HuagongsheHuagongshe Chemie-Druckbericht · Nur für Forschungszwecke
Pentadecafluoroctansure
Pfoa · PERFLUOROOCTANOIC ACID · PERFLUOROOCTANOATE · PERFLUORO-N-OCTANOIC ACID · N-PERFLUOROOCTANOIC ACID · Perfluoroctanoic acid · PERFLUOROCAPRYLIC ACID · Perfluorooctanoic acid(PFOA)
Identifikatoren & physikalische Daten
| CAS No. | 335-67-1 |
|---|---|
| Summenformel | C8HF15O2 |
| Durchschnittliche Molmasse | 414,07 g/mol |
| Monoisotopische Masse | 413,97370257 g/mol |
| SMILES | O=C(O)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)F |
| InChIKey | SNGREZUHAYWORS-UHFFFAOYSA-N |
| PubChem CID | 9554 |
| ChEMBL | CHEMBL172988 |
| ChEBI | CHEBI:35549 |
| EC No. | 206-397-9 |
| DTXSID | DTXSID8031865 |
| Lokaler Name | Pentadecafluoroctansure |
Chemische & physikalische Eigenschaften
| XLogP | 4,9 |
|---|---|
| Polarare Oberfläche (TPSA) | 37,3 |
| H-Brücken-Donoren | 1 |
| H-Brücken-Akzeptoren | 17 |
| Frei drehbare Bindungen | 6 |
| Schwere Atome | 25 |
| Formalladung | 0 |
| Komplexität | 530 |
| Stoffklassen | Other Classes -> Perfluoroalkyl AcidsIonic LiquidsIonic Liquids -> Fluorinated Ionic Liquids |
| PFAS | PFAS -> Perfluorocarboxylic acidsPFAS -> PFAS with analytical method availablePFAS -> Other/unspecified |
| LogP (Verteilungskoeffizient) | 6.3 |
| Dichte | 1.792 g/mL at 20 °C1.79 g/cm³1.792 @ 20°C1,7 g/cm3 |
| Color/Form | White to off-white powder |
| Löslichkeit | When heated to decomposition it emits toxic vapors of F(-).In water, 3300 mg/L at 25 °CIn water, 4340 mg/L at 24.1 °CSolubility in water: none3.4g/l3.4 g/L |
| Endocrine Disruptors | Potential endocrine disrupting compound |
| Siedepunkt | 192 °C189 °C189 °C @760 [mm Hg]189 °C/736 mmHg (lit.) |
| Decomposition | When heated to decomposition it emits toxic vapors of /flourine/. |
| Schmelzpunkt | 54.3 °C52-54 °C55-56 °C (lit.) |
| Dampfdruck | 0.15 [mmHg]3.16X10-2 mm Hg at 25 °C0.15 [mm Hg] @20 °C0.37 ± 0.01 [log Psd at 298.15 K (Pa)] |
| Surface Tension | 15.2 dynes/cm |
| Flammpunkt | 189-192°C |
| Lagerbedingungen | 2-8°C |
| Aggregatzustand | Crystalline Powder |
| pKa (Säurekonstante) | 0.50±0.10(Predicted) |
| Wichte | 1.7 |
| Farbe | White |
| pH | 2.6 (1g/l, H2O, 20℃) |
| BRN | 1809678 |
| Henry-Konstante | 4.9×10-2 mol/(m3Pa) at 25℃, Kutsuna and Hori (2008) |
| Stabilität | Stable. Incompatible with bases, oxidizing agents, reducing agents. |
| Hauptanwendungen | PFAS testingcleaning productscosmeticsenvironmentalfood and beveragespersonal care |
| InChI | 1S/C8HF15O2/c9-2(10,1(24)25)3(11,12)4(13,14)5(15,16)6(17,18)7(19,20)8(21,22)23/h(H,24,25) |
| InChIKey | SNGREZUHAYWORS-UHFFFAOYSA-N |
| SMILES | OC(=O)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)C(F)(F)F |
| CAS Datenbank | 335-67-1(CAS DataBase Reference) |
| NIST chemische Informationen | Octanoic acid, pentadecafluoro-(335-67-1) |
| EPA chemische Informationen | Perfluorooctanoic acid (335-67-1) |
Sicherheit & Vorschriften
| GHS-Einstufung | DangerH302: 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)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) |
|---|---|
| Regulatorische Informationen | Chemical: Octanoic acid, pentadecafluoro-Hazard Traits - BioaccumulationCarcinogenicityDevelopmental ToxicityEnvironmental PersistenceHepatotoxicity and Digestive System ToxicityReproductive ToxicityRegulation (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 |
| Weitere Sicherheitsinformationen | IMAP assessments - Perfluorooctanoic acid (PFOA) and its direct precursors: Environment tier II assessment |
| Brandgefahren | Not combustible. Gives off irritating or toxic fumes (or gases) in a fire. Risk of fire and explosion on contact with bases, oxidants or reducing agents. |
| Gefahrenübersicht | 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 tractInhalation 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] |
| EG-Einstufung | Symbol: T, XnR: 40-61-48/23-48/21/22-41-64S: 53-45 |
| UN-Einstufung | UN Hazard Class: 8UN Pack Group: III |
| Special Reports | 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 alTreatment of poly- and perfluoroalkyl substances in U.S. full-scale water treatment systems. Water Res 51: 246-55 (2014)] |
| Chemical Dangers | 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. |
| Packaging and Labelling | Do not transport with food and feedstuffs. Unbreakable packaging. Put breakable packaging into closed unbreakable container. |
| Toxic Combustion Products | Special hazards arising from the substance or mixture: Carbon oxides, Hydrogen fluoride |
| Hazard Classes and Categories | Acute Tox. 4 (95.5%)Acute toxicity - category 3Reproductive toxicity - Category 1BAcute toxicity (Oral) - Category 4Carcinogenicity - Category 2Carc. 2 |
| Landesrichtlinien für Trinkwasser | 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 acidCAS Registry No.: 335-67-1Analytical Method: EPA 537Minimum Reporting Level: 0.02 ug/LSampling 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 |
| Brandbekämpfung | Use water spray, carbon dioxide, dry powder, foam. |
| Erste-Hilfe-Maßnahmen | 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 . |
| Sichere Lagerung | Store only in original container. Separated from food and feedstuffs and incompatible materials. See Chemical Dangers. |
| Expositionsschutz und Persönliche Schutzausrüstung | 0.005 [mg/m3], inhalable fraction[German Research Foundation (DFG)] |
| Brandbekämpfungsverfahren | 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. |
| Lagerbedingungen | Keep container tightly closed in a dry and well-ventilated place. |
| Reinigungsverfahren | 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 dustEnvironmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drainsMethods 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. |
| Entsorgungsverfahren | 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 qualitypotential migration in air, soil or watereffects on animal, aquatic and plant lifeand 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 scrubberContaminated packaging: Dispose of as unused product. |
| Verschüttetes entsorgen | 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. |
| Preventive Measures | 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. |
| Eye Prevention | Wear safety goggles or eye protection in combination with breathing protection if powder. |
| Fire Prevention | NO contact with incompatible substances. See Chemical Dangers. |
| Körperbelastung | 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 lipidsamples were collected in 2009(6). Perfluorooctanoic acid was frequently detected in 30 human hair samplesconcentrations 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, Germanysamples 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 populationsamples 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/Lsamples 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. |
| Wechselwirkungen | ... 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. |
| Ökotoxizitätswerte | EC50Species: Isochrysis galbana (Haptophyte) Exponential Growth Phase, 10000 cells/mLConditions: saltwater, static, 20 °CConcentration: 163600 ug/L for 72 hrEffect: decreased population growth rate /96% purity/Species: Pseudokirchneriella subcapitata (Green Algae) 3000000 cells/mLConditions: freshwater, staticConcentration: 1.807 mM for 4.5 hr (95% confidence interval: 1.76-1.86 mM)Effect: population, decreased photosynthesis /96% purity/Species: Chydorus sphaericus (Water Flea) age <24 hr neonateConditions: freshwater, static, 20 °CConcentration: 0.426 mM for 24 hr (95% confidence interval: 0.223-0.537 mM)Effect: intoxication, immobilization /96% purity/Concentration: 0.282 mM for 48 hr (95% confidence interval: 0.122-0.345 mM)For more Ecotoxicity Values (Complete) data for Perfluorooctanoic acid (17 total), please visit the HSDB record page. |
| Umweltverhalten | 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). |
| Lebensmitteluntersuchungswerte | Perfluorooctanoic acid was detected in four tap water samples from Amsterdam, The Netherlands at 3.2-4.3 ng/Lmixed 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 agethese 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. |
| Unerwünschte Wirkungen | Dermatotoxin - Skin burns. |
| Expositionspfade | The substance can be absorbed into the body by inhalation of its aerosol, through the skin and by ingestion. |
| Milk Concentrations | 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] |
| Toxizitätsübersicht | 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. |
| Average Daily Intake | 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] |
| Ökotoxizitätsauszüge | /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. |
| Plant Concentrations | Perfluorooctanoic acid concentration was reported in lichen, plants and mushrooms growing in the northern Yukon Territory and Northwest Territories of Canadasamples 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] |
| Wassergefährdungsklasse (WGK) | 2 |
| TSCA-Inventar-Status | TSCA listed |
| UN-Transportnummer | UN 3261 8/PG 3 |
| Zollcode | 29159080 |
| RTECS-Nr. | RH0781000 |
| R-Sätze (R) | 22-34-52/53-39/23/24/25-23/24/25-11 |
| Toxizität | dnd-esc 50 mmol MUREAV 89,95,81 |
| Gefahrensymbole | C,Xi,T,F |
| hazard_note | Corrosive |
| Sicherheitshinweise (S) | 26-36/37/39-45-36/37-16-7 |
| Gefahrenklasse | 8Acute Tox. 3 DermalAcute Tox. 3 InhalationAcute Tox. 3 OralFlam. Liq. 2STOT SE 1 |
| Verpackungsgruppe | III |
| Lagerklasse | 3 - Flammable liquids |
| Gefahrstoffdaten | 335-67-1(Hazardous Substances Data) |
Anwendungen & Verwendung
Beschreibung
Concerns about the potential environmental and toxicological impacts of long-chain perfluoroalkyl sulfonates and carboxylic acids have led to: (1) the phaseout of production of perfluorooctane sulfonate (PFOS) and related compounds and perfluorooctanoic acid (PFOA) by their major global manufacturer in 2000–02; (2) the conclusion of a stewardship agreement between the United States Environmental Protection Agency (US EPA) and eight leading global companies to reduce emissions and product content of PFOA and related chemicals by 95% by 2010 and to work toward their elimination by 2015; (3) a similar agreement between the Canadian environmental and health authorities and five companies to restrict perfluorinated carboxylic acids in products; (4) a European Union Marketing and Use Directive restricting the use of ‘PFOSs’ in the European Union; and (5) the inclusion of PFOS in the Stockholm Convention on Persistent Organic Pollutants as an Annex B substance, i.e., restricted in its use; and other regulatory and voluntary initiatives intended to reduce environmental emissions of this family of compounds.
Verwenden
Perfluorooctanoic acid (PFOA) is fluorinated surfactant used, primarily as its ammonium salt (APFO), as an aid in the chemical synthesis of fluoropolymers and fluoroelastomers. As such, it may be found in nonstick cookware and utensils, stain-repellant fabric treatments, and water-proofing treatments for garments. Although an effort is underway by the U.S. EPA to reduce use of and replace perfluoroalkyls with other substances, PFOA is still used in United States industry. Perfluorooctanoic acid (PFOA, C8, pentadecafluorooctanoic acid, perfluoro caprylic acid) is an eightcarbon compound in the perfluoroalkyl family of chemicals. Perfluorooctane sulfonate is used in a variety of applications, including nonstick cookware, waterproof clothing, leather products, cleaning products, and pesticides. Its main use was as a stain repellent on carpet, furniture, and other consumer products. In 2006, the U.S. Protection Agency along with eight major companies that utilized PFOA embarked on a program to reduce emissions and use of the chemical by 2015 (USEPA, 2012).