Ammonium perfluorooctanoate

Perfluorooctanoic acid

| Section8 = }} Perfluorooctanoic acid (PFOA), also known as C8, is a man-made surfactant. PFOA can designate the acid itself, its principal salts (like ammonium perfluorooctanoate, also known as APFO), or its dissociated conjugate base perfluorooctanoate (also known as PFO).

PFOS is a related compound.

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 PFOA. In 1968, organofluorine content was detected in human blood serum. In 1976, it was hypothesized PFOA was in the blood of consumers. 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 EPA 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. After the PFOA-phaseout by 3M, increased attention has been directed towards PFOA.

Manufacture and uses

PFOA has four main synthesis routes: electrochemical fluorination of octanoic acid, oxidation of perfluoroiodooctane, carboxylation of perfluoroiodooctane, and fluorotelomer olefin oxidation. Using publicly available information, total global PFOA production during 1951-2004 was estimated at 7.2 - 11.4 million pounds with production sites located in the United States, Belgium, Italy, Japan, and Germany.

PFOA has widespread applications. It is used as an emulsifier for the processing of fluoropolymers such as polytetrafluoroethylene (PTFE, or Teflon) and polyvinylidene fluoride (PVDF). 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 fluoroelastomers. 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, EPA 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 perfluorinated 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 perfluorinated "tail" is hydrophobic and lipophobic, like other perfluorocarbons, because the "tail" is non-polar and resistant to van der Waals interactions. As a surfactant, the carboxylate group anchors PFOA to the surface of liquids. PFOA is a surfactant because perfluorinated carboxylates are surfactants when they possess 5-9 carbons. PFOA is an excellent surfactant because perfluorinated surfactants can lower the surface tension of water twice as low as the amount attained with hydrocarbon surfactants. Additionally, the eight-carbon chain lengths of PFOA (and PFOS) make them the most effective.

PFOA is a very stable compound due to the multitude of carbon-fluorine (C-F) bonds. C-F bonds are naturally rare and the strongest in organic chemistry. C-F bonds also strengthen the underlying backbone carbon-carbon bonds. Ironically, the stability of PFOA is desired industrially, but a cause of concern environmentally. PFOA does not break down by natural processes, such as metabolism, hydrolysis, photolysis, or biodegradation.

PFOA is found in environmental and biological fluids as the anion perfluorooctanoate, fully dissociated from its salts. The oxygens on PFOA are how it binds proteins with fatty acid or hormone substrates such as serum albumin, liver fatty acid-binding protein, and the nuclear receptor PPARα. PFOA is also involved in enterohepatic circulation. Therefore, PFOA is mainly present in the liver, blood serum, and kidney of humans and other animals. PFOA does not accumulate in fat tissue, unlike other 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 occurence

PFOA is dispersed globally. PFOA has been detected in the Arctic and Antartic regions. PFOA has been detected in the central Pacific Ocean and at higher 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 has been detected in rivers, lakes, air particulates, precipitation, groundwater, and tap water.

Sources

Industrial sites

PFOA is released directly from industrial sites. For example, the DuPont Teflon Washington Works facility in Washington, WV estimated total PFOA emissions of 80,000 lbs in 2000 and 1,700 lbs in 2004. A 2006 study, with two of four authors DuPont empolyees, 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.

PFOA precursors

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 (H(CF₂)₈CH₂CH₂OH), polyfloroalkyl phosphate surfactants (PAPS), and N-EtFOSE alcohol (F(CF₂)₈SO₂N(Et)CH₂CH₂OH). The 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.

Waste water treatment plants (WWTPs) are sites where PFOA precursors rinsed down domestic, commercial, and industrial drains are degraded into PFOA. This is evidenced by an increase in water contamination of PFOA output compared to PFOA intake, with WWTPs acting as the primary sources of PFOA in local rivers.

Sources to People

Contaminated water and food are considered the major exposure route to PFOA, while PFOA or PFOA precursor contaminated food contact papers/coatings are considered a minor source. Eating increased fish has been linked with increased PFOA levels in one study. Household dust has been implicated as a possible exposure route. Citizens that lived in the PFOA contaminated area around DuPont's Washington Works facility were found to have higher levels of PFOA in their blood from contaminated drinking water. Individuals who drank more tap water, ate locally grown fruits and vegetables, or ate local meat, were all associated with having higher PFOA levels. In this study, local fish consumption was not found to be associated with an increased level of PFOA. Residents that used home 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, including those intended for food contact. In an U.S. Food and Drug Administration (FDA) study, 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 ppb PFOA, while microwave popcorn bags contained 6-290 ppb PFOA, and residual PFOA was also detected in finished PTFE products including PTFE/Teflon cookware. In a New York State Department of Health study, PFOA was detected in the gas phase coming from new nonstick cookware and microwave popcorn bags; this research was funded by a 2005-2006 $17,700 grant from the Consumers Union. Fluorotelomer-based paper coatings are used in direct food contact because of their lipophobicity; the coatings give papers resistance to oil soaking in from fatty foods. 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 used in food contact papers. 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.

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 ppb), mill-treated carpeting (200-600 ppb), treated apparel (up to 1400 ppb), and treated home textiles (up to 1400 ppb). PFOA was detected in the low-ppb range in industrial floor waxes and wax removers, latex paint, and home and office cleaners. Upon extraction PFOA was also detected in treated upholstery.

Health concerns

PFOA induced liver tumors, Leydig cell tumors, and pancreatic acinar tumors in rats fed 300 ppm PFOA for 2 years. PFOA is also a developmental toxicant. Studies with pregnant mice fed PFOA in the low ppm range resulted in litters of pups with developmental delays and lower birth weight.

For humans, blood serum levels of PFOA have been linked to lower fetal growth factors such as birth weight, birth length, abdominal circumference, and head circumference. The study within the Danish National Birth Cohort used a sample size of 1400 and maternal serum while the Baltimore, MD study used a sample size of 293 and umbilical cord serum. Taken together, these studies suggest PFOA lowers human fetal growth factors; however, findings between the two studies regarding birth length were not replicated. These findings have prompted scientific discussion. A Canadian study with a sample size of 101 pregnant mothers used maternal serum and umbilical cord blood in their analysis but they did not find any inverse relationship between PFOA levels and birth weight.

Low ppb levels of PFOA and related compounds (PFOS, PFNA, and PFHxS) have been detected in the blood serum of nearly all Americans; in a Centers for Disease Control and Prevention (CDC) paper, PFOA was detected in 99.7% of National Health and Nutrition Examination Survey (NHANES) 2003-2004 samples, with a geometric mean of 3.9 ng/mL (≈ppb) and a LOD of 0.1 ng/mL (≈ppb). In the years between 1999-2000 and 2003-2004, PFOA concentrations decreased by about 25% in the blood serum of Americans. The durability of PFOA can lead to bioaccumulation in food chains, especially in Atlantic marine animals. In light of concerns about its pervasiveness, its major U.S. manufacturer, 3M, announced in May 2000 that it would cease producing the PFOA. DuPont, one of the largest U.S. users of PFOA, then built its own plant in Fayetteville, North Carolina to manufacture PFOA.

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 long-term health effects.

In 2002 Burger King stopped using fluorotelomer coated boxes.

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.

U.S. Federal Government Actions

In 2004, DuPont was investigated by the Environmental Protection Agency (EPA) for allegedly covering up knowledge of possible health effects of PFOA exposure in a study of pregnant employees, including evidence of PFOA in umbilical cord blood. The EPA pursued charges against DuPont for failure to report violations filed under the Toxic Substances Control Act and the Resource Conservation and Recovery Act.

In October 2005, a U.S. Food and Drug Administration (FDA) study was published revealing PFOA and PFOA precursor chemicals in food contact and PTFE/Teflon products.

On January 25, 2006, the EPA announced a long-term, voluntary program with eight major companies to reduce PFOA emissions and to eliminate PFOA use in products by the year 2015. While a New York Times article the next day claimed that companies would "stop using" PFOA, the EPA described its objective as "elimination of PFOA...from emissions and products" but not as a chemical intermediate to produce other substances.

On February 15, 2006, the EPA's Science Advisory Board recommended that PFOA should be considered a likely carcinogen.

On May 26, 2006, an EPA Science Advisory Board (SAB) letter was addressed to Administrator Stephen L. Johnson. It showed that only about 1/4 of the SAB advisers agreed with the EPA's own PFOA hazard descriptor of “suggestive evidence of carcinogenicity, but not sufficient to assess human carcinogenic potential" while about 3/4 of the SAB thought the stronger designation of PFOA as "likely to be carcinogenic" was warranted.

On November 21, 2006, EPA 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 0.50 parts per billion (ppb). This measure lowered action level and replaced the previous 150 ppb threshold that had been 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.

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 ppb 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 ppb to 0.5 ppb, 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 ppb. The German Federal Environmental Agency issued guidelines for the sum of PFOA and PFOS concentrations in drinking water: 0.1 ppb for precaution and 0.3 ppb for a health based lifelong safe exposure value. Residents were found to have a 4-8 factor increase of PFOA blood plasma levels over the general population, with geometric mean concentrations in the 22-25 ppb range. An expert panel concluded that "concentrations were considered too low to cause overt adverse health effects in the exposed population.