||This article needs more medical references for verification or relies too heavily on primary sources. (November 2013)|
|Jmol-3D images||Image 1|
|Molar mass||414.07 g/mol|
|Melting point||40 to 50 °C (104 to 122 °F; 313 to 323 K)|
|Boiling point||189 to 192 °C (372 to 378 °F; 462 to 465 K)|
|Solubility in water||soluble, 9.5 g/L (PFO)|
|Solubility in other solvents||polar organic
|R-phrases||R22 R34 R52/53|
|S-phrases||S26 S36/37/39 S45|
|Main hazards||Strong Acid, Causes Burns|
|Related compounds||Perfluorooctanesulfonic acid (PFOS), Perfluorononanoic acid (PFNA), Perfluorooctanesulfonamide (PFOSA), Trifluoroacetic acid (TFA)|
|Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)|
|(what is: / ?)|
Perfluorooctanoic acid (PFOA), also known as C8 and perfluorooctanoate, is a synthetic perfluorinated carboxylic acid and fluorosurfactant. One industrial application is as a surfactant in the emulsion polymerization of fluoropolymers. It has been used in the manufacture of such prominent consumer goods as Teflon. In 2013, Gore-Tex eliminated the use of PFOAs in the manufacture of its weatherproof functional fabrics. PFOA has been manufactured since the 1940s in industrial quantities. It is also formed by the degradation of precursors such as some fluorotelomers.
PFOA persists indefinitely in the environment. It is a toxicant and carcinogen in animals. PFOA has been detected in the blood of more than 98% of the general US population in the low and sub-parts per billion range, and levels are higher in chemical plant employees and surrounding subpopulations. How general populations are exposed to PFOA is not completely understood. PFOA has been detected in industrial waste, stain resistant carpets, carpet cleaning liquids, house dust, microwave popcorn bags, water, food, some cookware and PTFE such as Teflon.
As a result of a class-action lawsuit and community settlement with DuPont, three epidemiologists conducted studies on the population surrounding a chemical plant that was exposed to PFOA at levels greater than in the general population. The studies concluded that there was probably an association between PFOA exposure and six health outcomes: kidney cancer, testicular cancer, ulcerative colitis, thyroid disease, hypercholesterolemia (high cholesterol), and pregnancy-induced hypertension.
- 1 History
- 2 Synthesis
- 3 Applications
- 4 Properties
- 5 Global occurrence and sources
- 6 Regulatory status
- 7 Health concerns
- 8 Legal actions
- 9 See also
- 10 References
- 11 External links
In 1947, 3M began producing PFOA by electrochemical fluorination. In 1951, DuPont started using PFOA in the manufacturing of fluoropolymers in Washington, WV. In 1961, DuPont was aware of hepatomegaly in mice fed with PFOA. In 1968, organofluorine content was detected in the blood serum of consumers, and in 1976 it was suggested to be PFOA or a related compound such as PFOS. In the 1980s and 1990s researchers investigated the toxicity of PFOA.
In 1999, the United States Environmental Protection Agency (USEPA) began investigating perfluorinated chemicals after receiving data on the global distribution and toxicity of PFOS. For these reasons, and USEPA pressure, in May 2000, 3M announced the phaseout of the production of PFOA, PFOS, and PFOS-related products. 3M stated that they would have made the same decision regardless of USEPA pressure.
Because of the 3M phaseout, in 2002 DuPont built its own plant in Fayetteville, NC to manufacture the chemical. The chemical has received attention due to litigation from the PFOA-contaminated community around DuPont's Washington Works Washington, WV facility, along with USEPA focus. Research on PFOA has demonstrated ubiquity, animal-based toxicity, and some associations with human health parameters and potential health effects. Additionally, advances in analytical chemistry in recent years have allowed the routine detection of low- and sub-parts per billion levels of PFOA in a variety of substances.
A settlement of $235 million was awarded to those who brought action against the company, "DuPont". C8 was known to cause health issues by DuPont but the company kept this fact in the closet for years until uncovered in the lawsuit. A team of experts revealed that it has found a "probable link" between C8 and human cancers, rebuffing DuPont Co.'s longstanding contention that exposure to the chemical is harmless. - See more at: http://www.wvgazette.com/News/201204160035#sthash.6jRuGBfr.dpuf
The panel found the kidney cancer rate among residents exposed to higher levels of C8 was between 20 percent and 60 percent higher than lesser-exposed residents, depending on the chemical concentrations. For testicular cancer, rates were between 80 percent and 170 percent higher among residents with higher exposures, the panel said. - See more at: http://www.wvgazette.com/News/201204160035#sthash.6jRuGBfr.dpuf
PFOA has two main synthesis routes, electrochemical fluorination (ECF) and telomerization. The equation below represents the ECF route with hydrofluoric acid reacting with octanoic acid chloride.
- H(CH2)7COCl + 17 HF → H(CH2)7COF + C7H16 + 2 C8F16O + HCl + H2
The equation above shows the multiple products of ECF. The target product, F(CF2)7COF (not represented) is produced as only 10–15% of the total product, while the main products are perfluorinated cyclic ether isomers, including FC-75. To yield PFOA, the perfluorinated acid fluoride is hydrolyzed. The PFOA formed by this method is a mixture of straight chain (78%), terminally branched (13%), and internally branched (9%) molecules, as ECF rearranges the carbon "tail" of the acid chloride. ECF also results in production wastes. 3M synthesized ECF PFOA at their Cottage Grove, MN facility from 1947 to 2002 and was the world's largest producer. ECF production continues on a smaller scale in Europe and Asia.
- C2F5I + 3 C2F4 → C2F5(C2F4)3I
The product is oxidized by SO3 to form PFOA. Under reaction conditions, telomers form with varying length chains containing an even number of carbon atoms, as products mostly contain two to six tetrafluoroethylene taxogens. After oxidation, distillation is used to separate PFOA from the other perfluorinated carboxylic acids. The telomerization synthesis of PFOA was pioneered by DuPont, and it is not well suited to the laboratory. PFOA formed by telomerization is completely linear, in contrast to the mixture of structures formed by ECF.
PFOA has widespread applications. In 1976, PFOA was reported as a water and oil repellent "in fabrics and leather and in the production of floor waxes and waxed papers"; however, it is believed that paper is no longer treated with perfluorinated compounds, but with fluorotelomers with less than 0.1% PFOA. The compound is also used in "insulators for electric wires, planar etching of fused silica", fire fighting foam, and outdoor clothing. As a protonated species, the acid form of PFOA was the most widely used perfluorocarboxylic acid used as a reactive intermediate in the production of fluoroacrylic esters.
As a salt, the dominant use is as an emulsifier for the emulsion polymerization of fluoropolymers such as polytetrafluoroethylene (PTFE, or Teflon), polyvinylidene fluoride, and fluoroelastomers. For this use, 3M subsidiary Dyneon has a replacement emulsifer despite DuPont stating PFOA is an "essential processing aid". PFOA is used in the production of Gore-Tex as it is PTFE-based. In PTFE processing, PFOA is in aqueous solution and forms micelles that contain tetrafluoroethylene and the growing polymer. PFOA can be used to stabilize fluoropolymer and fluoroelastomer suspensions prior to further industrial processing and in ion-pair reversed-phase liquid chromatography it can act as an extraction agent. PFOA also finds uses in electronic products and as an industrial fluorosurfactant.
In a 2009 USEPA study of 116 products—purchased between March 2007 and May 2008 and found to contain at least 0.01% fluorine by weight—the concentrations of PFOA were determined. Concentrations shown below range from not detected, or ND, (with the detection limit in parenthesis) to 6750 with concentrations in nanograms of PFOA per gram of sample—or parts per billion—unless stated otherwise.
|Pre-treated carpeting||ND (<1.5) to 462|
|Carpet-care liquids||19 to 6750|
|Treated apparel||5.4 to 161|
|Treated upholstery||0.6 to 293|
|Treated home textiles||3.8 to 438|
|Treated non-woven medical garments||46 to 369|
|Industrial floor wax and wax removers||7.5 to 44.8|
|Stone, tile, and wood sealants||477 to 3720|
|Membranes for apparel||0.1 to 2.5 ng/cm2|
|Food contact paper||ND (<1.5) to 4640|
|Dental floss/tape||ND (<1.5) to 96.7|
|Thread sealant tape||ND (<1.5) to 3490|
|PTFE cookware||ND (<1.5) to 4.3|
The carboxylate "head" of PFOA is hydrophilic while the fluorocarbon tail is hydrophobic and lipophobic. The "tail" is hydrophobic due to being non-polar and lipophobic because fluorocarbons are less susceptible to the London dispersion force than hydrocarbons. PFOA is an ideal surfactant because it can lower the surface tension of water more than hydrocarbon surfactants while possessing exceptional stability due to the presence of multiple carbon–fluorine bonds. The stability of PFOA is desired industrially, but a cause of concern environmentally. PFOA is resistant to degradation by natural processes such as metabolism, hydrolysis, photolysis, or biodegradation making it persist indefinitely in the environment.
PFOA is found in environmental and biological fluids as the anion perfluorooctanoate. PFOA is absorbed from ingestion and can penetrate skin. The oxygens on PFOA are responsible for how it binds proteins with fatty acid or hormone substrates such as serum albumin, liver fatty acid-binding protein, and the nuclear receptors PPARα and possibly CAR. In animals, PFOA is mainly present in the liver, blood, and kidneys. PFOA does not accumulate in fat tissue, unlike traditional organohalogen persistent organic pollutants. In humans, PFOA has an average elimination half-life of about 3 years. Because of this long half-life, PFOA has the potential to bioaccumulate.
Global occurrence and sources
PFOA contaminates every continent. PFOA has been detected in the central Pacific Ocean at low parts per quadrillion ranges, and at low parts per trillion levels in coastal waters. Due to the surfactant nature of PFOA, it has been found to concentrate in the top layers of ocean water. PFOA is detected widely in surface waters, and is present in numerous mammals, fish, and bird species. However, wildlife has much less PFOA than humans, unlike PFOS and other longer perfluorinated carboxylic acids; in wildlife, PFOA is not as bioaccumulative as longer perfluorinated carboxylic acids.
Most industrialized nations have average PFOA blood serum levels ranging from 2 to 8 parts per billion; the highest consumer sub-population identified was in Korea—with about 60 parts per billion. In Peru, Vietnam, and Afghanistan blood serum levels have been recorded to be below one part per billion. In 2003–2004 99.7% of Americans had detectable PFOA in their serum with an average of about 4 parts per billion, and concentrations of PFOA in US serum have declined by 25% in recent years. Despite a decrease in PFOA, the longer perfluorinated carboxylic acid PFNA is increasing in the blood of US consumers.
PFOA is released directly from industrial sites. For example, the DuPont Washington Works facility in Washington, WV estimated total PFOA emissions of 80,000 pounds (lbs) in 2000 and 1,700 pounds in 2004. A 2006 study, with two of four authors DuPont employees, estimated about 80% of historical perfluorocarboxylate emissions were released to the environment from fluoropolymer manufacture and use. PFOA can be measured in water from industrial sites other than fluorochemical plants. PFOA has also been detected in emissions from the carpet, paper and electronics industries. The most important emission sources are carpet and textile protection as well as fire-fighting foams.
PFOA can form as a breakdown product from a variety of precursor molecules. PFOA precursors can be transformed to PFOA by metabolism, biodegradation, or atmospheric processes. Examples include 8:2 fluorotelomer alcohol (F(CF2)8CH2CH2OH), polyfluoroalkyl phosphate surfactants (PAPS), and possibly N-EtFOSE alcohol (F(CF2)8SO2N(Et)CH2CH2OH). When PTFE is degraded by heat (pyrolysis) it can form PFOA as a minor product. The Organisation for Economic Co-operation and Development (OECD) has compiled a list of 615 chemicals that have the potential to break down into perfluorocarboxylic acids (PFCA) including PFOA. However, not all 615 have the potential to break down to form PFOA.
A majority of waste water treatment plants (WWTPs) that have been tested output more PFOA than is input, and this increased output has been attributed to the biodegradation of fluorotelomer alcohols. A current PFOA precursor concern are fluorotelomer-based polymers; fluorotelomer alcohols attached to hydrocarbon backbones via ester linkages may detach and be free to biodegrade to PFOA.
Sources to people
Food, drinking water, outdoor air, indoor air, dust, and food packagings are all implicated as sources of PFOA to people. However, it is unclear which exposure routes dominate because of data gaps. When water is a source, blood levels are approximately 100 times higher than drinking water levels.
People who lived in the PFOA contaminated area around DuPont's Washington Works Washington, WV facility were found to have higher levels of PFOA in their blood from drinking water. The highest PFOA levels in drinking water were found in the Little Hocking water system, with an average concentration of 3.55 parts per billion during 2002–2005. Individuals who drank more tap water, ate locally grown fruits and vegetables, or ate local meat, were all associated with having higher PFOA levels. Residents who used water carbon filter systems had lower PFOA levels.
Food contact surfaces
PFOA is also formed as an unintended byproduct in the production of fluorotelomers and is present in finished goods treated with fluorotelomers, including those intended for food contact. Fluorotelomers are applied to food contact papers because they are lipophobic: they prevent oil from soaking into the paper from fatty foods. Also, fluorotelomers can be metabolized into PFOA. In a U.S. Food and Drug Administration (USFDA) study, lipophobic fluorotelomer-based paper coatings (which can be applied to food contact paper in the concentration range of 0.4%) were found to contain 88,000–160,000 parts per billion PFOA, while microwave popcorn bags contained 6–290 parts per billion PFOA. Toxicologists estimate that microwave popcorn could account for about 20% of the PFOA levels measured in an individual consuming 10 bags a year if 1% of the fluorotelomers are metabolized to PFOA. Fluorotelomer coatings are used in fast food wrappers, candy wrappers, and pizza box liners. PAPS, a type of paper fluorotelomer coating, and PFOA precursor, is also used in food contact papers.
Despite DuPont's asserting that "cookware coated with DuPont Teflon non-stick coatings does not contain PFOA," residual PFOA was also detected in finished PTFE products including PTFE cookware (4–75 parts per billion). However, PFOA levels ranged from undetectable (<1.5) to 4.3 parts per billion in a more recent study. Also, non-stick cookware is heated—which should volatilize PFOA; PTFE products that are not heated, such as PTFE sealant tape, had higher (1800 parts per billion) levels detected. Overall, PTFE cookware is considered an insignificant exposure pathway to PFOA.
Potential path: sludge to food
PFOA and PFOS were detected in "very high" (low parts per million) levels in agricultural fields for grazing beef cattle and crops around Decatur, AL. The approximately 5000 acres of land were fertilized with "treated municipal sewage sludge, or biosolids." PFOA was also detected in the blood of the cattle. The water treatment plant received process wastewater from a nearby perfluorochemical manufacturing plant. 3M says they managed their own wastes, but Daikin America "discharged process wastewater to the municipal waste treatment plant." If traced to meat, it would be the first time perfluorochemicals were traced from sludge to food. However, the USDA reported—with a detection limits of 20 parts per billion—non-detectable levels for both PFOA and PFOS in cattle muscle tissue.
Drinking water and products
While there is no "legally enforceable federal standard" for the level of PFOA in drinking water in the US, on January 15, 2009, the U.S. Environmental Protection Agency (USEPA) set a "provisional health advisory" of 0.4 parts per billion in response to the detection of PFOA in agricultural soil. However, the advisory is not meant to protect the public from long term exposure but might protect individuals for "a couple of years." While water companies are not required to test for PFOA, it is a potential candidate for regulation under the Safe Drinking Water Act. As for consumer products, there is no federal safety standard for PFOA in the US.
California and food packaging
An attempt to regulate PFOA in food packaging occurred in the US state of California in 2008. A bill, sponsored by State Senator Ellen Corbett and the Environmental Working Group, was passed in the house and senate that would have banned PFOA, PFOS, and related seven or more fluorinated carbon compounds in food packaging starting in 2010, but the bill was vetoed by Governor Schwarzenegger. The bill would have affected fluorochemical manufacturers outside of the state. Schwarzenegger said the compound should be reviewed by the newly established, and more comprehensive, state program.
Fluorotelomer-based products are under extended investigation to determine their potential to degrade to PFOA; these studies could lead the USEPA to require DuPont and others to reformulate products with a value over $1 billion.
PFOA is a carcinogen, liver toxicant, a developmental toxicant, an immune system toxicant, and also exerts hormonal effects including alteration of thyroid hormone levels. Animal studies show developmental toxicity from reduced birth size, physical developmental delays, endocrine disruption, and neonatal mortality. PFOA alters lipid metabolism. It is an agonist of PPARα and is a peroxisome proliferator in rodents contributing to a well understood form of oxidative stress. Humans are considered less susceptible to peroxisome proliferation than rodents. However, PFOA has been found to be a liver carcinogen in rainbow trout via a potential estrogenic mechanism, which may be more relevant to humans.
A USEPA review notes PFOA has not "been shown to be mutagenic in a variety of assays". PFOA has been described as a member of a group of "classic non-genotoxic carcinogens". However, a provisional German assessment notes that a 2005 study found PFOA to be genotoxic via a peroxisome proliferation pathway that produced oxygen radicals in HepG2 cells, and a 2006 study demonstrated the induction and suppression of a broad range of genes; therefore, it states that the indirect genotoxic (and thus carcinogenic) potential of PFOA cannot be dismissed. Criteria have been proposed that would allow PFOA, and other perfluorinated compounds, to be classified as "weakly non-specific genotoxic."
The levels of PFOA exposure in humans vary widely. While an average American might have 3 or 4 parts per billion of PFOA present in his blood serum, individuals occupationally exposed to PFOA have had blood serum levels over 100,000 parts per billion (100 parts per million or 0.01%) recorded. In a study of individuals living around DuPont's Washington Works WV plant, those who had no occupational exposure had a median blood serum level of 329 parts per billion while the median of those with occupational exposure was 775 parts per billion. While no amount of PFOA in humans is legally recognized as harmful, DuPont was "not satisfied" with data showing their Chinese workers accumulated an average of about 2,250 parts per billion of PFOA in their blood from a starting average of around 50 parts per billion less than a year prior.
In late 2012, scientists at Emory University compared health risks in workers at a DuPont chemical plant in West Virginia with high PFOA exposure to the risks of the same diseases in other regional DuPont factory workers and in the US population. In comparison with the other DuPont workers, workers at the high-PFOA plant were at roughly three times the risk of dying of mesothelioma or chronic kidney disease, and roughly twice the risk of dying of diabetes mellitus. Workers were at similarly elevated risk for kidney cancer and for non-cancer kidney diseases. In rodents, PFOA concentrates in the kidneys.
Single cross-sectional studies on consumers have been published noting multiple associations. Blood serum levels of PFOA were associated with an increased time to pregnancy—or "infertility"—in a 2009 study. PFOA exposure was associated with decreased semen quality, increased serum alanine aminotransferase levels, and increased occurrence of thyroid disease. In a study of 2003–2004 US samples, a higher (9.8 milligram per deciliter) total cholesterol level was observed when the highest quartile was compared to the lowest. Along with other related compounds, PFOA exposure was associated with an increased risk of attention deficit hyperactivity disorder (ADHD) in a study of US children aged 12–15. In a paper presented at the 2009 annual meeting of the International Society of Environmental Epidemiology, PFOA appeared to act as an endocrine disruptor by a potential mechanism on breast maturation in young girls. A C8 Science Panel status report noted an association between exposure in girls and a later onset of puberty.
PFOA has been associated with signs of reduced fetal growth including lower birth weight. However, other studies have not replicated the lower birth weight finding including a study on the DuPont exposed community. PFOA exposure in the Danish general population was not associated with an increased risk of prostate, bladder, pancreatic, or liver cancer. Maternal PFOA levels were not associated with an offspring's increased risk of hospitalization due to infectious diseases, behavioral and motor coordination problems, or delays in reaching developmental milestones.
Employees and DuPont exposed community
In 2010, the three members of the C8 Science Panel published a review of the epidemiological evidence on PFOA exposure in Environmental Health Perspectives. Insufficient evidence exists to conclude PFOA causes adverse health effects in humans, but consistent evidence exists on associations with higher cholesterol and uric acid. Whether or not these potential effects result in an increase in cardiovascular disease is unknown. Further data on the 69,030 member cohort that is being studied by the panel is scheduled for release through 2012.
Facial birth defects, an effect observed in rat offspring, occurred with the children of two out of seven female DuPont employees from the Washington Works facility from 1979 to 1981. Bucky Bailey is one of the affected individuals, however, DuPont does not accept any liability from the toxicity of PFOA. While 3M sent DuPont results from a study that showed birth defects to rats administered PFOA and DuPont moved the women out of the Teflon production unit, subsequent animal testing led DuPont to conclude there was no reproductive risk to women, and they were returned to the production unit. However, data released in March 2009 on the community around DuPont's Washington Works plant showed "a modest, imprecise indication of an elevation in risk ... above the 90th percentile ... based on 12 cases in the uppermost category", which was deemed "suggestive of a possible relationship" between PFOA exposure and birth defects.
Industry and legal actions
DuPont has used PFOA for over 50 years at its Washington Works plant near Parkersburg, WV. Area residents sued DuPont in August 2001, and claimed DuPont released PFOA in excess of their community guideline of 1 part per billion resulting in lower property values and increased risk of illness. The class was certified by Wood Circuit Court Judge George W. Hill. As part of the settlement, DuPont is paying for blood tests and health surveys of residents believed to be affected. Participants number 69,030 in the study, which will be reviewed by three epidemiologists—the C8 Science Panel—to determine if any health effects are the likely result of exposure.
On December 13, 2005, DuPont announced a settlement with the EPA in which DuPont will pay US$10.25 million in fines and an additional US$6.25 million for two supplemental environmental projects without any admission of liability.
On September 30, 2008, Chief Judge Joseph R. Goodwin of the United States District Court for the Southern District of West Virginia denied the certification of a class of Parkersburg residents exposed to PFOA from DuPont's facility because they did not "show the common individual injuries needed to certify a class action." On September 28, 2009, Judge Goodwin dismissed the claims of those residents except for medical monitoring.
U.S. federal government actions
In 2002, a panel of toxicologists, including several from the USEPA, proposed a level of 150 parts per billion for drinking water in the PFOA contaminated area around DuPont's Washington Works WV plant; this level was much higher than any known environmental concentration.
In July 2004, the USEPA filed a suit against DuPont alleging "widespread contamination" of PFOA near the Parkersburg, WV, plant "at levels exceeding the company's community exposure guidelines;" the suit also alleged that "DuPont had—over a 20 year period—repeatedly failed to submit information on adverse effects (in particular, information on liver enzyme alterations and birth defects in offspring of female Parkersburg workers)."
On January 25, 2006, the USEPA announced a voluntary program with several chemical companies to reduce PFOA and PFOA precursor emissions by the year 2015.
On May 26, 2006, the USEPA's SAB addressed a letter to Stephen L. Johnson. Three-quarters of advisers thought the stronger "likely to be carcinogenic" descriptor was warranted, in opposition to the USEPA's own PFOA hazard descriptor of "suggestive evidence of carcinogenicity, but not sufficient to assess human carcinogenic potential."
On November 21, 2006, the USEPA ordered DuPont company to offer alternative drinking water or treatment for public or private water users living near DuPont's Washington Works plant in West Virginia (and in Ohio), if the level of PFOA detected in drinking water is equal to or greater than 0.5 parts per billion. This measure sharply lowered the previous action level of 150 parts per billion that was established in March 2002.
According to a May 23, 2007, Environmental Science & Technology Online article, U.S. Food and Drug Administration research regarding food contact papers as a potential source of PFOA to humans is ongoing.
On January 15, 2009, the USEPA set a provisional health advisory level of 0.4 parts per billion in drinking water.
U.S. state government actions
On February 13, 2007, the New Jersey Department of Environmental Protection issued a preliminary health-based guidance level of 0.04 parts per billion in drinking water, due to PFOA being found at "elevated levels in the system's drinking water near DuPont's massive Chambers Works chemical plant."
On March 28, 2007, the Minnesota Department of Health lowered its Health Based Value for PFOA in drinking water from 1.0 parts per billion to 0.5 parts per billion, where "the sources are landfilled industrial wastes from a 3M manufacturing plant."
PFOA contaminated waste was incorporated into soil improver and spread on agricultural land in Germany, leading to PFOA drinking water contamination of up to 0.519 parts per billion. The German Federal Environmental Agency issued guidelines for the sum of PFOA and PFOS concentrations in drinking water: 0.1 parts per billion for precaution and 0.3 parts per billion for a threshold. Residents were found to have a 6–8 factor increase of PFOA serum levels over unexposed Germans, with average PFOA concentrations in the 22–27 parts per billion range. An expert panel concluded that "concentrations were considered too low to cause overt adverse health effects in the exposed population."
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