Perfluorooctanesulfonamide

499.142

499.14

212-046-0

80AM718FML

DTXSID3038939

2942000000

68.5

5.8(est)

Clear liquid

1.8±0.1 g/cm3

151-152 °C

227.2±50.0 °C at 760 mmHg

91.2±30.1 °C

1.310

In water, 8.04X10-3 mg/L at 25 deg C (est)

0.31 mm Hg at 25 deg C (est)

LD50 orl-rat: >172 mg/kg ATDAEI 15(Suppl 1),S104,1996

Henry's Law constant = 1.8 atm-cu m/mol at 25 °C (est)

170.13 Ų [M-H]-

When heated to decomposition it emits toxic vapors of SOx, Nox, and F(-)

53

S22-S24/25

Xi: Irritant;

P261, P264, P270, P271, P273, P280, P301+P310, P302+P352, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P337+P313, P362, P391, P403+P233, P405, P501

H301

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. 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 soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

|Danger|H301 (50%): Toxic if swallowed [Danger Acute toxicity, oral]|P261, P264, P270, P271, P273, P280, P301+P310, P302+P352, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P337+P313, P362, P391, P403+P233, P405, and P501|Aggregated GHS information provided by 3 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Perfluorooctanesulfonamide was not detected in sewage effluent samples from Finland, Norway and the Faeroe Islands nor in landfill effluent samples taken from Finland and Norway(1).

SEDIMENT: Sediment samples, collected from the Hudson Bay region of northeastern Canada May to Sept 1999 to 2003, had perfluorooctanesulfonamide concentrations in 22% of <0.01-0.04 ng/g dry weight(1). Perfluorooctanesulfonamide was not detected (detection limit 1.5 ng/g dry weight) in five sediment samples taken from the Ariake Sea in Jan 2004(2). Perfluorooctanesulfonamide was detected in river sediments at <0.1-6.5 ng/g dry weight in samples from five rivers in Kyoto, Japan, samples were collected Dec 2003 and Feb and March 2005(3).

URBAN/SUBURBAN: Perfluorooctanesulfonamide was detected in atmospheric samples from Barsbuttel, Germany at a maximum concentration of 0.5 pg/cu m, each sample was collected over a three to four day time span and the study was run April 2007 to June 2008(1).|INDOOR: Perfluorooctanesulfonamide was not detected in 40 indoor air samples from Oslo, Norway households(1).|RUARL/REMOTE: Although there is limited data for atmospheric concentrations of perfluorooctanesulfonamide(SRC, 2012), perfluoroalkyl contaminants have been shown to be widespread(1-2).

Perfluorooctanesulfonamide was detected in 41 dust samples from Norwegian households at 0.22 to 41 ng/g(1). Perfluorooctanesulfonamide was found in indoor dust samples with a mean value of 0.56 ng/g dry weight and a range of <0.19-0.88 ng/g dry weight, samples were collected from homes in Nanchang, Shanghai, Beijing and Tianjin, China(2).

LD50 Rat Oral: >172 mg/kg

/BIRDS and MAMMALS/ Contamination levels of perfluorinated compounds (PFCs), including perfluorooctanesulfonate (PFOS), perfluorononanoic acid (PFNA), perfluorooctane sulfonamide (PFOSA), perfluorohexanesulfonate (PFHS), and perfluorooctanoic acid (PFOA), were determined in the livers of wild common cormorants (Phalacrocorax carbo) from Lake Biwa, Japan. Potential effects of PFCs alone and combined effects by complex mixture of PFCs and dioxins and related compounds (DRCs) were also assessed by gene expression profiling using a cormorant oligo array. Perfluorooctanesulfonate, PFNA, and PFOSA were detected in almost all liver samples analyzed, while concentrations of PFHS and PFOA were below the limit of quantification. The microarray data analyses revealed that hepatic PFC levels were correlated with the expression of 74 genes. Real-time reverse-transcript polymerase chain reaction data demonstrated that PFOS concentration was positively correlated with mRNA levels of glutathione peroxidase 1 and glutathione S-transferase alpha 3 and negatively correlated with levels of heat shock 70-kDa protein 8 and tumor rejection antigen 1 mRNAs. These results suggest the induction of antioxidant enzymes in response to oxidative stress caused by PFCs and the suppression of molecular chaperones, leading to reduction in protein stability. Moreover, multiple regression analyses identified seven significant models in which certain genes showed expression levels altered by accumulation of PFCs and DRCs. The regression models explained associations with cytochrome P450 1A mRNA and protein expression levels, and its catalytic activity, ethoxy-resorufin-O-deethylase of both PFNA and the 2,3,7,8-tetrachlorodibenzo-p-dioxin toxic equivalent levels. Thus, the regression models suggested the potential of PFCs to enhance toxicities of DRCs. Since mixture toxicity is an urgent issue, further study is required to understand the effects of mixtures of PFCs and DRCs in wild cormorants.|/BIRDS and MAMMALS/ Perfluoroalkyl substances were determined in polar bears (Ursus maritimus) collected in East Greenland (69 deg 00'N to 74 deg 00''N) to compare with other populations and to examine effects of age and gender on concentrations of these contaminants. Hepatic tissue (n=29) was analyzed for perfluorooctane sulfonate (PFOS), perfluorooctanoate (PFOA), perfluorohexane sulfonate, heptadecafluorooctane sulfonamide (PFOSA), and perfluoroalkyl carboxylates (PFCAs) with C9-C15 perfluorinated carbon chains by liquid chromatography tandem mass spectrometry. Concentrations of PFOS found in samples from East Greenland (mean = 2,470 + or - 1,320 ng/g wet weight) were similar to Hudson Bay, Canada, and both populations had significantly greater concentrations than those reported for Alaska, suggesting a spatial trend. Male bears showed a significant increase in concentration up to age six for PFCAs with C10-C14 carbon chains (r2=0.50, p=0.05). Significant correlations were found between adjacent chain length PFCAs, (e.g., PFNA to PFDA: p<0.05; r2=0.90). This may indicate a common source for these chemicals, although the specifics of source and mode of transport are unknown. No significant correlations were found between concentrations of PFCAs in liver tissue and previously reported polychlorinated biphenyl (PCB) congeners analyzed in fat samples from the same bears.|/AQUATIC SPECIES/ Perfluorinated surfactants (PFSs) in Asian freshwater fish species were analyzed to investigate tissue distribution, temporal trends, extent of pollution, and level of PFS exposure through food intake. Freshwater fish species, namely carp, snakehead, and catfish, were collected in Japan, Vietnam, India, Malaysia, and Thailand, and 10 PFSs, including perfluorooctanesulfonate (PFOS) and perfluorooctanoate, were analyzed by liquid chromatography-tandem mass spectrometry. PFSs in carp in Tokyo were more concentrated in kidneys (sum of 10 PFSs = 257 +/- 95 ng/g wet weight [ww]) and livers (119 +/- 36 ng/g ww) than in ovaries (43 +/- 2 ng/g ww) and muscles (24 +/- 17 ng/g ww). Concentrations of PFOS and its precursor, perfluorooctane sulfonamide, in livers of carp and in waters in Tokyo showed a dramatic decrease during the last decade, probably because of 3 M's phasing-out of the manufacture of perfluorooctanesulfonyl-fluoride-based products in 2000. In contrast, continuing contamination by long-chain perfluorocarboxylates (PFCAs) with > or =9 fluorinated carbons was seen in multiple media, suggesting that these compounds continue to be emitted. PFS concentrations in freshwater fish species in tropical Asian countries were generally lower than those in developed countries, such as Japan, e.g., for PFOS in muscle, Vietnam < 0.05-0.3 ng/g ww; India < 0.05-0.2 ng/g ww; Malaysia < 0.05-0.2 ng/g ww; Thailand < 0.05 ng/g ww; and Japan (Tokyo) = 5.1-22 ng/g ww. Daily intake of short-chain PFCAs with < or =8 fluorinated carbons from freshwater fish species in Japan was approximately one order of magnitude lower than that from drinking water, whereas daily intake of PFOS and long-chain PFCAs with > or =9 fluorinated carbons from freshwater fish species was comparable with or greater than that from drinking water. Because the risk posed by exposure to these compounds through intake of fish species is a matter of concern, we recommend the continued monitoring of PFS levels in Asian developing countries. /Perfluorinated surfactants/

Perfluorochemicals like perfluorooctanesulfonamide 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). Perfluorooctanesulfonamide'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 3.6X10+5(SRC), determined from a structure estimation method(2), indicates that perfluorooctanesulfonamide is expected to be immobile in soil(SRC). Volatilization of perfluorooctanesulfonamide from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.8 atm-cu m/mole(SRC), using a fragment constant estimation method(3). However, adsorption to soil is expected to attenuate volatilization(SRC). Perfluorooctanesulfonamide is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 0.31 mm Hg at 25 °C(SRC), determined from a fragment constant method(4). Biodegradation data in soil were not available(2012, SRC).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 3.6X10+5(SRC), determined from a structure estimation method(2), indicates that perfluorooctanesulfonamide is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 1.8 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 6.5 hours and 8.8 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond is 11 years if adsorption is considered(5). According to a classification scheme(6), an estimated BCF of 3100(SRC), from an estimated log Kow of 5.8(7) and a regression-derived equation(8), suggests the potential for bioconcentration in aquatic organisms is very high(SRC). Biodegradation data in water were not available(2012, SRC). Perfluorooctanesulfonamide is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), perfluorooctanesulfonamide, which has an estimated vapor pressure of 0.31 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 perfluorooctanesulfonamide is not expected to react with photochemically-produced hydroxyl radicals(SRC). Perfluorooctanesulfonamide 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).

Vapor-phase perfluorooctanesulfonamide is not expected to react with photochemically-produced hydroxyl radicals or be susceptible to direct photolysis by sunlight(SRC). Perfluorooctanesulfonamide is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Perfluorooctanesulfonamide does not contain chromophores that absorb at wavelengths >290 nm(1) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 3100 was calculated in fish for perfluorooctanesulfonamide(SRC), using an estimated log Kow of 5.8(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is very high(SRC), provided the compound is not metabolized by the organism(SRC). Trophic level biomagnification factors were reported as: ringed seal:cod 0.1, beluga:cod 31, beluga:herring 52, beluga:Artic cisco 26, cod:calanus hyperboreus 0.5, cod:themisto libellula 1.2(4). Ringed seal appear to metabolize perfluorooctanesulfonamide more readily than beluga whales do(4).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of perfluorooctanesulfonamide can be estimated to be 3.6X10+5(SRC). According to a classification scheme(2), this estimated Koc value suggests that perfluorooctanesulfonamide is expected to be immobile in soil. The log Koc for perfluorooctanesulfonamide was 4.1 measured in three sediments(3).

The Henry's Law constant for perfluorooctanesulfonamide is estimated as 1.8 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that perfluorooctanesulfonamide is expected to volatilize rapidly from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 6.5 hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 8.8 days(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The volatilization half-life from a model pond is about 11 years when adsorption is considered(3). Perfluorooctanesulfonamide's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). Perfluorooctanesulfonamide is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 0.31 mm Hg(SRC), determined from a fragment constant method(4).

GROUNDWATER: Perfluorooctanesulfonamide was not detected (detection limit 0.00052 ng/L) in groundwater samples from the Highland Creek watershed, Canada, taken Feb to March 2010(1).|DRINKING WATER: Municipal drinking water samples were collected at 40 different locations from five different zones of Catalonia, Spain, perfluorooctanesulfonamide was detected in 11 of the 40 samples at a concentration of <0.03 to 1.80 ng/L(1).|SURFACE WATER: Surface water samples taken from US streams in the Great Lakes basin tested positive for perfluorooctanesulfonamide in 78% of 18 samples taken 1994 to 2000 at concentrations of 0.0001 to 0.0050 ug/L(1). Perfluorooctanesulfonamide was not detected (detection limit 10 ng/L) in water samples taken from the Raisin and St Clair Rivers, Michigan, samples collected March and April 2001, respectively(2). Perfluorooctanesulfonamide was not detected (detection limit 2.5 ng/L) in 51 samples from nine major water bodies in New York State, samples were collected July 2004(3). Perfluorooctanesulfonamide was detected in surface water samples from the Highland Creek watershed, Canada, taken Feb to March 2010 at 0.0039 to 0.32 ng/L(4).|SURFACE WATER: Perfluorooctanesulfonamide was not detected in seawater samples taken from Finland, Denmark or the Faeroe Islands, in lake water from Norway, or in rain water samples taken from Finland and Sweden(1). Five stream flowing into Lake Shihwa, Korea had perfluorooctanesulfonamide concentrations of <0.05 to 2.36 ng/L, concentrations in Lake Shihwa and Gyeonggi Bay were <0.05 ng/L, all samples were collected in Dec of 2004(2). Perfluorooctanesulfonamide was not detected (detection limit 3.7 ng/L) in river water samples from Kyoto area in Japan, samples were collected Feb and March 2005(3). Water samples taken from tributaries of the Pearl River in Guangzhou and along the Yangtze River had perfluorooctanesulfonamide concentrations of 0.073-0.34 and <0.005-0.053 ng/L, respectively(4). Perfluorooctanesulfonamide was detected in sea water samples from six locations around Hong Kong, eight locations from the Pearl River Delta and South China Sea at <0.005-0.07 pg/mL, samples were collected July and Sept 2003 and Jan 2004(5). Water samples collected from 11 locations along the west and south coasts of South Korea contained perfluorooctanesulfonamide at <0.005-0.33 pg/mL(5). Perfluorooctanesulfonamide was detected in Mid Atlantic Ocean water at 2.7-3.7 pg/L, in the Sulu Sea at 2.7 pg/L, in the Eastern Pacific Ocean at 2.2-2.8 pg/L and in the Central to Western Pacific Ocean at <1.0-0.3 pg/L(6).|For more Environmental Water Concentrations (Complete) data for Perfluorooctanesulfonamide (6 total), please visit the HSDB record page.

Perfluorooctanesulfonamide was not detected (detection limit 0.7 ng/mL) in two human milk samples, collection information was not provided(1).

Occupational exposure to perfluorooctanesulfonamide may occur through inhalation and dermal contact with this compound at workplaces where perfluorooctanesulfonamide is produced or used. Monitoring data indicate that the general population are exposed to perfluorooctanesulfonamide via ingestion of food and drinking water(SRC). Studies have found perfluorooctylsulfonate chemicals in very small quantities in the blood of the general human population as well as in wildlife, indicating that exposure to the chemicals, including pristine environments, is widespread(1).

Perfluorooctanesulfonamide was detected in 26% of 299 cord blood serum samples taken from singletons born in 2004 to 2005 in Baltimore, MD at a range of not detected (detection limit 0.05 ng/mL) to 0.8 ng/mL(1). Perfluorooctanesulfonamide was detected (detection limit 0.05 ng/mL) in all serum samples from the US population (1562 participants) as studied in the National Health and Nutrition Examination Survey (NHANES) conducted 1999 thru 2000, with a mean concentration of 0.4 ng/mL(2). Perfluorooctanesulfonamide was also detected (detection limit 0.05 ng/mL) in all serum samples from the NHANES survey conducted 2001 thru 2002 (1832 participants), with a mean concentration of 0.19 ng/mL(3). In the NHANES survey conducted 2003 thru 2004 perfluorooctanesulfonamide was detected (detection limit 0.2 ug/L) in 22.2% of the 2094 serum samples analyzed(4). Perfluorooctanesulfonamide was detected in five of 65 human sera samples obtained from US biological supply companies at concentrations of 1.5 to 2.2 ppb(5). The concentration of perfluorooctanesulfonamide in the serum of 20 Atlanta residents was <0.2 to 0.7 ng/mL, samples were collected July 2003(6). Perfluorooctanesulfonamide was not detected (detection limit 0.7 ng/mL) in two human milk samples, collection information was not provided(6). Perfluorooctanesulfonamide concentrations in human sera were <1.3-23.5 and 1.3-26 ng/mL in samples from Michigan and Kentucky(7).|Perfluorooctanesulfonamide levels in New York State infants using Newborn Screening Programs dried blood spots analysis(1).[Table#8008]|Perfluorooctanesulfonamide was detected in human blood samples at 1.3-1.7 ng/mL in 12.5% of females and 1.5-2.3 ng/mL in 9.5% of males collected at local hospitals in Siena, Italy(1). Perfluorooctanesulfonamide concentration was <0.050 ng/mL (1977), increased to 0.69 ng/mL (1989) and then decreased to <0.05 ng/mL (2003) in 24 pooled serum samples from men, age 40 to 50 years, representing 1977 to 2006(2). Pooled samples were obtained from archived serum samples from a biobank at the Norwegian Institute of Public Health(2). Perfluorooctanesulfonamide was not detected (detection limit 1.0 ng/mL) in 15 maternal and 15 cord blood samples taken Feb to July 2003 at Hospitals in Hokkaido, Japan(3). Perfluorooctanesulfonamide concentrations in human sera were <0.4-5.6, <0.4-2.3, <1.3-2.3, <0.4-7.7, <3, <3, 1.3-11, <0.1-7.2 and <2.6-9.5 ng/mL in samples from Colombia, Brazil, Italy, Poland, Belgium, India, Malaysia, Korea and Japan, respectively(4). Whole blood samples collected in Sweden, 1997-2000 contained 0.4-22.9 pg/uL of perfluorooctanesulfonamide(5). Perfluorooctanesulfonamide was found in 40 pooled serum samples collected from 3802 Australian residents collected Nov 2002 to April 2003 at 0.36 to 2.4 ng/mL(6). Perfluorooctanesulfonamide was detected in 24% of 84 pools of human blood serum taken from 2420 Queensland, Australia donors in 2006 to 2007, concentrations reported were <0.1-5 ng/mL(7). Human blood samples from volunteer donors from five Chinese cities (Shenyang, Beijing, Gulyang, Jintan, Nanjing) collected in 2004 had perfluorooctanesulfonamide concentrations of 0.0347 to 3.10 ng/mL(8).|Concentration of perfluorooctanesulfonamide in adult (age 19-62) human blood, 15 samples from each category, taken from citizens of Gdansk, Poland and nearby villages. Blood donations were all collected July 2003(1).[Table#8009]|For more Body Burden (Complete) data for Perfluorooctanesulfonamide (6 total), please visit the HSDB record page.

Oxidative stress has been hypothesized to provide a mechanism by which apparently unrelated chemicals can nevertheless produce similar developmental neurotoxic outcomes. /Researchers/ used differentiating PC12 cells to compare the effects of agents from four different classes and then to evaluate antioxidant amelioration: fipronil, perfluorooctanesulfonamide (PFOSA), dieldrin and chlorpyrifos. The rank order for lipid peroxidation corresponded to the ability to evoke cell loss: fipronil>PFOSA>dieldrin>chlorpyrifos. The same sequence was found for an index of cell enlargement (protein/DNA ratio) but the effects on neurite outgrowth (membrane/total protein) diverged, with fipronil producing a decrease and PFOSA an increase. Cotreatment with antioxidants reduced (ascorbate) or eliminated (Vitamin E) lipid peroxidation caused by each of the agents but failed to protect against cell loss, with the sole exception of chlorpyrifos, for which /they/ earlier showed partial protection by Vitamin E; addition of higher NGF concentrations protected neither against oxidative stress nor cell loss. Despite the failure to prevent cell loss, ascorbate protected the cells from the effects of PFOSA on neuritic outgrowth; NGF, and to a lesser extent, ascorbate, offset the effects of fipronil on both cell enlargement and neuritogenesis. At the same time, the ameliorant treatments also worsened some of the other toxicant effects. /The/ results point out the problems in concluding that, just because a neurotoxicant produces oxidative stress, antioxidant therapy will be effective in preventing damage. Instead, additional mechanisms for each agent may provide alternative routes to neurotoxicity, or may be additive or synergistic with oxidative stress.

/SRP:/ 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/|/SRP:/ 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/|/SRP:/ 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 /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's 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 or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/BIOMONITORING/ /Reaserchers/ studied occurrence and levels of PFCs in human milk in relation to maternal serum together with the temporal trend in milk levels between 1996 and 2004 in Sweden. Matched, individual human milk and serum samples from 12 primiparous women in Sweden were analyzed together with composite milk samples (25-90 women/year) from 1996 to 2004. Eight PFCs were detected in the serum samples, and five of them were also above the detection limits in the milk samples. Perfluorooctanesulfonate (PFOS) and perfluorohexanesulfonate (PFHxS) were detected in all milk samples at mean concentrations of 0.201 ng/mL and 0.085 ng/mL, respectively. Perfluorooctanesulfonamide (PFOSA), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) were detected less frequently. The total PFC concentration in maternal serum was 32 ng/mL, and the corresponding milk concentration was 0.34 ng/mL. The PFOS milk level was on average 1% of the corresponding serum level. There was a strong association between increasing serum concentration and increasing milk concentration for PFOS (r(2) = 0.7) and PFHxS (r(2) = 0.8). PFOS and PFHxS levels in composite milk samples were relatively unchanged between 1996 and 2004, with a total variation of 20 and 32% coefficient of variation, respectively. The calculated total amount of PFCs transferred by lactation to a breast-fed infant in this study was approximately 200 ng/day. Lactation is a considerable source of exposure for infants, and reference concentrations for hazard assessments are needed.

DESFA

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