Perfluorooctanoic acid

Perfluorooctanoic acid
Names
IUPAC name
pentadecafluorooctanoic acid
Other names
perfluorooctanoic acid, PFOA, C8, perfluorooctanoate, perfluorocaprylic acid, FC-143, F-n-octanoic acid, PFO
Identifiers
335-67-1 YesY
3D model (Jmol) Interactive image
ChEBI CHEBI:35549 YesY
ChEMBL ChEMBL172988 YesY
ChemSpider 9180 YesY
ECHA InfoCard 100.005.817
EC Number 206-397-9
PubChem 9554
RTECS number RH0781000
Properties
C8HF15O2
Molar mass 414.07 g/mol
Appearance colorless liquid
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
Main hazards Strong Acid, Causes Burns
Safety data sheet [1]
R-phrases R22 R34 R52/53
S-phrases S26 S36/37/39 S45
NFPA 704
Flammability code 0: Will not burn. E.g., water Health code 3: Short exposure could cause serious temporary or residual injury. E.g., chlorine gas Reactivity code 0: Normally stable, even under fire exposure conditions, and is not reactive with water. E.g., liquid nitrogen Special hazards (white): no codeNFPA 704 four-colored diamond
0
3
0
Related compounds
Related compounds
 Perfluorooctanesulfonic acid (PFOS), Perfluorononanoic acid (PFNA), Perfluorooctanesulfonamide (PFOSA), Trifluoroacetic acid (TFA)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
YesY verify (what is YesYN ?)
Infobox references

Perfluorooctanoic acid (PFOA) (conjugate base perfluorooctanoate), also known as C8, 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 polytetrafluoroethylene (commercially known as Teflon). PFOA has been manufactured since the 1940s in industrial quantities.[6] 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.[7]

The primary manufacturer of PFOS – 3M (known as Minnesota Mining and Manufacturing Company from 1902 to 2002) – began a production phase-out in 2002 in response to concerns by the United States Environmental Protection Agency (USEPA also known as EPA)[8]:2 and eight other companies agreed to gradually phase them out by 2015.[8]:3

By 2014 the USEPA had listed PFOA – free acid and PFOS -potassium salt – emergent contaminants.[8]:1

[PFOA and PFOS] are extremely persistent in the environment and resistant to typical environmental 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 and bioaccumulation potential of PFOS and PFOA pose potential adverse effects for the environment and human health.
— USEPA March 2014 page 1

History

3M (then Minnesota Mining and Manufacturing Company) began producing PFOA by electrochemical fluorination in 1947.[2] Starting in 1951, DuPont purchased PFOA from 3M for use in the manufacturing of specific fluoropolymers—commercially branded as Teflon, but DuPont internally referred to the material as C8.[9][10]

In the fall of 2000, lawyer Rob Bilott, a partner at Taft 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, products manufactured with PFOA were such an integral part of DuPont's earnings, $1 billion in annual profit, they chose to continue using PFOA.[9] Billott 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 of hepatomegaly in mice fed with PFOA.[9][11][12]

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.[13][14][15]

Bilott exposed how DuPont had been knowingly polluting water with PFOAs in Parkersburg, West Virginia since the 1980s.[9] In the 1980s and 1990s researchers investigated the toxicity of PFOA.[12]

In 1999, the United States Environmental Protection Agency (USEPA) ordered companies to examine the effects of perfluorinated chemicals after receiving data on the global distribution and toxicity of PFOS.[16] For these reasons, and USEPA pressure,[17] in May 2000, 3M announced the phaseout of the production of PFOA, PFOS, and PFOS-related products—the company's best-selling repellent.[18] 3M stated that they would have made the same decision regardless of USEPA pressure.[19]

Because of the 3M phaseout, in 2002 DuPont built its own plant in Fayetteville, NC to manufacture the chemical.[20] 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.[15] In 2013, Gore-Tex eliminated the use of PFOAs in the manufacture of its weatherproof functional fabrics.[21]

Synthesis

PFOA has two main synthesis routes, electrochemical fluorination (ECF) and telomerization.[2] The equation below represents the ECF route with hydrofluoric acid reacting with octanoyl chloride.[22]

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.[22] 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.[22] ECF also results in production wastes.[23] 3M synthesized ECF PFOA at their Cottage Grove, MN facility from 1947 to 2002 and was the world's largest producer.[2][23] ECF production continues on a smaller scale in Europe and Asia.[2]

PFOA is also synthesized by the telomerization represented below, where the telogen is the organoiodine compound and the taxogen is the unsaturated tetrafluoroethylene.[22][24]

C2F5I + 3 C2F4 → C2F5(C2F4)3I

The product is oxidized by SO3 to form PFOA.[22] 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.[22] After oxidation, distillation is used to separate PFOA from the other perfluorinated carboxylic acids.[22] The telomerization synthesis of PFOA was pioneered by DuPont,[22] and it is not well suited to the laboratory.[24] PFOA formed by telomerization is completely linear, in contrast to the mixture of structures formed by ECF.

Applications

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";[25] however, it is believed that paper is no longer treated with perfluorinated compounds, but with fluorotelomers with less than 0.1% PFOA.[26] The compound is also used in "insulators for electric wires, planar etching of fused silica",[24] fire fighting foam,[2][27] and outdoor clothing.[28] 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.[29][30]

ADONA, ammonium 4,8-dioxa-3H-perfluorononanoate, is 3M's PFOA replacement in the emulsion polymerization of fluoropolymers.[31]

As a salt, its dominant use is as an emulsifier for the emulsion polymerization of fluoropolymers such as polytetrafluoroethylene (PTFE, or Teflon), polyvinylidene fluoride, and fluoroelastomers.[32][33] For this use, 3M subsidiary Dyneon has a replacement emulsifer[34] despite DuPont stating PFOA is an "essential processing aid".[35] PFOA is used in the production of Gore-Tex[36] as it is PTFE-based. In PTFE processing, PFOA is in aqueous solution and forms micelles that contain tetrafluoroethylene and the growing polymer.[37] PFOA can be used to stabilize fluoropolymer and fluoroelastomer suspensions before further industrial processing and in ion-pair reversed-phase liquid chromatography it can act as an extraction agent.[38] PFOA also finds uses in electronic products and as an industrial fluorosurfactant.[36][39]

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.[40] 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.

Product Range
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

Properties

Strong polarized carbon–fluorine bonds make PFOA environmentally persistent.

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.[41] PFOA is an ideal surfactant because it can lower the surface tension of water more than hydrocarbon surfactants while having exceptional stability due to the presence of multiple carbon–fluorine bonds.[39][41] The stability of PFOA is desired industrially but is a cause of concern environmentally. PFOA is resistant to degradation by natural processes such as metabolism, hydrolysis, photolysis, or biodegradation[29] making it persist indefinitely[42] in the environment.

PFOA is found in environmental and biological fluids as the anion perfluorooctanoate.[43] PFOA is absorbed from ingestion and can penetrate skin.[13] 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[33] and possibly CAR.[44] In animals, PFOA is mainly present in the liver, blood, and kidneys.[13] PFOA does not accumulate in fat tissue, unlike traditional organohalogen persistent organic pollutants.[45] In humans, PFOA has an average elimination half-life of about 3 years.[46][47][48] Because of this long half-life,[49] PFOA has the potential to bioaccumulate.

Global occurrence and sources

PFOA contaminates every continent.[50] 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.[51] Due to the surfactant nature of PFOA, it has been found to concentrate in the top layers of ocean water.[52] PFOA is detected widely in surface waters, and is present in numerous mammals, fish, and bird species.[50] 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.[9] However, wildlife has much less PFOA than humans, unlike PFOS[53] and other longer perfluorinated carboxylic acids;[54] in wildlife, PFOA is not as bioaccumulative as longer perfluorinated carboxylic acids.[45]

Most industrialized nations have average PFOA blood serum levels ranging from 2 to 8 parts per billion;[55] the highest consumer sub-population identified was in Korea—with about 60 parts per billion.[53] In Peru,[56] Vietnam,[57] and Afghanistan[58] 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,[59] and concentrations of PFOA in US serum have declined by 25% in recent years.[60] Despite a decrease in PFOA, the longer perfluorinated carboxylic acid PFNA is increasing in the blood of US consumers.[59]

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.[10] 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.[2] PFOA can be measured in water from industrial sites other than fluorochemical plants. PFOA has also been detected in emissions from the carpet,[61] paper[62] and electronics industries.[63] The most important emission sources are carpet and textile protection as well as fire-fighting foams.[64]

Precursors

8:2 fluorotelomer alcohol, (8:2 FTOH), degrades environmentally to PFOA

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[65] and by simple abiotic reaction with water.[66] It has been argued that fluorotelomer-based polymers already produced might be major sources of PFOA globally for decades to come.[66] Other precursors that degrade to PFOA include 8:2 fluorotelomer alcohol (F(CF2)8CH2CH2OH), polyfluoroalkyl phosphate surfactants (PAPS),[67] and possibly N-EtFOSE alcohol (F(CF2)8SO2N(Et)CH2CH2OH).[50][68] When PTFE is degraded by heat (pyrolysis) it can form PFOA as a minor product.[69][70] 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.[71] 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.[72] 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.[73]

Sources to people

Food,[74] drinking water, outdoor air, indoor air,[75] dust, and food packagings[76] are all implicated as sources of PFOA to people.[67] However, it is unclear which exposure routes dominate[42] because of data gaps. When water is a source, blood levels are approximately 100 times higher than drinking water levels.[77][78]

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.[10] 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

Microwave popcorn bags can contain residual PFOA from fluorotelomers

PFOA is also formed as an unintended byproduct in the production of fluorotelomers[79] 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.[80] 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.[81] 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.[80]

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, journalist Peter 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.[82][83]

Fluorotelomer coatings are used in fast food wrappers, candy wrappers, and pizza box liners.[84] PAPS, a type of paper fluorotelomer coating, and PFOA precursor, is also used in food contact papers.[67]

Despite DuPont's asserting that "cookware coated with DuPont Teflon non-stick coatings does not contain PFOA",[85] residual PFOA was also detected in finished PTFE products including PTFE cookware (4–75 parts per billion).[81] However, PFOA levels ranged from undetectable (<1.5) to 4.3 parts per billion in a more recent study.[40] 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.[86] Overall, PTFE cookware is considered an insignificant exposure pathway to PFOA.[87][88]

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[42] and crops[89] around Decatur, AL.[90] The approximately 5000 acres of land were fertilized with "treated municipal sewage sludge, or biosolids".[42] PFOA was also detected in fodder grass grown in these soils[91] and the blood of the cattle feeding on this grass.[92] 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".[42] If traced to meat, it would be the first time perfluorochemicals were traced from sludge to food.[42] 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.[93]

Regulatory status

Drinking water and products

On May 25, 2016, the U.S. Environmental Protection Agency established drinking water health advisories for PFOA and PFOS. The lifetime health advisories and health effects support documents to assist federal, state, tribal, and local officials and managers of drinking water systems in protecting public health when these chemicals are present in drinking water. The levels of PFOS and PFOA concentrations under which adverse health effects are not anticipated to occur over a lifetime of exposure are 0.07 parts per billion (70 parts per trillion) [94]

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 seven or more related fluorinated carbon compounds in food packaging starting in 2010,[95][96] but the bill was vetoed by Governor Schwarzenegger.[97] 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.[97]

Fluorotelomers

Main article: Fluorotelomer

Fluorotelomer-based products have been shown to degrade to PFOA over periods of decades;[65] [66] these studies could lead the USEPA to require DuPont and others to reformulate products with a value over $1 billion.[98]

Health concerns

Toxicology data

PFOA is a carcinogen, a liver toxicant, a developmental toxicant, and an immune system toxicant, and also exerts hormonal effects including alteration of thyroid hormone levels.[33] Animal studies show developmental toxicity from reduced birth size, physical developmental delays, endocrine disruption, and neonatal mortality.[50][99] PFOA alters lipid metabolism.[50] It is an agonist of PPARα and is a peroxisome proliferator in rodents contributing to a well understood form of oxidative stress.[100] 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.[100]

A USEPA review notes PFOA has not "been shown to be mutagenic in a variety of assays".[33] PFOA has been described as a member of a group of "classic non-genotoxic carcinogens".[101] 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.[102] Criteria have been proposed that would allow PFOA, and other perfluorinated compounds, to be classified as "weakly non-specific genotoxic".[103]

Human data

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 their blood serum,[104] individuals occupationally exposed to PFOA have had blood serum levels over 100,000 parts per billion (100 parts per million or 0.01%) recorded.[105] 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.[10] 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.[20]

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.[106]

Consumers

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.[107] PFOA exposure was associated with decreased semen quality,[108] increased serum alanine aminotransferase levels,[109] and increased occurrence of thyroid disease.[49] 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.[110] 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.[111] In a paper presented at the 2009 annual meeting of the International Society of Environmental Epidemiology,[112] PFOA appeared to act as an endocrine disruptor by a potential mechanism on breast maturation in young girls.[113] A C8 Science Panel status report noted an association between exposure in girls and a later onset of puberty.[114]

PFOA has been associated with signs of reduced fetal growth including lower birth weight.[115][116][117] However, other studies have not replicated the lower birth weight finding[118][119] including a study on the DuPont exposed community.[120] PFOA exposure in the Danish general population was not associated with an increased risk of prostate, bladder, pancreatic, or liver cancer.[121] Maternal PFOA levels were not associated with an offspring's increased risk of hospitalization due to infectious diseases,[122] behavioral and motor coordination problems,[123] or delays in reaching developmental milestones.[124]

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.[47] 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.[125] Further data on the 69,030 member cohort[126] that is being studied by the panel is scheduled for release through 2012.[127] A 2011 epidemiological study demonstrated ‘‘probable link’’ between PFOA and kidney cancer, testicular cancer, thyroid disease, high cholesterol, pre-eclampsia and ulcerative colitis.[9][128]

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.[12][129] Bucky Bailey is one of the affected individuals, however, DuPont does not accept any liability from the toxicity of PFOA.[130] 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,[12] subsequent animal testing led DuPont to conclude there was no reproductive risk to women, and they were returned to the production unit.[131] 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.[132][133]

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.[12] The class was certified by Wood Circuit Court Judge George W. Hill.[134] As part of the settlement, DuPont is paying for blood tests and health surveys of residents believed to be affected.[135] 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.[136]

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".[137] On September 28, 2009, Judge Goodwin dismissed the claims of those residents except for medical monitoring.[134][138] By 2015, more than three thousand plaintiffs have filed personal-injury lawsuits against DuPont.[9]

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.[36]

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)."[12]

In October 2005, a USFDA study was published revealing PFOA and PFOA precursor chemicals in food contact and PTFE products.[81]

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.[139]

On February 15, 2005, the USEPA's Science Advisory Board (SAB) voted to recommended that PFOA should be considered a "likely human carcinogen".[140]

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".[141]

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.[142]

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.[67]

In November 2007, the Centers for Disease Control and Prevention (CDC) published data on PFOA concentrations comparing 1999–2000 vs. 2003–2004 NHANES samples.[59]

On January 15, 2009, the USEPA set a provisional health advisory level of 0.4 parts per billion in drinking water.[92]

On May 19, 2016, the EPA established a health advisory level of 0.07 parts per billion for PFOA and PFOS.[143]

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".[144]

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,[145] where "the sources are landfilled industrial wastes from a 3M manufacturing plant".[144]

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.[146][147] 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.[103] 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.[50] An expert panel concluded that "concentrations were considered too low to cause overt adverse health effects in the exposed population".[103]

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 in Dordrecht. 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".[148] As a result of this, the government commissioned several further studies, including blood tests and measurements in drinking water.

Australian action

On August 10, 2016, Australian litigation funder IMF Bentham announced an agreement to fund a class action led by the law firm Gadens against the Australian Department of Defence for economic loses to homeowners, fishers, and farmers resulting from the use of aqueous film forming foam (containing PFOA) at RAAF Base Williamtown.[149]

See also

References

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