Perfluorobutanesulfonic acid

300.1

300.10

206-793-1

1FV02N6NVO

DTXSID5030030

Colorless liquid

2904909090

62.8

1.82 (est)

1.811 g/mL at 25 deg C

211 °C

>230 °F

1.318

In water, 510 mg/L, temperature not specified

2-8°C

2.68X10-2 mm Hg at 25 deg C (est)

LD50 orl-rat: 430 mg/kg ATDAEI 15(Suppl 1),S105,1996

Henry's Law constant = 1.44X10-5 atm-cu m/mol at 25 °C (est)

pKa = -3.31 (est)

133.28 Ų [M-H]-

Hydroxyl radical reaction rate constant = 1.40X10-13 cu cm/molec-sec at 25 °C (est)

CORROSIVE

UN 3265 8/PG 2

3

14-22-34

26-36/37/39-45

EK5930000

C

Stable under recommended storage conditions.

P280-P305 + P351 + P338-P310

H302-H314

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.

Reacts violently with water.|Incompatible materials: Strong oxidizing agents

|Warning|H319: Causes serious eye irritation [Warning Serious eye damage/eye irritation]|P264, P280, P305+P351+P338, and P337+P313|Danger|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P260, P264, P270, P280, P301+P312, P301+P330+P331, P303+P361+P353, P304+P340, P305+P351+P338, P310, P321, P330, P363, P405, and P501

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. Flame retardant protective clothing. 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).

Suitable extinguishing media: Dry powder|Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas; Environmental precautions: Do not let product enter drains; Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Do not flush with water. Keep in suitable, closed containers for disposal.

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.

Perfluorobutanesulfonic acid was detected at a maximum of 2300 ng/L in leachate from six landfills from four locations in the US(1). Perfluorobutanesulfonic acid was detected in influent and effluent samples collected from 10 wastewater treatment facilities located throughout the US at not detected to 27 and not detected to 20 ng/L, respectively(2). Samples of effluent from 13 sewage treatment plants located in the Hayabuchi River region of Japan contained 0.9-10.7 ng/L of perfluorobutanesulfonic acid; samples were collected Jan 9, 2007(3).|Perfluorobutanesulfonic acid concentrations in the influent or effluent samples from waste water treatment plants along the Glatt Valley Watershed, Switzerland were reported; all samples were collected Feb to March 2006(1).[Table#8311]

SEDIMENT: Sediment samples from Resolute, Char and Amituk lakes on Cornwallis Island, Nunavut, Canada contained perfluorobutanesulfonic acid at <0.029-0.11, <1.1 and <0.046-0.068 ng/g dry weight, respectively(1). Perfluorobutanesulfonic acid was detected at <0.1-<1.1 ng/g dry weight (quantification limit 2.2 ng/g dry weight) in sediment samples from Kamo, Uji, Tenjin, Katsura and Osaka rivers, Japan; samples were collected Feb-March 2005 or Dec 2003(2).

INDOOR AIR: Perfluorobutanesulfonic acid was not detected in air samples from a home in Edmonton, Canada sampled Sept 2008(1). Perfluorobutanesulfonic acid was not detected in 40 indoor air samples from Oslo, Norway households(2).

Dust samples were collected from 102 homes and 10 daycare centers in North Carolina and Ohio from 2000 to 2001 from vacuum cleaner bags during the US Environmental Protection Agency's Children's Total Exposure to Persistent Pesticides and Other Persistent Organic Pollutants study, perfluorobutanesulfonic acid was detected in 33.0% of the samples at a mean, median and maximum concentration of 41.7, 9.11 and 1150 ng/g, respectively(1). Perfluorobutanesulfonic acid was not detected in dust or carpet samples from a home in Edmonton, Canada sampled Sept 2008(2). Perfluorobutanesulfonic acid was detected in 41 dust samples from Norwegian households at 0.17-9.8 ng/g(3).

IDENTIFICATION AND USE: Perfluorobutanesulfonic acid (PFBS) can be in the form of a colorless liquid or a corrosive solid. Esters of perfluoroalkanesulfonic acids are used as strong alkylating agents in preparative chemistry. HUMAN EXPOSURE AND TOXICITY: Children with asthma have been shown to have significantly different serum PFBS levels compared to children without asthma. Inhibitory potencies of four perfluoroalkylated substances on human and rat 11beta-HSD2 were tested, one of which was PFBS. PFBS showed the lowest potency for the inhibition of human and rat 11beta-HSD2 activities. In an in vitro study, PFBS did not generate ROS or DNA damage in HepG2 cells. PFBS inhibited PHA-induced IL-10 release and prevented LPS-induced I-kappaB degradation. ANIMAL STUDIES: PFBS modestly reduced plasma triglycerides in mice. A 90-day rat oral gavage study was conducted with potassium salt of PFBS (K(+)PFBS). No treatment-related mortality, body weight, or neurological effects were noted. Chromorhinorrhea (perioral) and urine-stained abdominal fur were observed in males at 600 mg/kg-day. Red blood cell counts, hemoglobin, and hematocrit values were reduced in males receiving 200 and 600 mg/kg-day. Total protein and albumin were lower in females at 600 mg/kg-day. Microscopic changes were observed only at the highest dose in the stomach. Histopathological changes were observed in the kidneys, consisting of minimal-to-mild hyperplasia of the epithelial cells of the medullary and papillary tubules and the ducts in the inner medullary region. A two-generation reproductive rat study was conducted with K(+)PFBS. In the 300 and 1000 mg/kg/day dose group rats, there were increased liver weight and corresponding increased incidence of adaptive hepatocellular hypertrophy, and increased incidence of minimal to mild microscopic findings in the medulla and papilla of the kidneys. There were no K(+)PFBS treatment-related effects on fertility or reproduction among the P or the F1 rats. There were no microscopic changes in male or female reproductive organs, and no biologically relevant effects on sperm parameters, mating, estrous cycles, pregnancy, and natural delivery in the P- or F1-generations. There were no K(+)PFBS treatment-related effects on survival of pups. Litter size and average pup birth weight per litter were not statistically significantly different from controls in any dose group. In the F1-generation, terminal body weight was reduced in males at 1000 mg/kg/day. Preputial separation was slightly delayed at this dose, a finding consistent with the body weight reduction. Essentially no effects were observed in the F1 females. F2 pups had normal body weights. ECOTOXICITY STUDIES: In a study of tadpoles, PFBS did not have a significant effect on survival and growth. However, it caused hepatohistological impairment at higher concentrations. PFBS had no effect on the sex ratio and gonadal histology. It promoted expression of estrogen receptor (ER) and androgen receptor (AR), but did not affected aromatase expression in the brain.

LD50 Rat oral 430 mg/kg

/BIRDS and MAMMALS/ The present pilot study examined emerging per- and polyfluoroalkyl substances (PFASs), i.e., a suite of short chain perfluoroalkyl acids (PFAAs), PFAA precursors and replacement chemicals, and legacy PFASs (long chain length PFAAs) in livers from ringed seals, polar bears and, for the first time, killer whales from East Greenland collected in 2012-2013. Among the emerging PFASs, perfluorobutanesulfonic acid (PFBS) and F-53B (a chlorinated polyfluorinated ether sulfonic acid) were detected in Arctic wildlife, albeit at concentrations approximately four orders of magnitude lower compared to perfluorooctanesulfonic acid (PFOS). PFOS was positively correlated with F-53B, but not PFBS in all three species. A total of 17 PFASs were detected in killer whales, including in a mother-fetus pair, demonstrating maternal transfer. /Total/ PFAS concentrations in killer whales (269 +/- 90 ng/g) were comparable to concentrations found in ringed seals (138 +/- 7 ng/g), however, an order of magnitude lower compared to concentrations found in polar bear livers (2336 +/- 263 ng/g). Patterns of long chain PFAAs in killer whales differed from the pattern in ringed seals and polar bears. Of the monitored PFAA precursors, only perfluorooctanesulfonamide (FOSA) was detected in all three species, and FOSA/PFOS ratios and isomer patterns indicated that killer whales have a potential lower metabolic capacity to degrade FOSA compared to polar bears and ringed seals.|/AQUATIC SPECIES/ Perfluorobutanesulfonate (PFBS), as a substitute for perfluorooctanesulfonate (PFOS), is widespread in the environment and biotic samples as well as PFOS. To investigate effects of PFOS and PFBS on the growth and sexual development of amphibians, we exposed Xenopus laevis tadpoles at a series of concentrations of PFOS and PFBS (0.1; 1; 100; 1,000 ug/L) as well as 17-beta-estradiol (E2, 100 ng/L) and 5 alpha-androstan-17-beta-ol-3-one (DHT, 100 ng/L) from stage 46/47 to 2 months postmetamorphosis. ...Neither PFOS nor PFBS had a significant effect on the survival and growth. However, they caused hepatohistological impairment at higher concentrations (100; 1,000 ug/L). Unlike E2, PFOS at all concentrations did not alter the sex ratio and induce intersex, but caused degeneration of spermatogonia in testes except for the lowest concentration. PFBS had no effect on the sex ratio and gonadal histology. PFOS and PFBS promoted expression of estrogen receptor (ER) and androgen receptor (AR), but not affected aromatase expression in the brain. The increase in expression of ER and AR suggests an increase in the responsiveness to the corresponding sex hormone and potential effects on sexual development. ...Results show that PFBS as well as PFOS have adverse effects on hepato-histology and sexual development on X. laevis. Also, PFOS- and PFBS-induced increase in ER and AR expression highlights the need to further study effects of PFOS and PFBS on subsequent gonadal development, sexual dimorphism, and secondary sex characteristics in X. laevis. It is debatable that PFBS is widely used as a substitute of PFOS.|/AQUATIC SPECIES/ The toxicity of perfluorinated surfactants perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorobutane sulfonate (PFBS) and PF-656 as well as the sulfosuccinate surfactant docusate sodium has been examined using two bioluminescence inhibition assays based on the marine bacterium Vibrio fischeri and the self-luminescent cyanobacterial recombinant strain Anabaena CPB4337. Multigenerational toxicity towards the growth of the algae Pseudokirchneriella subcapitata /was also determined/ with EC(50) values in the 43-75 mg/L range, docusate sodium exhibited a higher toxicity towards the three organisms than PFOS, PFOA, PF-656 and PFBS ...|/OTHER TOXICITY INFORMATION/ A multigeneration toxicity test on Chironomus riparius was performed with the aim of investigating the evolutionary consequences of exposure to perfluoralkyl substances (perfluorooctane sulfonic acid, PFOS; perfluorooctanoic acid, PFOA; perfluorobutane sulfonate, PFBS). Six-hundred larvae were bred per treatment and per generation until emergence and egg deposition under a nominal concentration of 10 ug/L of contaminants. Newborn larvae were used to start the next generation. Evolution of genetic variability was evaluated along a total of 10 consecutive generations based on 5 microsatellite loci. Analysis of life-history traits (survival, sex ratio and reproduction) was also carried out. Rapid genetic variability reduction was observed in all treatments, including controls, across generations due to the test conditions. Nevertheless, an increased mutation rate determined a stronger conservation of genetic variability in PFOS and, at minor extent, in PFBS exposed populations compared to controls. No significant effects were induced by exposure to PFOA. Direct mutagenicity or induced stress conditions may be at the base of increased mutation rate, indicating the potential risk of mutational load caused by exposure to PFOS and PFBS. The test provided the opportunity to evaluate the use of approximate Bayesian computation (ABC) and coalescent approaches in evolutionary ecotoxicology. A weak performance was evidenced for ABC, either in terms of bias or dispersion of effective population sizes and of estimates of mutation rate. On the contrary, coalescent simulations proved the sensitivity of traditional genetic endpoints (i.e. heterozygosity and number of alleles) to the alteration of mutation rate, but not to erosion of genetic effective size.

Perfluorobutanesulfonic acid does not occur naturally in the environment(1).

Perfluorochemicals like perfluorobutanesulfonic acid have been widely used since the 1950s in many industrial and consumer products, including protective coatings for fabrics and carpet, paper coatings, insecticide formulations, and surfactants(1). Perfluorobutanesulfonic acid may be a degradation product of perfluorooctanesulfonyl fluoride-derived materials that have previously been used as surfactants(2). Perfluorobutanesulfonic acid's production and use may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 180(SRC), determined from a structure estimation method(2), indicates that perfluorobutanesulfonic acid is expected to have moderate mobility in soil(SRC). The estimated pKa of perfluorobutanesulfonic acid is -3.31(3), indicating that this compound will exist 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 of perfluorobutanesulfonic acid from moist soil surfaces is not expected(SRC) given the estimated pKa(3). Perfluorobutanesulfonic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 0.027 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation of <3% of the Theoretical Oxygen Demand of perfluorobutanesulfonic acid in aerobic studies indicates that it is not expected to biodegrade in soil(5).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 180(SRC), determined from a structure estimation method(2), indicates that perfluorobutanesulfonic acid is expected to adsorb to suspended solids and sediment(SRC). An estimated pKa of -3.31(3) indicates perfluorobutanesulfonic 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). According to a classification scheme(4), a reported BCF of 0.71 in rainbow trout(5), suggests bioconcentration in aquatic organisms is low(SRC). Biodegradation of <3% of the Theoretical Oxygen Demand of perfluorobutanesulfonic acid in aerobic studies indicates that it is not expected to biodegrade in water(6).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), perfluorobutanesulfonic acid, which has an estimated vapor pressure of 0.027 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase perfluorobutanesulfonic 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). Perfluorobutanesulfonic acid does not contain chromophores that absorb at wavelengths >290 nm(3) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of perfluorobutanesulfonic acid with photochemically-produced hydroxyl radicals has been estimated as 1.4X10-13 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 115 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Perfluorobutanesulfonic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Perfluorobutanesulfonic acid does not contain chromophores that absorb at wavelengths >290 nm(2) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

Perfluorobutanesulfonic acid was not found to bioaccumulate in laboratory experiments in rainbow trout (Onchorynchus mykiss) with a reported BCF of 0.71(1). According to a classification scheme(2), this BCF suggests bioconcentration in aquatic organisms is low(SRC). The average log bioaccumulation factor in eel (Anguilla anguilla) was 1.26, sampled from 23 locations in The Netherlands(3).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of perfluorobutanesulfonic acid can be estimated to be 180(SRC). According to a classification scheme(2), this estimated Koc value suggests that perfluorobutanesulfonic acid is expected to have moderate mobility in soil. The estimated pKa of perfluorobutanesulfonic acid is -3.31(3), indicating that this compound will exist 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 log Koc for perfluorobutanesulfonic acid in three sediments was reported as 1.42 in 23 sediments(5).

An estimated pKa of -3.31(1) indicates perfluorobutanesulfonic acid will exist entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water and moist soil surfaces is not expected to be an important fate process(SRC). Perfluorobutanesulfonic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 0.027 mm Hg(SRC), determined from a fragment constant method(2).

DRINKING WATER: The concentration of perfluorobutanesulfonic acid was monitored through a water treatment facility in Amsterdam, The Netherlands; intake concentration from Lek canal was 31-42 ng/L, finished water was 17-24 ng/L, concentrations at monitored steps ranged from 11 to 34 ng/L(1). Perfluorobutanesulfonic acid was not detected (detection limit 0.045 ng/L) in drinking water samples collected in three homes that receive water from different water works in Oslo, Norway, samples were collected between Oct 2008 and Jan 2009(2). Perfluorobutanesulfonic acid was detected at a maximum of 13 ng/L in drinking water samples collected in Arnsberg-Neheim, Germany(3).|DRINKING WATER: The USEPA Unregulated Contaminant Monitoring Rule (UCMR3) program monitors for 30 contaminants (including perfluorobutanesulfonic acid) in PWSs (public water systems)(1). All PWSs serving more than 10,000 people and 800 representative PWSs serving 10,000 or fewer people were monitored beginning in January 2013. The April 2016 Data Summary reports that 4,864 systems contained perfluorobutanesulfonic acid, 8 of which were at or above the minimum reporting level (MRL) of 0.09 ug/L(2).|SURFACE WATER: Perfluorobutanesulfonic acid was detected in open ocean water at <1.6-60, <1.6 and <1.6 pg/L in 40 samples from the North Atlantic, 10 samples from the Middle Atlantic and 10 samples from the South Atlantic Ocean, respectively, samples were collected April, Oct and Nov of 2007(1). Perfluorobutanesulfonic acid was detected in 48 samples collected in August 2007 from the coastal waters of the German Bight at 3.38-17.7 ng/L(2). Perfluorobutanesulfonic acid was detected at 7.7, 2.8 and 2.3 ng/L in river water samples collected from the Glatt River at Schwerzenbach, Oberglatt and Rheinsfelden, Switzerland, respectively(3). Five streams flowing into Lake Shihwa, Korea had perfluorobutanesulfonic acid concentrations of <0.50-24.03 ng/L, concentrations in Lake Shihwa were <0.50-1.03 ng/L and in Gyeonggi Bay were <0.50-2.53 ng/L, all samples were collected in Dec of 2004(4). Concentrations of perfluorobutanesulfonic acid were reported as <1.7 ng/L in the Tenjin and Katsura rivers, Japan; samples were collected March 2005(5). Water samples taken from tributaries of the Pearl River in Guangzhou and along the Yangtze River, China had perfluorobutanesulfonic acid concentrations of <0.03-3.4 and <0.005-2.1 ng/L, respectively(6).

Perfluorobutanesulfonic acid was sampled in food, tea and milk purchased in grocery stores in Oslo, Norway between Oct 2008 and Jan 2009, concentrations were (pg/g fresh weight): chicken meat (3.2), egg (2.0), fish sticks (5.0), salmon (2.2). All other products (lettuce, carrot, potato, cheese, margarine, milk, bread, strawberry jam, pork meat, beef, canned mackerel, cod, cod liver and tea) were listed at less than detection limit (detection limits varied)(1).

Perfluorobutanesulfonic acid was not detected (detection limit 0.24 ng/g) in 12 raw and 49 retail milk samples collected at locations across the US(1). Perfluorobutanesulfonic acid was not detected (detection limit 0.7 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). Perfluorobutanesulfonic acid was not detected (detection limit 0.24 pg/g) in milk samples purchased at grocery stores in Oslo, Norway between Oct 2008 and Jan 2009(3).|Perfluorobutanesulfonic 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#8313]

Occupational exposure to perfluorobutanesulfonic acid may occur through inhalation and dermal contact with this compound at workplaces where perfluorobutanesulfonic acid is produced or used. Monitoring data indicate that the general population may be exposed to perfluorobutanesulfonic acid via inhalation of dust, ingestion of food and drinking water, and dermal contact with consumer products containing perfluorobutanesulfonic acid. (SRC)

In the National Health and Nutrition Examination Survey (NHANES) survey conducted 2003 thru 2004, perfluorobutanesulfonic acid was detected (detection limit 0.4 ng/mL) in <0.5% of the 2094 serum samples analyzed(1). Perfluorobutanesulfonic acid was detected at 0.610 ng/mL in the serum of a 23 year old male living in a home with a history of carpet Scotchgard application; it was not detected (detection limit 0.05 ng/mL and 2.50 ng/g, respectively) in the urine or stool of this person(2). Perfluorobutanesulfonic acid was not detected in the serum, urine or stool of any other residence (males ages 52, 21, 17, 15; females ages 48, 18) living in the home; samples were collected Nov 2008(2). Perfluorobutanesulfonic acid was not detected (detection limit 2 pg/mL) in 60 human blood samples (adult ages 19-62) collected from Gdansk, Poland and nearby villages in July of 2003(3). Perfluorobutanesulfonic acid concentration was 0.074 ng/mL (1977), increased to 0.18 ng/mL (1980), and then stabilized at 0.065 to 0.12 ng/mL (1981-2000) and then dropped to <0.050 from 2001-2006 in 24 pooled serum samples from men, age 40 to 50 years, representing 1977 to 2006(4). Perfluorobutanesulfonic acid was not detected (detection limit 0.02 ng/mL) in human blood samples from volunteer donors from five Chinese cities (Shenyang, Beijing, Gulyang, Jintan, Nanjing) collected in 2004(5). Perfluorobutanesulfonic acid was detected in one of 55 umbilical cord and one of 15 infertile man serum samples at 1.48 and 0.77 ng/mL, respectively; perfluorobutanesulfonic acid was not detected (detection limit 0.1 ng/mL) in the serum of 50 men working in manufacturing; all samples were collected Dec 2008 to Aug 2009 from residents of Wenzhou, China(6). Perfluorobutanesulfonic acid was not detected (detection limit 0.008 ng/mL) in 420 human blood samples collected from volunteer residents from Halle and Munster, Germany; samples were collected 1982 to 2009(7). Perfluorobutanesulfonic acid was frequently detected in 30 human hair samples(8).|Perfluorobutanesulfonic acid was detected in blood plasma of men, women and children from German population in samples collected Sept to Nov 2006 at the following concentrations(1):[Table#8310]

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.|PFBS was not detected in maternal sera (n = 20), cord sera (n = 20) or human milk (n = 17) taken from the general population of Seoul, South Korea (LOD of 0.1, 0.05 and 0.0011 ng/mL, respectively)|Materials derived from perfluorobutanesulfonyl fluoride (PBSF, C(4)F(9)SO(2)F) have been introduced as replacements for eight-carbon homolog products that were manufactured from perfluorooctanesulfonyl fluoride (POSF, C(8)F(17)SO(2)F). Perfluorobutanesulfonate (PFBS, C(4)F(9)SO(3)(-)) is a surfactant and potential degradation product of PBSF-derived materials. The purpose of this series of studies was to evaluate the pharmacokinetics of PFBS in rats, monkeys, and humans, thereby providing critical information for human health risk assessment. Studies included: (1) intravenous (i.v.) elimination studies in rats and monkeys; (2) oral uptake and elimination studies in rats; and (3) human serum PFBS elimination in a group of workers with occupational exposure to potassium PFBS (K(+)PFBS). PFBS concentrations were determined in serum (all species), liver (rats), urine (all species), and feces (rats). In rats, the mean terminal serum PFBS elimination half-lives, after i.v. administration of 30 mg/kg PFBS, were: males 4.51 +/- 2.22 hr (standard error) and females 3.96 +/- 0.21 hr. In monkeys, the mean terminal serum PFBS elimination half-lives, after i.v. administration of 10 mg/kg PFBS, were: males 95.2 +/- 27.1 hr and females 83.2 +/- 41.9 hr. Although terminal serum half-lives in male and female rats were similar, without statistical significance, clearance (CL) was significantly greater in female rats (469 +/- 40 mL/hr) than male rats (119 +/- 34 mL/hr) with the area under the curve (AUC) significantly larger in male rats (294 +/- 77 ug.hr/mL) than female rats (65 +/-5 ug.hr/mL). These differences were not observed in male and female monkeys. Volume of distribution estimates suggested distribution was primarily extracellular in both rats and monkeys, regardless of sex, and urine appeared to be a major route of elimination. Among 6 human subjects (5 male, 1 female) followed up to 180 days, the geometric mean serum elimination half-life for PFBS was 25.8 days (95% confidence interval 16.6-40.2). Urine was observed to be a pathway of elimination in the human. Although species-specific differences exist, these findings demonstrate that PFBS is eliminated at a greater rate from human serum than the higher chain homologs of perfluorooctanesulfonate (PFOS) and perfluorohexanesulfonate (PFHxS). Thus, compared to PFOS and PFHxS, PFBS has a much lower potential for accumulation in human serum after repeated occupational, non-occupational (e.g., consumer), or environmental exposures.|The toxicokinetics of perfluorohexanoic acid (PFHxA) and nonafluoro-1-butanesulfonic acid (PFBS) were evaluated in Sprague-Dawley rats and cynomolgus monkeys. Systemic exposure to PFHxA was lower than for PFBS following single equivalent intravenous or oral (rat only) doses. Serum clearance was more rapid for PFHxA than for PFBS. In rats, exposure to PFHxA and PFBS was up to 8-fold (intravenous) and 4-fold (oral) higher for males than females and serum clearance of PFHxA and PFBS was more rapid in females than males; however, there was no appreciable difference in the extent or rate of urinary elimination between compounds or genders. There were no apparent differences between genders in the serum half-life for PFHxA following 26 days of repeated oral dosing in rats; exposure decreased upon repeated dosing.|Perfluorobutanesulfonyl fluoride (PBSF) has been introduced as a replacement for its eight-carbon homolog perfluorooctanesulfonyl fluoride (POSF) in the manufacturing of fluorochemicals. Fluorochemicals derived from PBSF may give rise to perfluorobutanesulfonic acid (PFBS) as a terminal degradation product. Although basic mammalian toxicokinetic data exist for PFBS, information on its tissue distribution has only been reported in one study focused on rat liver. Therefore, here we characterized the tissue distribution of PFBS in mice in the same manner as we earlier examined its eight-carbon homolog perfluorooctanesulfonate (PFOS) to allow direct comparisons. Following dietary exposure of adult male C57/BL6 mice for 1, 3 or 5d to 16 mg (35)S-PFBS/kg/d, both scintillation counting and whole-body autoradiography (WBA) revealed the presence of PFBS in all of the 20 different tissues examined, demonstrating its ability to leave the bloodstream and enter tissues. After 5d of treatment the highest levels were detected in liver, gastrointestinal tract, blood, kidney, cartilage, whole bone, lungs and thyroid gland. WBA revealed relatively high levels of PFBS in male genital organs as well, with the exception of the testis. The tissue levels increased from 1 to 3 d of exposure but appeared thereafter to level-off in most cases. The estimated major body compartments were whole bone, liver, blood, skin and muscle. This exposure to PFBS resulted in 5-40-fold lower tissue levels than did similar exposure to PFOS, as well as in a different pattern of tissue distribution, including lower levels in liver and lungs relative to blood.

In rats, the mean terminal serum PFBS elimination half-lives, after i.v. administration of 30 mg/kg PFBS, were: males 4.51 +/- 2.22 hr (standard error) and females 3.96 +/- 0.21 hr. In monkeys, the mean terminal serum PFBS elimination half-lives, after i.v. administration of 10 mg/kg PFBS, were: males 95.2 +/- 27.1 hr and females 83.2 +/- 41.9 hr. Although terminal serum half-lives in male and female rats were similar, without statistical significance, clearance (CL) was significantly greater in female rats (469 +/- 40 mL/hr) than male rats (119 +/- 34 mL/hr) with the area under the curve (AUC) significantly larger in male rats (294 +/- 77 ug.hr/mL) than female rats (65 +/-5 ug.hr/mL). These differences were not observed in male and female monkeys. Volume of distribution estimates suggested distribution was primarily extracellular in both rats and monkeys, regardless of sex, and urine appeared to be a major route of elimination. Among 6 human subjects (5 male, 1 female) followed up to 180 days, the geometric mean serum elimination half-life for PFBS was 25.8 days (95% confidence interval 16.6-40.2).

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) or lorazepam (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/EPIDEMIOLOGY STUDIES/ In /a/ study ..., perfluorobutanesulfonic acid (PFBS) serum levels were reported to be significantly different between children with (n = 231) or without (n = 225) asthma. However, it was not clear which was the higher group as the means and medians for both groups were given as 0.5 ng/mL. The AOR in the highest quartile (> 0.6 ng/mL), compared with the lowest (< 0.4 ng/mL), was significantly increased at 1.90 (95 % CI = 1.08-3.37), and a significant dose-response trend was reported (p = 0.021). Of the immunological biomarkers only, AEC showed a significant dose-response trend among asthmatics. Exposure to other polyfluoroalkyl substances (PFASs) also measured were not controlled for in the analysis, and therefore may have biased the results.|/BIOMONITORING/ In the recent years hair has been increasingly used as alternative matrix in human biomonitoring (HBM) of environmental pollutants. Sampling advantages and time integration of exposure assessment seem the most attractive features of hair matrix. In the current study, a novel miniaturized method was developed and validated for measuring 15 perfluoroalkyl substances (PFAS), including perfluoro n-butanoic acid (PFBA), perfluoro n-pentanoic acid (PFPeA), perfluoro n-hexanoic acid (PFHxA), perfluoro n-heptanoic acid (PFHpA), perfluor n-octanoic acid (PFOA), perfluoro n-nonanoic acid (PFNA), perfluoro tetradecanoic acid (PFTeDA), perfluorobutane sulfonic acid (PFBS), perfluoro pentane sulfonic acid (PFPeS), perfluorohexane sulfonic acid (PFHxS), perfluoroheptane sulfonic acid (PFHpS), perfluorooctane sulfonic acid (PFOS), perfluorononane sulfonic acid (PFNS), perfluorodecane sulfonic acid (PFDS) and perfluorododecane sulfonic acid (PFDoS) in human hair by liquid chromatography tandem mass spectrometry (LC-MS/MS). After extraction using ethyl acetate, dispersive ENVI-Carb was used for clean-up. Good intra- and inter-day precision for low (LQ 5 ng/g hair) and high spike (HQ 15 ng/g) levels were achieved (in general RSD <10%). The accuracy was assessed using recoveries (%), which ranged between 68-118% (LQ) and 70-121% (HQ). The instrumental limit of detection (LODi) and limit of quantification (LOQi) were between 1-4 pg/g hair and 3-13 pg/g hair, respectively. The method limit of quantification (LOQm) ranged between 6 and 301 pg/g hair. The PFAS levels were measured in 30 human hair samples indicating that the levels are low (14-1534 pg/g hair). Some PFAS were not present in any hair sample (e.g. PFHpA, PFTeDA, PFNA, PFPeS, PFHpS, PFOS and PFNS), while other PFAS were frequently detected (PFBA, PFPeA, PFHxA, PFOA, PFBS, PFHxS, PFOS, PFDS and PFDoS) in human hair. Although levels in general were low, there is evidence of higher human exposure to some analytes, such as PFBA, PFPeA, PFHxA, PFOA, PFBS, PFHxS, and PFDoS. The current study shows that hair is a suitable alternative non-invasive matrix for exposure assessment of PFAS.|/ENDOCRINE MODULATION/ 11beta-Hydroxysteroid dehydrogenase 2 (11beta-HSD2) regulates active glucocorticoid access to glucocorticoid and mineralocorticoid receptors by metabolizing it to an inactive form. Perfluoroalkylated substances (PFASs) are man-made polyfluorinated compounds that are widely used and persistent in the environment. We tested the inhibitory potencies of four PFASs including perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorohexanesulfonate (PFHxS) and perfluorobutane sulfonate (PFBS) on human and rat 11beta-HSD2. PFOS was a potent inhibitor of both human (IC(50)=48 nM) and rat (IC(50)=293 nM) 11beta-HSD2 activities. The potencies for the inhibition of human and rat 11beta-HSD2 activities were PFOS>PFOA>PFHxS>PFBS. PFASs showed competitive inhibition of both human and rat 11beta-HSD2 activities. This observation indicates that PFOS is a potent endocrine disruptor for glucocorticoid metabolism.|/ALTERNATIVE and IN VITRO TESTS/ ... COS-1 cells were transfected with mouse or human PPARalpha plasmids to investigate the effects of different Perfluoroalkylated substances (PFASs) on PPARalpha activation. Greater PPARalpha activity was induced by PFASs with longer chain lengths and sulphonates were more potent than carboxylates. Perfluorobutanesulfonic acid (PFBS) (mouse, 317 uM; human, 206 uM) was least potent at activating PPARalpha followed by perfluorooctane sulfonate (PFOS) (94 uM; 262 uM), perfluorohexane sulfonic acid (PFHxS) (76 uM; 81 uM), PFBA (51 uM; 75 uM), perfluoro n-hexanoic acid (PFHxA) (38 uM; 471 uM), perfluorodecyl acrylate (PFDA) (20 uM; human not active), perfluorooctanoic acid (PFOA) (6 uM; 16 uM) and perfluoro n-nonanoic acid (PFNA) (5 uM; 11 uM).|For more Human Toxicity Excerpts (Complete) data for Perfluorobutanesulfonic acid (7 total), please visit the HSDB record page.

perfluorobutane sulfonate

1-Butanesulfonic acid, 1,1,2,2,3,3,4,4,4-nonafluoro-: ACTIVE

Method: EPA-ORD/EPA-OST 537; Procedure: liquid chromatography/tandem mass spectrometry; Analyte: perfluorobutanesulfonic acid; Matrix: drinking water; Detection Limit: 3.1 nanogram/L.

In the recent years hair has been increasingly used as alternative matrix in human biomonitoring (HBM) of environmental pollutants. Sampling advantages and time integration of exposure assessment seems the most attractive features of hair matrix. In the current study, a novel miniaturized method was developed and validated for measuring 15 perfluoroalkyl substances (PFAS), including perfluoro n-butanoic acid (PFBA), perfluoro n-pentanoic acid (PFPeA), perfluoro n-hexanoic acid (PFHxA), perfluoro n-heptanoic acid (PFHpA), perfluor n-octanoic acid (PFOA), perfluoro n-nonanoic acid (PFNA), perfluoro tetradecanoic acid (PFTeDA), perfluorobutane sulfonic acid (PFBS), perfluoro pentane sulfonic acid (PFPeS), perfluorohexane sulfonic acid (PFHxS), perfluoroheptane sulfonic acid (PFHpS), perfluorooctane sulfonic acid (PFOS), perfluorononane sulfonic acid (PFNS), perfluorodecane sulfonic acid (PFDS) and perfluorododecane sulfonic acid (PFDoS) in human hair by liquid chromatography tandem mass spectrometry (LC-MS/MS). After extraction using ethyl acetate, dispersive ENVI-Carb was used for clean-up. Good intra- and inter-day precision for low (LQ 5 ng/g hair) and high spike (HQ 15 ng/g) levels were achieved (in general RSD <10%). The accuracy was assessed using recoveries (%), which ranged between 68-118% (LQ) and 70-121% (HQ). The instrumental limit of detection (LODi) and limit of quantification (LOQi) were between 1-4 pg/g hair and 3-13 pg/g hair, respectively. The method limit of quantification (LOQm) ranged between 6 and 301 pg/g hair. The PFAS levels were measured in 30 human hair samples indicating that the levels are low (14-1534 pg/g hair). Some PFAS were not present in any hair sample (e.g. PFHpA, PFTeDA, PFNA, PFPeS, PFHpS, PFOS and PFNS), while other PFAS were frequently detected (PFBA, PFPeA, PFHxA, PFOA, PFBS, PFHxS, PFOS, PFDS and PFDoS) in human hair. Although levels in general were low, there is evidence of higher human exposure to some analytes, such as PFBA, PFPeA, PFHxA, PFOA, PFBS, PFHxS, and PFDoS. The current study shows that hair is a suitable alternative non-invasive matrix for exposure assessment of PFAS.

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