengers were incapacitated, and five were given oxygen. The heating system was suspected of being a source of toxic fumes and was turned off.
Although a fusilage hatch was opened to provide ventilation, some passengers continued to complain. On arrival, three passengers required hospitalization, and everyone aboard the plane except one co-pilot had experienced effects, which persisted after the plane landed.
To characterize the illness, Nuttall et al  interviewed and gave questionnaires to all crew members and passengers.
The answers to the questionnaire revealed a toxic reaction pattern similar to that of influenza, with onset of symptoms occurring within 2-6 hours after exposure to the unidentified agent. Typical symptoms were chest discomfort, difficulty in breathing deeply, chills, muscular aches, fever, dull headache, and general malaise. Respiratory symptoms were not present in all cases, and nausea and aversion to cigarettes was often reported. The number of smokers aboard the plane was unspecified, and it was not stated whether smoking was permitted during the flight. Recovery was complete within 24 hours in most cases, including those of the three hospitalized patients. The authors noted that examination of these three patients showed elevated temperatures, increased white blood cell counts with a shift to the left (indicative of an increased proportion of young cells), and rapid pulse rates. They emphasized the similarity of the reported symptoms to those of metal or polymer fume fever, characterizing 50% of the cases as "typical" examples of this syndrome. The questionnaire data indicated that 6 cases were severe, 12 were moderate, and 9 were mild.
Although 12 of those aboard the flight did not complete questionnaires because they could not be located, the flight surgeons who had interviewed everyone on the plane at the time of the incident reported that they also had been affected to some extent.
Nuttall and coworkers  conducted an extensive investigation to determine the cause of the illness. Air samples were collected in the grounded aircraft and analyzed for total metals and zinc with negative results. The four who collected samples developed a typical fume fever reaction. Six volunteers were exposed to fumes from the APU for 40 minutes. All six developed symptoms similar to those of the affected passengers and crew members 1-3 hours after exposure. All had elevated temperatures and elevated white blood cell counts, with polymorphonuclear leukocytosis and a shift to the left. A trip made by the same plane 2 days later, after a new APU had been installed, was uneventful.
The tape used to wrap the exhaust manifolds of the old APU was subjected to a variety of tests  . Five volunteers were exposed to fumes emitted from the APU before the manifold was wrapped with tape. No symptoms were reported after 35 minutes of exposure. Next, the APU exhaust manifolds were wrapped with an unspecified amount of asbestos tape salvaged from the old wrappings of the manifold, and used APU oil was placed on the wrapping.
In this instance, two of six subjects exposed for 35 minutes reported symptoms, and small quantities of uncharacterized fumes were observed around the wrappings. Carbon monoxide levels were below 50 ppm in both these runs. The authors noted elevated temperatures and mild leukocytoses in the two affected subjects, but suggested that the reported effects were questionable. This second run was repeated, whereupon two of the six subjects exposed for 35 minutes developed mildly elevated temperatures and leukocytosis. Subsequent exposure of four subjects to oil fumes alone for 40 minutes failed to produce symptoms. Nuttall et al  concluded that the asbestos tape was the source of toxic fumes, although the oil might have been a modifying agent. New asbestos tape of the same type that had been used to wrap the manifolds of the APU was analyzed with an infrared spectrometer. This examination revealed the presence of PTFE, a finding that was later confirmed by the manufacturer.
In a final experiment, one subject was exposed to fumes emitted from an unspecified amount of the tape pyrolyzed in a platinum dish at 800-1,000 In 1967, Barnes and Jones  gave the results of an investigation of an outbreak of respiratory illness affecting 4 of 19 workers at a factory that made abrasive wheels. The affected workers were male press operators, aged 20-32 years, whose employment histories were not given.
Their work involved placing by hand a mixture of phenol-formaldehyde resin, furfural, abrasive grain, a small amount of hexamethylenetetramine, and, occasionally, a rectifying oil containing cresylic acid on cold presses in a tray. The wheels thus formed were removed from the press room and placed in batches in an oven heated to 177 C for curing. The investigators noted that the factory consisted of one large shed and that the press room was not physically closed off from the area where the mixture was made. The press room was mechanically ventilated by recirculated, cooled air, and the mixing area was air-conditioned.
In describing these four case histories, Barnes and Jones  noted that these workers were moderate to heavy smokers who smoked on the job.
All four had suffered recurrent bouts of illness over a 2-to 4-month period and had experienced respiratory distress characterized as either tightness of the chest or difficulty in breathing deeply. Typical symptoms of these attacks included uncontrollable shivering lasting 1-2 hours in two workers, pain in the retrosternal area in one worker, sore throat in one worker, and severe headache in one worker. Physical examinations at the time of the plant visit revealed scattered rhonchi in the chest of one worker, congested throat and congested soft palate in a second worker who had not complained of a sore throat, congested pharynx in a third, and no signs in a fourth worker who had been transferred to the packing room 2 weeks earlier.
The authors discovered during their investigation of the plant that the use of powdered PTFE as a mold-release agent had been initiated approximately 3 months earlier. They noted that, although the pressing and curing processes were carried out at temperatures below 300 C, all the affected workers handled the PTFE-treated plates and all smoked while working. They further stated that PTFE powder was detected on the hands of the press operators and that there was ample opportunity for the skin to become contaminated in the plant. Smoking on the job was then prohibited. The authors reported that, according to the plant manager, there had been no recurrence of symptoms during the 2 months after the reported illnesses and the prohibition of smoking in the work area.
Although the decomposition products of PTFE may have been the cause of the illness, some of the typical polymer fume fever symptoms were not present.
In 1974, Wegman and Peters  reported the investigation of a similar outbreak of influenza-like illness in workers in a textile mill that produced imitation crushed velvet. The fabric was made of nylon and rayon, and the final stage of its production was a flocking process that consisted of the addition of a liquid fluorocarbon polymer to the material, with subsequent dipping, rolling, and squeezing of the mixture, curing at 150-155 C, mechanical crushing and steaming at 135 C, and final static elimination. In an initial interview, the plant manager revealed that a number of workers involved in the flocking process had reported symptoms of weakness, muscle aches, fever, chills, and shortness of breath.
The authors  interviewed and examined all workers in the flocking division, 10 men and 3 women, ranging in age from 19 to 61 years. Those complaining of symptoms had been employed in this division for from 2 months to 6 years. Seven of these workers, six men and one woman, described symptoms of cough, muscular aching or weakness, fever, and chills. Four of these seven workers also had experienced shortness of breath.
All had suffered repeated bouts of illness, three of the seven workers having experienced as many as six attacks during an unspecified period of time. In several instances, symptoms were of such severity that affected workers had to leave the plant. Onset of symptoms was generally gradual and illness persisted for 6-72 hours, most workers reporting recovery within 24 hours. Of the six workers who did not report such attacks, one nonsmoking man had experienced headache on five occasions and possibly some coughing; a second had had an isolated bout of cough, fever, and chills, which the authors attributed to a common cold. One woman who did not report typical attacks had an unspecified number of attacks of coughing, fever, chills, and shortness of breath, but these were of rapid onset and short duration. One of the six men experienced severe weakness, chest discomfort, and shortness of breath on one occasion. The affected workers experienced symptoms only when they worked in the area where the fluorocarbon polymer-treated material was cured.
The authors  considered four materials as possible causes of the symptoms: ammonia, formaldehyde, nylon, and the fluorocarbon polymer.
Analysis of the air of the workplace found air concentrations of less than 50 ppm of ammonia and less than 1 ppm of formaldehyde.
The nylon was reported to be of nonrespirable size. The authors maintained that exposure could not have resulted from the flocking process itself, since the maximum temperatures at which the fluorocarbon was applied and cured were at or below 165 C. However, the authors noted that all seven workers who had "typical" symptoms of polymer fume fever were cigarette smokers, and that all but two of the other workers experiencing symptoms were also smokers.
They observed that workers engaged in applying the polymer to the material had frequent hand contact with both liquid and cured polymer and that they often smoked during breaks without first washing their hands. The authors concluded that the source of the illness was polymer fume generated by the smoking of PTFE-contaminated tobacco. No further symptoms were reported after smoking in the work area was prohibited and the workers were instructed to wash their hands before smoking or eating.
In 1973, Evans  reported a case of respiratory illness in a 49year-old man who had been using an oxyacetylene torch to dismantle a metal table used to hold PTFE-coated molds. The molds had been sprayed with S-143, a dispersion of TFE telomer in unspecified fluorocarbon solvents. In 1975, Blandford et al  described a case of nonoccupational respiratory illness in a man who had inhaled fumes from a PTFE-coated pan that had contained only water and had boiled dry when left unattended on an electric stove.
When he removed the pan from the stove, the man noticed that the fumes "took his breath." No smoke was visible. Five cockatiels kept caged in an adjoining room died within 30 minutes after the incident.
The patient's wife, who was in the same room as the birds during the incident, was unaffected. About 60 minutes postexposure, the patient experienced shortness of breath and a paroxysm of coughing when he tried to smoke a cigarette. About 80 minutes after the incident, the man's symptoms included shivering, dizziness, and nausea. He felt cold and noted a painful tightening of the chest. The next day, on awakening after 8 hours of sleep, he had a severe headache, which subsided during the morning. The tightness of the chest persisted for the remainder of the day. The subsequent recovery was complete and uneventful, although the patient had difficulty remembering events following the death of his birds and felt that the fumes had affected his level of consciousness. The authors noted that this was an unusually clearcut case of polymer fume fever, because there had been no smoke and the pan had contained only water. The data as reported by the authors demonstrated that PTFE produced toxic decomposition products that were more lethal to birds than to humans.
In 1967, Clayton  published the results of investigations conducted by Kligman for the Haskell Laboratory for Toxicology and

# Industrial
Medicine to determine the effects on humans of smoking cigarettes contaminated with known amounts of a TFE fluorocarbon telomer.
The sex, age, medical and employment histories, and smoking histories of the subjects were not reported, and the author did not specify whether the same or different subjects were exposed at the various dose levels.
The first experiment evaluated the effects of smoking a cigarette to which 0.05, 0.10, 0.20, or 0.40 mg of a TFE fluorocarbon telomer had been added. Ten volunteers smoked one cigarette apiece with each of the added amounts of telomer.
Results indicated that 0.40 mg telomer in each cigarette was necessary to cause an increase in body temperature and pulse rate. No symptoms were reported at the lower levels, although average maximum pulse rates were slightly elevated at an unspecified interval after smoking. At the 0.40 mg dose level, the author reported that 9 of 10 subjects had what he considered to be typical symptoms of polymer fume fever, with cough as the first symptom in 6 subjects. The symptoms reported by the nine affected subjects were headache, muscular aches, chills, malaise, sluggishness, excessive perspiration, and weakness. Onset of symptoms occurred 1-3.5 hours after smoking, with a mean latency period of 2 hours. From 2.5 to 5.5 hours after the volunteers smoked, the average temperature of the nine affected volunteers increased to 100.5 F from a mean preexposure value of 98.1. From 2.5 to 4.5 hours after they smoked, The other four subjects expressed well-defined symptoms of polymer fume fever after smoking six to eight cigarettes; the first symptom to appear was chills.
Other symptoms were the same as those of subjects in the first experiment, except that coughing was not reported by any of the subjects.
Clear symptoms first appeared 3-5 hours (average 3.8) after the subjects smoked. Five to 6 hours after smoking, average temperatures of these four subjects increased from 98.3 to 101.4 F. From 1 to 9.5 hours (average 5.4) after smoking, the average pulse rate of the four affected subjects increased from 87 to 111. Recovery time in the subjects with well-defined attacks was 7.5-12.5 hours (average 9.8), but the author did not explain the criteria for recovery. The cumulative amount of added telomer necessary to elicit signs and symptoms of illness in these four patients was 0.30-0.40 mg.
Clayton  noted that the cumulative amount of telomer (0.30-0.40 mg) needed to produce well-defined symptoms in four subjects coincided with the amount of telomer (0.40 mg) needed to produce symptoms in subjects who smoked one cigarette. The sequence of events was similar in subjects given both single and cumulative exposures, but the signs and symptoms differed.
Six of 10 subjects complained about a cough in the first experiment but none of the 4 subjects in the second experiment complained of cough.
Clayton suggested that subjects receiving single large exposures to fluorocarbon telomer had an initial respiratory tract irritation that was not experienced by subjects receiving cumulative exposures because the latter were subjected to irritant substances at lower concentrations. The same amount of telomer, however, produced fever in both experiments.
Clayton concluded that there is no obligatory sequence of effects in polymer fume fever and that the absence of cough does not preclude a diagnosis of this illness. He emphasized that the total clinical picture should be considered by anyone contemplating a diagnosis of polymer fume fever, and that objective measurements such as temperature, pulse rate, and white blood cell counts should be relied on as indices of illness; however, he did not report white blood cell counts. The interval between the smoking of cigarettes was also not specified, and any individual differences in the subjects that might have explained their differing reactions were not discussed. Nevertheless, these experiments indicate that smoking cigarettes contaminated with a TFE-telomer can result in a syndrome commonly referred to as polymer fume fever.
In 1965, Makulova  reported five cases of perfluoroisobutylene (PFIB) poisoning in two male and three female laboratory workers. A 34year -old woman had worked with this compound for approximately 2.5 years with no previous ill effects. The ages and employment histories of the other patients were not specified. Four of the five workers reported that exposure to PFIB lasted less than 1 minute, during which time they inhaled two to five times. All patients described symptoms of coughing, difficulty in breathing, and chest pains immediately after exposure. These symptoms became progressively more severe, and by 6-8 hours after exposure, all patients had developed headaches and other symptoms and had begun to expectorate sputum.
Makulova   Chest X-rays of all patients showed significant pulmonary changes that came on rapidly 4-6 hours postexposure and became fully developed approximately 48 hours postexposure.
In four patients, these changes consisted of bilateral, confluent pulmonary edema, especially in the middle lobes, with emphysematous lateral borders and segments above the diaphragm. In the other patient, multiple clearly defined small foci of intense opacity were found.
The author  noted that treatment was largely symptomatic and consisted of calcium chloride, ascorbic acid, glucose, unspecified cardiac medication, and oxygen administration to combat the pulmonary edema.
Penicillin or streptomycin in combination with sulfonamides was given during the first few hours postexposure. Symptomatic improvement was noted in some patients within 4-6 days postexposure, and complete resolution of breathing difficulties and pulmonary rales occurred 7-10 days after exposure. At 10-13 days postexposure, pulmonary damage observed in X-rays had been resolved, and leukocytosis and eosinopenia improved 15-20 days postexposure. Three patients were discharged from the clinic in good health 13-23 days after exposure, and a followup 2 years later revealed no complications. One patient developed exudative pleurisy and remained in the clinic for more than 2 months.
The fifth patient, the 34-year-old woman, died 2 days after exposure.
Makulova  described the last patient's history and illness in detail, noting that she had suffered from influenzal pneumonia 2 months before poisoning. She was unable to give any information on the duration or degree of her exposure to PFIB on the day she became ill. Her symptoms were similar to those already described, and clinical findings were similar to those for the other patients. She was admitted to the clinic with a where gaskets were produced, 0.2-2.9 mg/cu m in the machine shop, and 2.5-2.9 mg/cu m in a sample for a worker who operated the ring-grinding machines.
A questionnaire was completed by 77 workers (about 75% of the workers in the plant)  . Sixty of the production workers (86%) said that they had experienced polymer fume fever at some time in the past, but only 50% had experienced polymer fume fever during the past year. Fourteen percent of the workers stated that they had had more than three episodes in the preceding year. Only 10% of those who had experienced polymer fume fever In the fabrication techniques studied by Sherwood , the polymer was pressed into a mold or "pre-form" and sintered at 350-380 C to form a finished product or a material suitable for machining to final specifications. Variations of this technique included prebaking before molding, repressing after sintering, and extrusion. Machining was carried out on standard metal-working machines, and waste was recovered for reuse.
Tape was produced by veneering followed by a heat treatment, which is known as tensilating. In 1963, Adams  conducted an investigation to determine the cause of polymer fume fever in employees in a plant where PTFE was processed.
Altogether, 30 wage and 8 staff employees were interviewed by a medical
-fficer. An investigation of the plant was also conducted. Of the 30 wage employees, 14 had experienced symptoms of polymer fume fever in the 2 months previous to the interview. A total of 32 incidents of polymer fume fever were reported by these 14 workers. Only employees working in the finishing room had been affected.
Of the 18 men who worked in the finishing room, 12 who were smokers accounted for 30 incidents and 2 nonsmokers accounted for the other 2 attacks.
A detailed investigation showed that 6 men who rolled their own cigarettes had had 21 of the attacks of polymer fume fever. Of the eight staff employees, only one, a pipe smoker, had had an attack of polymer fume fever.
In the finishing room, PTFE was dried, sifted, and packed . In an unspecified drying operation, a small amount of PTFE was occasionally heated beyond the normal drying temperatures. Air samples were taken by an unidentified method at points close to the drying ovens and the ovens where the polymer was further heated when required. Adams found concentrations of hydrogen chloride as high as 35 ppm on occasions when PTFE was heated only to normal drying temperatures. When oven temperatures exceeded 300 C , the author found up to 6 ppm of hydrogen fluoride. Although acetic acid is usually used to coagulate PTFE latex, it is possible that hydrogen chloride was used and that residues of this acid provided the HC1. HC1 boils at 110 C whereas something like 250 C is required to liberate HF from PTFE.
Adams  concluded that the majority of incidents of polymer fume fever resulted from the smoking of PTFE-contaminated tobacco. He noted that precautions must be taken to prevent particles of polymer from lodging beneath nails, in hair, or on clothing. Adams did not report the method of analysis used to detect hydrogen fluoride. That the hydrogen chloride in the vicinity of the drying ovens came from PTFE per se is highly unlikely because this polymer contains no chlorine atoms.

# Animal Toxicity
A list of compounds that have been identified as pyrolysis products of fluorine-containing polymers, as stated previously in the section on In addition to the various molecular species mentioned in the preceding paragraph, there is the particulate material that may be the principal cause of polymer fume fever . Harris  had found in 1957 that heating PTFE at temperatures above 300 C produced the deposition of a solid material within his exposure chamber and also liberated an acid into the air of the chamber. Four rats exposed to such atmospheres developed congested or hemorrhagic lungs and pulmonary edema. Harris concluded that PTFE heated to 300 C or more produced a sublimate or an acid that induced pulmonary edema and killed rats thereby.
In 1968, Waritz and Kwon  and Birnbaum et al  suggested that the particulate material may carry adsorbed toxic materials (perhaps hydrofluoric acid, carbonyl fluoride, octafluoroisobutene, or chlorotrifluoroethylene) into the alveoli, the latter group of researchers  having found that the mean particle size of this material was 0.5 jum and that 99% of the particles had diameters of less than 2 m. These dimensions place the polymer fume in the category of inhalable dusts.
Waritz and Kwon  found that removal of the particulate material by  produced minimal mortality in rabbits and rats, respectively. Hyperemia of the liver, hemorrhage in spleen and lungs, dystrophic changes in the epithelium of the renal tubules, atelectasis and emphysema in the lungs, and desquamation of the bronchial epithelium were the principal changes attributed to the monomer. Clayton  reported that the LC50 for the rat exposed to tetrafluoroethylene for 4 hours was 163,600 mg/cu m.
For CTFE, the LC50 for rabbits and white rats exposed for 2 hours was reported to be 24,000 mg/cu m .
The "absolutnaya smertelyenya kontsentratsiya," meaning probably the LC100, was said to be 26,400 mg/cu m for the rabbit and 36,000 mg/cu m for the white rat. No actual data on the numbers of deaths after exposure at any concentration were provided.
Clayton, in a series of papers  all probably referring to a single estimation of the inhalation toxicity of CTFE, has reported that the LC50 for the rat exposed for 4 hours was 1,000 ppm (4,770 mg/cu m ) .
More recently, Hood et al  have exposed rats, guinea pigs, rabbits, and dogs to chlorotrifluoroethylene at concentrations of 300 ppm
(1,431 mg/cu m) for 4 hours/day, 5 days/week, for a total of 18 exposures.
One of 10 male guinea pigs died after the sixth exposure. One of 10 male rabbits died after 4 exposures and another after 5. None of 10 rats of to have increased more than that of the control animals; the increase was stated to have become progressively larger throughout exposure in the exposed rabbits. The exposed animals also were said to have recovered from the orthostatic tachycardia more slowly than the control animals. These observations suggest that exposure to CTFE altered the properties of the sympathetic nervous system, including possibly such centers in the brain stem as the bulbar vasomotor mechanisms. The exposed rats were reported to have undergone a significant decrease in the ability to summate subthreshold stimuli (presumably applied to the motor nerve of some unidentified effector).
Hood et al  exposed rats of both sexes, male guinea pigs, male rabbits, and dogs for 6 hours/day, 5 days/week, for 14 months to CTFE at concentrations starting at 15 ppm (about 71.6 mg/cu m) and increasing progressively, at irregular intervals of time, to 30, 50, 100, and 150 ppm (715.5 mg/cu m ) . These exposures produced no significant pathologic effects in rabbits and guinea pigs but produced severe tubular necrosis in rats.
Two of four exposed dogs began to exhibit signs of neurologic disturbances after 27 and 64 exposures, respectively, at 150 ppm. These consisted of stiffness and weakness of the legs and unsteadiness in standing. One of two other dogs that were added to the exposed group at the beginning of exposure at 100 ppm (477 mg/cu m) died after 56 exposures at that concentration followed by 54 exposures at 150 ppm. The second of these dogs was reported to have become very irritable at this same time.
Degenerative changes in the central and peripheral portions of the somatic nervous system were found, most severe in samples of nerve tissue from the dog that had exhibited the most marked neurologic signs (temporary prostration at the end of each period of exposure, ataxia, and difficulty in swallowing). This dog was found to have atrophy of the muscles of the hindlegs.
Clayton  reported that a mixture of 80% hexafluoroethane with 20% oxygen (about 4,515,000 mg/cu m of hexafluoroethane) was an approximate lethal concentration for the rat exposed to it for 4 hours. The data in these paragraphs allow arrangement of the compounds on which information is available in a hierarchy of decreasing toxicity, albeit with some uncertainty.
There is little doubt that perfluoro isobutylene is the most toxic compound and that octafluorocyclobutane and hexafluoroethane are the least toxic. The ranking of inhalation toxicity for the rat, based largely on single exposures, that NIOSH has derived from the information stated above is as follows, going from the most toxic to the least: perfluoroisobutylene, hydrofluoric acid, carbonyl fluoride, silicon tetrafluoride, chlorotrifluoroethylene, hexafluoropropene, tetrafluoroethylene, tetrafluoromethane, hexafluoroethane, and octafluorocyclobutane.
In addition to the information summarized above on the breakdown The other general approach to assessing the toxicity of the pyrolysis products of fluorinated polymers, ie, exposing experimental animals to mixed decomposition products of polymers heated to various temperatures, has been used by a number of investigators.
In 1955, Zapp et al  pointed out that the intact PTFE polymer is nearly inert but that products of its thermal decomposition are not. Polymer fume fever has been recognized to be a consequence of exposure to heated PTFE since its description in 1951 by Harris .
Studies of the toxicity of the pyrolysis products of PTFE had been started at the Haskell Laboratory in 1943, but polymer fume fever had not been reproduced in experimental animals. Lethal activity had been demonstrated, however .
Strips of PTFE subjected to temperatures of 200 and 250 C in a stream of air passing into an exposure chamber containing 2 rats caused no deaths of the rats after a 6-hour exposure , Similar exposures to air passing over strips of PTFE heated to 300 and 350 C did result in the death of rats, the higher temperature having a more marked effect with "Teflon 6," described as a low-molecular-weight polymer, than with "Teflon 1," a highmolecular-weight polymer.
Clayton et al  reported that, when "Teflon 1" and "Teflon 6" were subjected to temperatures of 300, 325, and 350 C in tubes of either glass or stainless steel, the materials heated in glass tubes yielded more toxic pyrolysis products than those heated in the stainless steel tubes. The differences were most marked for "Teflon 6" at 300 C and for "Teflon 1" at 350 C. Samples of "Teflon 6" that yielded comparatively large amounts of particulate material were more toxic than those that yielded less.
Filtration of the pyrolysis products with a filter having a pore size of 0.45 j i r n i lowered the mortality of rats exposed to the pyrolysis products from 43/48 to 7/48.
"Teflon 6" manufactured before 1958 was reported  to yield toxic breakdown products at 350 C, whereas "Teflon 6" manufactured "currently"
(1959 and thereafter) yielded pyrolysis products of approximately equal toxicity only when the temperature was raised to 425 C .

# Cavagna et al
 reported they had been able to produce attacks of fever in rabbits subjected to inhalation of aerosolized 20% acetic acid, in an undisclosed concentration in the inspired air, for 10 minutes, followed 16 hours later by exposure for 30 minutes to an atmosphere containing 10-12 mg/cu m of hydrogen fluoride and 1.0-1.7 billion particles/cu m with diameters greater than 0.7 jum, which had been generated by heating PTFE in a tube furnace at 400-500 C. Seven of 11 rabbits had temperature increases of 0.5-1.5 C. These appeared after a latency period of about 5 hours, during which a decrease in body temperature, leukopenia, and cough and rhinorrhea were observed. The fever lasted 6-7 hours and coincided approximately in onset, but not in duration, with leukocytosis. Exposures of naive rabbits to fumes from heated PTFE produced initial hypothermia and irritation of the respiratory tract but no fever. the particles produced. Some of this powder was used at once, another aliquot was washed with water to remove the gaseous products of decomposition, and a third portion was stored for 6 months before being used. These three samples of powder were compared with a powder produced by grinding PTFE that had not been pyrolyzed and with powdered chalk.
The powders were administered to rabbits by iv injection of 1-1.5 mg/kg in suspension in sterile, apyrogenic saline. Control rabbits received only saline.
Only the unwashed pyrolyzed particles produced a febrile reaction in the rabbits. This was preceded by leukopenia, which was frequently succeeded by leukocytosis.
A similar response was induced in rabbits by inhalation exposure to the unwashed pyrolyzed particles at a concentration of 122.8 mg/cu m for 2.5 hours.
The succession of leukopenia, pyrexia, and leukocytosis reported by Blagodarnaya  in the rabbits exposed to unwashed pyrolyzed particles from PTFE is reminiscent of the febrile response to gram-positive bacteria injected iv into rabbits  . The failure of washed pyrolyzed particles to produce fever in these experiments indicates that the response is not to particulate agents alone. The presumption is that some water-soluble and volatile component of pyrolyzed PTFE adsorbed on the surfaces of the particulate material render the particles capable of interacting with the leukocytes of the blood and releasing the leukocytic pyrogen as suggested by Cavagna et al  . Some further study of the pyrogenic process after exposure to pyrolyzed fluorocarbon polymers seems desirable.
Treon et al  compared the toxicities of the pyrolysis products of PTFE and of two polymers of PCTFE differing in extent of polymerization, so that one (FL) was a liquid and the other (KF) was a solid. The liquid polymer (FL) was dropped into an Inconel tube heated by an electric current through resistance wire wound around the tube. The solid polymers (PTFE and KF) were prepared as strips which were inserted into the cold Inconel tube.
The tube was then raised to the planned temperature as rapidly as possible. Air or nitrogen (PTFE only) was passed through the furnace at a rate of 31.8 liters/minute and into the 800 liter exposure chamber. PTFE was pyrolyzed at temperatures of 375-878 C. FL was pyrolyzed at either 371 or 482 C, whereas KF was heated to temperatures of 803-813 C.
Groups of five mice, six rats, four guinea pigs, four rabbits, one cat, and one dog (PTFE only) were exposed in the chamber to various concentrations of pyrolysis products (graded by the rate at which the polymer was fed into the furnace) and for different spans of time .
The exposures to pyrolysis products of PTFE lasted for 30-180 minutes, most being less than 60 minutes in duration.
Exposures to the pyrolysis products of FL were for 2, 7, or 24 hours, whereas those to the pyrolysis products of KF were for 32-34 minutes.
Dogs, mice, and rabbits were the most resistant species to PTFE pyrolyzed at temperatures of 739-813 C in the presence of air. When PTFE was pyrolyzed at temperatures of 811-878 in nitrogen, rabbits, guinea pigs, and rats were more resistant than mice. Cats and dogs were not used in these last tests. When the temperature of pyrolysis was 491-527 C in the presence of air, rats and rabbits were more resistant to a lethal effect than mice and guinea pigs. Cats and dogs were not included in these studies either. Pyrolysis of PTFE in the presence of air yielded pyrolysis products of greater toxicity than those produced in nitrogen. Lowering the temperature of the pyrolysis apparatus from 739-813 to 491-527 C decreased the toxicity of the pyrolysis products to rats, rabbits, and mice, but slightly increased the toxicity to guinea pigs.
Cats and rats were the most resistant species to the lethal effect of the pyrolysis products of FL heated at 482 C  . When the pyrolysis temperature of this polymer was lowered to 371 C, no animals were killed during exposures of 2 or 7 hours. Mice, cats, and rabbits were more resistant to the lethal action of the pyrolysis products of KF than were guinea pigs and rats.
When PTFE was pyrolyzed in the presence of nitrogen, pyrolysis at a rate of 1.99 g/hour produced no fatalities in any of the four species exposed . When PTFE was pyrolyzed in air, pyrolysis at a rate of 2.60
g/hour at 506 C produced death of only 1/6 rats, 1/4 rabbits, 0/5 mice, and 0/4 guinea pigs after an exposure of 36 minutes. Pyrolysis at a rate of 1.67 g/hour at 805 C produced death of 3/6 rats, 2/4 rabbits, 2/5 mice, and 0/4 guinea pigs after an exposure of 33 minutes.
Pyrolysis of FL at 482 C at rates of 3.18 g/hour or 1.02 g/hour killed no animals after exposures of 2 and 7 hours, respectively .
Pyrolysis of KF at 805 C at a rate of 0.88 g/hour killed no mice, rats, guinea pigs or rabbits after an exposure of 34 minutes .
The Treon et al  data are difficult to interpret in a comparative way because of the various conditions of pyrolysis and exposure of the experimental animals. A higher temperature of pyrolysis seems generally to produce more toxic pyrolysis products. The observations that species sensitivity to the pyrolysis products of the three polymers varies not only with the polymer but also with the conditions of pyrolysis indicate that, under similiar conditions, the two polymers of PCTFE probably yield different pyrolytic products, despite their monomeric identity, and that a single polymer yields different products under different conditions of pyrolysis. Pyrolysis in the presence of an inert gas seems to be less hazardous than that in the presence of air. The pyrolysis products from FL may be less hazardous than those from either PTFE or K F , but this conclusion cannot be supported satisfactorily by the data provided. Good comparative data would be useful.
Zapp  gave a little further information about the pyrolysis of PCTFE, finding that it, like PTFE, undergoes degradation when exposed to a temperature of 300 C but not when exposed to one of 250 C.
Birnbaum et al  exposed rats to the products of pyrolysis of PCTFE heated to temperatures of either 375 C or 400 C, determining the rate at which a rod of PCTFE had to be fed into a pipe heated to the desired temperature in an electric furnace to maintain an LC50 of pyrolysis products within an exposure chamber fed with air passed through the furnace at a rate of 4 liters/minute. The exposure periods were either 1 or 3 hours.
One-hour exposures at 375 C did not result in sufficient mortality to yield valid estimates of the LC50 at the highest rate of feed of the PCTFE rod into the heated tube. The 3-hour exposure to the products of pyrolysis at this temperature yielded an estimate that 31.5 g/hr of the polymer had to be subjected to pyrolysis to maintain an LC50 of the pyrolysis products within the chamber. Exposure for 1 hour at the higher temperature of pyrolysis (400 C) yielded an estimate that 23.5 g/hr of the polymer had to be pyrolyzed at this temperature to maintain an LC50 of the pyrolysis products within the chamber. The particles in the pyrolysis products ranged in diameter from about 0.15 to 3.0 jiim, 85% of the particles being less than 1 /nm in diameter and 99% less than 2 /um. Infrared and mass spectrometers were used to obtain some idea of the molecular species present in the exposure atmosphere; these two techniques indicated the presence of perhaps as many as 13 different materials in the pyrolysis products.
Comparatively little information about pyrolysis products of fluorocarbon polymers other than PTFE and PCTFE has been found. Clayton  reported studies of the inhalation toxicities of two samples of a copolymer of vinylidene fluoride and hexafluoropropylene for the rat. One Hydrogen fluoride was the only pyrolysis product whose concentration in the exposure chamber seemed to be related to mortality in the exposed rats. The principal effects of the exposure on rats were irritation of the respiratory tract, pulmonary edema, hemorrhage in the lungs, congestion of the liver, vacuolation of hepatocytes, tubular necrosis in the kidneys, and proteinaceous material in the renal tubules.
Ehrsam  has shown that the pyrolysis products of PTFE are more toxic to birds than to mice or guinea pigs. Similarly, Griffith et al  has reported that Japanese quail and parakeets were killed by effluvia from a frying pan coated with PTFE and heated to 330 C and 280 C, respectively, whereas rats appeared not to be harmed until the pan was heated to 450 C . Some investigators  have reported that subcutaneous implantation of PTFE into rats resulted in the formation of fibrosarcomas.
However, Bryson and Bischoff  were unable to duplicate these results.

# Correlation of Exposure and Effects
The most frequently reported effect of workplace exposure to the pyrolysis products of PTFE is an influenza-like syndrome designated polymer fume fever .
No effects of workplace exposure to the pyrolysis products of other fluorocarbon polymers were found in the literature.
The major signs and symptoms associated with polymer fume fever are chest discomfort , fever , leukocytosis , headache , chills 40,41], achy feeling , and weakness .
Complete recovery usually occurred within 12-48 hours after the exposure ended .
Other effects reported in humans exposed to the pyrolysis products of PTFE were nausea , malaise , congested throat and pharynx , basal rales of the lungs , pulmonary edema , hyperpnea , and increased pulse rate ,
Damage to the respiratory tract, occasionally severe enough to result in pulmonary edema, was found in humans exposed to the pyrolysis products of PTFE  and in animals exposed to the pyrolysis products of PTFE , PCTFE , VF2-HFP , VF2-HFP-TFE , and E-CTFE . Effects such as leukocytosis and elevated temperature were difficult to produce in animals .
Polymer fume fever has resulted when there was an insufficient amount of ventilation in molding operations  and when PTFE processing temperatures were not controlled because of malfunctioning thermostats . Polymer fume fever has also resulted from the smoking of PTFEcontaminated tobacco . As little as 0.3 mg of a TFE fluorocarbon telomer added to the cigarettes of volunteers produced polymer fume fever Without these data, it is difficult to determine whether the authors' conclusions were justified.
Clayton et al  also concluded that the toxicity of the pyrolysis products of PTFE heated at 350 C was caused by a particulate. Seven of 36 (19.4%) rats were killed when the pyrolysis products of PTFE heated at 350 C were filtered (Millipore filter, 0.45 jum pore size). The expected mortality was 100%. When PTFE was pyrolyzed at 325 C, the unfiltered fume killed 6/16 rats (37.5%). The same pyrolysis products after filtration through a filter of 0.45 m. pore size killed 0/8 rats. These results are in agreement with the findings of Waritz and Kwon , since filtration of the pyrolysis products reduced mortality. However, Waritz and Kwon  reported that the unfiltered pyrolysis products of PTFE heated at 400 C were not lethal to rats. This discrepancy may be related to the finding of Clayton et al  that low-molecular-weight PTFE yielded pyrolysis products more toxic than those from high-molecular-weight PTFE; Clayton et al and Waritz and Kwon perhaps used samples of PTFE of different molecular weights.
In animal studies, Scheel  found a correlation of lethality with the amount of hydrolyzable fluoride produced when E-CTFE was pyrolyzed at 550 C, but the amount of hydrolyzable fluoride produced was not correlated with the amount of E-CTFE pyrolyzed.
Other investigators found no correlation of lethality with the amount of hydrolyzable fluoride produced by pyrolysis of PCTFE , VF2-HFP , or VF2-HFP-TFE .
Waritz and Kwon  reported that traces of perfluoroisobutylene (PFIB) were produced when PTFE was pyrolyzed at 475 C and that pyrolysis at 480 C produced 5 ppm of PFIB. Clayton  has reported that the LC50 for PFIB in rats after a 6-hour exposure was 0.5 ppm. Although PFIB appears to be the most toxic gas produced by the pyrolysis of PTFE, no studies correlating the concentration of PFIB with the toxicity of the pyrolysis products of PTFE were found in the literature.
In the absence of pertinent data, no useful correlation can be made between the type and extent of exposure and the degree of human intoxication produced by the decomposition products of fluorocarbon polymers. However, compiling and summarizing the signs and symptoms reported in humans is a useful first step in the attempt to understand the adverse effects of these substances.     dust counts were of the order of 1,000 particles/cc with diameters smaller than 5 m , 15 particles/cc with diameters between 0.5 and 1.0 urn, and 1 particle/cc with a diameter greater than 1 jum.

# Carcinogenicity, Mutagenicity, Teratogenicity, and Effects on Reproduction
Adams  sampled air in a finishing room where PTFE was dried, sifted, and packed. At collection sites close to ovens which were heated occasionally to above 300 C, he found concentrations of hydrogen fluoride up to 6 ppm. This assumption was used because the toxic effects of decomposition products of PTFE are associated with a particulate substance which is a small fraction of the total decomposition products. Waritz and Kwon  observed that test animals died after being exposed to the particles at a concentration of 1.4 mg/cu m (equivalent to 1.2 ppm by weight at ambient conditions).  NIOSH maintains that the most important feature of an exhaust ventilation system is its design. Guidance for designing a local exhaust ventilation system can be found in Industrial Ventilation-A Manual of Recommended Practice  and in Fundamentals Governing the Design and Operation of Local Exhaust Systems . Ventilation systems of this type require regular inspection and maintenance to ensure effective operation.
Regularly scheduled inspections should include face-velocity measurements of the collecting hood and inspection of the air mover and collector.
In addition to providing adequate ventilation, it may be appropriate, under certain circumstances, to isolate a process or system in an especially designed enclosure to minimize exposure. Other control measures may be intentionally redundant temperature monitoring systems and alarms to signal harmful thermal excursions.  In all extrusion processes, the handling precautions described above must be observed. As in sintering operations, the temperature to which the fluorocarbon polymer is subjected must not be allowed to exceed the manufacturer's recommended processing temperature, and an appropriate temperature cutout system must be used. Local exhaust ventilation must be installed at the orifice from which the melt is extruded to keep decomposition products from entering the work area. An appropriate alarm system must be incorporated into the exhaust ventilation system.

# Biologic Evaluation
In thermoforming, compression molding, and coining, and in all processes in which the temperature of the fluorocarbon polymer approaches its melting point, ovens must be fitted with exhaust ventilation and temperature-regulating systems. These systems must be equipped with appropriate alarms and must be serviced at regular intervals.
Coagulated dispersion polymers are usually processed by "paste extrusion." This involves mixing the fluorocarbon polymer with a lubricant, generally a volatile petroleum fraction. This use of flammable liquids adds a potential hazard. The lubricant may be removed in a drying oven or in a continuous oven constructed in series with the extruder and a sintering oven. Precautions must be taken to minimize the risk of forming explosive mixtures of vapor and air and to prevent their ignition if they should form. These precautions might include controlling the rate of solvent removal, increasing the exhaust ventilation in the solvent-removal area, and locating the solvent-removal zone apart from the sintering area.
If flammable vapor enters the sintering oven, it probably will ignite.
Removal of all traces of the lubricant before sintering is necessary. As in sintering operations, appropriate temperature-regulating and exhaustventilation systems should be used on ovens where solvent removal takes place. Fire-extinguishing equipment should also be readily available.  (29 CFR 1910(29 CFR .1000).

# Basis for the Recommended Standard
The most frequently reported effect of exposure in the workplace to the pyrolysis products of fluorocarbon polymers has been an influenza-like syndrome, polymer fume fever, which was described first by Harris  in 1951 and subsequently by several other investigators . The major signs and symptoms associated with polymer fume fever are chest discomfort , fever , leukocytosis , Other effects found in humans exposed to the pyrolysis products of fluorocarbon polymers were nausea , malaise , congested throat and pharynx , rales in the bases of the lungs , pulmonary edema , hyperpnea , and increased pulse rate . Respiratory irritation and pulmonary edema have been reported in humans  and animals  exposed to the pyrolysis products of fluorocarbon polymers.
No reports of serious injury or of long-term effects of polymer fume fever were found in the literature.
The syndrome outlined above has been described most frequently as a result of exposure to fumes from heated PTFE. Since there are now a number of other fluorinated polymers whose breakdown products are almost entirely unidentified and untested for toxicity, there seems to be no basis for attempting to set an occupational exposure limit that will apply to breakdown products of fluorinated polymers in general. Accordingly, NIOSH suggests that exposure of employees to breakdown products of polymers of fluorinated monomers be limited to the greatest extent possible by designing production processes to restrict heating of these polymers to the lowest temperature that permits the desired operation, to limit access of air and oxygen to heated polymers to the greatest extent feasible, and to take the greatest possible advantage of local ventilation of sites from which polymer fumes may enter the occupational environment. Such steps, in conjunction with effective general ventilation of the workplace and good work practices, should go far toward protecting employees from deleterious effects from breakdown products of the materials with which they work.
Although these deleterious effects are more likely to be incapacitating than dangerous, their avoidance is certainly desirable.

# (c) Medical
Several studies on humans  and animals  showed that exposure to fluorocarbon polymer decomposition products produced respiratory irritation and pulmonary edema.    Chemical substances should be listed according to their complete name derived from a recognized system of nomenclature.
Where possible, avoid using common names and general class names such as "aromatic amine,"
"safety solvent," or "aliphatic hydrocarbon" when the specific name is known.
The "%" may be the approximate percentage by weight or volume (indicate basis) which each hazardous ingredient of the mixture bears to the whole mixture. This may be indicated as a range or maximum amount, ie, "10-40% vol" or "10% max wt" to avoid disclosure of trade secrets.
Toxic hazard data shall be stated in terms of concentration, mode of exposure or test, and animal used, eg, "100 ppm LC50-rat," "25 mg/kg LD50skin-rabbit," "75 ppm LC man," or "permissible exposure from 29 CFR The "Health Hazard Data" should be a combined estimate of the hazard of the total product. This can be expressed as a TWA concentration, as a permissible exposure, or by some other indication of an acceptable standard. Other data are acceptable, such as lowest LD50 if multiple components are involved.
Under "Routes of Exposure," comments in each category should reflect the potential hazard from absorption by the route in question. Comments should indicate the severity of the effect and the basis for the statement if possible. The basis might be animal studies, analogy with similar products, or human experiences. Comments such as "yes" or "possible" are not helpful. Typical comments might be:
Skin Contact-single short contact, no adverse effects likely; prolonged or repeated contact, possibly mild irritation.
Eye Contact-some pain and mild transient irritation; no corneal scarring.
"Emergency and First Aid Procedures" should be written in lay language and should primarily represent first-aid treatment that could be provided by paramedical personnel or individuals trained in first aid.
Information in the "Notes to Physician" section should include any special medical information which would be of assistance to an attending physician including required or recommended preplacement and periodic medical examinations, diagnostic procedures, and medical management of overexposed employees. Respirators shall be specified as to type and NIOSH or US Bureau of Mines approval class, ie, "Supplied air," "Organic vapor canister," etc.
Protective equipment must be specified as to type and materials of construction.

# C E N T E R F O R D I S E A S E C O N T R O L N A T ' O N A L I N S T I T U T E F O R O C C U P A T I O N A L S A F E T Y A N D H E A L T H R O B E R T A T A F T L A B O R

# MATERIAL SAFETY DATA SHEET 1 PRODUCT IDENTIFICATION M A N U F A C T U R E R S N A M E R E G U L A R T E LE P H O N E NO

# % V O L A T IL E S BY V O L E V A P O R A T IO N R A TE BUTYL A C E T A T E 11 A P P E A R A N C E A N O ODOR

# IV FIRE AND EXPLOSION DATA