ARCHIVED - State of the Science Report for a Screening Health Assessment: Perfluorooctane Sulfonate, Its Salts and Its Precursors that Contain the C8F17SO2 or C8F17SO3 Moiety

2006
ISBN: 0-662-44200-8
Cat. No.: H128-1/06-482E
HC Pub.: 4447


Table of Contents

Formula

Introduction

Under the Canadian Environmental Protection Act, 1999 (CEPA 1999) the Minister of Health may gather information, conduct investigations and evaluations, including screening assessments, relevant for the purpose of assessing whether a substance is entering or may enter the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health.

Screening health assessments focus initially on conservative assessment of hazard or effect levels for critical endpoints and upper-bounding estimates of exposure, after consideration of all relevant identified information.  Decisions based on the nature of the critical effects and margins between conservative effect levels and estimates of exposure take into account confidence in the completeness of the identified databases on both exposure and effects, within a screening context.  Additional background information on screening health assessments conducted under this program is available at http://www.hc-sc.gc.ca/ewh-semt/contaminants/existsub/index_e.html.

A screening health assessment was undertaken on perfluorooctane sulfonate (PFOS), its salts and its precursors containing the C8F17SO2 or C8F17SO3 moiety on the basis that some of these compounds were included in the Domestic Substances List pilot phase for screening and in response to a request to the Minister of the Environment to add these compounds to the Priority Substances List.

The State of the Science Report for a screening assessment and associated unpublished supporting working documentation were prepared by evaluators within the Existing Substances Division of Health Canada; the content of these documents was reviewed at several meetings of senior Divisional staff. The draft Report was subsequently externally reviewed for adequacy of data coverage and defensibility of the conclusions.  The draft report was also reviewed during a 60-day public comment period. The supporting working documentation is available upon request by e-mail from ExSD@hc-sc.gc.ca

Information identified as of September 2003 was considered for inclusion in this screening health assessment. Additional information identified after that time and its relevance to the scientific assessment is presented in the last section of this document. The critical information and considerations upon which the assessment is based are summarized below.

Identity, Uses and Sources of Exposure

PFOS, its salts and its precursors form part of a larger chemical class of fluorochemicals typically referred to as perfluorinated alkyl compounds (PFAs). Depending upon the intended use, the various precursors of PFOS are formed via derivatization of perfluorooctanesulfonylfluoride (POSF: C8F17SO2F) (OECD, 2002), yielding molecules with the general chemical formula of CF3(CF2)7SO2-R. The screening health assessment of PFOS, its salts and its precursors containing the C8F17SO2 or C8F17SO3 moiety covers some 50 substances, many of which are on the Domestic Substances List (see Appendix 1).

The results of a survey of Canadian industry conducted in 2000 under Section 71 of CEPA 1999 to determine the manufacture, import, export and uses of specific PFAs, their derivatives and polymers indicated that there was no known manufacture of PFAs, including PFOS, in Canada. Almost 600 000 kg of PFAs were imported into Canada between 1997 and 2000, PFOS representing only a very small proportion of this total (Environment Canada, 2001). PFOS and its precursors were imported into Canada as chemicals or in various products. As noted elsewhere (OECD, 2002), the principal applications for PFOS and its precursors are for water, oil, soil and grease repellents for use on surface and paper-based applications, such as rugs and carpets, fabric and upholstery and food packaging, as well as use in specialized chemical applications, such as fire-fighting foams, hydraulic fluids, carpet spot removers, mining and oil well surfactants and other specialized chemical formulations. Owing to these use patterns, the exposure of humans to such substances would likely result from contact with, and/or the use of, certain consumer products (3M, 1999a).

The screening health assessment on PFOS, its salts and its precursors containing the C8F17SO2 or C8F17SO3 moiety is based upon a comparison of the margin between the levels of PFOS in the blood and liver of laboratory animals[1] that are associated with the development of toxicological effects and the levels in the blood and liver of humans. The following considerations were taken into account in developing the approach for the screening health assessment of PFOS, its salts and precursors listed herein:

  • Chemical, environmental and metabolic processes can lead to the removal of the perfluorinated moiety, ultimately yielding PFOS (3M, 1999a,b).
  • PFOS is persistent and is not further degraded or metabolically converted to other compounds (3M, 1999a,b).
  • On the basis of CATABOL modelling (Mekenyan and Dimitrov, 2002), the substances listed in Appendix 1 of this assessment were considered to have the potential to biodegrade to PFOS.
  • Since PFOS is likely the ultimate perfluorinated degradation or metabolic product of the group of substances listed in Appendix 1, the level of this compound in human tissue provides a useful indicator of exposure to this group of substances from all potential sources.
  • Biomonitoring in humans (and animal species) has focused on PFOS, which has been detected in the blood of non-occupationally exposed humans in North America and Europe.
  • The toxicity profile of those PFOS precursors examined here (see table below) appears to be generally similar to that of PFOS itself. Available data indicate that effects associated with the PFOS precursors occur at exposures that are similar to or slightly higher than those for PFOS.

Toxicological data relevant to this screening health assessment report were identified for the following substances on the Domestic Substances List (see following table), and these data were used as the basis for assessing the PFOS precursors listed in Appendix 1:

Substance

Designation

CAS No.

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

(perfluorooctane sulfonate)

PFOS

2795-39-3 (potassium salt)

29081-56-9 (ammonium salt)

70225-14-8 (diethanolamine salt)

1-Octanesulfonamide, N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-N-(2-hydroxyethyl)-

(N-ethylperfluorooctane sulfonamidoethanol)

N-EtFOSE

1691-99-2

1-Octanesulfonamide, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-N-(2-hydroxyethyl)-N-methyl-

(N-methylperfluorooctane sulfonamidoethanol)

N-MeFOSE

24448-09-7

1-Octanesulfonamide, N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-

(N-ethyl perfluorooctane sulfonamide)

N-EtFOSA

4151-50-2

1-Octanesulfonamide, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-N-methyl-

(N-methyl perfluorooctane sulfonamide)        

N-MeFOSA

31506-32-8

Glycine, N-ethyl-N-[(heptadecafluorooctyl)-sulfonyl]-, potassium salt

(potassium-N-ethyl-N((heptadecafluorooctyl)-sulfonyl)-glycinate)

PFOSAA

2991-51-7

Ethanaminium, N,N,N-trimethyl-2-[(2-methyl-1-oxo-2-propenyl)oxy]-, chloride, polymer with 2-ethoxyethyl 2-propenoate, 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl 2-propenoate and oxiranylmethyl 2-methyl-2-propenoate

92265-81-1

Exposure Assessment and Hazard Characterization

Although the identified data for some of these substances (see table above) were variable and limited, the available information indicates that toxicological effects of these precursors of PFOS are similar to those of PFOS itself (Table 1). Moreover, based upon the data identified, health-related effects associated with exposure to these substances would appear to be somewhat less severe and/or are observed at higher exposures (doses) than those associated with exposure to PFOS itself.

Studies considered critical to the screening health assessment of PFOS, its salts and its precursors (i.e., those with lowest effect levels) are long-term repeated-dose investigations conducted with rodents and primates. In rats receiving PFOS in the diet for 2 years, histopathological effects in the liver were observed in males and females at intakes as low as 0.06-0.23 mg/kg-bw per day and 0.07-0.21 mg/kg-bw per day, respectively (Covance Laboratories, Inc., 2002a). The mean levels of PFOS in the serum and liver of males and females with these intakes were 7.6 and 20.2 µg/ml and 26.4 and 55.1 µg/g, respectively, after 2 years of exposure (3M Environmental Laboratory, 2001). Evidence of increased thymic atrophy (in females) and reduced serum high-density lipoprotein, cholesterol, bilirubin and triiodothyronine levels (in males) were observed in monkeys administered 0.03 mg PFOS/kg-bw per day for 26 weeks (Covance Laboratories, Inc., 2002b).[2] The mean levels of PFOS in the serum of the males and females after 26 weeks on study were 15.8 and 13.2 µg/ml, respectively (3M Environmental Laboratory, 2000). The mean levels of PFOS in the liver of males and females after 27 weeks on study were 17.3 and 22.2 µg/g, respectively.

Based upon data from chronic exposure studies, there is evidence for the carcinogenicity of PFOS (increased incidence of hepatocellular adenoma in males and females) and N-EtFOSE (increased incidence of hepatocellular adenoma in females; thyroid follicular cell adenoma in males) in rats. In both of these studies, statistically significant increases in tumour incidence were observed only at the highest doses tested -- that is, at doses that were above those associated with the development of non-neoplastic effects in these animals. PFOS and its related substances evaluated here are not genotoxic based upon the results of a wide range of identified in vitro and in vivo assays.

Identified data included investigations on health effects in workers occupationally exposed to PFOS. Although a significantly elevated risk of bladder cancer has been observed for one group of workers exposed to PFOS, the identified epidemiological studies of workers occupationally exposed to PFOS are considered inadequate to assess the potential of this substance (and its precursors) to induce cancer in humans. Workers were exposed to other substances, and the observed number of cause-specific and overall deaths was relatively small. Moreover, the database is inadequate as a basis to assess aspects of weight of evidence of causality, such as consistency.

In other surveys of occupationally exposed workers in which potential relationships between exposure to PFOS (assessed by monitoring serum PFOS levels in workers, which ranged as high as 10 µg/ml) and effects upon clinical chemistries and haematological and hormonal parameters were assessed, consistent associations have not been observed. The sensitivity of these investigations is limited by low participation rates and employee turnover during study periods at certain facilities.

In a recent study providing preliminary analytical data on the occurrence and distribution of selected organic perfluorinated compounds in the blood of 56 volunteer non-occupationally exposed adult Canadians, PFOS was detected in 100% of the samples (Kubwabo et al., 2002). Measured concentrations of PFOS in the serum ranged from 0.0037 to 0.065 µg/ml; the overall mean and 95th-percentile concentrations were 0.0288 and 0.0631 µg/ml, respectively. These levels are similar to those measured in other contemporary biomonitoring studies conducted in the United States and Europe (OECD, 2002).

In one study of 599 children (aged 2-12 years) in the United States conducted between 1994 and 1995, the geometric mean concentration of PFOS in the serum was 37.5 ppb (i.e., 0.0375 µg/ml); the 95th percentile was 97 ppb (0.097 µg/ml), with a small number of samples (<20) exceeding this value. Individual values ranging widely from 7 to 515 ppb (i.e., 0.0067-0.515 µg/ml) (3M Medical Department, 2002).

In view of the physical/chemical properties of PFOS, the substance is not expected to accumulate in breast milk. Although biomonitoring data in very young children have not been identified, PFOS levels in the sera of fetuses and very young offspring do not exceed those of exposed dams in experimental studies (Argus Research Laboratories, 1999e,f).

In analyses of liver samples collected from 30 cadavers in the United States, levels of PFOS ranged from <0.0045 (limit of quantitation) to 0.057 µg/g (Olsen et al., 2003). The mean and geometric mean concentrations were 0.0188 and 0.0152 µg/g, respectively.

Confidence in the effects assessment for PFOS and N-EtFOSE is high, owing to the available database, which covers a wide range of toxicological endpoints. Although confidence in the effects assessment for the remaining PFOS-related compounds is low, due to the lack of identified data, this is mitigated to some degree by the consideration that these compounds are likely converted to PFOS in environmental and biological media. Confidence in the measure of the "internal dose" of PFOS (i.e., levels of PFOS in serum and liver) to assess exposure of the general population to this group of compounds is high. Although the size of the sampled population of individuals in Canada is relatively small, the mean measured concentration is similar to that reported elsewhere for samples collected from other non-occupationally exposed populations in the United States and Europe. Although there may be somewhat less confidence in the available data on the levels of PFOS in human liver, owing to the small sample size in the single report, use of this exposure metric takes into account aspects related to both the toxicokinetics and metabolism of such substances.

Conclusion for Human Health

The two laboratory studies considered critical for the margin of exposure analysis are the chronic toxicity study in rats, with a large number of animals per dose group exposed for nearly their lifetime, and the study in which small groups of monkeys (considered as better surrogates for humans) received PFOS for 26 weeks. The levels of PFOS in the serum and liver of these animals at the critical effect level are less than those associated with the critical effect in the F0 and F1 rats in the two-generation reproduction/developmental toxicity study.

Most often in the screening health assessment of Existing Substances under CEPA 1999, margins of exposure are based upon a comparison of the doses (intakes) administered to laboratory animals at which substance-induced effects were observed with the upper-bound estimate of human intake. While such estimates of intake for PFOS are included in the supporting working document, they are less reliable as a basis for development of margins than those based on serum levels. In this case, therefore, comparisons have been based upon information on the levels of PFOS in the serum and liver from animals administered PFOS and data from human biomonitoring studies. This obviates the need to take into account the significant uncertainty associated with a determination of the upper-bound estimate of human intake of PFOS, owing to the limited available data on levels of PFOS and precursors in air, foodstuffs, drinking water and breast milk and resulting from contact with household materials treated with such perfluorinated substances. Moreover, the levels of PFOS in human tissues provide a useful indicator of the combined exposure from all sources.

Comparisons of the levels of PFOS in the serum and liver of animals at the critical effect level with levels in serum and/or liver from human adult and children biomonitoring studies are presented in the following table:

Critical study and effect

PFOS dose metric at critical effect

Metric(s) of human exposure to PFOS

Margin of exposure

(critical effect/human exposure)

Microscopic changes in the liver of rats (m + f) receiving PFOS in the diet for 2 years1

Serum PFOS level:

13.9 µg/ml2

Mean serum PFOS level in adults in Canada3:

0.028 µg/ml

496

95th percentile of human serum PFOS level in adults in Canada3:

0.0631 µg/ml

220

Mean serum PFOS level in children in the United States4:

0.0375 µg/ml

371

95th percentile of serum PFOS level in children in the United States4:

0.097 µg/ml

143

Liver PFOS level:

40.8 µg/g5

Mean6 liver PFOS level:

0.0188 µg/g

21707

Thymic atrophy (f), reduced serum high-density lipoprotein (m), cholesterol (m), triiodothyronine (m) and total bilirubin (m) in monkeys administered PFOS for 26 weeks1

Serum PFOS level:

14.5 µg/ml8

Mean serum PFOS level in adults in Canada3:

0.028 µg/ml

518

95th percentile of human serum PFOS level in adults in Canada3:

0.0631 µg/ml

230

Mean serum PFOS level in children in the United States4:

0.0375 µg/ml

387

95th percentile of serum PFOS level in children in the United States4:

0.097 µg/ml

149

Liver PFOS level:

19.8 µg/g9

Mean10 liver PFOS level:

0.0188 µg/g

105311

1 Covance Laboratories, Inc. (2002a).
2 Average of mean levels in males (7.6 :g/ml) and females (20.2 :g/ml).
3 Kubwabo et al. (2002).
4 3M Medical Department (2002).
5 Average of mean levels in males 26.4 (:g/g) and females (55.1 :g/g).
6 Mean level of PFOS in livers from 30 cadavers (Olsen et al., 2003).
7  Published data on 95th percentile not available. Margin of exposure based upon highest level of PFOS in human liver from this study (0.057 :g/g) is 716.
8  Average of mean levels in males (15.8 :g/ml) and females (13.2 :g/ml) (week 26).
9  Average of mean levels in males 17.3 (:g/g) and females (22.2 :g/g) (week 27).
10  Mean level of PFOS in livers from 30 cadavers (Olsen et al., 2003).
11  Published data on 95th percentile not available. Margin of exposure based upon highest level of PFOS in human liver from this study (0.057 :g/g) is 347.

These margins are considered adequate to address elements of uncertainty, including intraspecies variation, interspecies variation and biological adversity or severity of the effects considered critical here. These margins will also be protective for the increased incidence of tumours observed in the chronic study of PFOS in rats, since the tumours were observed only at doses of PFOS that were higher than those that induced non-neoplastic effects and since the weight of evidence indicates that PFOS (and its precursors) are not genotoxic. While the margins for blood levels in children are somewhat less (approximately 145 for the 95th-percentile values), more appropriate margins for comparison with the effect level from long-term studies are those for adults (approximately 225 for the 95th-percentile values), since they are exposed for a greater portion of their life span. In addition, the critical lowest-observed-effect levels selected for development of these margins of exposure are very conservative, being about an order of magnitude less than values in other studies (i.e., for effects observed in reproductive studies with rats). The margins are also based on more relevant metrics of exposure to PFOS than dose in experimental studies and deterministic estimates of daily intake in children and adults and, as a result, account for a significant portion of the uncertainties associated with interspecies and intraspecies differences in pharmacokinetics (usually accounted for by 4-fold and 3.2-fold default uncertainty factors, respectively). The higher margins for values in liver, although based on limited data, take into account even a greater proportion of uncertainty in toxicokinetics. The margins also take into account limitations of the database for human exposure. Use of the 95th percentiles for the serum levels is also more conservative than deterministic estimates of exposure, which are based on mean intakes of environmental media.

Additional Information Identified After Cut-Off Date

The concentration of PFOS measured in 10 maternal pools of plasma obtained from populations residing in Northern Canada ranged from about 20 to 60 ng/mL; overall mean was 36.9 ng/mL  (Tittlemier  et al, 2004). The mean level of PFOS in 13 cord blood pools was 16.7 ng/mL. In a study involving pregnant Japanese women, blood PFOS levels were higher than those measured in the matching cord blood samples (Inoue et al., 2004).  In a study conducted in the United States, Olsen et al. (2005) reported no statistically significant increase in the median concentrations of PFOS, between 1989 and 2001. The median level in sample collected in 1989, were statistically higher than in samples obtained in 1974.  Kannan et al. (2004) reported on the levels of PFOS obtained from samples collected in 10 countries; the overall range of mean concentrations (in males or females) was from 1.7 to 73.2 ng/mL.


[1] Available data from identified epidemiological studies were considered inadequate for such analysis.

[2] Also reported in Seacat et al. (2002).

Table 1: Summary of health effects information for PFOS and related compounds

Endpoint

PFOS

N-EtFOSE

N-EtFOSA

N-MeFOSE

N-MeFOSA

PFOSAA

Ethana-
minium...

Acute toxicity: oral

Oral LD50
rat (m/f)

LD50 = 251 mg/kg-bw

(International Research and Development Corporation, 1978a)

[Additional studies: Hazleton Laboratories America, Inc., 1987a; Hazleton Wisconsin, Inc., 1994a; Corning Hazleton, Inc., 1997a]

Oral LD50 rat (m/f)

LD50 = 1467 mg/kg-bw

(International Research and Development Corporation, 1978b)

Oral LD50
rat (m/f)

LD50 = >
500 and <5000 mg/kg-bw

(Riker Laboratories, Inc., 1981b)

[Additional study: Riker Laboratories, Inc., 1987]

Oral LD50 rat (m/f)

LD50 = >1000 and <5000 mg/kg-bw

(Riker Laboratories, Inc., 1979)

Oral LD50 rat (m/f)

LD50 = 350 mg/kg-bw

(Hazleton Laboratories America, Inc., 1985a)

[Additional studies: Riker Laboratories, Inc., 1981c; Hazleton Laboratories America, Inc., 1985b]

Oral LD50 rat (m/f)

LD50 = >0.5 and <5 ml/kg-bw

(Biosearch, Inc., 1978c)

[Additional studies: Biosearch, Inc., 1978a; Hazleton Laboratories America, Inc., 1988a]

Oral LD50 rat (m/f)

LD50 = >5 g/kg-bw

(Hazleton Wisconsin, Inc., 1991a)

Acute toxicity: dermal

Dermal LD50 rabbit (m/f) 24-hour covered

LD50 = >2000 mg/kg-bw

(Hazleton Laboratories America, Inc., 1988b)

Acute toxicity: inhalation

Inhalation LC50 rat (m/f) LC50 = 5200 mg/m3

(Bio/Dynamics, Inc., 1979a)

Inhalation
LC50
rat (m/f) LC50 = >6.5 g/m3

(Hazleton Laboratories America, Inc., 1981)

Inhalation LC50 rat (m/f)

LC50 = >22 g/m3 and <66 g/m3

(Bio/Dynamics, Inc., 1979b)

Irritation: ocular

Severe irritation: rabbit 0.1 ml ocular application, washout after 5 or 30 seconds

(Riker Laboratories, Inc., 1981a)

[Additional studies: mild to moderate irritation: Warf Institute, Inc., 1974, 1975; Hazleton Laboratories America, Inc., 1987b; Hazleton Wisconsin, Inc., 1994b; Corning Hazleton, Inc., 1997b]

Minimal irritation: rabbit (f) 0.1 g ocular application

(Riker Laboratories, Inc., 1984)

No irritation:

rabbit 0.1 g ocular application

(Biosearch, Inc., 1978b)

Minimal irritation: rabbit (f) 0.09 g ocular application

(Hazleton Laboratories America, Inc., 1985c)

[Additional study: Hazleton Laboratories America, Inc., 1985d]

Mild irritation: rabbit 0.1 ml ocular application (unwashed)

(Hazleton Laboratories America, Inc., 1988c)

[Additional study: Biosearch, Inc., 1978d]

Moderate irritation: rabbit 0.1 ml ocular application (unwashed)

(Hazleton Wisconsin, Inc., 1991b)

Short-term repeated-dose toxicity

Oral gavage LOAEL rat (m/f), 28 days

LOAEL = 3 mg/kg-bw per day

hepatocellular hypertrophy (m/f); increased relative liver weight (m/f); increased relative kidney weight (f); reduced body weight (f)

(NOTOX, 1999)

[Additional study: Austin et al., 2003]

Dietary LOEL rat (m/f), at least 4 weeks

LOEL (m/f) = 2.4-4.1 mg/kg-bw per day

increased relative liver weight (f), hepatocellular hypertrophy (m) (investigators give LOAEL of 35-63 mg/kg-bw per day, ignoring liver effects at lower doses)

(Covance Laboratories, Inc., 2000a)

Subchronic toxicity

Oral gavage LOEL rhesus monkey (m/f), 90 days

LOEL = 0.5 mg/kg-bw per day

clinical signs of toxicity and increased leukocytes

(International Research and Development Corporation, 1978e)

[Additional study: International Research and Development Corporation, 1978c]

Oral diet
LOEL
rat (m/f), 90 days

LOEL (m) = 2 mg/kg-bw per day

slight hepatocellular vacuolization; decreased hemoglobin
and hematocrit

(International Research and Development Corporation, 1978d)

[Additional study: International Research and Development Corporation, 1979]

Oral diet LOEL rat (m/f), 13 weeks LOEL (m) = 2 mg/kg-bw per day

increased relative brain, kidney, liver and testis weights; histopathological changes in the liver, reductions in serum cholesterol and triglycerides

(Covance Laboratories, Inc., 1999d)

Carcinogenicity/

chronic

Oral diet LOAEL rat (m/f), 104 weeks

LOAEL = 0.06-0.23 mg/kg-bw per day

increased incidence of non-neoplastic changes in the liver (statistically significant increased incidence of hepatocellular adenoma in males and females at intakes of 0.64-2.21 mg/kg-bw per day)

(Covance Laboratories, Inc., 2002a)

Oral LOEL cynomolgus monkey (m/f), 26 weeks

LOEL (m/f) = 0.03 mg/kg-bw per day

m: reduced high-density lipoprotein and triiodothyronine levels, thymic atrophy

f: thymic atrophy

(Covance Laboratories, Inc., 2002b)

Oral diet LOEL rat (m/f) 104-week cancer bioassay with
N-EtFOSE
narrow range (98.1%)

LOEL (m) =
0.86-2.618 mg/kg-bw
per day

LOEL (f) =
4.213-10.166 mg/kg-bw
per day

m/f:
increased incidence of histopatho-
logical effects
in liver

f: significant
(p < 0.05) reduced
serum triglycerides after 104
weeks

(statistically significant increased incidences of thyroid
follicular adenoma in males at intakes of
3.1-8.72 mg/kg-bw
per day and
of hepato-
cellular adenoma in females at intakes of 4.213-10.166 mg/kg-bw per day)

(Covance Laboratories, Inc., 2001)

[Additional study: Riker Laboratories, Inc., 1983]

Genotoxicity and related endpoints: in vivo

Negative: mouse (m/f) bone marrow micronucleus 950 mg/kg-bw; acute oral gavage

(Corning Hazleton, Inc., 1996b)

Negative: mouse (m/f) bone marrow micronucleus 2200 mg/kg-bw; acute oral gavage

(Corning Hazleton, Inc., 1996a)

[Additional studies: Corning Hazleton,
Inc., 1993; Hazleton Washington, Inc., 1993a]

Negative: mouse (m/f) bone marrow micronu-
cleus, 4000 mg/kg-bw, acute oral gavage

(Corning Hazleton, Inc., 1996c)

Negative: rat (m/f) bone marrow micronucleus, 5000 mg/kg-bw, acute oral gavage, and rat hepatic unscheduled DNA synthesis in vivo/in vitro

(Hazleton Washington, Inc., 1993b,c)

Genotoxicity and related endpoints: in vitro

Negative: with/without metabolic activation: Ames Salmonella/E. coli mutagenicity, S. cerevisiae mitotic recombinogenicity, rat hepatocyte unscheduled DNA synthesis and human lymphocyte chromosomal aberration in vitro assays

(Litton Bionetics, Inc., 1978; SRI International, 1978, 1980, 1981; Covance Laboratories, Inc., 1999a,b,c)

Negative
(-S9), questionable (+S9):
mouse lymphoma L5178Y;
in vitro
mutation -S9/+S9

(NOTOX,
1998)

[Additional negative
in vitro study: Covance Laboratories, Inc., 2000b]

Negative:

Ames Salmonella mutagenicity and Chinese hamster
ovary sister chromatid exchange in vitro assays

(U.S. EPA, 1989)

Negative: with/without metabolic activation: Ames Salmonella mutagenicity, mouse L5178Y lymphoma mutation and human lymphocyte chromosomal aberration in vitro assays

(NOTOX, 1994a,b,c)

Negative: with/without metabolic activation: Ames Salmonella mutagenicity and yeast recombination in vitro assays

(SRI International, 1985)

Negative: with/without metabolic activation: Ames Salmonella mutagenicity and yeast recombination in vitro assays

(SRI International, 1982)

Reproductive/ developmental toxicity, rat

LOEL maternal/LOEL fetal rat (f) oral gavage, days 6-15 of gestation

LOEL maternal = 5 mg/kg-bw per day

LOEL fetal = 1 mg/kg-bw per day

maternal: decreased weight gain; decreased body weight minus gravid uterine weight; clinical effects

fetal: incomplete skull closure twice that of controls

(Hazleton Laboratories America, Inc., 1983b)

[Additional studies: Riker Laboratories, Inc., 1980; Argus Research Laboratories, Inc., 1999e,f]

LOEL
maternal/
LOEL fetal

rat (f) oral gavage, days 6-17 of gestation

LOEL
maternal =
10 mg/kg-bw per day

LOEL fetal =
10 mg/kg-bw per day

maternal: reduced body weight gain

fetal: reduced live fetal body weight and increased skeletal alterations, ossification alterations

(Argus Research Laboratories, Inc., 1998)

[Additional studies: Riker Laboratories, Inc., 1981d; Hazleton Laboratories America, Inc., 1983a, 1984]

Reproductive/ developmental toxicity, rat two-generation

LOEL F0/LOEL F1/LOEL F2: rat (m/f) oral gavage, F0 males: from 6 weeks before to the end of mating, F0 females: from 6 weeks before mating through to the 21st day of lactation (DL 21), F1 males: from 22 days after birth to the end of mating (started 90 days after birth), F1 females: from 22 days after birth to DL 21 (for F2)

LOEL F0 (m) = 0.4 mg/kg-bw per day

LOEL F0 (f) = 1.6 mg/kg-bw per day

LOEL F1 (m/f) = 1.6 mg/kg-bw per day

LOEL F2 (m/f) = >0.4 mg/kg-bw per day

F0 (m) reduced body weight gains, F0 (f) reduced body weight gains during precohabitation, F1 (m/f) significantly reduced litter sizes and both viability and lactation indices; reductions in development, including delayed eye opening, surface righting, pinna unfolding and air righting reflex

(Argus Research Laboratories, Inc., 1999a)

[Additional study: Argus Research Laboratories, Inc., 2000]

LOEL F0/
LOEL F1/
LOEL F2:
rat (m/f) oral gavage, F0 males: from
28 days
before to end of mating, females: from 28 days before through to the 21st day of lactation (DL 21), F1 males from 22 days after birth to end of mating (started 90 days after birth), F1 females: from 22 days after birth through
to DL 21
(for F2)

LOEL F0 (m/f) = 5 mg/kg-bw per day

LOEL F1 (m/f) = 1 mg/kg-bw per day

LOEL F2 (m/f) = 5 mg/kg-bw per day

F0reduced
body weight gains (m/f); increased relative left testis weight; reduced duration of gestation, F1 reduced body weight gains (m/f), F2 reduced
viability and lactation indices; reduced mean litter weight

(Argus Research Laboratories, Inc., 1999b)

Reproductive/ developmental toxicity, rabbit

LOEL maternal/ LOEL fetal rabbit (f) oral gavage, days 7-20 of gestation

LOEL maternal = 1.0 mg/kg-bw per day

LOEL fetal = 2.5 mg/kg-bw per day

maternal: reduced body weight gain over entire exposure period

fetal: decreased ossification of sternal centres per fetus per litter; reduced body weight

(Argus Research Laboratories, Inc., 1999d)

LOEL maternal/
LOEL fetal
rabbit (f) oral gavage, days 7-20 of gestation LOEL maternal = 2.5 mg/kg-bw
per
day

LOEL fetal = >3.75 mg/kg-bw per day

maternal: reduced body weight gain; increased late resorptions and abortions

(Argus Research Laboratories, Inc., 1999c)

[Additional study: Riker Laboratories, Inc., 1981e]

LOEL offspring rabbit (f)
oral gavage; days 19-28
of gestation

LOEL offspring = 0.3 mg/kg-bw per day

increased neonatal mortality throughout pre-weaning period

(Stump et
al., 1997)

LOEL = lowest-observed-effect level; LOAEL = lowest-observed-adverse-effect level; LC50 = median lethal concentration; LD50 = median lethal dose; m = male; f = female; bw = body weight.

References

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APPENDIX 1

PFOS AND RELATED SUBSTANCES

CAS No. Chemical name Molecular formula

N/A

1-Octanesulfonate, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-

C8F17SO3-

1691-99-2

1-Octanesulfonamide, N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-N-(2-hydroxyethyl)-

C12H10F17NO3S

2250-98-8

1-Octanesulfonamide, N,N',N''-[phosphinylidynetris(oxy-2,1-ethanediyl)]tris[N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-

C36H27F51N3O10PS3

2795-39-3

1-Octanesulfonic acid, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-, potassium salt

C8HF17O3S·K

2991-51-7

Glycine, N-ethyl-N-[(heptadecafluorooctyl)sulfonyl]-, potassium salt

C12H8F17NO4S·K

4151-50-2

1-Octanesulfonamide, N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-

C10H6F17NO2S

24448-09-7

1-Octanesulfonamide, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-N-(2-hydroxyethyl)-N-methyl-

C11H8F17NO3S

29081-56-9

1-Octanesulfonic acid, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-, ammonium salt

C8HF17O3S·H3N

29117-08-6

Poly(oxy-1,2-ethanediyl), α-[2-[ethyl[(heptadecafluorooctyl)sulfonyl]amino]ethyl]-ω-hydroxy-

(C2H4O)nC12H10F17NO3S

30381-98-7

1-Octanesulfonamide, N,N-[phosphinicobis(oxy-2,1-ethanediyl)]bis[N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-, ammonium salt

C24H19F34N2O8PS2·H3N

31506-32-8

1-Octanesulfonamide, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-N-methyl-

C9H4F17NO2S

25268-77-3

2-Propenoic acid, 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl ester

C14H10F17NO4S

423-82-5

2-Propenoic acid, 2-[ethyl[(heptadecafluorooctyl)sulfonyl]amino]ethyl ester

C15H12F17NO4S

38006-74-5

1-Propanaminium, 3-[[(heptadecafluorooctyl)sulfonyl]amino]-N,N,N-trimethyl-, chloride

C14H16F17N2O2S·Cl

52550-45-5

Poly(oxy-1,2-ethanediyl), α-[2-[[(heptadecafluorooctyl)sulfonyl]propylamino]ethyl]-ω-hydroxy-

(C2H4O)nC13H12F17NO3S

56773-42-3

Ethanaminium, N,N,N-triethyl-, salt with 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-1-octanesulfonic acid (1:1)

C8H20N·C8F17O3S

57589-85-2

Benzoic acid, 2,3,4,5-tetrachloro-6-[[[3-[[(heptadecafluorooctyl)sulfonyl]oxy]phenyl]amino]carbonyl]-, monopotassium salt

C22H6Cl4F17NO6S·K

67939-88-2

1-Octanesulfonamide, N-[3-(dimethylamino)propyl]-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-, monohydrochloride

C13H13F17N2O2S·ClH

67969-69-1

1-Octanesulfonamide, N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-N-[2-(phosphonooxy)ethyl]-, diammonium salt

C12H11F17NO6PS2·H3N

68298-11-3

1-Propanaminium, 3-[[(heptadecafluorooctyl)sulfonyl](3-sulfopropyl)amino]-N-(2-hydroxyethyl)-N,N-dimethyl-, hydroxide, inner salt

C18H23F17N2O6S2

68298-62-4

2-Propenoic acid, 2-[butyl[(heptadecafluorooctyl)sulfonyl]amino]ethyl ester, telomer with 2-[butyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-propenoate, methyloxirane polymer with oxirane di-2-propenoate, methyloxirane polymer with oxirane mono-2-propenoate and 1-octanethiol

(C17H16F17NO4S·C16H16F15NO4
S·W99·W99)x·C8H18S

68298-78-2

2-Propenoic acid, 2-methyl-, 2-[[[[5-[[[2-[ethyl[(heptadecafluorooctyl)sulfonyl]amino]ethoxy]carbonyl]amino]-2-methylphenyl]amino]carbonyl]oxy]propyl ester, telomer with butyl 2-propenoate, 2-[[[[5-[[[2-[ethyl[(nonafluorobutyl)sulfonyl]amino]ethoxy]carbonyl]amino]-2-methylphenyl]amino]carbonyl]oxy]propyl 2-methyl-2-propenoate, 2-[[[[5-[[[2-[ethyl[(pentadecafluoroheptyl)sulfonyl]amino]ethoxy]carbonyl]amino]-2-methylphenyl]amino]carbonyl]oxy]propyl 2-methyl-2-propenoate, 2-[[[[5-[[[2-[ethyl[(tridecafluorohexyl)sulfonyl]amino]ethoxy]carbonyl]amino]-2-methylphenyl]amino]carbonyl]oxy]propyl 2-methyl-2-propenoate, 2-[[[[5-[[[2-[ethyl[(undecafluoropentyl)sulfonyl]amino]ethoxy]carbonyl]amino]-2-methylphenyl]amino]carbonyl]oxy]propyl 2-methyl-2-propenoate, 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl 2-propenoate, 2-[methyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-propenoate and 1-octanethiol

(C28H28F17N3O8S·C27H28F15N3O8
S·C26H28F13N3O8S·C25H28F11N3O8
S·C24H28F9N3O8S·C14H10F17NO4
S·C13H10F15NO4S·C12H10F13NO4
S·C11H10F11NO4S·C10H10F9NO4
S·C7H12O2)x·C8H18S

68329-56-6

2-Propenoic acid, eicosyl ester, polymer with 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl 2-propenoate, hexadecyl 2-propenoate, 2-[methyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-propenoate and octadecyl 2-propenoate

(C23H44O2·C21H40O2·C19H36O2
·C14H10F17NO4S·C13H10F15NO4
S·C12H10F13NO4S·C11H10F11NO4
S·C10H10F9NO4S)x

68555-90-8

2-Propenoic acid, butyl ester, polymer with 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl 2-propenoate, 2-[methyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-propenoate and 2-[methyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-propenoate

(C14H10F17NO4S·C13H10F15NO4
S·C12H10F13NO4S·C11H10F11NO4
S·C10H10F9NO4S·C7H12O2)x

68555-91-9

2-Propenoic acid, 2-methyl-, 2-[ethyl[(heptadecafluorooctyl)sulfonyl]amino]ethyl ester, polymer with 2-[ethyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[ethyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[ethyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate and octadecyl 2-methyl-2-propenoate

(C22H42O2·C16H14F17NO4S·C15
H14F15NO4S·C14H14F13NO4S·C13
H14F11NO4S·C12H14F9NO4S)x

68555-92-0

2-Propenoic acid, 2-methyl-, 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl ester, polymer with 2-[methyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[methyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[methyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[methyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate and octadecyl 2-methyl-2-propenoate

(C22H42O2·C15H12F17NO4S·C14
H12F15NO4S·C13H12F13NO4S·C12
H12F11NO4S·C11H12F9NO4S)x

68586-14-1

2-Propenoic acid, 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl ester, telomer with 2-[methyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-propenoate, α-(2-methyl-1-oxo-2-propenyl)-ω-hydroxypoly(oxy-1,2-ethanediyl), α-(2-methyl-1-oxo-2-propenyl)-ω-[(2-methyl-1-oxo-2-propenyl)oxy]poly(oxy-1,2-ethanediyl), 2-[methyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-propenoate and 1-octanethiol

(C14H10F17NO4S·C13H10F15NO4
S·C12H10F13NO4S·C11H10F11NO4
S·C10H10F9NO4S·(C2H4O)nC8H10O3
·(C2H4O)nC4H6O2)x·C8H18S

68649-26-3

1-Octanesulfonamide, N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-N-(2-hydroxyethyl)-, reaction products with N-ethyl-1,1,2,2,3,3,4,4,4-nonafluoro-N-(2-hydroxyethyl)-1-butanesulfonamide, N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,7,7,7-pentadecafluoro-N-(2-hydroxyethyl)-1-heptanesulfonamide, N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,6-tridecafluoro-N-(2-hydroxyethyl)-1-hexanesulfonamide, N-ethyl-1,1,2,2,3,3,4,4,5,5,5-undecafluoro-N-(2-hydroxyethyl)-1-pentanesulfonamide, polymethylenepolyphenylene isocyanate and stearyl alc.

N/A

68867-62-9

2-Propenoic acid, 2-methyl-, 2-[ethyl[(heptadecafluorooctyl)sulfonyl]amino]ethyl ester, telomer with 2-[ethyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[ethyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[ethyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[ethyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 1-octanethiol and α-(1-oxo-2-propenyl)-ω-methoxypoly(oxy-1,2-ethanediyl)

(C16H14F17NO4S·C15H14F15NO4
S·C14H14F13NO4S·C13H14F11NO4
S·C12H14F9NO4S·(C2H4O)nC4H6O2)x·C8H18S

68877-32-7

2-Propenoic acid, 2-methyl-, 2-[ethyl[(heptadecafluorooctyl)sulfonyl]amino]ethyl ester, polymer with 2-[ethyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[ethyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[ethyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-[ethyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate and 2-methyl-1,3-butadiene

(C16H14F17NO4S·C15H14F15NO4
S·C14H14F13NO4S·C13H14F11NO4
S·C12H14F9NO4S·C5H8)x

68891-96-3

Chromium, diaquatetrachloro[µ-[N-ethyl-N-[(heptadecafluorooctyl)sulfonyl]glycinato-O':O" ]]µ-hydroxybis(2-methylpropanol)di-

C18H28Cl4Cr2F17NO9S

68958-61-2

Poly(oxy-1,2-ethanediyl), α-[2-[ethyl[(heptadecafluorooctyl)sulfonyl]amino]ethyl]-ω-methoxy-

(C2H4O)nC13H12F17NO3S

70225-14-8

1-Octanesulfonic acid, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-, compd. with 2,2-iminobis[ethanol] (1:1)

C8HF17O3S·C4H11NO2

70776-36-2

2-Propenoic acid, 2-methyl-, octadecyl ester, polymer with 1,1-dichloroethene, 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl 2-propenoate, N-(hydroxymethyl)-2-propenamide, 2-[methyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-propenoate and 2-[methyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-propenoate

(C22H42O2·C14H10F17NO4S·C13
H10F15NO4S·C12H10F13NO4S·C11
H10F11NO4S·C10H10F9NO4S·C4H7
NO2·C2H2Cl2)x

71487-20-2

2-Propenoic acid, 2-methyl-, methyl ester, polymer with ethenylbenzene, 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl 2-propenoate, 2-[methyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-propenoate, 2-[methyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-propenoate and 2-propenoic acid

(C14H10F17NO4S·C13H10F15NO4
S·C12H10F13NO4S·C11H10F11NO4
S·C10H10F9NO4S·C8H8
·C5H8O2·C3H4O2)x

92265-81-1

Ethanaminium, N,N,N-trimethyl-2-[(2-methyl-1-oxo-2-propenyl)oxy]-, chloride, polymer with 2-ethoxyethyl 2-propenoate, 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl 2-propenoate and oxiranylmethyl 2-methyl-2-propenoate

(C14H10F17NO4S·C9H18NO2·C7H12
O3·C7H10O3·Cl)x

94313-84-5

Carbamic acid, [5-[[[2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethoxy]carbonyl]amino]-2-methylphenyl]-, 9-octadecenyl ester, (Z)-

C38H50F17N3O6S

98999-57-6

Sulfonamides, C7-8-alkane, perfluoro, N-methyl-N-[2-[(1-oxo-2-propenyl)oxy]ethyl], polymers with 2-ethoxyethyl acrylate, glycidyl methacrylate and N,N,N-trimethyl-2-[(2-methyl-1-oxo-propenyl)oxy]ethanaminium chloride

(C14H10F17NO4S·C9H18NO2·C7H12
O3·C7H10O3·Cl)x

178094-69-4

1-Octanesulfonamide, N-[3-(dimethyloxidoamino)propyl]-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-, potassium salt

C13H12F17N2O3S·K

N/A

2-(Perfluoro-N-methyl-C4-8-1-alkanesulfonamido)ethyl esters of trimers of C18 unsaturated fatty acids

N/A

29457-72-5

1-Octanesulfonic acid, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-, lithium salt

C8HF17O3S·Li

68909-15-9

2-Propenoic acid, eicosyl ester, polymers with branched octyl acrylate, 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl acrylate, 2-[methyl[(nonafluorobutyl)sulfonyl]amino]ethyl acrylate, 2-[methyl[(pentadecafluoroheptyl)sulfonyl]amino ]ethyl acrylate, 2-[methyl[(tridecafluorohexyl)sulfonyl]amino]ethyl acrylate, 2-[methyl[(undecafluoropentyl)sulfonyl]amino]ethyl acrylate, polyethylene glycol acrylate Me ether and stearyl acrylate

(C23H44O2·C21H40O2·C14H10F17
NO4S·C13H10F15NO4S·C12H10F13
NO4S·C11H10F11NO4S·C10H10F9
NO4S·(C2H4O)nC4H6O2·Unspecified)x

148684-79-1

Sulfonamides, C4-8-alkane, perfluoro, N-(hydroxyethyl)-N-methyl, reaction products with 1,6-diisocyanatohexane homopolymer and ethylene glycol

N/A

30295-51-3

1-Octanesulfonamide, N-[3-(dimethyloxidoamino)propyl]-1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-

N/A

91081-99-1

Sulfonamides, C4-8-alkane, perfluoro, N-(hydroxyethyl)-N-methyl, reaction products with epichlorohydrin, adipates (esters)

N/A

N/A

Fatty acids, C18-unsatd., dimers, 2-[methyl[(perfluoro-C4-8-alkyl)sulfonyl]amino]ethyl esters

N/A

68081-83-4

Carbamic acid, (4-methyl-1,3-phenylene)bis-, bis[2-[ethyl[(perfluoro-C4-8-alkyl)sulfonyl]amino]ethyl] ester

68608-14-0

Sulfonamides, C4-8-alkane, perfluoro, N-ethyl-N-(hydroxyethyl), reaction products with 1,1'-methylenebis[4-isocyanatobenzene]

307-35-7

1-Octanesulfonyl fluoride, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-

N/A

376-14-7

2-Propenoic acid, 2-methyl-, 2-[ethyl[(heptadecafluorooctyl)sulfonyl]amino]ethyl ester

N/A

14650-24-9

2-Propenoic acid, 2-methyl-, 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl ester

N/A

94133-90-1

1-Propanesulfonic acid, 3-[[3-(dimethylamino)propyl][(heptadecafluorooctyl)sulfonyl]amino]-2-hydroxy-, monosodium salt

N/A

127133-66-8

2-Propenoic acid, 2-methyl-, polymers with Bu methacrylate, lauryl methacrylate and 2-[methyl[(perfluoro-C4-8-alkyl)sulfonyl]amino]ethyl methacrylate

N/A

179005-06-2

Sulfonamides, C4-8-alkane, perfluoro, N-[3-(dimethyloxidoamino)propyl], potassium salts

N/A

179005-07-3

Sulfonamides, C4-8-alkane, perfluoro, N-[3-(dimethyloxidoamino)propyl]

N/A

ROF

Residual Organic Fluorochemicals (impurities)

N/A

1763-23-1

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

C8HF17O3S

N/A = not available; Me = methyl; Bu = butyl

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