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 Perfluorooctanoic acid visible in an emulsion | |
| Names | |
|---|---|
| Preferred IUPAC name Pentadecafluorooctanoic acid | |
| Other names Perfluorooctanoic acid, PFOA, C8, Perfluorooctanoate, PFO, Perfluorocaprylic acid, C8-PFCA, FC-143, F-n-octanoic acid | |
| Identifiers | |
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3D model (JSmol) | |
| ChEBI | |
| ChEMBL | |
| ChemSpider |
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| ECHA InfoCard | 100.005.817 |
| EC Number |
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| RTECS number |
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| UNII | |
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| Properties | |
| C8HF15O2 | |
| Molar mass | 414.07 g/mol |
| Appearance | White solid |
| Density | 1.8 g/cm3[1] |
| Melting point | 40 to 50 °C (104 to 122 °F; 313 to 323 K)[1] |
| Boiling point | 189 to 192 °C (372 to 378 °F; 462 to 465 K)[1] |
| Soluble, 9.5 g/L (PFO)[2] | |
| Solubility in other solvents | Polar organic solvents |
| Acidity (pKa) | ~0[3][4][5] |
| Hazards | |
| Occupational safety and health (OHS/OSH): | |
Main hazards | Strong acid, knowncarcinogen andpersistent organic pollutant |
| GHS labelling: | |
   | |
| Danger | |
| H302,H318,H332,H351,H360,H362,H372 | |
| P201,P202,P260,P263,P264,P270,P271,P280,P281,P301+P312,P304+P312,P304+P340,P305+P351+P338,P308+P313,P310,P312,P314,P330,P405,P501 | |
| NFPA 704 (fire diamond) | |
| Safety data sheet (SDS) | [1] |
| Related compounds | |
Related compounds |
|
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Perfluorooctanoic acid (PFOA;conjugate baseperfluorooctanoate; also known colloquially asC8, from its chemical formula C8HF15O2) is aperfluorinated carboxylic acid produced and used worldwide as an industrialsurfactant in chemical processes and as a chemical precursor. PFOA is considered a surfactant, or fluorosurfactant, due to its chemical structure, which consists of a perfluorinated,n-heptyl "tail group" and acarboxylic acid "head group". The head group can be described ashydrophilic while thefluorocarbon tail is bothhydrophobic andlipophobic.[6]
TheInternational Agency for Research on Cancer (IARC) has classified PFOA as carcinogenic to humans.[7] PFOA is one of many syntheticorganofluorine compounds collectively known asper- and polyfluoroalkyl substances (PFASs). Many PFAS such asPFOS, PFOA are a concern because they do not break down via natural processes and are commonly described aspersistent organic pollutants or "forever chemicals".[8] They can also move through soils and contaminate drinking water sources and can build up (bioaccumulate) in fish and wildlife.[8]Residues have been detected in humans and wildlife.[8][9]
PFOA is used in several industrial applications, including carpeting, upholstery, apparel, floor wax, textiles, fire fighting foam and sealants. PFOA serves as a surfactant in theemulsion polymerization offluoropolymers and as a chemical precursor for the synthesis of perfluoroalkyl-substituted compounds, polymers, and polymeric materials. PFOA has been manufactured since the 1940s in industrial quantities.[10] It is also formed by thedegradation ofprecursors such as somefluorotelomers. PFOA is used as a surfactant because it can lower thesurface tension of water more thanhydrocarbon surfactants while having exceptional stability due to having perfluoroalkyl tail group.[6][11] The stability of PFOA is desired industrially but is a cause of concern environmentally.
The primary manufacturer ofperfluorooctanesulfonic acid (PFOS),3M, began a production phase-out in 2002 in response to concerns expressed by theU.S. Environmental Protection Agency (EPA).[12]: 2 Eight other companies agreed to gradually phase out the manufacturing of the chemical by 2015.[12]: 3
By 2014, EPA had listed PFOA and perfluorooctanesulfonates (salts of perfluorooctanesulfonic acid, PFOS) asemergent contaminants:
PFOA and PFOS are extremely persistent in the environment and resistant to typicalenvironmental degradation processes. [They] are widely distributed across the higher trophic levels and are found in soil, air and groundwater at sites across the United States. The toxicity, mobility andbioaccumulation potential of PFOS and PFOA pose potential adverse effects for the environment and human health.[12]: 1
In 2024 EPA published drinking water regulations for PFOA and five other PFAS.[13]
3M (then the Minnesota Mining and Manufacturing Company) began producing PFOA byelectrochemical fluorination in 1947.[2] Starting in 1951,DuPont purchased PFOA from 3M for use in the manufacturing of specificfluoropolymers—commercially branded as Teflon—but DuPont internally referred to PFOA as C8.[14][15][16]
In 1968,organofluorine content was detected in theblood serum of consumers, and in 1976 it was suggested to be PFOA or a related compound such asPFOS.[17][18][19]
In 1999, EPA ordered companies to examine the effects of perfluorinated chemicals after receiving data on the global distribution and toxicity of PFOS.[20] For these reasons, and EPA pressure,[21] in May 2000, 3M announced the phaseout of the production of PFOA, PFOS, and PFOS-related products—the company's best-selling repellent.[22] 3M stated that they would have made the same decision regardless of EPA pressure.[23]
Because of the 3M phaseout, in 2002, DuPont built its own plant inFayetteville, North Carolina, to manufacture the chemical.[24] The chemical has received attention due to litigation from the PFOA-contaminated community around DuPont'sWashington Works facility inWashington, West Virginia, along with EPA focus. In 2004,ChemRisk—an "industry risk assessor" that had been contracted by Dupont, reported that over 1.7 million pounds of C8 had been "dumped, poured and released" into the environment from Dupont's Parkersburg, West Virginia-based Washington Works plant between 1951 and 2003.[25]
Research on PFOA has demonstrated ubiquity, animal-based toxicity, and some associations with human health parameters and potential health effects. Additionally, advances inanalytical chemistry in recent years have allowed the routine detection of low- and sub-parts per billion levels of PFOA in a variety of substances.[19] In 2013,Gore-Tex eliminated the use of PFOAs in the manufacture of its weatherproof functional fabrics.[26] Major companies producing PFOA signed with the Global PFOA Stewardship Program with the goal of elimination of PFOA by 2015.[27] Since then it has been eliminated from the production of non-stick materials used in cookware.GenX has been introduced as a replacement for PFOA, but in a 2015 study which tested the effects on rats, GenX caused many of the same health problems as PFOA, but required much higher concentrations. This is because GenX (C3) is a short chain alternative to PFOA. GenX also has a significantly shorter half-life than PFOA so it is not as bio-persistent as PFOA or other long chain perfluorinated chemicals.[28]
In the Autumn of 2000, lawyerRobert Bilott, a partner atTaft Stettinius & Hollister, won a court order forcing DuPont to share all documentation related to PFOA. This included 110,000 files, consisting of confidential studies and reports conducted by DuPont scientists over decades. By 1993, DuPont understood that "PFOA caused cancerous testicular, pancreatic and liver tumors in lab animals" and the company began to investigate alternatives. However, because products manufactured with PFOA were such an integral part of DuPont's earnings, $1 billion in annual profit, they chose to continue using PFOA.[14] Bilott learned that both "3M and DuPont had been conducting secret medical studies on PFOA for more than four decades", and by 1961 DuPont was aware ofhepatomegaly in mice fed with PFOA.[14][29][30]
Bilott exposed how DuPont had been knowingly polluting water with PFOAs inParkersburg, West Virginia, since the 1980s.[14] In the 1980s and 1990s, researchers investigated thetoxicity of PFOA.[30] Regarding a secret agreement between 3M and the government ofJersey (UK) to not perform group testing of residents and to help 3M avoid a class action, Billott toldThe Guardian: "I've not seen something like this where there's an agreement to try to help the company against claims by others, Particularly if it's something affecting public health and safety or research."[31]
For his work in the exposure of the contamination, Bilott received several awards includingThe Right Livelihood Award in 2017.[32] In film, this battle with DuPont has been depicted in the documentaryThe Devil We Know[33] and the legal thrillerDark Waters.
PFOA has two main synthesis routes,electrochemical fluorination (ECF) andtelomerization.[2] The ECF route seesoctanoyl chloride (theacid chloride ofoctanoic acid) reacted withhydrofluoric acid.[34] Multiple products are formed by ECF with the targetacid fluoride F(CF2)7COF being produced as only 10–15% of the yield, while the main products areperfluorinated cyclicetherisomers, includingFC-75.[34] This acid fluoride is hydrolyzed to yield PFOA as a mixture of straight-chain (78%), terminally branched (13%), and internally branched (9%) molecules, because ECF induces rearrangements in the carbon tail of the acid chloride.[34] ECF also results in production wastes.[35]3M synthesized ECF PFOA at theirCottage Grove, Minnesota facility from 1947 to 2002 and was the world's largest producer.[2][35] ECF production continues on a smaller scale in Europe and Asia.[2]
PFOA is also synthesized by thetelomerization represented below, where the telogen is theorganoiodine compound and the taxogen is thetetrafluoroethylene.[34][36] Each step is anaddition reaction where the carbon-iodine bond of the telogen is added across the carbon-carbon double bond of theunsaturated taxogen, resulting in the formation of a new telogen.
The product isoxidized bySO3 to form PFOA.[34] Since each addition produces a new teleomer,fluorotelomers like these form with varying length chains containing an even number of carbon atoms, depending on reaction conditions. Typically, most products within will contain between two and six taxogens (that is, from CF3(CF2)5I to CF3(CF2)13I).[34] After oxidation,distillation is used to separate PFOA from the other perfluorinated carboxylic acids.[34] The telomerization synthesis of PFOA was pioneered byDuPont,[34] and is not well suited to the laboratory.[36] 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 andwaxed papers";[37] however, it is believed that paper is no longer treated withperfluorinated compounds, but withfluorotelomers with less than 0.1% PFOA.[38] The compound is also used in "insulators forelectric wires, planar etching offused silica",[36]fire fighting foam,[2][39] and outdoor clothing.[40] 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.[41][42]
As asalt, its dominant use is as anemulsifier for theemulsion polymerization of fluoropolymers such as PTFE,polyvinylidene fluoride, andfluoroelastomers.[44][45] For this use, 3M subsidiary Dyneon has a replacement emulsifer[46] despite DuPont stating PFOA is an "essential processing aid".[47] In the past PFOA was used in the production ofGore-Tex[48] as it is PTFE-based. In PTFE processing, PFOA is inaqueous solution and formsmicelles that containtetrafluoroethylene and the growingpolymer.[49] PFOA can be used to stabilize fluoropolymer and fluoroelastomer suspensions before further industrial processing and inion-pairreversed-phase liquid chromatography it can act as an extraction agent.[50] PFOA also finds uses in electronic products and as an industrialfluorosurfactant.[48][11]
In a 2009 EPA 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.[51] Concentrations shown below range from not detected, or ND, (with thedetection limit in parentheses) to 6750 with concentrations innanograms of PFOA pergram of sample (parts per billion) unless stated otherwise.
| Product | Range, ng/g |
|---|---|
| Pre-treatedcarpeting | ND (<1.5) to 462 |
| Carpet-care liquids | 19 to 6750 |
| Treatedapparel | 5.4 to 161 |
| Treatedupholstery | 0.6 to 293 |
| Treated hometextiles | 3.8 to 438 |
| Treated non-woven medical garments | 46 to 369 |
| Industrial floorwax and wax removers | 7.5 to 44.8 |
| Stone, tile, and woodsealants | 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 |
PFOA contaminates everycontinent.[52] Two of the most common types of PFAS (more precisely, PFOS and PFOA) were phased out of production in the United States (US) in 2002 and 2015 respectively, but are still present in some imported products. PFOA and PFOS are found in every American person's blood stream in the parts per billion range, though those concentrations have decreased by 70% for PFOA and 84% for PFOS between 1999 and 2014, which coincides with the end of the production and phase out of PFOA and PFOS in the US.[53] PFOA has been detected in the central Pacific Ocean at lowparts per quadrillion ranges, and at lowparts per trillion (ppt) levels incoastal waters.[54] Due to the surfactant nature of PFOA, it has been found to concentrate in the top layers of ocean water.[55] PFOA is detected widely insurface waters, and is present in numerous mammals, fish, and bird species.[52] PFOA is in the blood or vital organs of Atlantic salmon, swordfish, striped mullet, gray seals, common cormorants, Alaskan polar bears, brown pelicans, sea turtles, sea eagles, Midwestern bald eagles, California sea lions and Laysan albatrosses on Sand Island, a wildlife refuge on Midway Atoll, in the middle of the North Pacific Ocean, about halfway between North America and Asia.[14] Because PFAS are ubiquitous in households, consumer products, food, and the environment generally, some trace levels reflecting this ubiquitous broad use of these compounds will make their way into thewastewater andsolid waste streams.[56]
However, wildlife has much less PFOA than humans, unlikePFOS[57] and other longerperfluorinated carboxylic acids;[58] in wildlife, PFOA is not as bioaccumulative as longer perfluorinated carboxylic acids.[59] Municipal wastewater andlandfillleachates are considered as important sources of PFOA to the environment.[60][61]
Most industrialized nations have average PFOAblood serum levels ranging from 2 to 8parts per billion;[62] the highest consumer sub-population identified was in Korea—with about 60parts per billion.[57] InPeru,[63]Vietnam,[64] andAfghanistan[65] 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,[66] and concentrations of PFOA in US serum have declined by 25% in recent years.[67] Despite a decrease in PFOA, the longer perfluorinated carboxylic acidPFNA is increasing in the blood of US consumers.[66] PFAS are also found in paper mill residuals, digestates, composts, and soils. Given the ubiquity of PFAS, and the comparative background levels which may be found in wastewater, biosolids, and leachates, setting requirements near analytical detection limits on these sources may not provide a discernable benefit to protecting public health.[56]
PFOA is released directly from industrial sites. For example, the estimate for the DuPont Washington Works facility is a total PFOA emissions of 80,000 pounds (lbs) in 2000 and 1,700 pounds in 2004.[15] A 2006 study, with two of four authors being DuPont employees, estimated about 80% of historical perfluorocarboxylate emissions were released to the environment fromfluoropolymer manufacture and use.[2] PFOA can be measured in water from industrial sites other than fluorochemical plants. PFOA has also been detected in emissions from thecarpet industry,[68] paper[69] and electronics industries.[70] The most important emission sources are carpet and textile protection products, as well as fire-fighting foams.[71]
PFOA can form as a breakdown product from a variety of precursor molecules. In fact, the main products of the fluorotelomer industry, fluorotelomer-based polymers, have been shown to degrade to form PFOA and related compounds, with half-lives of decades, both biotically[72] and by simple abiotic reaction with water.[73] It has been argued that fluorotelomer-based polymers already produced might be major sources of PFOA globally for decades to come.[73] Other precursors that degrade to PFOA include 8:2fluorotelomer alcohol (F(CF2)8CH2CH2OH), polyfluoroalkyl phosphate surfactants (PAPS),[74] and possiblyN-EtFOSE alcohol (F(CF2)8SO2N(Et)CH2CH2OH).[52][75] When PTFE (Teflon) is degraded by heat (pyrolysis) it can form PFOA as a minor product.[76][77] TheOrganisation for Economic Co-operation and Development (OECD) has compiled a list of 615 chemicals that have the potential to break down intoperfluorocarboxylic acids (PFCA) including PFOA.[78] However, not all 615 have the potential to break down to form PFOA.
A majority ofwaste 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.[79]A current PFOA precursor concern arefluorotelomer-based polymers; fluorotelomer alcohols attached to hydrocarbon backbones viaester linkages may detach and be free to biodegrade to PFOA.[80]
Food,[81]drinking water,[82] outdoorair, indoor air,[83]dust, andfood packagings[84] are all implicated as sources of PFOA to people.[74] However, it is unclear which exposure routes dominate[85] because of data gaps. When water is a source, blood levels are approximately 100 times higher than drinking water levels.[86][87]
People who lived in the PFOA-contaminated area around DuPont's Washington Works 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.[15] 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 watercarbon filter systems had lower PFOA levels.
In Jersey, UK, 18% of residents of an area were found to have elevated levels of PFOA, downstream from 3M fire retardant tests in weekly fire-service practice from the 1960s to the mid 1990s.[31] Bloodletting is used for these residents at a cost of $4500 per patient. The potatoes of the island were found to contain 10x the EU limit of PFOS.
PFOA is also formed as an unintended byproduct in the production offluorotelomers[88] and is present in finished goods treated with fluorotelomers, including those intended for food contact. Fluorotelomers are applied to food contact papers because they arelipophobic: they prevent oil from soaking into the paper from fatty foods. Also, fluorotelomers can bemetabolized into PFOA.[89] In aU.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 before application, while the oil frommicrowave popcorn bags contained 6–290 parts per billion PFOA after heating.[90] 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.[89]
In 2008 as news stories began to raise concerns about PFOA in microwaved popcorn, Dan Turner, DuPont's global public relations chief, said, "I serve microwave popcorn to my three-year-old." Five years later, journalistPeter Laufer wrote to Turner to ask if his child was still eating microwave popcorn. "I am not going to comment on such a personal inquiry", Turner replied.[91][92]
Fluorotelomer coatings are used in fast food wrappers, candy wrappers, and pizza box liners.[93] PAPS, a type of paper fluorotelomer coating, and PFOA precursor, is also used in food contact papers.[74]
Despite DuPont's assertion that "cookware coated with DuPont Teflon non-stick coatings does not contain PFOA",[94] residual PFOA was also detected in finishedPTFE products including PTFE cookware (4–75 parts per billion).[90] However, PFOA levels ranged from undetectable (<1.5) to 4.3 parts per billion in a more recent study.[51] Also, non-stick cookware is heated—which shouldvolatilize PFOA; PTFE products that are not heated, such as PTFE sealant tape, had higher (1800 parts per billion) levels detected.[95] Overall, PTFE cookware is considered an insignificant exposure pathway to PFOA.[96][97]
PFOA andPFOS were detected in "very high" (lowparts per million) levels in agricultural fields for grazing beef cattle[85] and crops[98] aroundDecatur, Alabama.[99] The approximately 5000acres of land were fertilized with "treated municipal sewagesludge, orbiosolids".[85] PFOA was also detected in fodder grass grown in these soils[100] and the blood of the cattle feeding on this grass.[101] The water treatment plant received process wastewater from a nearbyperfluorochemical manufacturing plant. 3M says they managed their own wastes, butDaikin America "discharged process wastewater to the municipal waste treatment plant".[85] If traced to meat, it would be the first time perfluorochemicals were traced from sludge to food.[85] However, theUSDA reported—with a detection limits of 20 parts per billion—non-detectable levels for both PFOA and PFOS in cattle muscle tissue.[102]
PFOA is frequently found in household dust, making it an important exposure route for adults, but more substantially, children. Children have higher exposures to PFOA through dust compared to adults.[103] Hand-to-mouth contact and proximity to high concentrations of dust make them more susceptible to ingestion, and increases PFOA exposure.[104] One study showed significant positive associations were recognized between dust ingestion and PFOA serum concentrations.[103] However, an alternate study found exposure due to dust ingestion was associated with minimal risk.[105]
In 2024 it was reported that a brand ofmenstrual pad was found to contain PFOA.[106]
In April 2024 EPA issued a final drinking water rule for PFOA, PFOS, GenX, PFBS, PFNA, and PFHxS.Public water systems must remove these six PFAS to near-zero levels by 2027. Grant funding is available from EPA to assist utilities in water testing and development of treatment systems.[13][107][108][109]
TheState of New Jersey published drinking water standards for PFOA and PFOS in 2020.[110] A standard for PFNA was published in 2018. This was the first state to publish PFAS standards in the absence of federal regulations.[111]SeeU.S. state government actions.
In 2018 theState of New York adopted drinking water standards of 10 ppt for PFOA and 10 ppt for PFOS, the most stringent such standards in the United States. The standards apply topublic water systems and took effect in 2019 after a public comment period.[112]
Using information gained through aFreedom of Information Act request, in May 2018 it was learned that January 2018 emails between theEPA, theOffice of Management and Budget, theDepartment of Defense, and theDepartment of Health and Human Services showed an effort to suppress the release of a draft report on the toxicology of PFOS and PFOA done by theAgency for Toxic Substances and Disease Registry. The report found that these chemicals endanger human health at a far lower level than EPA has previously called safe.[113] After media accounts of the effort surfaced, the regional EPA administrator for Colorado denied that EPA had anything to do with suppressing the report.[114] The report was released on June 21, 2018.[82]
The new ATSDR analysis derives provisionalMinimal Risk Levels (MRLs) of 3x10−6 mg/kg/day for PFOA and 2x10−6 mg/kg/day for PFOS during intermediate exposure.[115] The European Food Safety Authority opinion sets a provisional tolerable weekly intake (TWI) of 6 x10−6 mg/kg body weight per week for PFOA.[116]
An attempt to regulate PFOA in food packaging occurred in the US state of California in 2008. A bill, sponsored by State SenatorEllen Corbett and theEnvironmental Working Group, was passed in the house and senate that would have banned PFOA,PFOS, and seven or more related fluorinated carbon compounds in food packaging starting in 2010,[117][118] but the bill was vetoed byGovernor Schwarzenegger.[119] 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.[119]
Fluorotelomer-based products have been shown to degrade to PFOA over periods of decades;[72][73] these studies could lead EPA to require DuPont and others to reformulate products with a value over $1 billion.[120]
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PFOA is a possiblecarcinogen, a possible liver toxicant, a possible developmental toxicant, and a possibleimmune system toxicant, and also exertshormonal effects including alteration ofthyroid hormone levels at very high concentrations.[45] Animal studies show developmental toxicity from reduced birth size, physical developmental delays,endocrine disruption, andneonatal mortality.[52][121] PFOA alterslipid metabolism.[52]
In 2008, PFOA has been described as a member of a group of "classic non-genotoxic carcinogens".[122] However, a provisional German assessment notes that a 2005 study found PFOA to begenotoxic via a peroxisome proliferation pathway that producedoxygen radicals inHepG2 cells, and a 2006 study demonstrated the induction and suppression of a broad range ofgenes; therefore, it states that the indirectgenotoxic (and thus carcinogenic) potential of PFOAcannot be dismissed.[123] As of November 2023, theInternational Agency for Research on Cancer (IARC) has classified PFOA as carcinogenic to humans (Group 1) based on "sufficient" evidence for cancer in animals and "strong" mechanistic evidence in exposed humans.[7]
An additional study has shown PFOA to be developmentally toxic, hepatotoxic, immunotoxic, and to have negative effects of thyroid hormone production.[45]
PFOA is resistant to degradation by natural processes such asmetabolism,hydrolysis,photolysis, orbiodegradation[41] and has been found to persist in the environment.[85] PFOA is found in environmental and biological fluids as the anion perfluorooctanoate.[124] PFOA can be absorbed from ingestion and can penetrateskin.[17] The acid headgroup of PFOA enables binding toproteins withfatty acid orhormonesubstrates such asserum albumin, liver fatty acid-binding protein, and thenuclear receptorsPPARα[45] and possiblyCAR.[125]
In animals, PFOA is mainly present in theliver,blood, andkidneys.[17] PFOA does not accumulate infat tissue, unlike traditionalorganohalogenpersistent organic pollutants.[59] In humans, PFOA has an averageelimination half-life of about three years.[126][127][128] Because of this long half-life,[129] PFOA has the potential tobioaccumulate.
The levels of PFOA exposure in humans vary widely. While an average American might have 3 or 4parts per billion of PFOA present in their blood serum,[130] individuals occupationally exposed to PFOA have had blood serum levels over 100,000 parts per billion (100parts per million or 0.01%) recorded.[131] 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.[24]
Singlecross-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.[132] PFOA exposure was associated with decreasedsemen quality,[133] increased serumalanine aminotransferase levels,[134] and increased occurrence ofthyroid disease.[129] In a study of 2003–2004 US samples, a higher (9.8 milligram perdeciliter) total cholesterol level was observed when the highestquartile was compared to the lowest.[135] Along with other related compounds, PFOA exposure was associated with an increased risk ofattention deficit hyperactivity disorder (ADHD) in a study of US children aged 12–15.[136] In a paper presented at the 2009 annual meeting of the International Society of Environmental Epidemiology,[137] PFOA appeared to act as anendocrine disruptor by a potential mechanism onbreast maturation in young girls.[138] A C8 Science Panel status report noted an association between exposure in girls and a later onset ofpuberty.[139]
PFOA exposure on thyroid function has also been a topic of concern, and has found to negatively impact thyroid stimulating hormone even at low levels when exposed during fetal development.[140] PFOA is also shown to have obesogenic effects, and an experimental study found a positive correlation to low-dose prenatal exposure of PFOA and prevalence of overweight and high waist circumference in females at age 20.[141] A correlation between in utero PFOA exposure and mental performance has yet to be established, as many studies have resulted in insignificant results. For example, a study conducted near Parkersburg, West Virginia did not find a significant association between in utero PFOA exposure and performance of math skills or reading performance in children ages 6 to 12 living in the PFOA-contaminated water district.[142] Based on a cohort study conducted in the Mid-Ohio Valley, no clear association was found between prenatal exposure to PFOA and birth defects, although a possible association with brain defects was observed and requires further research and assessment.[143]
Extrapolated epidemiological data suggests a slight association between PFOA exposure and low birth weight.[144] This was consistent based on blood levels of PFOA metabolites regardless of the geographic residence of subjects.[144] Generally, the findings among human fetuses exposed to the chemical were considerably less drastic than what was seen in mice studies.[144] Because of this, studies linking exposure to low birth weight can be considered inconclusive.[144] PFOA exposure in the Danish general population was not associated with an increased risk ofprostate,bladder,pancreatic, orliver cancer.[145] Maternal PFOA levels were not associated with an offspring's increased risk of hospitalization due to infectious diseases,[146] behavioral and motor coordination problems,[147] or delays in reaching developmental milestones.[148]
In 2010, the three members of the C8 Science Panel[149] published areview of theepidemiological evidence on PFOA exposure inEnvironmental Health Perspectives.[127] 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 incardiovascular disease is unknown.[150] Further data on the 69,030 member cohort[151] that is being studied by the panel is scheduled for release through 2012.[152][obsolete source] A 2011 epidemiological study demonstrated "probable link" between PFOA and kidney cancer, testicular cancer, thyroid disease, high cholesterol, pre-eclampsia and ulcerative colitis.[14][153]
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.[30][154] Bucky Bailey is one of the affected individuals; DuPont, however, does not accept any liability from the toxicity of PFOA.[155] 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,[30] subsequent animal testing led DuPont to conclude there was no reproductive risk to women, and they were returned to the production unit.[156] 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.[157][158]
PFOA was proposed for listing under theStockholm Convention on Persistent Organic Pollutants in 2015, and on May 10, 2019, PFOA, its salts, and PFOA-related compounds were added to Annex A of the Stockholm Convention by the Conference of the Parties.[159] Several hundred salts and precursors of PFOA fall within the scope of the restriction.[160][161] A few specific exemptions remained. Among them is a time-bound exemption for PFOA in fire-fighting foam.
DuPont has used PFOA for over 50 years at its Washington Works plant. 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.[30] The class was certified by Wood Circuit Court Judge George W. Hill.[162] As part of the settlement, DuPont has paid forblood tests andhealth surveys of residents believed to be affected.[163] Participants numbered 69,030 in the study, which was reviewed by threeepidemiologists—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 would payUS$10.25 million in fines and an additional US$6.25 million for two supplemental environmental projects without any admission of liability.[164]
On September 30, 2008, Chief Judge Joseph R. Goodwin of theUnited 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".[165] On September 28, 2009, Judge Goodwin dismissed the claims of those residents except for medical monitoring.[162][166] By 2015, more than three thousand plaintiffs have filed personal-injury lawsuits against DuPont.[14] In 2017, DuPont reached a $670.7 million cash settlement[167] related to 3,550 personal injury lawsuits tied to PFOA contamination of drinking water in the Parkersburg area. Chemours, which was spun off from DuPont in 2015, agreed to pay half the settlement. Both companies denied any wrongdoing.
The government of Jersey signed a confidential agreement with 3M in 2005, agreeing to not pursue legal claims for £2.6m. Jersey must assist 3M in the defense of future claims.
A source told the Guardian that Jersey needed 3M's permission to proceed with blood tests to avoid 3M punitive measures. "The state got an agreement to do individual blood tests, but not screening, as that could be the first step towards a possible class action lawsuit."[31]
In 2002, a panel of toxicologists, including several from EPA, proposed a level of 150 ppb fordrinking water in the PFOA contaminated area around DuPont's Washington Works plant. This initially proposed level was much higher than any known environmental concentration[48] and was over 2,000 times the level EPA eventually settled on for the drinking water health advisory.
In July 2004, EPA filed a suit against DuPont alleging "widespread contamination" of PFOA near the Parkersburg, West Virginia 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)."[30]
In October 2005, a USFDA study was published revealing PFOA and PFOA precursor chemicals in food contact andPTFE products.[90]
On January 25, 2006, EPA announced a voluntary program with several chemical companies to reduce PFOA and PFOA precursor emissions by the year 2015.[168]
On February 15, 2005, EPA's Science Advisory Board (SAB) voted to recommended that PFOA should be considered a "likely humancarcinogen".[169]
On May 26, 2006, EPA's SAB addressed a letter to AdministratorStephen L. Johnson. Three-quarters of advisers thought the stronger "likely to be carcinogenic" descriptor was warranted, in opposition to EPA's own PFOA hazard descriptor of "suggestive evidence of carcinogenicity, but not sufficient to assess human carcinogenic potential".[170]
On November 21, 2006, EPA ordered DuPont 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.[171]
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.[74]
In November 2007, theCenters for Disease Control and Prevention (CDC) published data on PFOA concentrations comparing 1999–2000 vs. 2003–2004NHANES samples.[66]
In October 2021 the EPA proposed to designate PFOA and PFOS as hazardous substances in its PFAS Strategic Roadmap.[172][173] In September 2022 the EPA proposed to designate as hazardous substances under theSuperfund Comprehensive Environmental Response, Compensation, and Liability Act of 1980 (CERCLA).
In 2024 EPA published drinking water regulations for PFOA and five other PFAS.[13]
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In 2007 theNew Jersey Department of Environmental Protection (NJDEP) announced that it found PFOA at "elevated levels in the system's drinking water near DuPont's massiveChambers Works chemical plant".[174]
In 2018 the state published a drinking water standard for PFNA.Public water systems in New Jersey are required to meet amaximum contaminant level (MCL) standard of 13 ppt.[111][175]
In 2019 New Jersey filed lawsuits against the owners of two plants that had manufactured PFASs (the Chambers Works and the Parlin plant inSayreville), and two plants that were cited for water pollution from other chemicals. The companies cited are DuPont, Chemours and 3M.[176]
In 2020 the NJDEP set a PFOA standard at 14 ppt and a PFOS standard at 13 ppt.[110]
In 2018 theNew York State Department of Health adopted drinking water standards of 10 ppt for PFOA and 10 ppt for PFOS, effective in 2019 after a public comment period.[112]
In November 2017, the Michigan PFAS Action Response Team (MPART) was created to address growing pollution concerns after multiple sites contaminated by PFAS were identified. MPART is a multi-agency team tasked with investigating PFAS contamination sites and sources in the state, protecting drinking water, enhancing interagency communication and keeping the public informed.[177]
In January 2018, Michigan established a legally enforceable groundwater cleanup level of 70 ppt for both PFOA and PFOS. Two science advisory committees were also created and joined MPART to "coordinate and review medical and environmental health, PFAS science and develop evidence-based recommendations".[178]
In August 2020, theMichigan Department of Environment, Great Lakes, and Energy adopted stricter drinking water standards in the form ofMCLs, lowering acceptable levels from the 2018 enforceable groundwater cleanup levels of 70 ppt to 8 ppt for PFOA and 16 ppt for PFOS and adding MCLs for 5 previously unregulated PFAS compounds PFNA,PFHxA,PFHxS,PFBS, andHFPO-DA.[179][180]
In 2007, theMinnesota Department of Health lowered its Health Based Value for PFOA in drinking water from 1.0 ppb to 0.5 ppb,[181] where "the sources are landfilled industrial wastes from a 3M manufacturing plant".[174]
PFOA contaminated waste was incorporated into soil improver and spread on agricultural land in Germany, leading to PFOA drinking water contamination of up to 0.519parts per billion.[182][183] The German Federal Environmental Agency issued guidelines for the sum of PFOA andPFOS concentrations in drinking water: 0.1 parts per billion for precaution and 0.3 parts per billion for a threshold.[184] 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.[52] An expert panel concluded that "concentrations were considered too low to cause overt adverse health effects in the exposed population".[184]
In the Netherlands, after questions by members of Parliament, the minister of Environment ordered a study into the potential exposure to PFOA of people living in the vicinity of the DuPont factory inDordrecht. The report was published in March 2016 and concluded that "prior to 2002 residents were exposed to levels of PFOA at which health effects could not be ruled out".[185] As a result of this, the government commissioned several further studies, including blood tests and measurements in drinking water.
PFOA was identified as aPBT substance in the EU in 2013. It was then included in the candidate list ofsubstances of very high concern. In 2017, PFOA, its salts and PFOA-related substances were added to annex XVII (restriction) of theREACH Regulation.[186]
The EU adopted the listing of PFOA in Annex A of the Stockholm Convention with Commission Delegated Regulation (EU) 2020/784 of 8 April 2020 and introduced a limit value of 0,025 mg/kg for PFOA including its salts, and at 1 mg/kg for the individual PFOA-related compounds or a combination of those compounds.[187] They also included some specific exemptions. Among them is a time-bound exemption for PFOA in fire-fighting foam.
On August 10, 2016, Australianlitigation funder IMF Bentham announced an agreement to fund a class action led by the law firmGadens against the Australian Department of Defence for economic losses to homeowners, fishers, and farmers resulting from the use ofaqueous film forming foam (containing PFOA) atRAAF Base Williamtown.[188]
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