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Perfluorooctanoic acid
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Perfluorooctanoic acid (PFOA), also known as C8 and perfluorooctanoate, is a synthetic, stable perfluorinated carboxylic acid and fluorosurfactant. One industrial application is as surfactant in the emulsion polymerization of fluoropolymers. PFOA has been produced since the 1940s in industrial synthesis. It is also formed by the degradation of precursors such as 8:2 fluorotelomer alcohol.
PFOA is a toxicant and carcinogen in animals, persistent in the environment, and detected in the blood of general populations in the low parts per billion range where it has been linked to infertility.
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Encyclopedia
Perfluorooctanoic acid (PFOA), also known as C8 and perfluorooctanoate, is a synthetic, stable perfluorinated carboxylic acid and fluorosurfactant. One industrial application is as surfactant in the emulsion polymerization of fluoropolymers. PFOA has been produced since the 1940s in industrial synthesis. It is also formed by the degradation of precursors such as 8:2 fluorotelomer alcohol.
PFOA is a toxicant and carcinogen in animals, persistent in the environment, and detected in the blood of general populations in the low parts per billion range where it has been linked to infertility. In people with higher exposures, PFOA is linked to birth defects, increased cancer rates, and changes to lipid levels, the immune system, and liver, effects identified in animals.
PFOA has been detected in industrial waste and consumer products including stain resistant carpets, microwave popcorn bags, food packaging, and Teflon (PTFE). PFOA is also found in food and water.
History
In 1947, 3M began producing PFOA by the electrochemical fluorination method. 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 likely be PFOA. In 1980, PFOA was identified as the primary organofluorine present in the blood serum of fluorochemical production workers. In the 1980s and 1990s researchers investigated the toxicity of PFOA. In 1999, the USEPA began investigating perfluorinated chemicals after receiving data on the global distribution and toxicity of PFOS. For these reasons, in May of 2000, 3M announced the phaseout of the production of PFOA, PFOS, and PFOS-related products. Because of the 3M phaseout, in 2002 DuPont built its own plant in Fayetteville, NC to manufacture the chemical. The PFOA contaminated community around DuPont's Washington Works Washington, WV facility, along with research demonstrating the ubiquity, toxicity, and links to human effects have increased scrutiny towards the chemical. Additionally, advances in analytical chemistry in recent years have allowed the routine detection of low- and sub-parts per billion levels of PFOA in water, food, wildlife, and humans.
Synthesis
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 + HF ? H(CH2)7COF + C7H16 + 2C8F16O + HCl + H2
The equation demonstrates the inefficiency of ECF for the production of PFOA. 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%), 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 1947-2002 and was the world's largest producer. ECF production continues on a smaller scale in Europe and Asia.
PFOA is also synthesized by the telomerization represented below where the telogen is the organoiodine compound while the taxogen is the unsaturated tetrafluoroethylene.
- C2F5I + 3C2F4 ? C2F5(C2F4)3I
The product is oxidized by reaction with SO3 to form PFOA. Under reaction conditions, telomers form with different carbon chain lengths of an even number, 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 for the laboratory. PFOA formed by telomerization is completely linear, in contrast to a minority of branched PFOA isomers formed by ECF.
Applications
PFOA has widespread applications. Historically, the acid form was the dominant perfluorinated carboxylic acid used as a reactive intermediate in the production of fluoroacrylic esters. Currently, the salt form is used as an emulsifier for the emulsion polymerization of fluoropolymers such as polytetrafluoroethylene (PTFE, or Teflon), polyvinylidene fluoride, and fluoroelastomers. In PTFE processing, PFOA is in aqueous solution and forms micelles that contain tetrafluoroethylene and the growing polymer. PFOA is used in the production of stain-resistant carpets and Gore-Tex. Carpet manufacturers of brands such as STAINMASTER have stated that PFOA production and emission from plants are the result of PFOA being an "unwanted byproduct." However, USEPA scientist John Washington wrote in an email that "...the industry has claimed that PFOA is an unintended impurity, I now suspect that it has been intended---or at least very [c]onvenient---because it helps to stabilize the...particles."
PFOA is used in aircraft production processes, electronic products, personal care products, and as a fluorocarbon-based industrial surfactant. PFOA is also used in the automotive, chemical, medical, and building/construction industries.
Properties
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 suceptible 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.
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 how it binds proteins with fatty acid or hormone substrates such as serum albumin, liver fatty acid-binding protein, ß-lipoproteins, and the nuclear receptor PPARa. PFOA is involved in enterohepatic circulation and is mainly present in the liver, blood serum, and kidney of humans and other animals. PFOA does not accumulate in fat tissue, unlike most organohalogen persistent organic pollutants. In humans, PFOA has an elimination half-life of about 4 years. Because of this long half-life, PFOA has the to 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 and may even concentrate further into sea spray aerosols. PFOA is detected widely in surface waters, and is present in numerous mammal, fish, and bird species. However, wildlife has much less PFOA than humans, unlike PFOS and other longer chained perfluorinated carboxylic acids. PFOA has been detected in humans globally with the highest average consumer concentrations found in Korea, at about 60 parts per billion in blood serum. While in 2003-2004 99.7% of Americans had detectable PFOA in their blood serum with an average of about 4 parts per billion, concentrations of PFOA in US blood serum have declined by 25% in recent years. Despite a decrease in PFOA, the related chemical PFNA, a longer chained perfluorinated carboxylic acid, is increasing in the blood of US consumers.
Industrial sources
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 flurochemical plants. PFOA has also been detected in emissions from the carpet industry and paper industry.
Precursors
, (8:2 FTOH), degrades environmentally to PFOA]]
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), polyfloroalkyl phosphate surfactants (PAPS), and N-EtFOSE alcohol (F(CF2)8SO2N(Et)CH2CH2OH). The Organisation for Economic Co-operation and Development (OECD) has compiled a list of chemicals that have the potential to break down into perfluorocarboxylic acids (PFCA) including PFOA. The OECD identified 615 chemicals that potentially break down to form PFCA. However, not all of these chemicals 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 the stability of fluoropolymers themselves; fluorotelomer alcohols attached to products via ester linkages and fluoroacrylic esters may 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. Contaminated food and drinking water are thought to be the largest contributors, while consumer products such as impregnation sprays (textile treatments), treated carpets, and coated food contact materials are considered as minor. Citizens that 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.
Fluorotelomer and Teflon 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 an 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 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/Teflon cookware. Additionally, a New York State Department of Health study detected PFOA in the gas phase coming from new nonstick cookware and microwave popcorn bags in research funded by a 2005-2006 $17,700 grant from the Consumers Union. However, PTFE cookware is considered an insignificant source of PFOA.
Other products
Residual PFOA is found in aqueous film forming foam (AFFF), a component of fire-fighting foams. Residual PFOA has also been detected in stain-resistant carpet (200-2000 parts per billion), mill-treated carpeting (200-600 parts per billion), treated apparel (up to 1400 parts per billion), and treated home textiles (up to 1400 parts per billion). PFOA was detected in the low-parts per billion range in industrial floor waxes and wax removers, latex paint, and home and office cleaners. Upon extraction PFOA was also detected in treated upholstery.
Potential 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.
Regulatory status
While there is no "legally enforceable federal standard" for the level of PFOA in drinking water in the US, on January 15, 2009 the Bush administration 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.
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 approved 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 impacted fluorochemical manufacturers outside of the state, and Schwarzenegger was lobbied by the chemical industry to veto. Schwarzenegger said the compound should be reviewed by the newly established, and more comprehensive, state program.
Health concerns
Animal data
PFOA is a carcinogen, liver toxicant, a developmental toxicant, an immune system toxicant, and also exerts hormonal effects. PFOA alters lipid metabolism. Animal studies show developmental toxicity from reduced birth size, physical developmental delays, endocrine disruption, and neonatal mortality. PFOA alters thyroid hormone levels. PFOA causes liver cancer in rodents and also induces testicular and pancreatic cancer through induction of Leydig cell tumors and pancreatic acinar cell tumors. PFOA is an agonist of PPARa and is a peroxisome proliferator in rodents contributing to a well understood form of oxidative stress. However, humans are considered less susceptible to peroxisome proliferation than rodents, and recently PFOA was found to be a liver carcinogen in rainbow trout via an estrogenic mechanism, which may be more relevant to humans.
While PFOA has been found to cause oxidative DNA damage in the liver of animals, classifying PFOA as mutagenic or genotoxic is proposed but not widely accepted by regulatory agencies. A 2007 USEPA toxicology review states, regarding PFOA and PFOS, that "neither compound has been shown to be mutagenic in a variety of assays" and then cites three sources: one authored by 3M, one authored by 3M, DuPont, Covance, Atofina, and Ineos Chlor, and one from the USEPA. As early as 1991 researchers from Japan demonstrated oxidative liver DNA damage in an experiment with rats. In Germany criteria have been proposed that would allow PFOA, and other perfluorinated compounds, to be classified as "weakly non-specific genotoxic."
Human data
The levels of PFOA exposure in humans varies widely. While an average American might have 3 or 4 parts per billion of PFOA present in their blood serum, individuals occupationally exposed to PFOA have had blood serum levels over 100,000 parts per billion (100 parts per million) 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.
Consumers
For general populations, blood serum levels of PFOA have been linked to infertility in a 2009 study from UCLA researchers. The 2009 infertility study measured levels of PFOS and PFOA and the "results showed a very strong statistical relationship between...levels and time to pregnancy. Women who had large amounts...in their blood were more than twice as likely to have taken more than a year to fall pregnant (or to have needed infertility treatment) than those with low levels." PFOA might also contribute to decreased semen quality.
PFOA has also been associated with lower birth weight in babies in two 2007 studies. In response to media coverage from the two studies, the American Council on Science and Health (ACSH) labeled the idea that "PFOA Causes Low Birth Weight Babies" as #4 on their Top Ten Unfounded Health Scares of 2007. The ACSH said that "PFOA affecting birth weight by four ounces does not imply any real harm to the babies - they were all of normal weight." While the ACSH implied causality, more recently, a smaller Canadian study did not find any inverse relationship between PFOA levels and birth weight. Additionally, a study on the DuPont exposed community found no association with PFOA levels and birth weight.
Employees and DuPont exposed community
Occupationally exposed female workers have demonstrated troubling data concerning PFOA exposure. 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 1979-1981. Bucky Bailey is one of the affected individuals, however, DuPont does not accept any responsibility from the toxicity of PFOA. With empolyees, a 2000 3M epidemiology study recorded statistically significant increases in cholesterol, triglyceride, and triiodothyronine levels and a statistically significant decrease in HDL with increasing levels of PFOA. A 3M funded study found workers who were highly exposed to PFOA had twice the odds of dying from prostate cancer and stroke when compared to other workers at the same plant; in response, 3M's spokesman said, "nothing in this study changes our conclusion that there are no adverse health effects from PFOA." A DuPont report on the rate of occurrence of carcinoid tumors at their Washington, WV plant gave "preliminary evidence for a cancer cluster." DuPont responded by stating that they did not have any reason to believe the increase from the Washington Works plant was due to any specific chemical. In a May 2008 preliminary report released by West Virginia University (WVU), PFOA was linked to liver, thyroid, immune system, and cholesterol changes considered harmful in the population around DuPont's Washington, WV plant. In a quick response to the release of the WVU report, DuPont's spokesman highlighted the preliminary nature and the legal issue of the C8 Science Panel being the only court appointed authority on study results. The C8 Science Panel also criticized the WVU release, labeling the graphs as "simple" that related PFOA to several blood tests because they did not represent a thorough data analysis. In October 2008, when the C8 Science Panel released findings, PFOA was only linked to high levels of cholesterol. Despite evidence PFOA may harm humans, DuPont's position is that the data does not prove PFOA causes health effects.
A 2008 legal opinion stated that health concerns from PFOA exposed citizens around DuPont's Washington Works WV plant were justified. Chief Judge Joseph R. Goodwin wrote that the "plaintiffs have presented compelling evidence that exposure to C-8 may be harmful to human health, and the evidence certainly justifies the concerns expressed by the plaintiffs in this case."
Legal actions
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 2001, claiming that the chemical contaminated area drinking water (DuPont and C-8). As part of the settlement, DuPont is paying for blood tests and health surveys of residents believed to be affected. Up to 60,000 people are expected to participate in the study, which will be reviewed by epidemiologists to determine any likely health effects.
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 because residents exposed to PFOA from DuPont's Washington Works WV facility did not "show the common individual injuries needed to certify a class action."
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)."
In October 2005, a USFDA study was published revealing PFOA and PFOA precursor chemicals in food contact and PTFE/Teflon products.
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. Since then, it has become obvious that other companies and industries operate outside of the voluntary program.
On February 15, 2005, the USEPA's Science Advisory Board (SAB) voted to recommended that PFOA should be considered a "likely human carcinogen."
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.
In November 2007, the Centers for Disease Control and Prevention (CDC) published data on PFOA concentrations comparing 1999-2000 vs. 2003-2004 NHANES samples.
On January 15, 2009 the USEPA set 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 1, 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."
European action
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."
See also
External links
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