Heptadecafluoroctan-1-sulfonsure

The surface active properties of the potassium salt of PFOS make a direct determination of the octanol-water partition coefficient impossible. In a preliminary study reported by 3M an inseparable emulsion was formed. 3M determined the solubility of PFOS (K salt) in octanol as 56 mg/L, and calculated the log Kow from the ratio of solubilities, giving a log Kow value of -1.08. /Potassium salt/

Water solubility of the potassium salt: A value of 570 mg/L was reported from a 1999 study by 3M for pure water. A more recent 3M assessment found values of 519 and 680 mg/L at 20 and 25 °C, respectively, in pure water. Solubility in salt water is reduced from that in pure water. In natural seawater a solubility of 12.4 mg/L at 22-23 °CC was measured. A value of 20.0 mg/L was obtained for a sodium chloride solution at 3.5% salinity, the same as the natural seawater. /Perfluorooctane sulfonic acid, potassium salt/

249 °C

BP: 133 °C at 6 mm Hg

VP: 3.31X10-4 Pa at 20 °C (2.48X10-6 mm Hg) measured by OECD Method 104 ... however, a note in the 3M assessment comments that this result is thought to be due to volatile impurities in the substance. /Perfluorooctane sulfonic acid, potassium salt/

2.0X10-3 mm Hg at 25 °C /estimated by extrapolation of the boiling pt and two reduced pressure boiling pts (6 mm Hg at 133 °C and 10 mm Hg at 145 °C) via Antoine method fit/

Henry's Law constant (potassium salt): direct measurement by 3M found the air-water partition coefficient to be very low and much less than the Henry's Law constant of water (4.34X10-7 atm-cu m/mol). /Perfluorooctane sulfonic acid, potassium salt/

Negative

2.77

10.5

Agilent XCT

Electrospray ionization

ammonia (10nM)

Danger

H302: Harmful if swallowed [Warning Acute toxicity, oral]；H332: Harmful if inhaled [Warning Acute toxicity, inhalation]；H351: Suspected of causing cancer [Warning Carcinogenicity]；H360D ***: May damage the unborn child [Danger Reproductive toxicity]；H362: May cause harm to breast-fed children [Reproductive toxicity, effects on or via lactation]；H372 **: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]；H411: Toxic to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]

P203, P260, P261, P263, P264, P270, P271, P273, P280, P301+P317, P304+P340, P317, P318, P319, P330, P391, P405, and P501 (click each P-code to see the statement)

Danger

Hazard Traits - Bioaccumulation; Carcinogenicity; Developmental Toxicity; Environmental Persistence; Immunotoxicity; Reproductive Toxicity；Authoritative List - CA NLs; CECBP - Priority Chemicals; EC Annex VI CMRs - Cat. 1B; IARC Carcinogens - 2B; OSPAR Priority Action Part A; Prop 65; WA PBTs；Report - regardless of intended function of ingredient in the product

Regulation (EC) No 178/2002 (amended)

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

Substance: Heptadecafluorooctane-1-sulphonic acid；EC: 217-179-8；Date of inclusion in the POPs Regulation: 24-Aug-2010；POPs Regulation Annex: Annex I, part A; Annex IV

Animals given high doses develop liver enlargement and elevated cholesterol. The presence of PFOS in nonoccupationally exposed populations and wildlife has raised concerns about the environmental and health effects of PFOS and prompted the phase-out of the production of POSF-based chemicals by the major producer. A study of 1895 employees in PFOS-exposed jobs, no increased risks for several cancers, low birth weights, or other common health problems were found. [Reference #1] Caused severe eye irritation in rabbits in one study, and mild to moderate irritation in several others; Histopathological changes to the liver observed in two year feeding study with rats with doses as low as 0.06-0.23 (males) and 0.007-0.21 (females) mg/kg body weight; Increased frequency of hepatocellular adenomas seen in chronic animal studies at the highest doses (greater than doses which caused non-neoplastic effects); No evidence of mutagenicity in various in vitro and in vivo assays; Teratogenic effects (incomplete skull closure) observed at doses below maternal NOEL in rats; Effects in a multi-generational study with rats (F1 generation) include significant reductions in litter sizes, viability and lactation indices, and slower development pups; [Reference #2] Corrosive to skin and eyes; A respiratory tract irritant; Can be absorbed through skin; Animal studies conducted on organic fluorochemicals which are present in this product indicate effects including liver disturbances, weight loss, loss of appetite, lethargy, and neurological, pancreatic, adrenal and hematologic effects. There are no known human health effects from anticipated exposure to these organic fluorochemicals when used as intended and instructed. [MSDSonline: 3M MSDS] Serum PFAS concentrations were not associated with increased cardiometabolic risk measures in this population of firefighters. [PMID 33105404]

OECD; Hazard Assessment of Perfluorooctane Sulfonate (PFOS) and its Salts. 21-Nov-02. Paris, France: Organization for Economic Co-operation and Development, Environ Direct, Joint Mtg Chem Comm, Working Party Chem, Pest, Biotechnol. ENV/JM/RD(2002)17/FINAL.[Available from, as of November 22, 20010 http://www.oecd.org/document/58/0,2340,en_2649_37465_2384378_1_1_1_37465,00.html]

EPA. 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]

Certain Perfluoroalkyl Sulfonates. Chemical substances and significant new uses subject to reporting. 1-Octanesulfonic acid, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro- is included on this list.

EPA is issuing a significant new use rule (SNUR) under section 5(a)(2) of the Toxic Substances Control Act (TSCA) for 75 substances including perfluorooctanesulfonic acid (PFOSH) and certain of its salts (PFOSS), perfluorooctanesulfonyl fluoride (POSF), certain higher and lower homologues of PFOSH and POSF, and certain other chemical substances, including polymers, that are derived from PFOSH and its homologues. These chemicals are collectively referred to as perfluoroalkyl sulfonates, or PFAS. This rule requires manufacturers and importers to notify EPA at least 90 days before commencing the manufacture or import of these chemical substances for the significant new uses described in this document. EPA believes that this action is necessary because the PFOSH component of these chemical substances may be hazardous to human health and the environment. The required notice will provide EPA with the opportunity to evaluate an intended new use and associated activities and, if necessary, to prohibit or limit that activity before it occurs. ... The significant new uses described in this document are: 1. Any manufacture or import for any use of any chemical listed in Table 1, Unit I.A., on or after January 1, 2003, except as noted in Unit II.A.2. 2. Manufacture or import of any chemical listed in Table 1, Unit I.A., solely for one or more of the following specific uses shall not be considered as a significant new use subject to reporting under this section: i. Use as an anti-erosion additive in fire-resistant phosphate ester aviation hydraulic fluids. ii. Use as a component of a photoresist substance, including a photo acid generator or surfactant, or as a component of an anti-reflective coating, used in a photomicrolithography process to produce semiconductors or similar components of electronic or other miniaturized devices. iii. Use in coatings for surface tension, static discharge, and adhesion control for analog and digital imaging films, papers, and printing plates, o

PFCs have been manufactured in Decatur since the 1960s by the 3M Corporation (3M), and later by Daikin America, Inc. (Daikin). Additionally, Toray Carbon Fibers America, Inc. (Toray) in Decatur historically used PFCs. In the past, 3M disposed of PFC waste on-site as well as in local landfills. Wastewater containing PFCs from the three industrial facilities was treated at the Decatur Utilities. In 2007, a local industry notified EPA that it had inadvertently discharged large quantities of a PFC to Decatur Utilities. At that time, biosolids from Decatur Utilities was being applied as a fertilizer on about 5000 acres of privately owned agricultural fields in Alabama's Lawrence, Morgan and Limestone counties. This practice had been ongoing since 1996. EPA regulations under the Clean Water Act allow biosolids to be applied as a fertilizer as long as certain operating and monitoring requirements are followed. PFCs are a class of man-made chemicals that, in most cases, are not regulated by EPA. Therefore, biosolids are typically not required to be tested for PFCs. In response to the notification, EPA tested biosolids and a limited set of soil samples from two agricultural sites where biosolids from Decatur Utilities had been applied. The results indicated elevated levels of perfluorooctyl sulfonate (PFOS), perfluorooctanoic acid (PFOA) and other PFCs when compared with sampling results from industrial and residential sites.

Acute Tox. 4 (100%)；Skin Corr. 1B (79.2%)；Acute Tox. 4 (100%)；Carc. 2 (100%)；Repr. 1B (97.9%)；Lact. (100%)；STOT RE 1 (100%)；Aquatic Chronic 2 (100%)

Carcinogenicity - category 2；Reproductive toxicity - category 1B；Specific target organ toxicity (repeated exposure) - category 1；Acute toxicity - category 4；Reproductive toxicity - effects on or via lactation；Hazardous to the aquatic environment (chronic) - category 2

Acute toxicity (Oral) - Category 3；Acute toxicity (Inhalation: Dusts and mists) - Category 4；Serious eye damage/eye irritation - Category 2B；Carcinogenicity - Category 2；Reproductive toxicity - Category 1A, Additional category: Effects on or via lactation；Specific target organ toxicity - Repeated exposure - Category 1 (liver, blood system)；Hazardous to the aquatic environment (Acute) - Category 2；Hazardous to the aquatic environment (Long-term) - Category 2

Acute toxicity (Oral) - Category 3；Serious eye damage/eye irritation - Category 2B；Reproductive toxicity - Category 1B；Hazardous to the aquatic environment (Acute) - Category 2；Hazardous to the aquatic environment (Long-term) - Category 2

Carcinogenicity - Category 2；Reproductive toxicity - Category 1B, Additional category for effects on or via lactation；Specific target organ toxicity - Repeated exposure - Category 1 (liver, immune system)

Carc. 2；Repr. 1B；Lact.；Acute Tox. 4 *；Acute Tox. 4 *；STOT RE 1；Aquatic Chronic 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: perfluorooctanesulfonic acid; CAS Registry No.: 1763-23-1; Analytical Method: EPA 537; Minimum Reporting Level: 0.04 ug/L; Sampling location: EPTDS (entry points to the distribution system); Period during which monitoring to be completed: 1/1/2013-12/31/2015.

Perfluorooctane Sulfonate (PFOS) Provisional Health Advisory: 0.2 ug/L. Provisional Health Advisory values are developed to provide information in response to an urgent or rapidly developing situation. They reflect reasonable, health-based hazard concentrations above which action should be taken to reduce exposure to unregulated contaminants in drinking water. They will be updated as additional information becomes available and can be evaluated. /Perfluorooctane Sulfonate/

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

Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas; Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided; Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. 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.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid inhalation of vapor or mist.

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.

Eye/face protection: Tightly fitting safety goggles. Faceshield (8-inch minimum). Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Skin protection: Handle with gloves.

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multipurpose combination (US) or type ABEK (EN 14387) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Perfluorooctane sulfonic acid was measured in blood sera of employees in the fluorochemical manufacturing industry at concentrations up to 12.8 ug/L(1). The compound has been detected in samples of human sera at concentrations ranging from 6.7 to 81.5 ng/mL, an average of 28.4 ng/mL(2). Perfluorooactane sulfonic acid concentrations in serum samples ranged from 3.6 to 164.0 ng/mL from 20 adults residents of Atlanta, GA analyzed in July 2003(3). The mean concentrations in blood samples from 47 males and 36 females in Sweden were 18.4 (1.7-37) and 17.8 (4.6-33) ppb, respectively, collected in 1997-2000(4). Mean concentrations in blood plasma levels of children, women, and men in Arnsberg, Germany, , were 5.4, 6.3, an 11.8 ug/L, sampled between September and November, 2006(5). The geometric mean in serum (ug/L) for the US population 12 years and older from data reported in the National Health and Nutrition Examination Survey 2003-2004 is 20.7, with females at 18.4 and males at 23.3 ug/L. The mean geometric concentrations reported in the 1999-2000 survey were 30.4, 28.0, and 33.4 ug/L for total, females, and males, respectively(6). A mean concentration of 20.8 ng/mL was reported for perfluorooctane sulfonic acid as a result of analysis of 3802 samples in pooled Australian serum, collected 2002-2003 in rural and urban areas(7). Serum concentrations in US samples collected in 1974 and 1989 were 29.5 ng/mL vs. 34.7 ng/mL, respectively(8). Mean serum concentrations reported in various studies from the United States through 2015 were 9.32-55.8 ng/mL(9). Based on results from the National Health and Nutrition Examination Survey (NHANES), the adjusted geometric mean perfluorooactane sulfonic acid concentration in US male serum samples has fallen from 34 ng/mL in 1999-2000 to 17.5 ng/mL in 2007-2008(10); US female serum sample levels have fallen from 30 ng/mL in 1999-2000 to 11 ng/mL in 2007-2008(10).

... 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.

... Curcumin is a natural polyphenolic compound abundant in the rhizome of the perennial herb turmeric. It is commonly used as a dietary spice and coloring agent in cooking and anecdotally as an herb in traditional Asian medicine. In this study, male rats were treated with three different PFOS doses (0.6, 1.25, and 2.5 mg/kg) and one dose of curcumin, from Curcuma longa (80 mg/kg), and combined three doses of PFOS with 80 mg/kg dose of curcumin by gavage for 30 d at 48 hr intervals. Here, we investigated the DNA damage via single-cell gel electrophoresis/comet assay and micronucleus test in rat peripheral blood in vivo. It is found that all doses of PFOS increased micronucleus frequency (p<0.05) and strongly induced DNA damage in peripheral blood in two different parameters; the damaged cell percent and genetically damage index, and curcumin prevented the formation of DNA damage induced by PFOS. Results showed that curcumin inhibited DNA damage including GDI at certain levels at statistical manner, 30.07%, 54.41%, and 36.99% for 0.6 mg/kg, 1.25 mg/kg, and 2.5 mg/kg.

LC50; Species: Pimephales promelas (Fathead minnow); Conditions: static; Concentration: 9.5 mg/L for 96 hr /Perfluorooctane sulfonate, potassium salt/

LC50; Species: Lepomis macrochirus (Bluegill sunfish); Conditions: static; Concentration: 7.8 mg/L for 96 hr /Perfluorooctane sulfonate, DEA salt/

LC50; Species: Oncorhynchus mykiss (Rainbow trout); Conditions: static; Concentration: 22 mg/L for 96 hr /Perfluorooctane sulfonate, potassium salt; 86.7% pure/

LC50; Species: Cyprinodon variegatus (Sheepshead minnow); Conditions: semi-static (24 hr renewal); Concentration: >15 mg/L for 96 hr /Perfluorooctane sulfonate, potassium salt; 86.7% pure/

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

TERRESTRIAL FATE: Based on a classification scheme(1), a laboratory measured Koc range of 250 to 50,100(2) indicates that perfluorooctane sulfonic acid is expected to have moderate mobility to immobility in soil(SRC); the average Koc value of 1000(2) indicates low mobility in soil(SRC). The pKa of perfluorooctane sulfonic acid is <1.0(3), indicating that this compound will exist almost 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). The strength of adsorption can vary depending on the nature of the adsorbing material with respect to pH, organic content, mineral content, and other factors(1,5). Although perfluoroalkyl anions will not volatilize from moist soil surfaces, their unique surfactant properties may prevent total dissociation in water(6). Therefore, some volatilization of perfluoroalkyls may occur since the neutral forms are considered to be volatile(6). Perfluorooctane sulfonic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.0X10-3 mm Hg(7), however, perfluoroalkyl neutral forms are considered to be volatile(6). Perfluorooctane sulfonic acid is resistant to biodegradation(6) and does not biodegrade under typical environmental conditions(8). Utilizing the Japanese MITI test(9), 0% of the Theoretical BOD was reached in 4 weeks indicating that biodegradation is not an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), a field-based Koc range of 126 to 39,800(2-4) indicates that perfluorooctane sulfonic acid can have low to very high adsorption to suspended solids and sediment(SRC). The strength of sorption to sediment and suspended material in water can vary depending on the nature of the sediment material with respect to pH, organic content, mineral content, salinity and other factors(2,5). In marine environments where suspended solid concentrations are low, perfluorooctane sulfonic acid may be transported in dissolved phase rather than being adsorbed to suspended solids(5). A pKa of <1.0(6) indicates perfluorooctane sulfonic acid will exist almost 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). However, unique surfactant properties of the compound may prevent total dissociation in water and some volatilization may occur since the neutral form of perfluoroalkyls are considered to be volatile(7). According to a classification scheme(8), a BCF range of 200-1500 measured in carp (Cyprinus carpio)(9) suggests the potential for bioconcentration in aquatic organisms is high to very high(SRC). Perfluorooctane sulfonic acid is resistant to biodegradation(7) and does not biodegrade under typical environmental conditions(10). Utilizing the Japanese MITI test(9), 0% of the Theoretical BOD was reached in 4 weeks indicating that biodegradation is not an important environmental fate process in soil(SRC). Hydrolysis is not expected to be an important environmental fate process since this compound has an extrapolated hydrolysis half-life of >41 years(11).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), perfluorooctane sulfonic acid, which has an estimated vapor pressure of 2.0X10-3 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase perfluorooctane sulfonic 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 115 days(SRC), calculated from its rate constant of 1.4X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Monitoring data has detected perfluorooctane sulfonic acid in both vapor and particulate phases in ambient air samples(3). Vapor-phase perfluorooctane sulfonic acid can adsorb to atmospheric particulate matter and be removed from the air by wet and dry deposition(4,5). It has been detected in rain and snow samples(3). Perfluorooctane sulfonic acid is not susceptible to direct photolysis by sunlight(4,5). Monitoring data from remote Arctic sites indicate the compound is subject to long-range transport either through atmospheric transport of precursor compounds followed by degradation to form PFOS or through atmospheric aerosol transport(4,5).

As a result of the 1998 Health Canada Total Diet Study, perfluorooctane sulfonic acid was detected as follows (ng/g wet wt): cold cuts <0.88; cookies <0.15; processed cheese 1.14; peppers <0.15; canned lunch meats <0.37; pizza <0.20; cheese 0.71; frozen dinner (beef) <0.17(1). The mean concentrations of perfluorooctane sulfonic acid in foods from a market in Catalan, Spain were reported as follows (ng/g fresh weight): vegetables 0.022; pulses <0.027; cereals <0.069; white fish 0.407; seafood 0.148; tinned fish 0.271; blue fish 0.654; pork 0.045; chicken 0.021; veal 0.028; lamb 0.040; eggs 0.082; dairy products 0.121; fruits <0.017; margarine <0.034; oil <0.099. Sampling was conducted in July 2006(2).

Food occurrence data for perfluorooctane sulfonic acid (PFOS) and other perfluoroalkylated substances were collected in 13 European countries during the period 2006 to 2012. A total of 54,195 analytical results were obtained for 7,560 food samples. PFOS was quantified in 29% of all food samples with fish and other seafoods having the most frequent detections. Across foods of plant origin, PFOS was found in vegetables and wild edible fungi in concentrations from 0.0043 to 1.54 ug/kg, in fruits in concentrations from 0.003 to 0.54 ug/kg, in one potato sample (1.2 ug/kg) and in one bean sample (0.0063 ug/kg)(1).；Table: Meat and meat products (including edible offal) [Table#6718]

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.；Reproductive Toxin - A chemical that is toxic to the reproductive system, including defects in the progeny and injury to male or female reproductive function. Reproductive toxicity includes developmental effects. See Guidelines for Reproductive Toxicity Risk Assessment.

Perfluorooctane sulfonic acid was detected in 3% of 2,449 "Milk and dairy products" samples collected in 13 European countries during the period 2006 to 2012(1); concentrations measured in liquid milk ranged from 0.0009 to 0.12 ug/kg(1). Human milk samples collected in 2003-2004 in the Kingston region of Ontario Canada were found to contain average and median perfluorooctane sulfonic acid concentrations of 0.055 and 0.026 ng/mL respectively(2). Perfluorooctane sulfonic acid was not detected in 60 raw and retail cow milk samples collected from across the US(3); a concentration of 0.16 ng/g was detected in a milk sample collected at a dairy farm that had applied perfluoroalkyl compound containing biosolids to its fields(3). The mean concentrations of perfluorooctane sulfonic acid in foods from a market in Catalan, Spain were reported as follows (ng/g fresh weight): dairy products 0.121; whole milk <0.014; skimmed milk <0.019. Sampling was conducted in July 2006(4).

IDENTIFICATION AND USE: Perfluorooctane sulfonic acid (PFOS) is a liquid. It is used as a chemical intermediate, an acid catalyst for photoresists, a surfactant in firefighting foam, a surfactant for alkaline cleaners, an emulsifier in floor polish, a mist suppressant for metal plating baths, a surfactant for etching acids for circuit boards, a pesticide active ingredient for ant bait traps, and an agricultural chemical. HUMAN EXPOSURE AND TOXICITY: Health effects of perfluoroalkyl-compounds on humans remain controversial, in spite of a number of experimental and epidemiological studies. In one study, subjects with Polycystic Ovary Syndrome had higher serum concentrations of PFOS. Some studies of women and infants found that PFOS levels negatively correlated with birth weight only in female infants, while other studies found the association to be small. Pre-natal exposure may be associated with immunosuppression in early childhood. Testosterone production may be compromised in individuals with high PFOS exposure. An occupational study conducted on volunteers working at two different 3M plants showed a relationship between higher PFOS serum levels and higher mean values for triglycerides, alkaline phosphatase, total bilirubin, ALT, and serum triiodothyronine, as well as a lower thyroid hormone binding ratio. In a mortality study, which followed workers for 37 years, a statistically significant risk of death from bladder cancer was reported. In a different study, PFOS altered the expression of crucial genes, reduced ATP production, induced ROS, and stimulated apoptosis during the early stages of cardiogenesis. It appears that that PFOS induces apoptosis in A549 cells through a reactive oxygen species-mediated mitochondrial dysfunction pathway mechanism. PFOS suppressed IL-2 production in both a human cell line and human primary cells at dose levels within the high end of the human exposure range. In a study on serum levels of men and women, higher concentrations of PF

Fish consumption and estimated perfluorooctane sulfonic acid intake among residents of the Lake Vattern and Baltic Seas regions, Sweden were reported as 8.3-83 g consumption/day with intake of 0.92-9.6 ng/kg body weight/day and 0-242 g consumption/day with intake of 0-4.5 ng/kg body weight/day, respectively(1). On average, the daily dietary intake of perfluorooctanesulfonic acid for a standard adult man in Tarrgona County, Spain ranged from 62.5 to 74.2 ng/day(2). Based on food monitoring in 13 European countries during the period 2006 to 2012, the dietary exposure for age groups was determined as follows (in ng/kg body wt/day): infants (0.29-11, min-max), toddlers (1.2-8.5, median), other children (1.5-7.1 median), adolescents (0.84-4.0 median), adults (0.8-3.0 median), elderly (1.0-3.2 median), very elderly (0.92-3.1 median)(3).

/BIRDS and MAMMALS/ ... Despite the widespread occurrence of perfluoroalkyl compounds (PFCs), little is known about the impact these contaminants have on the health of wildlife populations. The authors investigated the relationship between PFCs (including sigma-perfluorocarboxylates, sigma-perfluoroalkyl sulfonates, perfluorooctane sulfonate, perfluorooctanoic acid, and perfluorodecanoic acid) and the clinocopathologic and immune parameters in a highly exposed population (n=79) of Atlantic bottlenose dolphins (mean sigma-PFCs = 1970 ng/mL; range 574-8670 ng/mL) sampled from 2003 to 2005 near Charleston, South Carolina, USA. Age-adjusted linear regression models showed statistically significant positive associations between exposure to one or more of the PFC totals and/or individual analytes and the following immunological parameters: absolute numbers of CD2+ T cells, CD4+ helper T cells, CD19+ immature B cells, CD21+ mature B cells, CD2/CD21 ratio, MHCII+ cells, B cell proliferation, serum IgG1, granulocytic, and monocytic phagocytosis. Several PFC analyte groups were also positively associated with serum alanine aminotransferase, gamma-glutamyltransferase, creatinine, phosphorus, amylase, and anion gap and negatively associated with cholesterol levels, creatinine phosphokinase, eosinophils, and monocytes. Based on these relationships, the authors suggest that the PFC concentrations found in Charleston dolphins may have effects on immune, hematopoietic, kidney, and liver function. The results contribute to the emerging data on PFC health effects in this first study to describe associations between PFCs and health parameters in dolphins.

/AQUATIC SPECIES/ In this study, ...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. ...Also studied bone development in larvae, 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

/AQUATIC SPECIES/ ... We developed a novel partial life-cycle assay that incorporates exposures to brooding adult female mussels and used this method in combination with acute toxicity tests to assess adverse effects of perfluoroctanesulfonic acid (PFOS) and perfluoroctanoic acid (PFOA) on freshwater mussels. Fatmucket (Lampsilis siliquoidea) were exposed to PFOS at two life stages: brooding glochidia (in marsupia) for 36 d and free glochidia in water for 24 hr. In standard acute tests with glochidia (24-48 hr exposures) and juveniles (48-96 hr exposures) of fatmucket and black sandshell (Ligumia recta), glochidia were 8 to 25 times more sensitive than juveniles. Perfluoroctanesulfonic acid significantly reduced the duration of glochidia viability and reduced probability of metamorphosis at concentrations 3,000 times lower than the most sensitive acute endpoint (24-hr EC50). The partial life-cycle test is adaptable to a variety of endpoints and research objectives and is useful for identifying adverse effects at contaminant concentrations below those required for an acute lethal response.

/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.

For more Ecotoxicity Excerpts (Complete) data for Perfluorooctane sulfonic acid (42 total), please visit the HSDB record page.

Perfluorooctane sulfonic acid has been measured in blood sera of Laysan albatross (Phoebastria immutabilis) and Blackfooted albatross (P. nigripes) from the Midway Atoll in the North Pacific at concentrations of 3-26 ng/L(1). Blood samples from cormorants (Phalacrocorax auritus) and herring gulls (Larus argentatus) from the Great Lakes showed a 10-fold increase over that for the albatrosses(1). Blood plasma from 200 day old eagles (Aquila chrysaetos) from the Midwestern United States contained perfluorooctane sulfonic acid up to 2,570 ng/mL, with detectable levels >100 ng/mL reported in other fish-eating birds such as pelicans (Pelecanus erythrorhynchos) and loons (Gavia immer)(1). Concentrations in the eggs of Caspian terns (Hydroprogne caspia) from Lake Michigan waters were as great as 3,350 ng/g(1).

Mean concentrations in waterfowl livers collected from the Niagara River region of New York State in July of 2004(1). [Table#6712]

Perfluorooctane sulfonate was measured in 161 samples of liver, kidney, blood, or egg yolk from 21 species of fish-eating water birds collected in the United States, including albatrosses (Laysan albatross (Diomedea immutabilis); black-footed albatross (D. nigripes)) from Sand Island, Midway Atoll, in the central North Pacific Ocean. Concentrations of perfluorooctane sulfonate in the blood plasma of bald eagles (Haliaeetus leucocephalus) collected from the midwestern United States ranged from 13 to 2,220 ng/mL (mean: 330 ng/mL); concentrations of perfluorooctane sulfonate were greater in blood plasma than in whole blood. Among 82 livers from various species of birds from inland or coastal U.S. locations, Brandt's cormorant (Phalacrocorax penicillatus) from San Diego, CA, contained the greatest concentration of perfluorooctane sulfonate (1,780 ng/g, wet wt). Perfluorooctane sulfonate was also found in the sera of albatrosses from the central North Pacific Ocean at concentrations ranging from 3 to 34 ng/mL. Occurrence of perfluorooctane sulfonate in birds from remote marine locations suggests widespread distribution of perfluorooctane sulfonate and related fluorochemicals in the environment. Data were collected over 1991 to 1998(1).

Perfluorooctane sulfonic acid has been measured in mink (Neovison vison) livers from the Midwestern United States with concentrations ranging from 40-5,140 ng/g(1). Concentrations in the river otters (Lontra canadensis) collected in Oregon ranged from 33.6 to 329 ng/g(2). Perfluorooctane sulfonic acid mean plasma concentrations in mammals were reported as follows (genus species, location, concentration in ng/mL or ng/g wet weight): Amur tiger, Panthera tigris altaica, China, 1.41; polar bear, Ursus maritimus, Svalbard,1290; bottlenose dolphin, Tursiops truncates: Bermuda, 49; Indian River Lagoon, FL, 642; New Jersey, 751; Sarasota Bay, FL 780; Charleston, SC, 1315; giant panda, Ailuropoda melanoleuca, Beijing, China, 11.10; red panda, Ailurus fulgens, 15.65(3). Concentrations in various Japanese animals sampled in February 2005 were 35-238, 19-33, 25-61, and 0.15-13 ng/g wet weight for cormorant, racoon dog, eagle, and large-bill crow, respectively(4). Levels in thick-billed murres (Uria lomvia) sampled from 1975, 1993 and 2004 were not detected, 0.51 and 0.75 ng/g wet weight, respectively; levels in northern fulmars (Fulmaris glacialis) from 1975, 1987, 1993, and 2003 were not detected, 0.17, 0.57, and 0.4 ng/g wet weight, respectively. Both species are residents of Prince Leopold Island in the Canadian Arctic(5). Concentrations in melon-head whales (Peponocephala electra) stranded along the Japanese coast in 1982, 2001/2002, and 2006 were reported as 4.6 to 10.2, 17.8 to 117, and 49.2 to 60.6 ng/g met weight, respectively(6). Mean concentration trends from 1992-2007 in livers from northern sea otters (Enhydra lutris kenyoni) from South-Central Alaska were 2.3, 1.6, 10.4, 2.7, 6.0, 4.2, 5.1, 10.8, 21.2, 7.0, 4.2, <0.9, 1.3, 1.9, and 2.8 ng/g wet wt(7).

For more Animal Concentrations (Complete) data for Perfluorooctane sulfonic acid (9 total), please visit the HSDB record page.

EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPA; ICSS Dashboard Application; Available from, as of December 17, 2015: http://actor.epa.gov/dashboard/]

Hazard Traits - Bioaccumulation; Carcinogenicity; Developmental Toxicity; Environmental Persistence; Immunotoxicity; Reproductive Toxicity；Authoritative List - CA NLs; CECBP - Priority Chemicals; EC Annex VI CMRs - Cat. 1B; IARC Carcinogens - 2B; OSPAR Priority Action Part A; Prop 65; WA PBTs；Report - regardless of intended function of ingredient in the product

Regulation (EC) No 178/2002 (amended)

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

Substance: Heptadecafluorooctane-1-sulphonic acid；EC: 217-179-8；Date of inclusion in the POPs Regulation: 24-Aug-2010；POPs Regulation Annex: Annex I, part A; Annex IV

Certain Perfluoroalkyl Sulfonates. Chemical substances and significant new uses subject to reporting. 1-Octanesulfonic acid, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro- is included on this list.

EPA is issuing a significant new use rule (SNUR) under section 5(a)(2) of the Toxic Substances Control Act (TSCA) for 75 substances including perfluorooctanesulfonic acid (PFOSH) and certain of its salts (PFOSS), perfluorooctanesulfonyl fluoride (POSF), certain higher and lower homologues of PFOSH and POSF, and certain other chemical substances, including polymers, that are derived from PFOSH and its homologues. These chemicals are collectively referred to as perfluoroalkyl sulfonates, or PFAS. This rule requires manufacturers and importers to notify EPA at least 90 days before commencing the manufacture or import of these chemical substances for the significant new uses described in this document. EPA believes that this action is necessary because the PFOSH component of these chemical substances may be hazardous to human health and the environment. The required notice will provide EPA with the opportunity to evaluate an intended new use and associated activities and, if necessary, to prohibit or limit that activity before it occurs. ... The significant new uses described in this document are: 1. Any manufacture or import for any use of any chemical listed in Table 1, Unit I.A., on or after January 1, 2003, except as noted in Unit II.A.2. 2. Manufacture or import of any chemical listed in Table 1, Unit I.A., solely for one or more of the following specific uses shall not be considered as a significant new use subject to reporting under this section: i. Use as an anti-erosion additive in fire-resistant phosphate ester aviation hydraulic fluids. ii. Use as a component of a photoresist substance, including a photo acid generator or surfactant, or as a component of an anti-reflective coating, used in a photomicrolithography process to produce semiconductors or similar components of electronic or other miniaturized devices. iii. Use in coatings for surface tension, static discharge, and adhesion control for analog and digital imaging films, papers, and printing plates, o

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: perfluorooctanesulfonic acid; CAS Registry No.: 1763-23-1; Analytical Method: EPA 537; Minimum Reporting Level: 0.04 ug/L; Sampling location: EPTDS (entry points to the distribution system); Period during which monitoring to be completed: 1/1/2013-12/31/2015.

Perfluorooctane Sulfonate (PFOS) Provisional Health Advisory: 0.2 ug/L. Provisional Health Advisory values are developed to provide information in response to an urgent or rapidly developing situation. They reflect reasonable, health-based hazard concentrations above which action should be taken to reduce exposure to unregulated contaminants in drinking water. They will be updated as additional information becomes available and can be evaluated. /Perfluorooctane Sulfonate/

Perfluorooctane sulfonate (PFOS), an emerging persistent contaminant that is commonly encountered during daily life, has been shown to exert toxic effects on the central nervous system (CNS). However, the molecular mechanisms underlying the neurotoxicity of PFOS remain largely unknown. It has been widely acknowledged that the inflammatory mediators released by hyper-activated microglia play vital roles in the pathogenesis of various neurological diseases. In the present study, we examined the impact of PFOS exposure on microglial activation and the release of proinflammatory mediators, including nitric oxide (NO) and reactive oxidative species (ROS). We found that PFOS exposure led to concentration-dependent NO and ROS production by rat HAPI microglia. We also discovered that there was rapid activation of the ERK/JNK MAPK signaling pathway in the HAPI microglia following PFOS treatment. Moreover, the PFOS-induced iNOS expression and NO production were attenuated after the inhibition of ERK or JNK MAPK by their corresponding inhibitors, PD98059 and SP600125. Interestingly, NAC, a ROS inhibitor, blocked iNOS expression, NO production, and activation of ERK and JNK MAPKs, which suggested that PFOS-mediated microglial NO production occurs via a ROS/ERK/JNK MAPK signaling pathway. Finally, by exposing SH-SY5Y cells to PFOS-treated microglia-conditioned medium, we demonstrated that NO was responsible for PFOS-mediated neuronal apoptosis.

Zebrafish embryos were exposed to 1 ug/ mL PFOS or DMSO control from 6 hr post-fertilization (hpf) to 24 or 120 hpf. Subsequently, RNA was isolated from the embryo pool and the expression profiles of 219 known zebrafish miRNAs were analyzed using microarray. Finally, quantitative real-time polymerase chain reaction was used to validate several miRNAs expression of microarray data. The analysis revealed that PFOS exposure induced significant changes in miRNA expression profiles. A total of 39 and 81 miRNAs showed significantly altered expression patterns after PFOS exposure 24 and 120 hpf. Of the changed miRNAs, 20 were significantly up-regulated and 19 were significantly down-regulated (p < 0.01) at 24 hpf, whereas 41 were significantly up-regulated and 40 were significantly down-regulated (p < 0.01) at 120 hpf. These miRNAs were involved in development, apoptosis and cell signal pathway, cell cycle progression and proliferation, oncogenesis, adipose metabolism and hormone secretion ...

... PFOA and PFOS (50-200 umol/L) induced production of reactive oxygen species (ROS), dissipation of mitochondria membrane potential and apoptosis of Hep G2 cells. Moreover, activities of superoxide dismutase, catalase and glutathione reductase were increased, whereas activities of glutathione-S-transferase and glutathione peroxidase were decreased. Glutathione content was reduced. Differential expression of genes, such as p53, Bcl-2, caspase-9, was evident in PFOA or PFOS exposure groups. ...

Chicken embryo primary hepatocyte cultures (N=3 independent cell cultures) /were exposed/ to PFOS or fenofibrate, a mammalian PPAR-alpha agonist, and examined the expression of PPAR-alpha and we PPAR-alpha target genes using quantitative real-time PCR. The target genes examined were peroxisomal acyl-CoA oxidase (ACOX), liver fatty acid binding protein (L-FABP), enoyl-Coenzyme A, hydratase/3-hydroxyacyl Coenzyme A dehydrogenase bifunctional enzyme (BIEN), peroxisomal 3-ketoacyl thiolase (PKT), and malic enzyme (ME). All five target genes were induced in response to PFOS exposure and all of the target genes, except L-FABP, were induced in response to fenofibrate. PPAR-alpha mRNA expression was not altered by PFOS or fenofibrate. ...

Cultured hepatocytes were exposed to various concentrations of perfluorooctanyl sulfonate (PFOS), pentadecafluorooctanoic acid (PFOA), 1H, 1H, 2H, 2H-nonafluoro-1-hexanol (4:2 FTOH), 1H, 1H, 2H, 2H-perfluorooctanol (6:2 FTOH) and 1H, 1H, 2H, 2H-perfluoro-1-decanol (8:2 FTOH) for 48 hr, while 17beta-estradiol (E2) and 4-nonylphenol (4-NP) were used as positive controls. A dose-dependent induction of VTG was observed in E2-, 4-NP-, PFOS-, PFOA- and 6:2 FTOH-treated cells, whereas VTG levels remained unchanged in the 4:2 FTOH and 8:2 FTOH exposure groups at the concentrations tested. The estimated 48-hr EC(50) values for E2, 4-NP, PFOS, PFOA and 6:2 FTOH were 4.7 x 10-7, 7.1 x 10-6, 1.5 x 10-5, 2.9 x 10-5 and 2.8 x 10-5 M, respectively. In the time-course study, significant VTG induction took place at 24 hr (E2), 6 hr (4-NP), 48 hr (PFOS), 48 hr (PFOA), 72 hr (4:2 FTOH), 12 hr (6:2 FTOH), 72 hr (8:2 FTOH), and increased further after 96 h of exposure. Co-exposure to binary mixtures of individual PFCs and E2 for 48 hr significantly inhibited E2-induced hepatocellular VTG production in a dose-dependent manner except for 4:2 FTOH. The estimated 48-h IC(50) (concentration of a compound that elicits 50% inhibition of maximally E2-induced VTG) values for PFOS, PFOA, 6:2 FTOH and 8:2 FTOH were 3.1 x 10-7, 5.1 x 10-7, 1.1 x 10-6 and 7.5 x 10-7 M, respectively. In order to further investigate the estrogenic mechanism of PFCs, the hepatocytes were co-exposed to binary mixtures of individual chemicals (E2, 4-NP, PFOS, PFOA and 6:2 FTOH) and the known estrogen receptor inhibitor tamoxifen for 48 hr; tamoxifen significantly inhibited the ability of these chemicals to stimulate vitellogenesis. ... /Perfluorooctanyl sulfonate/

... Adult trout were exposed to ... perfluorooctane sulfonic acid (PFOS) ... via food over a time period of 28 d ... The ... estimated elimination half-lives were found to be ... between 8.4 d in muscle tissue and 20.4 d in the liver ...

There are species differences in the elimination half-life of PFOS. The half-life in serum is 7.5 days in adult rats and 200 days in Cynomolgus monkeys. In humans, it appears to be quite longer. A recent halflife analysis was conducted on 9 retired 3M chemical workers. PFOS samples were collected over 4 time periods spanning 180 days, measured in triplicate with all time points from each subject analyzed in the same analytical run. The mean half-life for PFOS was 8.67 years (range 2.29 - 21.3 years, SD = 6.12).

Serum PFOS levels in 3 retired male 3M chemical workers have been followed for 5 1/2 yr and suggest a mean elim half-life (t 1/2) of 1,428 days (approx 4 yr). /Perfluorooctyl sulfonates/

Female Sprague-Dawley rats were treated orally with N-ethyl perfluorooctanesulfonamidoethanol (N-EtFOSE), ciprofibrate or corn oil (vehicle) for 21 days, and levels of N-EtFOSE and its metabolites as well as markers of peroxisome proliferation and oxidative stress were assessed in serum, liver and/or uterus. The N-EtFOSE metabolite profile in liver and serum was in good agreement with reported in vitro biotransformation pathways in rats and the metabolite levels decreasing in the order perfluorooctanesulfonate >> perfluorooctanesulfonamide ~ N-ethyl perfluorooctanesulfonamidoacetate >> perfluorooctanesulfonamidoethanol approximately N-EtFOSE. Although N-EtFOSE treatment significantly decreased the growth rate, increased relative liver weight and activity of superoxide dismutases (SOD) in liver and uterus (total SOD, CuZnSOD and MnSOD), a metabolic study revealed no differences in the metabolome in serum from N-EtFOSE-treated and control animals. Ciprofibrate treatment increased liver weight and peroxisomal acyl Co-A oxidase activity in the liver and altered antioxidant enzyme activities in the uterus and liver. According to NMR metabolomic studies, ciprofibrate treated animals had altered serum lipid profiles compared to N-EtFOSE-treated and control animals, whereas putative markers of peroxisome proliferation in serum were not affected. ... /Perfluorooctane sulfonate/

PFOS can also be formed as a metabolite of other perfluorinated sulfonates. It does not appear to be further metabolized. /Perfluorooctyl sulfonates/

Tissue specific uptake and elimination of perfluoroalkyl acids (PFAAs) were studied in rainbow trout (Oncorhynchus mykiss). Adult trout were exposed to perfluorobutane sulfonic acid (PFBS), perfluorohexane sulfonic acid (PFHxS), perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA) and perfluorononanoic acid (PFNA) via food over a time period of 28 d. In the following 28-d depuration period the fish were fed PFAA-free food. At defined sampling times four animals were removed from the experimental tank, euthanized and dissected. Muscle, liver, kidneys, gills, blood, skin and carcass were examined individually. At the end of the accumulation phase between 0.63% (PFOA) and 15.5% (PFOS) of the absolute, applied quantity of PFAAs was recovered in the whole fish. The main target organ was the liver with recovery rates between 0.11% (PFBS) and 4.01% (PFOS) of the total amount of ingested PFAAs. Perfluoroalkyl sulfonic acids were taken up more readily and had longer estimated elimination half-lives than perfluoroalkyl carboxylic acids of the same chain length. The longest estimated elimination half-lives were found to be for PFOS between 8.4 d in muscle tissue and 20.4 d in the liver and for PFNA between 8.2 d in the blood and 11.6 d in the liver.

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.

Prenatal exposure to perfluoroalkyl substances (PFAS) has been associated with lower birth weight in epidemiologic studies. This association could be attributable to glomerular filtration rate (GFR), which is related to PFAS concentration and birth weight. We used a physiologically based pharmacokinetic (PBPK) model of pregnancy to assess how much of the PFAS-birth weight association observed in epidemiologic studies might be attributable to GFR. We modified a PBPK model to reflect the association of GFR with birth weight (estimated from three studies of GFR and birth weight) and used it to simulate PFAS concentrations in maternal and cord plasma. The model was run 250,000 times, with variation in parameters, to simulate a population. Simulated data were analyzed to evaluate the association between PFAS levels and birth weight due to GFR. We compared simulated estimates with those from a meta-analysis of epidemiologic data. The reduction in birth weight for each 1-ng/mL increase in simulated cord plasma for perfluorooctane sulfonate (PFOS) was 2.72 g (95% CI: -3.40, -2.04), and for perfluorooctanoic acid (PFOA) was 7.13 g (95% CI: -8.46, -5.80); results based on maternal plasma at term were similar. Results were sensitive to variations in PFAS level distributions and the strength of the GFR-birth weight association. In comparison, our meta-analysis of epidemiologic studies suggested that each 1-ng/mL increase in prenatal PFOS and PFOA levels was associated with 5.00 g (95% CI: -21.66, -7.78) and 14.72 g (95% CI: -8.92, -1.09) reductions in birth weight, respectively. Results of our simulations suggest that a substantial proportion of the association between prenatal PFAS and birth weight may be attributable to confounding by GFR and that confounding by GFR may be more important in studies with sample collection later in pregnancy.

For more Absorption, Distribution and Excretion (Complete) data for Perfluorooctane sulfonic acid (16 total), please visit the HSDB record page.

Used as a surfactant in fire-fighting foams, alkaline cleaners, floor polishes, metal plating baths, and etching acids for circuit boards; Also used as an acid catalyst for photoresists and the active ingredient for ant bait traps; [HSDB] PFOS and its precursors used as protective surface coatings (i.e. carpets, fabrics, and food packaging) and in specialty chemicals (i.e. fire-fighting foams, hydraulic fluids, mining and oil-well surfactants, and consumer products); [Reference #2] The manufacturing of PFOS began in the United States in 1948. In 2000, the major manufacturer, 3M Corporation, announced that it would stop making many of its well-known Scotchgard stain-repellent products after finding the PFOS persists in the environment and is found widely in numerous species, including humans. [PMID 21346631]

3M to phase out perfluorooctane sulfonates (PFOs) by 2001; [HSDB] PFOS use in new AFFFs [aqueous film-forming foams] and other products were banned in the European Union in 2011 and Canada in 2013. [PMID 31045850]

Electroplating [Category: Plate]；Semiconductor Manufacturing [Category: Industry]；Farming (Pesticides) [Category: Industry]；Textiles (Printing, Dyeing, or Finishing) [Category: Industry]

... Surface-active agents in aqueous media.

Chemical intermediate; acid catalyst for photoresists

Surfactant in fire fighting foam; surfactant for alkaline cleaners; emulsifier in floor polish; mist suppressant for metal plating baths; surfactant for etching acids for circuit boards; pesticide active ingredient for ant bait traps. /K, Li, DEA, NH4 Salts/

Perfluoroalkanesulfonyl fluorides are usually made by the Simons electrochemical fluorination process, in which a hydrocarbon sulfonyl fluoride is electrolyzed in anhydrous hydrogen fluoride at nickel electrodes ... The electrochemical yield is excellent for the first member of the series and decreases progressively with the increasing length of the carbon chain; the yield for octanesulfonyl fluoride is about 40%. Alkaline hydrolysis of perfluoroalkanesulfonyl fluorides gives the corresponding salts, which when acidified and distilled from concentrated sulfuric acid yield the anhydrous sulfonic acids. /Perfluoroalkanesulfonic Acids/

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

PFAS -> PFsulfonic acids (PFSA)

1-Octanesulfonic acid, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-: ACTIVE

The 3M Company, the primary manufacturer of PFOS, completed a voluntary phase-out of PFOS production in 2002 ... PFOS chemicals are no longer manufactured in the United States; however, EPA Significant New Use Rules (SNURs) allow for the continuation of a few, limited, highly technical applications of PFOS-related substances where no known alternatives are available. /Perfluoroalkyls/

3M, the principal manufacturer of PFAS worldwide, voluntarily committed to discontinue the production of the specific PFOS-based PFAS chemicals covered by this rule by December 31, 2002. Based on the information EPA possessed when the original proposed SNUR was published, EPA concluded that this action by 3M would reduce manufacture and importation of these chemicals to zero, with a corresponding reduction in the type, form, and duration of exposure to these chemicals. EPA therefore concluded that any subsequent new manufacture or importation of these chemicals would constitute a significant new use. /Prefluorooctane sulfonic acid (Cas No. 1763-23-1) is included in this SNUR/