Special Report: Teflon – its safety story doesn’t stick

Teflon® is the trade name for polymer polytetrafluoroethylene (PTFE), a thermoplastic found in a slew of domestic products (see box, page 21). More than 95 per cent of Americans now show traces of perfluorooctanic acid (PFOA), a breakdown product of PTFE and a potential carcinogen, in their blood (Regul Toxicol Pharmacol, 2004; 39: 363-80). That doesn’t bode well for the rest of the world either.

The US Environmental Protection Agency (EPA) became concerned about PFOA after removing PFOS (perfluorooctanic sulphonates) – the active ingredient in Scotchgard – from the market in 2000. PFOA belongs to the same class of environmentally hazardous, carcinogenic chemicals.

PTFE has been around for a good 50 years, but we’re only beginning to understand the health consequences of this prevalent polymer. Once again, the manufacturers (in this case, DuPont) have served up decades of scientific spin. In fact, the EPA is currently suing DuPont for failing to report information concerning PFOA.

In the meantime, these are the most pressing health hazards we know of so far.


A series of studies point to an increased risk of heart attack and stroke in workers exposed to PFOA. In 2001, onetime PFOA manufacturer 3M (who made Scotchgard) published its own study showing that workers consistently exposed to Teflon® for five to 10 years had a risk of fatal stroke that was 15 times higher than that of non-exposed workers (www.ewg.org/issues/pfcs/20041216/index.php).

More recently, DuPont released its own study linking PFOA to higher levels of cholesterol. According to a January 2005 DuPont press release, analysis of the blood and urine of 62 workers exposed to PFOA showed “an approximate 10 per cent increase in total cholesterol (most of which was in the LDL fraction) and a rise in triglycerides among some individuals having PFOA levels of greater than 1000 parts per billion”, which are levels at least 200 times higher than that found in the general population (www2.dupont.com/Media_Center/en_US/assets/downloads/pfoa/nr01_11_05a.pdf).

Polymer fume fever

PFOA isn’t the only Teflon® chemical of concern. A report by the Environmental Working Group (EWG), a Washington, DC-based non-profit research and advocacy organisation, showed that PTFE can break down when heated for as little as two to five minutes or, in one case, to just 396º F (202.2º C). The higher the temperature, the more chemicals are released. In addition to PFOA, these include global pollutants such as: TFE, a potential carcinogen; PFIB, an extremely toxic chemical warfare agent; and MFA, which is fatal at low doses. These fumes produce a flu-like illness (‘polymer fume fever’) as well as more severe conditions such as pulmonary oedema, pneumonitis and even death (Acta Astronaut, 1992; 27: 257-9). This can easily happen in any household if an unfilled PTFE-coated saucepan is heated or when such a pan boils dry, and is more likely to occur if the coating is worn or scratched. Considering that PTFE is heated daily in most kitchens (see box, page 21), this is very bad news. It’s even worse news for birds, which are even more susceptible than humans.

In days of yore, that was why canaries were placed in coalmines. Given their small size and high metabolic rates, birds are extremely efficient in exchanging gases and delivering oxygen. However, this also makes them more susceptible to airborne toxins. In one case report, five cockatiels died within 30 minutes of a PTFE-coated frying pan being accidentally overheated. And within an hour, their owner developed symptoms of polymer fume fever (Vet Rec, 1975; 96: 175-8). In another report, 264 broiler chicks, out of a flock of 2400, developed pulmonary oedema due to breathing a noxious gas – found to be emanating from PTFE-coated heat-lamp bulbs – and died over a six-week period of exposure. In another similar flock, 96 chicks died within just 24 hours of such exposure (Avian Dis, 2000; 44: 449-53).

Polymer fume fever (see box below) usually resolves itself within 48 hours but, in some people, it’s not so benign. In one instance, textile workers exposed to PTFE experienced recurring polymer fume fever that eventually led to permanent lung damage (J Occup Med, 1994; 36: 75-8). In a similar incident but in a domestic situation, a 26-year-old woman suffered respiratory distress for a month after exposure to a defective and melting PTFE microwave-oven part (Thorax, 1993; 48: 300-2). And, in a more recent report, three workers in a plastics factory suffered acute pulmonary oedema after inhaling heated PTFE, one of whom died as a result (Eur Respir J, 1997; 10: 1408-11). An epidemiological study of workers exposed to PFOA for 10 years revealed a more than threefold increase in prostate cancer mortality compared with workers not exposed (J Occup Med, 1993; 35: 950-4; J Occup Health, 2004; 46: 49-59). In rats, PFOA caused malignant pancreatic, testicular and liver tumours (Toxicol Appl Pharmacol, 1991; 111: 530-7; Toxicol Sci, 2001; 60: 44-55; Dis Markers, 2003-2004; 19: 19-25), although this may not necessarily apply to people.

Symptoms of polymer fume fever
* Chest tightness
* Difficulty breathing
* Dry, irritating cough
* Chills
* Fever
* Headaches
* Nausea and vomiting
* Sore throat
* Malaise
* A 100-104° F (37.8-40° C) temperature

Nevertheless, the EPA recently dubbed the chemical a ‘likely human carcinogen’ – a good example of understatement, given that PFOA meets the agency’s own criteria for labelling as a human carcinogen. For some reason, the EPA appears to be dragging its feet in fully condemning PFOA.

PTFE has also been shown to cause cancer of the liver and kidneys as well as leukaemia – but again, in rodents (Natl Toxicol Program Tech Rep Ser, 1997; 450: 1-321; Toxicol Pathol, 2004; 32: 222-8). However, based on this evidence, it is “reasonably anticipated to be a human carcinogen”, according to the US Department of Health and Human Services National Toxicology Program Report on Carcinogens (11th edition).

Birth defects

The EWG recently unearthed a decades-old internal DuPont company-research memo stating that PFOA had been found in the umbilical cord blood of an infant born to a company worker, and in the blood of another worker’s baby. In the same memo, serious birth defects in two of seven babies born to female Teflon®-plant workers were also recorded. According to the memo, one baby was born with “one nostril and eye defect”; the other had an “unconfirmed eye and tear duct defect”.

According to the EWG, DuPont did remove women from the plant, but these findings were never reported to the EPA. This revelation sparked off an EPA review of DuPont company practices concerning PFOA, including the potential contamination of the Lubeck, West Virginia, and Little Hocking, Ohio, tap-water systems for at least 17 years (www.ewg.org/issues/pfcs/20040617/index.php?print_ version=1).

Kim Wallace

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