Pentadecafluoroctansure

Other Classes -> Perfluoroalkyl Acids

Ionic Liquids

Ionic Liquids -> Fluorinated Ionic Liquids

PFAS -> Perfluorocarboxylic acids

PFAS

PFAS -> PFAS with analytical method available

PFAS -> Other/unspecified

PFAS

PFAS -> Other/unspecified

1.792 g/mL at 20 °C

1.79 g/cm³

1.792 @ 20°C

When heated to decomposition it emits toxic vapors of F(-).

In water, 3300 mg/L at 25 °C

In water, 4340 mg/L at 24.1 °C

Solubility in water: none

192 °C

189 °C

189 °C @760 [mm Hg]

54.3 °C

52-54 °C

0.15 [mmHg]

3.16X10-2 mm Hg at 25 °C

0.15 [mm Hg] @20 °C

0.37 ± 0.01 [log Psd at 298.15 K (Pa)]

Danger

H302: Harmful if swallowed [Warning Acute toxicity, oral]

P203, P260, P261, P263, P264, P264+P265, P270, P271, P280, P301+P317, P304+P340, P305+P354+P338, P317, P318, P319, P330, P405, and P501 (click each P-code to see the statement)

Danger

H302 (95.5%): Harmful if swallowed [Warning Acute toxicity, oral]

P203, P260, P261, P263, P264, P264+P265, P270, P271, P280, P301+P317, P301+P330+P331, P302+P361+P354, P304+P340, P305+P354+P338, P316, P317, P318, P319, P321, P330, P363, P405, and P501 (click each P-code to see the statement)

Chemical: Octanoic acid, pentadecafluoro-

Hazard Traits - Bioaccumulation; Carcinogenicity; Developmental Toxicity; Environmental Persistence; Hepatotoxicity and Digestive System Toxicity; Reproductive Toxicity

Regulation (EC) No 178/2002 (amended)

S - indicates a substance that is identified in a final Significant New Use Rule.

Substance: Pentadecafluorooctanoic acid (PFOA)

Substance: Pentadecafluorooctanoic acid

Danger of cutaneous absorption; [MAK] A skin, eye, and respiratory tract irritant; [ICSC] A corrosive substance that can cause injury to the skin, eyes, and respiratory tract; Inhalation may cause chemical pneumonitis; [MSDSonline] See Perfluorobutyric acid. See Perfluorooctane sulfonic acid. Serum PFAS concentrations were not associated with increased cardiometabolic risk measures in this population of firefighters. [PMID 33105404]

Perfluorooctanoic Acid and Fluorinated Telomers. This site provides information on PFOA and related chemicals and EPA's actions on these chemicals.[Available from, as of August 15, 2011: http://www.epa.gov/oppt/pfoa/index.html]

The near ubiquitous presence of poly- and perfluoroalkyl substances (PFASs) in humans has raised concerns about potential human health effects from these chemicals, some of which are both extremely persistent and bioaccumulative. Because some of these chemicals are highly water soluble, one major pathway for human exposure is the consumption of contaminated drinking water. This study measured concentrations of PFASs in 18 raw drinking water sources and 2 treated wastewater effluents and evaluated 15 full-scale treatment systems for the attenuation of PFASs in water treatment utilities throughout the U.S. A liquid-chromatography tandem mass-spectrometry method was used to enable measurement of a suite of 23 PFASs, including perfluorocarboxylic acids (PFCAs) and perfluorosulfonic acids (PFSAs). Despite the differences in reporting levels, the PFASs that were detected in >70% of the source water samples (n = 39) included PFSAs, perfluorobutane sulfonic acid (74%), perfluorohexane sulfonic acid (79%), and perfluorooctane sulfonic acid (84%), and PFCAs, perfluoropentanoic acid (74%), perfluorohexanoic acid (79%), perfluoroheptanoic acid (74%), and perfluorooctanoic acid (74%). More importantly, water treatment techniques such as ferric or alum coagulation, granular/micro-/ultra- filtration, aeration, oxidation (i.e., permanganate, ultraviolet/hydrogen peroxide), and disinfection (i.e., ozonation, chlorine dioxide, chlorination, and chloramination) were mostly ineffective in removing PFASs. However, anion exchange and granular activated carbon treatment preferably removed longer-chain PFASs and the PFSAs compared to the PFCAs, and reverse osmosis demonstrated significant removal for all the PFASs, including the smallest PFAS, perfluorobutanoic acid. /Perfluoroalkyls/[Appleman TD et al; Treatment of poly- and perfluoroalkyl substances in U.S. full-scale water treatment systems. Water Res 51: 246-55 (2014)]

Decomposes on heating above 300 °C . This produces toxic and corrosive gases including hydrogen fluoride (See ICSC 0283). The solution is a weak acid. Reacts with bases, oxidants and reducing agents. This produces flammable/explosive gas (hydrogen - see ICSC 0001). Attacks many metals.

Acute Tox. 4 (95.5%)

Acute toxicity - category 3

Reproductive toxicity - Category 1B

Acute toxicity (Oral) - Category 4

Carcinogenicity - Category 2

Carc. 2

Monitoring requirements for unregulated contaminants. (a) General applicability. This section specifies the monitoring and quality control requirements that must be followed if you own or operate a public water system (PWS) that is subject to the Unregulated Contaminant Monitoring Regulation (UCMR), as specified in paragraphs (a)(1) and (2) of this section. In addition, this section specifies the UCMR requirements for State and Tribal participation. For the purposes of this section, PWS "population served," "State," " PWS Official," "PWS Technical Contact," and "finished water" apply as defined in section 141.35(a). The determination of whether a PWS is required to monitor under this rule is based on the type of system (e.g., community water system, non-transient non-community water system, etc.), and its retail population, as indicated by SDWIS/Fed on December 31, 2010. ... Contaminant: perfluorooctanoic acid; CAS Registry No.: 335-67-1; Analytical Method: EPA 537; Minimum Reporting Level: 0.02 ug/L; Sampling location: EPTDS (entry points to the distribution system); Period during which monitoring to be completed: 1/1/2013-12/31/2015.

(MN) MINNESOTA 0.3 ug/L

(NJ) NEW JERSEY 0.04 ug/L

Fresh air, rest. Artificial respiration may be needed. Refer for medical attention.

Wear protective gloves when administering first aid. Remove contaminated clothes. Rinse and then wash skin with water and soap.

Rinse with plenty of water for several minutes (remove contact lenses if easily possible). Refer immediately for medical attention.

Rinse mouth. Give one or two glasses of water to drink. Refer for medical attention .

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust; Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains; Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber; Contaminated packaging: Dispose of as unused product.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Sweep spilled substance into covered non-metallic containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

Results from National Health and Nutrition Examination Survey conducted in the US of serum analysis for perfluorooctanoic acid were reported for 1999 to 2008 as follows(1):[Table#6754]

Serum concentrations of perfluorooctanoic acid in US samples collected in 1974 and 1989 were 2.3 and 5.6 ng/mL, respectively(1). Concentrations of perfluorooctanoic acid in 65 human serum samples purchased from various biological supply companies in the US ranged from <5 to 35.2 ng/mL(2). The concentration of perfluorooctanoic acid in the serum of 20 Atlanta, GA residents was 0.2-10.4 ng/mL, samples were collected July 2003(3). Perfluorooctanoic acid was detected at 0.9-4751.5 ug/L in serum, collected Aug 2005 to Aug 2006, of 108 participants from Ohio and West Virginia that drink well water that contains 0.006-13.3 ug/L of perfluorooctanoic acid(4). Perfluorooctanoic acid was detected at 1.1-8.9 ng/mL in the serum of 31 Boston, MA office workers in samples collected winter of 2009(5). Perfluorooctanoic acid was detected in the blood of all 12 California firefighters tested at 2-12 ng/g lipid; samples were collected in 2009(6). Perfluorooctanoic acid was frequently detected in 30 human hair samples; concentrations were not reported(7).

Perfluorooctanoic acid was not detected in the urine or stool of residents living in a home with a history of carpet Scotchgard application. The compound was detected in serum samples as follows (samples were collected Nov 2008)(1):[Table#6755]

Perfluorooctanoic acid was detected at 5.0-9.9 ng/mL (mean 7.6 ng/mL) in 40 pooled serum samples collected from 3802 Australian residents collected Nov 2002 to April 2003(1). Perfluorooctanoic acid concentration was 0.58 ng/mL (1977), increased to 5.2 ng/mL (1993), stabilized at 4.0 to 4.9 ng/mL (1994-2001), and then slowly decreased to 2.7 ng/mL by 2006 in 24 pooled serum samples from men, age 40 to 50 years, representing 1977 to 2006 in Norwegian residents(2). Perfluorooctanoic acid was detected in 66 human blood samples collected from 11 counties in Sweden during the period of 1997 to 2000, concentrations were 0.5-12.4 ng/mL(3). Perfluorooctanoic acid was detected at 0.092-39.4 ng/mL in 420 human blood samples collected from volunteer residents from Halle and Munster, Germany; samples were collected 1982 to 2009(4). Perfluorooctanoic acid was detected at 2.0-96.6, 0.7-99.7 and 1.1-77.5 ug/L in blood plasma samples of 170 children, 317 women and 204 men from the German population; samples were collected Sept to Nov 2006(5). Perfluorooctanoic acid was detected in blood serum samples collected July 1 through Sept 4, 2008 at 2.1-170 ug/L; samples were collected from 105 anglers (99 men, 6 women) that consumed fish from Lake Mohne, Germany(6). From 2006 to 2008, 233 human blood samples were taken from donors from the capital cities of 12 provinces or districts of China, perfluorooctanoic acid was detected as follows - city (ng/mL): Harbin (0.720), Hohhot (0.759), Lanzhou (1.40), Taiyuan (0.258), Shijiazhuang (1.50), Qingdao (1.42), Ningbo (3.87), Changsha (0.251), Chengdu (1.00), Chongqing (1.88), Kumming (1.13) and Guizhou (1.22)(7). Human blood samples from volunteer donors from five Chinese cities (Shenyang, Beijing, Gulyang, Jintan, Nanjing) collected in 2004 had perfluorooctanoic acid concentrations of <0.05-2.19 ng/mL(8).

For more Body Burden (Complete) data for Perfluorooctanoic acid (8 total), please visit the HSDB record page.

... This study assessed the effects of PFOS and PFOA on interleukin (IL)-2 production in the human Jurkat T-cell line and PFOS in healthy human primary T cells. Jurkat cells were stimulated with phytohemagglutinin (PHA)/phorbol myristate acetate (PMA), anti CD-3/anti CD-28, or anti CD-3, and dosed with 0, 0.05, 0.1, 0.5, 1, 5, 10, 50, 75, or 100 ug/mL PFOS or 0, 0.005, 0.01, 0.05, 0.1, 0.5, 1, 5, or 10 ug/mL PFOA. Jurkat cells stimulated with PHA/PMA or anti CD-3 exhibited decreased IL-2 production beginning at 50 ug PFOS/mL and 5 ug PFOS/mL respectively, but stimulation with anti-CD3/anti-CD28 resulted in no changes compared with the control. Addition of the PPAR-alpha antagonist GW6471 to PFOS-dosed cells stimulated with PHA/PMA resulted in decreases in IL-2 production starting at 50 ug PFOS/mL, which suggests PFOS affected T-cell IL-2 production via PPAR-alpha-independent mechanisms. Exposure to PFOA, PFOA + GW6471, or PFOS + PFOA in Jurkat cells resulted in no significant differences in IL-2 production. In vitro dosing studies using healthy primary human CD4+ T cells were consistent with the Jurkat results. These data demonstrated that PFOA did not impact IL-2 production, but PFOS suppressed IL-2 production in both a human cell line and human primary T cells at dose levels within the high end of the human exposure range. A decrease in IL-2 production is characteristic of autoimmune diseases such as systemic lupus erythematosus and should be further investigated.

... Considering liver is the primary toxic target organ for chlorinated phenols and perfluoroalkyl acids (PFAAs), it is interesting to evaluate the possible joint effects of them on liver. In this work, the combined toxicity of pentachlorophenol (PCP) and perfluorooctane sulfonate (PFOS) or perfluorooctanoic acid (PFOA) were investigated using HepG2 cells. The results indicated that PFOS and PFOA could strengthen PCP's hepatotoxicity. Further studies showed that rather than intensify the oxidative stress or promote the biotransformation of PCP, PFOS (or PFOA) might lead to strengthening of the oxidative phosphorylation uncoupling of PCP. By measuring the intracellular PCP concentration and the cell membrane properties, it was suggested that PFOS and PFOA could disrupt the plasma membrane and increase the membrane permeability. Thus, more cellular accessibility of PCP was induced when they were co-exposed to PCP and PFOS (or PFOA), leading to increased cytotoxicity ...

... In the present study, the single and combined toxicity of PFOA and PFOS to zebrafish (Danio rerio) embryos were investigated. PFOS was more toxic than PFOA for the single toxicity. In four mixtures, PFOS and PFOA showed complex interactive effects that changed from additive to synergistic effect, then to antagonistic effect, and at last turnover to synergic effect again, with increased molar ratios of PFOS. Neither the concentration-addition model nor the independent-action model could predict the combined effects when strong interactive effects existed. Although the interactive effects of PFOS and PFOA affected their combined toxicity, the trend of mixture toxicity still showed an increase with increasing molar ratios of PFOS in the mixture.

...Peroxisome proliferation caused by /perfluorooctanoic acid in diet of male mice/ is highly dependent on the vitamin A status of the mouse.

For more Interactions (Complete) data for Perfluorooctanoic acid (8 total), please visit the HSDB record page.

EC50; Species: Isochrysis galbana (Haptophyte) Exponential Growth Phase, 10000 cells/mL; Conditions: saltwater, static, 20 °C; Concentration: 163600 ug/L for 72 hr; Effect: decreased population growth rate /96% purity/

EC50; Species: Pseudokirchneriella subcapitata (Green Algae) 3000000 cells/mL; Conditions: freshwater, static; Concentration: 1.807 mM for 4.5 hr (95% confidence interval: 1.76-1.86 mM); Effect: population, decreased photosynthesis /96% purity/

EC50; Species: Chydorus sphaericus (Water Flea) age <24 hr neonate; Conditions: freshwater, static, 20 °C; Concentration: 0.426 mM for 24 hr (95% confidence interval: 0.223-0.537 mM); Effect: intoxication, immobilization /96% purity/

EC50; Species: Chydorus sphaericus (Water Flea) age <24 hr neonate; Conditions: freshwater, static, 20 °C; Concentration: 0.282 mM for 48 hr (95% confidence interval: 0.122-0.345 mM); Effect: intoxication, immobilization /96% purity/

For more Ecotoxicity Values (Complete) data for Perfluorooctanoic acid (17 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), log Koc values of 1.92-2.59(2), indicate that perfluorooctanoic acid is expected to have high to moderate mobility in soil(SRC). The pKa values of -0.5 to 4.2(3), indicate that perfluorooctanoic acid will exist entirely in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization from moist soil is not expected because the acid exists as an anion and anions do not volatilize(SRC). Perfluorooctanoic acid is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 0.0316 mm Hg at 19 °C(5). A 5% of Theoretical BOD using activated sludge in the Japanese MITI test(6) suggests that biodegradation is not an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), log Koc values of 1.92-2.59(2), indicate that perfluorooctanoic acid is expected to adsorb to suspended solids and sediment(SRC). pKa values of -0.5 to 4.2(3) indicate perfluorooctanoic acid will exist entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). Organic fluorochemical compounds, such as perfluorooctanoic acid, are expected to be resistant to hydrolysis and photolysis(4). According to a classification scheme(5), BCFs of <5.2-9.4 in carp(6) and 100-230 in mullet(7), suggest bioconcentration in aquatic organisms is low to high. Utilizing the Japanese MITI test, 5% of the Theoretical BOD was reached in 4 weeks(8) indicating that biodegradation is not an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), perfluorooctanoic acid, which has a vapor pressure of 0.0316 mm Hg at 19 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase perfluorooctanoic acid is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 31 days(SRC), calculated from its rate constant of 5.2X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Organic fluorochemical compounds, such as perfluorooctanoic acid, are expected to be resistant to photolysis(4).

Perfluorooctanoic acid was detected in four tap water samples from Amsterdam, The Netherlands at 3.2-4.3 ng/L; mixed cola and brewed coffee made from this tap water had perfluorooctanoic acid concentrations of <3.1 and <3.1-8.0 ng/L, respectively(1). Perfluorooctanoic acid was detected at 100, 0 and 0 pg/mL in blood plasma from three Japanese black beef cattle at 9 months of age; these concentrations changed to 70, 70 and 0 pg/mL at 27 months of age(2).

The perfluorooctanoic acid concentration in food items purchased from Flemish markets and farms were as follows(1):[Table#6762]

Canadian Total Diet Study conducted from 1992-2004 indicated the dietary exposure of Canadians to perfluorooctanoic acid via consumption of the following (1):[Table#6763]

The mean concentrations of perfluorooctanoic acid in foods collected July 2006 from local markets, large supermarkets and grocery stores from different locations of Tarragona County, Spain were reported as follows(1):[Table#6764]

For more Food Survey Values (Complete) data for Perfluorooctanoic acid (6 total), please visit the HSDB record page.

Perfluorooctanoic acid was not detected (detection limit 0.12 ng/g) in 12 raw and 49 retail milk samples collected at locations across the US(1). Perfluorooctanoic acid was not detected (detection limit 48.3 pg/mL) in 21 infant formula samples purchased from retail stores in Washington, DC and Boston, MA in 2007, or in 12 dairy milk samples purchased from retail stores and local farms in Albany, NY in 2008(2). Perfluorooctanoic acid was detected at 4.7 pg/g in milk samples purchased at grocery stores in Oslo, Norway between Oct 2008 and Jan 2009(3). In Nov 2009, milk samples randomly purchased in several Dutch retail stores contained perfluorooctanoic acid at 1 pg/g(4). Perfluorooctanoic acid was found at 0.056 ng/g fresh weight in whole milk but not detected in semi-skimmed milk (detection limit 0.028 ng/g fresh weight); samples were collected July 2006 from local markets, large supermarkets and grocery stores from different locations of Tarragona County, Spain(5).

Perfluorooctanoic acid was detected at <0.05-0.224 ug/L in 47 of 48 breast milk samples collected November 2007, one month postpartum, from French women(1). Perfluorooctanoic acid was detected at 0.082 ng/mL in pooled human milk samples collected 2003 to 2004 from women in the Kingston, Ontario, Canada region(2). Perfluorooctanoic acid was not detected (detection limit 0.2 ng/mL) in two human milk samples, collection data were not provided(3). The concentration or perfluorooctanoic acid was reduced by 7.87% per month in monthly breast milk samples collected two to 12 months after giving birth(4).

Perfluorooctanoic acid concentrations in breast milk samples, collected 1999 to 2005, from women primarily living in major cities from seven Asian Countries were reported as follows(1):[Table#6767]

IDENTIFICATION AND USE: Perfluorooctanoic acid (PFOA) is a white to off-white powder. PFOA is used primarily to produce its salts, which are used as essential processing aids in the production of fluoropolymers and fluoroelastomers. PFOA is also used as a water repellent, a surfactant in firefighting foams, and as an intermediate in the synthesis of fluoroacrylic esters. It is used in the process of making Teflon and similar chemicals (known as fluorotelomers), although it is burned off during the process and is not present in significant amounts in the final products, including Teflon-coated products. HUMAN EXPOSURE AND TOXICITY: Results of a thyroid study suggest that perfluoroalkyl substances are associated with subtle alterations in thyroid hormone levels in aging populations, and that these associations are likely to vary by age. Exposure to PFOA may reduce fecundability. At a plant in Cottage Grove, Minnesota, workers with 27 years of exposure in probable PFOA exposed jobs or those with 9 years of definite PFOA exposure were 3.3 times more likely to die of cerebrovascular disease than the general population. Based on workers studied at two different 3M plants, there was a statistically significant positive association between PFOA and serum cholesterol and triglycerides levels over time. It has been suggested that there is a significant dose response relationship between PFOA levels and ADHD. Maternal PFOA levels in early pregnancy were associated with smaller abdominal circumference and birth length. In another study, there was a positive association between the maternal concentrations of PFOA and the number of episodes of common cold for the children, and between PFOA and the number of episodes of gastroenteritis. In a study on blood serum levels of men and women, higher concentrations of PFOA were observed in men in comparison to women from the same populations. Simultaneous flow cytometric analysis of apoptosis-associated DNA strand breaks revealed DNA breaks in HepG2 cells exposed to 150 uM PFOA, prior to nuclear fragmentation. Epidemiologic evidence does not support the hypothesis of a causal association between PFOA exposure and cancer in humans. However, ten years of employment in PFOA exposed jobs was associated with a 3.3-fold increase in prostate cancer mortality compared to no employment in PFOA production, based on limited number of cancer deaths. ANIMAL STUDIES: Animal studies have indicated that PFOA cause a wide array of toxic effects including liver and brain dysfunction, carcinogenicity and reproductive and developmental toxicity. PFOA was demonstrated to be immunotoxic following dermal exposure of mice. Based on another study in mice, PFOA can induce airway inflammation and alter airway function. Histological examination of mice showed that the exposure to PFOA for 14 consecutive days led to serious hepatocellular injury and obvious inflammatory cell infiltration. In addition, malondialdehyde formation and hydrogen peroxide generation, indicators of oxidative stress, were significantly induced by PFOA treatment in the liver of mice. Furthermore, hepatic levels of interleukin-6, cyclooxygenase-2, and C-reactive protein, markers of inflammatory response, were markedly increased by exposure to PFOA. A study with perinatal exposure to PFOA in mice produced metabolic effects in adult offspring. PFOA-induced male reproductive disorders might be involved in developmental impairment and inhibition of NRF2-mediated antioxidant response in the testis of mice. In mice and rats, PFOA alone did not cause any neurotoxic symptoms. However, developmental neurotoxicity of PFOA described after neonatal exposure in mice. Neonatal exposure to PFOA affected the cholinergic system, manifested as a hypoactive response to nicotine, compared to a hyperactive response to nicotine in controls. PFOA was not mutagenic in the Ames test, using four strains of Salmonella typhimurium in the presence or absence of metabolic system. High-dose, short-term exposure of mice to PFOA augments inflammatory responses to lipopolysaccharide (LPS), a potent activator of innate immunity. ECOTOXICITY STUDIES: In rare minnows, PFOA was found to alter genes involved in lipid metabolism and transport, hormone action, immune responses, mitochondrial functions, fatty acid biosynthesis, and transport. In addition, PFOA inhibited genes responsible for thyroid hormone biosynthesis and significantly induced estrogen-responsive genes. A study on fruit flies indicated that the toxic effects of PFOA at the organismal level were associated with the developmental status of the organism, with larvae being most sensitive to this chemical.

The median daily intake of perfluorooctanoic acid was reported for pooled diets from composite food samples as follows(1):[Table#6751]

The average daily intake of perfluorooctanoic acid (ng/kg/day) in the Flemish population, based on reported soil, dust, outdoor air, and food and beverages concentrations were(1):[Table#6752]

/AQUATIC SPECIES/ ...The effect of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) on endocrine signalling, growth and development in Atlantic salmon (Salmo salar) embryos and larvae /was investigated/. Expression of genes related to the hypothalamic-pituitary-thyroid (HPT) axis, growth-hormone/insulin-like growth factor (GH/IGF) axis and the steroid hormone axis were used as indicators of endocrine disruption. ...Bone development in larvae /was also studied/, both by observing skeletal structure formation and by investigating expression of genes involved in ossification process. Atlantic salmon embryos, kept in plastic tanks at 5-7 °C, were exposed to 100 ug/L PFOA or PFOS from egg stage for a period of 52 days, followed by one-week recovery period. Sampling was performed at day 21, 35, 49 and 56 representing age 549, 597, 679 and 721 dd (dd or day degrees = number of days x temperature in degree Celsius: °C). Note that day 56 or 721 dd is the end of the 1-week recovery period. Larvae were divided into designated head and body regions for the purpose of gene expression analysis, except for genes that regulate ossification that were analyzed in whole larvae. Expression of thyroid receptor alpha and beta (TR-alpha and TR-beta), thyroid-stimulating hormone beta (TSH-beta), T(4) outer-ring deiodinase (T(4)ORD), growth hormone (GH), insulin-like growth factor-I and II (IGF-I and II), insulin-like growth factor I receptor (IGF-IR), and estrogen receptor alpha and beta (ER-alpha and ER-beta) were investigated using quantitative PCR. Both PFOS and PFOA exposure produced non-significant alterations in larvae weight (except after the recovery period when a decrease was observed), while larvae length was unaffected. PFOS and PFOA exposure produced body- and head region-specific alterations in expression of all the investigated gene transcripts. Expression of IGF-I and IGF-IR paralleled that of GH, indicating that perturbation of GH expression is a possible end point for disruption of the GH-IGF axis. We did not observe developmental changes related to angiogenesis, ossification and chondrogenesis after exposure to PFOS and PFOA. Transcriptional abnormalities may serve as indicators of chronic exposure, although the concrete mechanisms causing the observed effects remain ambiguous ...

/AQUATIC SPECIES/ ... The primary objective of this study was to determine whether multiple PFAAs enhance hepatic tumorigenesis in trout, an animal model that represents human insensitivity to peroxisome proliferation. A two-stage chemical carcinogenesis model was employed in trout to evaluate PFOA, perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluorooctane sulfonate (PFOS), and 8:2 fluorotelomer alcohol (8:2FtOH) as complete carcinogens or promoters of aflatoxin B(1) (AFB(1))- and/or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced liver cancer. A custom trout DNA microarray was used to assess hepatic transcriptional response to these dietary treatments in comparison with E2 and the classic peroxisome proliferator, clofibrate (CLOF). Incidence, multiplicity, and size of liver tumors in trout fed diets containing E2, PFOA, PFNA, and PFDA were significantly higher compared with AFB(1)-initiated animals fed control diet, whereas PFOS caused a minor increase in liver tumor incidence. E2 and PFOA also enhanced MNNG-initiated hepatocarcinogenesis. Pearson correlation analyses, unsupervised hierarchical clustering, and principal components analyses showed that the hepatic gene expression profiles for E2 and PFOA, PFNA, PFDA, and PFOS were overall highly similar, though distinct patterns of gene expression were evident for each treatment, particularly for PFNA. Overall, these data suggest that multiple PFAAs can promote liver cancer and that the mechanism of promotion may be similar to that of E2.

/AQUATIC SPECIES/ ... In this study, the effects of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) on the population growth rate and resting egg production of rotifer Brachionus calyciflorus were investigated. Reproductive bioassays indicated that PFOS increased the rotifer population growth rate at the concentration was greater than 2.0 mg/L, and inhibited it at higher concentrations. For PFOA, the inhibition of population growth rate was observed when the concentration was greater than 4.0 mg/L. Exposure to PFOS (0.25 mg/L) or PFOA (2.0 mg/L) increased the mictic ratios of unexposed rotifer offspring. Population variation and increased mictic ratios were likely the two major factors leading to decline of resting egg production. The resting eggs formed under exposure to PFOA/PFOS in the range of 0.125-2.0 mg/L showed higher hatching percentages in the control medium than that without PFOA/PFOS exposure. When the resting eggs were formed in the control medium and incubated in media with different levels of PFOA/PFOS, higher hatching percentages were induced by PFOS but lower hatching percentages induced by PFOA. The effects on the hatching rate of resting eggs with PFOA/PFOS exposure during the hatching period were greater than those with exposure during resting egg formation period, and the effect of PFOS was greater than that of PFOA. Both PFOA and PFOS exhibited slight effect on the hatching pattern.

/AQUATIC SPECIES/ ... environmental toxicity of two dominant PFCs, perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA), was examined in a sentinel species, green mussel Perna viridis, using a series of biomarkers corresponding to different biological levels (molecular, cellular, and physiological). Correlations among these biomarkers were also investigated. The results showed that the tested compounds can induce a series adverse effect at different biological levels, including oxidative stress, DNA damage, membrane instability, suppressed filtration rate, and reduced body weight. Correlation analysis revealed that excess production of reactive oxygen species could be the major toxic pathway. An indirect mode of toxic action was also explored where adverse impacts could be secondary effects of PFC exposure. The joint analysis of biomarkers from multiple biological levels resulted in a comprehensive understanding of how PFC exposure can influence the health of organisms. The correlations of these biomarkers also provided a new perspective of the ecological consequences of PFCs.

For more Ecotoxicity Excerpts (Complete) data for Perfluorooctanoic acid (21 total), please visit the HSDB record page.

Perfluorooctanoic acid concentration was reported in lichen, plants and mushrooms growing in the northern Yukon Territory and Northwest Territories of Canada; samples were collected June 24 to July 2, 2008 or Aug 2009(1).[Table#6768]

Perfluorooctanoic acid concentration was reported in vegetables grown in contaminated soil(1).[Table#6769]

Monitoring requirements for unregulated contaminants. (a) General applicability. This section specifies the monitoring and quality control requirements that must be followed if you own or operate a public water system (PWS) that is subject to the Unregulated Contaminant Monitoring Regulation (UCMR), as specified in paragraphs (a)(1) and (2) of this section. In addition, this section specifies the UCMR requirements for State and Tribal participation. For the purposes of this section, PWS "population served," "State," " PWS Official," "PWS Technical Contact," and "finished water" apply as defined in section 141.35(a). The determination of whether a PWS is required to monitor under this rule is based on the type of system (e.g., community water system, non-transient non-community water system, etc.), and its retail population, as indicated by SDWIS/Fed on December 31, 2010. ... Contaminant: perfluorooctanoic acid; CAS Registry No.: 335-67-1; Analytical Method: EPA 537; Minimum Reporting Level: 0.02 ug/L; Sampling location: EPTDS (entry points to the distribution system); Period during which monitoring to be completed: 1/1/2013-12/31/2015.

(MN) MINNESOTA 0.3 ug/L

(NJ) NEW JERSEY 0.04 ug/L

Perfluorooctanoic acid (PFOA) has been shown to cause hepatotoxicity and other toxicological effects. Though PPARalpha activation by PFOA in the liver has been well accepted as an important mechanism of PFOA-induced hepatotoxicity, several pieces of evidence have shown that the hepatotoxic effects of PFOA may not be fully explained by PPARalpha activation. In this study, we observed autophagosome accumulation in mouse livers as well as HepG2 cells after PFOA exposure. Further in vitro study revealed that the accumulation of autophagosomes was not caused by autophagic flux stimulation. In addition, we observed that PFOA exposure affected the proteolytic activity of HepG2 cells while significant dysfunction of lysosomes was not detected. Quantitative proteomic analysis of crude lysosomal fractions from HepG2 cells treated with PFOA revealed that 54 differentially expressed proteins were related to autophagy or vesicular trafficking and fusion. The proteomic results were further validated in the cells in vitro and livers in vivo after PFOA exposure, which implied potential dysfunction at the late stage of autophagy. However, in HepG2 cells, it seemed that further inhibition of autophagy did not significantly alter the effects of PFOA on cell viability. Although these findings demonstrate that PFOA blocked autophagy and disturbed intracellular vesicle fusion in the liver, the changes in autophagy were observed only at high cytotoxic concentrations of PFOA, suggesting that autophagy may not be a primary target or mode of toxicity. Furthermore, since altered liver autophagy was not observed at concentrations of PFOA associated with human exposures, the relevance of these findings must be questioned.

...Hepatomegaly caused by perfluorooctanoic acid depends on corticosterone, the major glucocorticoid in rodents. Liver growth caused by perfluorooctanoic acid appears to be predominantly hypertrophic in nature, and DNA synthesis in response to perfluorooctanoic acid predominates in periportal regions of the liver lobule. Data also show that although induction of peroxisomal beta-oxidation by perfluorooctanoic acid is independent of adrenal hormones, induction of catalase is dependent on the presence of these hormones. This study supports the contention that induction of activities of various peroxisomal enzymes is controlled by different regulatory mechanisms.

...This study ...investigated the involvement of reactive oxygen species (ROS), mitochondria, and caspase-9 in PFOA-induced apoptosis. Treatment with 200 and 400 microM PFOA was found to cause a dramatic increase in the /HepG2/ cellular content of superoxide anions and hydrogen peroxide after 3 hr. Measurement of the mitochondrial transmembrane potential (Delta Psi(m)) after PFOA treatment showed a dissipation of Delta Psi(m) at 3 hr. Caspase-9 activation was seen at 5 hr after treatment with 200 microM PFOA. In order to evaluate the importance of these events in PFOA-induced apoptosis, cells were cotreated with PFOA and N-acetylcysteine (NAC), a precursor of glutathione, or Cyclosporin A (CsA), an inhibitor of mitochondrial permeability transition pore (MPT pore). NAC reduced Delta Psi(m) dissipation, caspase 9 activation, and apoptosis, indicating a role for PFOA-induced ROS. In addition, CsA also reduced Delta Psi(m) dissipation, caspase 9 activation, and apoptosis, indicating a role for PFOA-induced opening of the MPT pore. ...

To determine the role of PPAR alpha in mediating PFOA transcriptional events, we compared the transcript profiles of the livers of wild-type or PPAR alpha-null mice exposed to PFOA or the PPAR alpha agonist WY-14,643 (WY). After 7 days of exposure, 85% or 99.7% of the genes altered by PFOA or WY exposure, respectively were dependent on PPAR alpha. The PPAR alpha-independent genes regulated by PFOA included those involved in lipid homeostasis and xenobiotic metabolism. Many of the lipid homeostasis genes including acyl-CoA oxidase (Acox1) were also regulated by WY in a PPAR alpha-dependent manner. The increased expression of these genes in PPAR alpha-null mice may be partly due to increases in PPAR gamma expression upon PFOA exposure. Many of the identified xenobiotic metabolism genes are known to be under control of the nuclear receptor CAR (constitutive activated/androstane receptor) and the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2). There was excellent correlation between the transcript profile of PPAR alpha-independent PFOA genes and those of activators of CAR including phenobarbital and 1,4-bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) but not those regulated by the Nrf2 activator, dithiol-3-thione. ...

For more Mechanism of Action (Complete) data for Perfluorooctanoic acid (12 total), please visit the HSDB record page.

The intrinsic elimination half-life of PFOA in humans is 2.4 years, representing the average of independent estimates of 2.5 years (95% CI, 2.4-2.7) and 2.3 years (95% CI, 2.1-2.4).

Rainbow trout (Oncorhynchus mykiss) confined to respirometer-metabolism chambers were dosed with perfluorooctanoate (PFOA) by intra-arterial (i.a.) injection and sampled to obtain concentration time-course data for plasma, urine, and expired water. The data were then analyzed by compartmental modeling to estimate rates of renal and branchial clearance. Averaged across all animals, the renal clearance rate (1.35 mL/hr/kg) was more than ten times greater than the branchial clearance rate (0.12 mL/hr/kg). The average whole-body elimination half-life was 12.6 d ...

... Biological half-life of PFOA is quite different between species and sexes and the difference is due mainly to the difference in renal clearance. ...

A half-life study on 27 retirees from the Decatur and Cottage Grove 3M plants was undertaken, in which serum samples were drawn every 6 months over a 5-yr period. Two interim reports describing the results thus far have been submitted. The first interim report suggested a median serum half-life of PFOA of 344 days, with a range of 109 to 1308 days. The two highest half-life calculations were for the 2 female retirees who participated in this study (654 and 1308 days).

For more Biological Half-Life (Complete) data for Perfluorooctanoic acid (8 total), please visit the HSDB record page.

Untargeted metabolic profiling of body fluids in experimental animals and humans exposed to chemicals may reveal early signs of toxicity and indicate toxicity pathways. Avian embryos develop separately from their mothers, which gives unique possibilities to study effects of chemicals during embryo development with minimal confounding factors from the mother. In this study we explored blood plasma and allantoic fluid from chicken embryos as matrices for revealing metabolic changes caused by exposure to chemicals during embryonic development. Embryos were exposed via egg injection on day 7 to the environmental pollutant perfluorooctanoic acid (PFOA), and effects on the metabolic profile on day 12 were compared with those caused by GW7647 and rosiglitazone, which are selective agonists to peroxisome-proliferator activated receptor alpha (PPARalpha) and PPARgamma, respectively. Analysis of the metabolite concentrations from allantoic fluid by Orthogonal Partial Least Squares Discriminant Analysis (OPLS-DA) showed clear separation between the embryos exposed to GW7647, rosiglitazone, and vehicle control, respectively. In blood plasma only GW7647 caused a significant effect on the metabolic profile. PFOA induced embryo mortality and increased relative liver weight at the highest dose. Sublethal doses of PFOA did not significantly affect the metabolic profile in either matrix, although single metabolites appeared to be altered. Neonatal mortality by PFOA in the mouse has been suggested to be mediated via activation of PPARalpha. However, we found no similarity in the metabolite profile of chicken embryos exposed to PFOA with those of embryos exposed to PPAR agonists. This indicates that PFOA does not activate PPAR pathways in our model at concentrations in eggs and embryos well above those found in wild birds. The present study suggests that allantoic fluid and plasma from chicken embryos are useful and complementary matrices for exploring effects on the metabolic profile resulting from chemical exposure during embryonic development.

PFOA is not metabolized and there is evidence of enterohepatic circulation of the compound.

Rainbow trout (Oncorhynchus mykiss) confined to respirometer-metabolism chambers were dosed with perfluorooctanoate (PFOA) by intra-arterial (i.a.) injection and sampled to obtain concentration time-course data for plasma, urine, and expired water. The data were then analyzed by compartmental modeling to estimate rates of renal and branchial clearance. Averaged across all animals, the renal clearance rate (1.35 mL/hr/kg) was more than ten times greater than the branchial clearance rate (0.12 mL/hr/kg). The average whole-body elimination half-life was 12.6 d, which is somewhat longer than values obtained in previous studies with smaller trout. The tissue distribution of PFOA was assessed by collecting tissues at the end of chambered exposures and in a separate tissue time-course experiment. From the time-course study it appeared that an internal steady-state was established within 24 hr of i.a. injection. Consistent with previous studies, the rank order of PFOA concentration in tissues at steady state was: plasma>liver>kidney>muscle. In a second set of chambered experiments, fish were exposed to PFOA in water to determine the rate of branchial uptake. Branchial uptake rates were too low to assess directly by measuring PFOA concentrations in inspired and expired water. Uptake rate constants (mean 0.19 L/d/kg; 0.1% uptake efficiency) were therefore estimated by compartmental modeling using plasma concentration time-course data and model parameters derived from the elimination experiments. It is clear from this effort that elimination of PFOA by trout occurs primarily via the renal route. This finding is consistent with numerous studies of mammals and suggests that trout possess membrane transporters that facilitate the movement of PFOA from plasma to urine.

Determination of the chemical clearance rate from human blood is a critical component of toxicokinetic exposure assessment. Analysis of temporal biomonitoring data without consideration of ongoing exposure results in calculation of apparent elimination half-life values that are longer than the intrinsic value. The intrinsic elimination half-life is solely a function of the rate of elimination while the apparent elimination half-life reflects the processes of both elimination and ongoing exposure. Confusion between intrinsic and apparent half-life values can lead to misinterpretation of biomonitoring data and can result in exaggerated predictions in subsequent modeling efforts. This work provides a review of the first-order equations that have been developed to calculate intrinsic and apparent half-life values and the potential bias that can result from confusing these two values. Published human biomonitoring data forperfluorooctanoic acid (PFOA) are analyzed using these equations to provide examples of low, medium and high bias in determination of the intrinsic elimination half-life from plasma or serum, the components of blood typically analyzed for PFOA. An approach is also provided to estimate the extent of exposure reduction that is indicated by declining longitudinal or cross-sectional biomonitoring data. Based on the evaluation methodology presented in this work, the intrinsic elimination half-life of PFOA in humans is 2.4 years, representing the average of independent estimates of 2.5 years (95% CI, 2.4-2.7) and 2.3 years (95% CI, 2.1-2.4). The declining concentration of PFOA in blood of the general USA adult population represents an estimated exposure reduction of 20-30% over the period 1999-2008.

Perfluorinated alkyl acids (PFAAs) have been detected in serum at low concentrations in background populations. Higher concentrations have been observed in adult males compared to females, with a possible explanation that menstruation offers females an additional elimination route. In this study, we examined the significance of blood loss as an elimination route of PFAAs. Pooled serum samples were collected from individuals undergoing a medical procedure involving ongoing blood withdrawal called venesection. Concentrations from male venesection patients were approximately 40% lower than males in the general population for perfluorohexane sulfonate (PFHxS), perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA). A simple pharmacokinetic model was used to test the hypothesis that blood loss could explain why adult males have higher concentrations of PFAAs than females, and why males undergoing venesections had lower concentrations compared to males in the general population. The model application generally supported these hypotheses showing that venesection might reduce blood serum concentrations by 37% (PFOA) and 53% (PFOS) compared to the observed difference of 44% and 37%. Menstruation was modeled to show a 22% reduction in PFOA serum concentrations compared to a 24% difference in concentrations between males and females in the background population. Uncertainties in the modeling and the data are identified and discussed.

... In this study, PFOS and PFOA were analyzed in 81 whole blood-urine paired samples from general adults and pregnant women in Tianjin, China. PFOS and PFOA were detected in 48 and 76% of adult urine (AU) samples, with geometric mean (GM) concentrations of 0.011 and 0.008 ng/mL, respectively; whereas relatively low PFOS and PFOA concentrations were found in maternal urine (MU) samples, with GM concentrations of 0.006 and 0.003 ng/mL, respectively. For PFOA, the coefficients of Pearson's correlation between whole blood concentrations and creatinine-adjusted and creatinine-unadjusted urinary concentrations were 0.348 (p=0.013) and 0.417 (p=0.002), respectively. The GM urinary elimination rates of PFOS (PFOSUER) and PFOA (PFOAUER) were 16 and 25%, respectively, for adults. These results indicate that urine is an important pathway of excretion of perfluoroalkyl substances (PFASs). The partitioning ratios of PFAS concentration between urine and whole blood (PFASU/B) in pregnant women (PFOSU/B, 0.0004; PFOAU/B, 0.0011) were significantly lower (p=0.025 for PFOSU/B, p=0.017 for PFOAU/B) than the ratios found in non-pregnant women (PFOSU/B, 0.0013; PFOAU/B, 0.0028). Furthermore, our results suggest a clear gender difference in the urinary elimination of PFOA, with male adults (31%) having significantly higher PFOAUER than that of female adults (19%). PFOSUER was significantly inversely correlated with age (r=-0.334, p=0.015); these findings suggest that urinary elimination of PFOS is faster in young adults than in the elderly.

For more Absorption, Distribution and Excretion (Complete) data for Perfluorooctanoic acid (26 total), please visit the HSDB record page.

Used to produce fire-fighting applications, cosmetics, greases, lubricants, paints, polishes, and adhesives; [HSDB]

. . . major US manufacturers of AFFF [aqueous film-forming foam] indicated they would no longer produce PFOA-based fluorosurfactant foams after 2015. [PMID 31045850]

In fire-fighting applications, cosmetics, greases and lubricants, paints, polishes and adhesives /Fluorinated surfactants/

Long-chain perfluoroalkanecarboxylic acids and their salts are surface-active chemicals (surfactants), which greatly reduce the surface tension (surface energy) of water, aqueous solutions, and organic liquids even at low concentrations. These acids (C6- C12) and derivatives are used as wetting, dispersing, emulsifying, and foaming agents. /Long-chain perfluoroalkanecarboxylic acids/

non-polymer PFAS -> Personal Care products and cosmetics -> Sunscreen

It has been used in the manufacture of such prominent consumer goods as Teflon and Gore-Tex. 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. Exposure has been associated with increased cholesterol and uric acid levels, and recently higher serum levels of PFOA were found to be associated with increased risk of chronic kidney disease in the general United States population, consistent with earlier animal studies. This association was independent of confounders such as age, sex, race/ethnicity, body mass index, diabetes, hypertension, and serum cholesterol level.

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. [Table#6770]

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: Octanoic acid, 2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-pentadecafluoro-. Aggregated National Production Volume: < 500,000 pounds.

Non-confidential 2012 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: Octanoic acid, 2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-pentadecafluoro-. National Production Volume: Withheld.

PFOA can be commercially manufactured by two major alternative processes: The Simons Electro-Chemical Fluorination (ECF) process, and a telomerization process. ... In the ECF process, an electric current is passed through a solution of anhydrous hydrogen fluoride and an organic feedstock of octanoic acid or a derivative. The ECF process replaces the carbon-hydrogen bonds on molecules of the organic feedstock with carbon-fluorine bonds. Perfluorination occurs when all the carbon-hydrogen bonds are replaced with carbon-fluorine ones. The ECF process yields between 30-45% straight chain (normal) perfluorooctanonyl fluoride (PFOF), along with a variable mixture of byproducts and impurities. The output of the ECF process consists of a complex combination of chemical substances with varying molecular weights, including higher and lower straight-chain homologues; branched-chain perfluoroalkyl fluorides of various chain lengths; straight-chain, branched, and cyclic perfluoroalkanes and ethers; and other byproducts. After disposal or recovery of some of the byproducts and impurities, the acid fluoride is base hydrolyzed in batch reactors to yield PFOA. The PFOA salts are synthesized by base neutralization of the acid to the salt in a separate reactor. In the telomerization process, tetrafluoroethylene is reacted with other fluorine-bearing chemicals to yield fluorinated intermediates which are readily converted into PFOA. This process yields predominantly straight-chain acids with an even number of carbon atoms. Distillation can be used to obtain pure components.

Long-chain perfluorocarboxylic acids are prepared by the Simons electrochemical fluorination of the corresponding acyl halide ... The acids are obtained by hydrolysis of the perfluoroacyl fluoride, followed by distillation. Some carbon - carbon bond scission occurs to form lower homologous acids along with inert fluorocarbons and cyclic ethers. The acid yield decreases with increasing chain length. /Long-chain perfluorocarboxylic acids/

Food Contaminant -> CONTAMINANT; Food Contaminant -> -> JECFA Functional Classes

PFAS -> PFcarboxylic acids (PFCA)

PFAS (per- and polyfluoroalkyl substances) -> OECD Category

PFAS

Octanoic acid, 2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-pentadecafluoro-: ACTIVE

Historically, most U.S. production was by 3M using the ECF /Electro-Chemical Fluorination/ process. 3M discontinued its manufacture of PFOA between 2000 and 2002, and other domestic producers are using the telomerization process exclusively.

In 2006, EPA and the eight major companies in the industry launched the 2010/15 Perfluorooctanoic Acid (PFOA) Stewardship Program, in which companies committed to reduce global facility emissions and product content of PFOA and related chemicals by 95 percent by 2010, and to work toward eliminating emissions and product content by 2015.

In May 2000, the 3M Company (St. Paul, MN) announced that it would discontinue the production of perfluorooctanoic acid.