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U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release 

Long-Chain Perfluorinated Chemicals (PFCs)

I. Overview

Long-chain perfluorinated chemicals (PFCs)1 are found world-wide in the environment, 

wildlife, and humans. They are bioaccumulative in wildlife and humans, and are persistent in the 

environment. They are toxic to laboratory animals and wildlife. To date, significant adverse 

effects have not been detected in humans. However, given the long half-life of these chemicals in 

humans (years), it can reasonably be anticipated that continued exposure could increase body 

burdens to levels that would result in adverse outcomes. 

Since 2000, the Agency has taken various actions to help minimize the potential impact 

of PFCs on human health and the environment, including the review of substitutes for these 

chemicals as part of its review process for new chemicals under EPA's New Chemicals Program. 

Although such actions are important steps to reducing exposure to these chemicals, EPA 

continues to be concerned with long-chain PFCs. Consequently, EPA intends to propose actions 

in 2012 under the Toxic Substances Control Act (TSCA) to address the potential risks from longchain PFCs. 

EPA intends to initiate a TSCA § 6 rule for managing long-chain PFCs. If EPA can make 

certain findings with respect to these chemicals, TSCA section 6 provides authority for EPA to 

ban or restrict the manufacture (including import), processing, and use of these chemicals. A rule 

addressing the PFAS sub-category could expand the reach of three SNURs that the Agency has 

promulgated over the past decade. For example, the rule could address PFAS-containing articles. 

A rule addressing the PFAC category could expand the reach of the 2010/15 PFOA Stewardship 

Program beyond the eight participating companies and further address the concerns for potential 

PFAC exposure through the use of PFAC-containing articles. 

As part of the Agency's efforts to address PFCs, EPA also intends to evaluate the 

potential for disproportionate impact on children and other sub-populations. Given that 

NHANES and other data have demonstrated that humans are exposed to PFCs in utero, as 

babies, and during puberty, and that animal studies have shown that the fetus and neonate are 

sensitive life stages to PFC exposures, EPA will consider effects to the developing fetus and 

children. 

II. Introduction

As part of EPA's efforts to enhance the existing chemicals program under the Toxic 

Substances Control Act (TSCA)2

, the Agency identified an initial list of widely recognized 

chemicals, including PFCs, for action plan development based on their presence in human blood; 

persistent, bioaccumulative, and toxic (PBT)3

 characteristics; use in consumer products; 

 

1

 The terms PFCs, PFAS, and PFAC in this document refer only to chemicals described in the chemical identity 

section including certain polymers that contain perfluorinated moieties. They do not include other PFCs, particularly 

those having shorter chain lengths. 

2 15 U.S.C. §2601 et seq. 3

 Information on PBT chemicals can be found on the EPA website at http://www.epa.gov/pbt/. 
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production volume; and other similar factors. This Action Plan is based on EPA’s initial review 

of readily available use, exposure, and hazard information4 on PFCs. EPA considered which of 

the various authorities provided under TSCA and other statutes might be appropriate to address 

potential concerns with PFCs in developing the Action Plan. The Action Plan is intended to 

describe the courses of action the Agency plans to pursue in the near term to address its 

concerns. The Action Plan does not constitute a final Agency determination or other final 

Agency action. Regulatory proceedings indicated by the Action Plan will include appropriate 

opportunities for public and stakeholder input, including through notice and comment 

rulemaking processes. 

The information used by EPA for this Action Plan includes the Organisation for 

Economic Co-operation and Development’s (OECD) assessments of PFOS (OECD, 2002) and 

PFOA (OECD, 2006), EPA’s Office of Pollution Prevention and Toxics’ (OPPT) draft risk 

assessment of PFOA (EPA, 2009d), Environment Canada’s assessment (Canada, 2006), the 

assessment of PFOS by the Stockholm Convention on Persistent Organic Pollutants (POPs, 

2009), and other sources. The summary of the toxicity information is based on these previous 

assessments, and where appropriate, additional information on lower and higher chain lengths is 

provided. 

III. Scope of Review

The PFC chemicals included in this review are a category defined by the similar 

molecular structure as provided for under 15 U.S.C. § 2625(c)(2)(A). The two related subcategories that comprise the PFC category are PFAS and PFAC chemicals. 

Continuing contributions of PFAS/PFAC to the environmental/human reservoir need to 

be addressed using a category approach because all the chemicals are PBT chemicals or degrade 

to PBT chemicals. A chemical-by-chemical analysis is not needed and would be impractical. 

The PFAS/PFAC precursors may be polymers that are coated on a specific substrate. This 

action is considering only the contribution of precursors as a source of PFAS/PFAC, and not the 

inherent toxic effects of the polymer or exposure to dust that contains fluorinated polymers. 

PFAS Sub-Category 

The PFAS sub-category includes perfluorohexane sulfonic acid (PFHxS)5

, 

perfluorooctane sulfonic acid (PFOS) 6, and other higher homologues. The category also includes 

 

4 Information sources customarily employed include Inventory Update Reporting (IUR) submissions; Toxic Release 

Inventory (TRI) reporting; data submitted to the HPV Challenge Program; existing hazard and risk assessments 

performed by domestic and international authorities including but not limited to U.S. Federal government agencies, 

the Organization for Economic Cooperation and Development, the Stockholm Convention on Persistent Organic 

Pollutants, Health and Environment Canada, the European Union; and others. Action plans will reference specific 

sources used. 

5

 CF3-(CF2)5-SO3H; CAS RN: [355-46-4]. 6

 CF3-(CF2)7-SO3H; CAS RN: [1763-23-1]. 
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the acid salts and precursors.

The similarities of the chemicals within the PFAS sub-category can be established when 

reviewing representative structures of the different category member compounds: 

a. CF3(CF2)n-SO3

-

M where M = H+ or any other group where a formal dissociation can be made; 

and 

b. CF3(CF2)n-S(=O)y-X where y = 0 – 2 and X is any chemical moiety. 

where n > 4. 

PFAC Sub-Category 

The PFAC sub-category includes perfluorooctanoic acid (PFOA) 7 and other higher 

homologues. The category also includes the acid salts and precursors.

These similarities within the PFAC sub-category can be established by reviewing 

representative structures of the different category member compounds: 

a. CF3(CF2)n-COOM where M = H+

 or any other group where a formal dissociation can be 

made; 

b. CF3(CF2)n-CH=CH2; 

c. CF3(CF2)n-C(=O)-X where X is any chemical moiety; 

d. CF3(CF2)m-CH2-X where X is any chemical moiety; and 

 

7

 CF3-(CF2)5-COOH; CAS RN: [335-67-1]. 
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e. CF3(CF2)m-Y-X where Y = non-S, non-N hetero atom and where X is any chemical moiety. 

where n > 5 or m > 6. 

IV. Uses and Substitutes Summary

Production Volume 

PFAS Chemicals 

Commercial production of PFAS chemicals began over half a century ago. Total 

production from 1970 to 2002 was estimated to be about 100,000 tons (Paul A.G., 2009). By 

2003, PFOS chemicals were no longer manufactured by 3M, the principal U.S. producer. 

However, production of PFOS-related chemicals is still ongoing in other countries, though to a 

much smaller extent than before 2003 (POPRC, 2007). As PFOS-based products became more 

strictly regulated in developed countries, production shifted to other countries. For example, 

manufacturers in China began large scale production in 2003 at the advent of 3M’s 2002 global 

PFOS phase-out. China had an annual production in 2004 of less than 50 tons, but has increased 

production dramatically in recent years, with an estimated production of more than 200 tons in 

2006. Approximately 100 tons of that amount is designated for export (POPs, 2008). 

PFAC Chemicals 

World-wide production of fluorotelomers was estimated at 20 million pounds in 2006. 

The United States accounts for more than 50 percent of world-wide fluorotelomer production. 

Textiles and apparel account for approximately 50 percent of the volume, with carpet and carpet 

care products accounting for the next largest share in consumer product uses. Coatings, including 

those for paper products, are the third largest category of consumer product uses. 

Fluorotelomer release sources, and consequent exposure to fluorotelomers, can be 

explained through the examination of the life cycle of this category of chemicals: 

Manufacture of Monomers  Manufacture of Polymers  Processing and Use  Product Life

The manufacture of non-polymeric chemicals (surfactants, wetting agents, cleansers, etc.) 

is included in the manufacture of monomers. Some residual monomers are present in the various 

raw materials and final products of the different steps of manufacturing. Because each 

intermediate contains the same Rf moiety, the polymers also contain this moiety. The 2010/15 

PFOA Stewardship Program encourages the elimination of PFAC precursors in product content. 

Companies reporting under PFOA Stewardship Program differentiate between the amounts of 

PFAC precursors present in the final polymer product as residuals and the amount present in the 

polymer as Rf moities. The availability of PFAC precursor from the content of residuals in 

fluorotelomer based polymer products (FTBP) would be small in comparison to the amount 

released should polymeric materials biodegrade in the environment. Potentially all monomeric, 
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5

not just the small amounts of residual monomers and other monomer raw material and 

intermediates released at each of the four steps in the sequence above, could be PFAC 

precursors. 

Uses

PFAS Chemicals 

PFOS is a synthetic chemical that does not occur naturally in the environment. PFAS 

chemicals, as defined in this action plan, are no longer manufactured in United States. However, 

there is a limited set of existing uses for which alternatives are not yet available, and which are 

characterized by low volume, low exposure potential, and low releases. 

The existing SNUR regulations on PFAS chemicals do not affect the continued use of 

existing stocks of the listed chemicals that had been manufactured or imported into the United 

States prior to the effective date of the SNURs. Existing products and formulations already in the 

United States containing these chemicals – for example, PFOS-based fire fighting foams 

produced before the rules took effect in 2002 – can also still be used without providing notice to 

the Agency. Because the PFAS SNURs exempt articles, PFOS may be imported or processed as 

part of an article without the Agency receiving prior notice. 

PFAC Chemicals 

PFOA is a synthetic chemical that does not occur naturally in the environment. PFOA is 

manufactured for use primarily as an aqueous dispersion agent [as the ammonium salt] in the 

manufacture of fluoropolymers, which are substances with special properties that have thousands 

of important manufacturing and industrial applications. 

PFOA also can be produced unintentionally by the degradation of some fluorotelomers, which 

are not manufactured using PFOA but could degrade to PFOA. Fluorotelomers are used to make 

polymers that impart soil, stain, grease, and water resistance to coated articles. Some 

fluorotelomer based products are also used as high performance surfactants in products where an 

even flow is essential, such as paints, coatings, cleaning products, and fire-fighting foams for use 

on liquid fuel fires. Fluorotelomer-based products can be applied to articles both at the factory 

and by consumers and commercial applicators in after-market uses such as carpet treatments and 

water repellent sprays for apparel and footwear. 

Fluoropolymers, such as polytetrafluoroethylene (PTFE), which may contain some PFAC 

contamination, or that use PFOA as an emulsion stabilizer in aqueous dispersions, have a large 

U.S. market. The wire and cable industry is one of the largest segments of the fluoropolymer 

market, accounting for more than 35 percent of total U.S. fluoropolymer use. Apparel makes up 

about 10 percent of total fluoropolymer use, based on total reported production volume. 

Fluoropolymers are used in a wide variety of mechanical and industrial components, such as 

plastic gears, gaskets and sealants, pipes and tubing, O-rings, and many other products. Total 

U.S. demand for fluoropolymers in 2004 was between 50,000 and 100,000 metric tons. The 
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United States accounted for less than 25 percent of the world consumption of PTFE in 2007, and 

between 25 and 50 percent of the world consumption of other fluoropolymers. PTFE is the most 

commonly used fluoropolymer, and the United States consumed less than 50,000 metric tons of 

PTFE in 2008. 

Substitutes 

EPA is reviewing substitutes for PFOS, PFOA, and other long-chain PFCs under the New 

Chemicals Program. EPA established the program under section 5 of TSCA to help manage the 

potential risk from chemicals new to the marketplace. 

EPA's review of alternatives to long-chain PFCs has been ongoing since 2000 and is 

consistent with the approaches to alternatives encouraged under the PFOA Stewardship Program. 

Through October 2009, EPA has received and reviewed over 100 perfluorinated alternatives of 

various types. EPA reviews the new substances against the range of toxicity, fate, and 

bioaccumulation issues that have caused past concerns with perfluorinated substances, as well as 

any issues that may be raised by new chemistries(EPA, 2009b). 

V. Hazard Identification Summary

World-Wide Distribution of PFAS and PFAC 

Presence in Humans

PFAS and PFAC have been detected in human blood samples throughout the world. 

Blood samples have been collected in countries world-wide including the United States, Japan, 

Canada, Peru, Colombia, Brazil, Italy, Poland, Germany, Belgium, Sweden, India, Malaysia, 

Korea, China, and Australia. In addition, PFAS and PFAC have been detected in breast milk, 

liver, umbilical cord blood, and seminal plasma. In most cases, the analytes most often detected 

in human matrices, and usually in the highest concentrations, were PFOS, PFOA, and PFHxS. 

Other PFAS and PFAC detected in human tissue include perfluorooctane sulfonamide (PFOSA), 

2-(N-methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH), 2-(Nethylperfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH or PFOSAA), 

perfluoroheptanoic acid (PFHpA), perfluorononanoate (PFNA), perfluorodecanoic acid (PFDeA 

or PFDA), perfluoroundecanoic acid (PFUA), perfluorododecanoic acid (PFDoA), 

perfluoropentanoic acid (PFPeA), perfluorohexanoic acid (PFHxA), and perfluorobutane 

sulfonate (PFBS). 

National Health and Nutrition Examination Survey (NHANES) data show that mean 

levels of PFOS, PFOA and PFHxS in the general U.S. population older than 12 years declined 

between the sampling period of 1999-2000 and 2003-2004 (Calafat, 2007). In addition, 3M 

reported a decline of the same chemicals from 2000 to 2006 in a group of 600 adult American 

Red Cross (ARC) blood donors (G. W. Olsen, Mari DC, Church TR, Ellefson ME, Reagen WK, 

Boyd TM, Herron RM, Medhdizadehkashi Z, Nobiletti JB, Rios JA, Butenhoff JL, Zobel LR 

2008). The biggest drop reported in both surveys was in PFOS (~30% in NHANES and ~60% in 
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the ARC study). Both reported ~25% decline in PFOA. NHANES reported a 10% decrease in 

PFHxS while the ARC study reported a 30% drop. Conversely, PFNA increased by 

approximately 50% over 4 years in NHANES and by 100% over 6 years in the ARC study. 3M 

also reported a 100% increase in PFDeA, while the increase in NHANES was 60%. 3M reported 

an 80% increase in PFUA. 

It appears that most of PFAS and PFAC do not vary much across adolescents 

participating in NHANES; however, pooled data from 2001-2002 indicate that most of the levels 

of perfluorinated compounds are higher in children ages 3-11 years compared to adults 

(individual samples 2001-2002), especially for PFHxS (Kato, 2009). More recent data on 

children are not available. 

It is clear that there are individuals who have been exposed to perfluorinated compounds 

at levels much higher than the majority of the population. Recent data indicate that individuals 

living near a U.S. facility that uses PFOA may have much higher PFOA serum concentrations 

than those currently reported for the general population (Calafat, 2007; Emmett, 2006). 

Presence in the Environment and Wildlife

Water 

Log Kow values for PFOA, PFOS and other commercially available ammonium salts 

range from -0.52 to > 6.8 (De Silva, 2008; Tomlin, 2005) and have water solubilities that range 

from 0.10 to > 500,000 (Hekster, 2003; Kissa, 2001). Long-chain PFAC have been measured in 

surface waters of remote areas such as the north shore of Lake Superior, the Hudson Bay region 

of Northeastern Canada, tributaries of the Pearl River in Guangzhou, China and the Yangtze 

River. Ice surface samples in the Canadian Arctic (Northwest Territories and Nunavut) had 

levels of that ranged from 5-246 pg/L for C9-C11 compounds. 

Multiple studies have reported a global distribution of PFAC and PFAS that have been 

reported in wildlife tissue and blood samples. PFAS have also been found in a variety of aquatic 

organisms. Most recently, four perfluorinated analytes (PFOS and PFAS: C10, C11, and C12) 

were found in fillets from bluegill in selected rivers in Minnesota and North Carolina (Delinsky, 

2009). In general, the highest concentrations in wildlife have been found in the livers of fisheating animals close to industrialized areas. 

Soil and Sediment 

PFOA and PFOS are considered to be resistant to degradation in soil. Levels of C9-C11 

PFAC have been found in remote Arctic region sediment ranging from 0.68 μg/kg – 2.58 μg/kg. 

PFAC are known to increase over time in sediment as observed in a 22-year study (1980-2002) 

of the Niagara River discharge. Sediment dwelling invertebrates such as amphipods, zebra 

mussels, and crayfish have also been found to have PFOA concentrations ranging from 2.5 – 90 

ng/g ww in the Raisin, St. Clair, and Calumet Rivers (MI)(Kannan, 2005). At the 3M Decatur, 

AL. site, PFOA concentrations in Asiatic clams ranged from 0.51 ng/g to 1.01 ng/g. Mussels and 
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oysters in Tokyo Bay were found to contain PFOA concentrations 0.660 ng/g ww and worms 

from the Ariake Sea in western Japan had concentrations of PFOA of 82 ng/g ww. 

PFAS and PFAC are Persistent, Bioaccumulative, and Toxic 

Persistence and Bioaccumulation in Humans and Laboratory Animals

Animal studies of the straight-chain PFAS and PFAC have shown that these compounds 

are well absorbed orally, but poorly eliminated; they are not metabolized, and they undergo 

extensive uptake from enterohepatic circulation. Studies of PFOS and PFOA have shown that 

these compounds are distributed mainly to the serum, kidney, and liver, with liver concentrations 

being several times higher than serum concentrations; the distribution is mainly extracellular. 

Both compounds have a high affinity for binding to B-lipoproteins, albumin, and liver fatty acidbinding protein. Studies have reported PFOS, PFOA, and several other PFAS and PFAC in 

umbilical cord blood indicating these chemicals cross the placenta. 

The elimination half-lives of several PFAS and PFAC are summarized in Table 1. In 

general, the rate of elimination decreases with increasing chain length, although the half-life of 

PFHxS (C6) is longer than the half-life of PFOS (C8) in humans. There is a tremendous species 

difference in elimination, and elimination is greatly reduced in humans. Thus, the half-life of 

PFOS is 7 days in rats, 150 days in monkeys, and 5.4 years in humans. There is a gender 

difference in the elimination of PFOA and other PFAC in laboratory animals. Studies of PFOA 

in rats have shown that the gender difference is developmentally regulated, and the adult pattern 

is achieved by sexual maturation. The reason for the species and gender differences in 

elimination are not well understood. These differences are hormonally controlled, and may also 

be due to the actions of organic anion transporters. A gender difference has not been found in 

humans, although uncertainty exists due to the small sample size. 

Table 1. Comparative Rates of Elimination*

Serum 

Half-life 

PFHxS 

(C6) 

PFOS 

(C8) 

PFOA 

(C8) 

PFNA 

(C9) 

PFDA 

(C10) 

Rat 7 days 2-4 hours 

6-7 days

2 days 

31 days 

59 days 

40 days 

Mouse 16 days 

22 days 

41 days 

64 days 

Monkey 87 days 

141 days 

150 days 30 days 

21 days 

 

Human 8.5 years 5.4 years 2.3-3.8 

years 

 

*Red – females; blue - males 

Regardless of chain length, it is critical to note that the half-lives of these compounds are 

measured in hours to days to months in rats, mice and monkeys, but years in humans. This means 

that these compounds will persist and bioaccumulate in humans, and comparatively low 

exposures can result in large body burdens. The gender and species differences in elimination 
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also indicate that comparisons of toxicological effects must utilize some measure of body burden 

rather than administered dose. 

Persistence and Bioaccumulation in the Environment

PFOS and longer chain PFAC (> C8) bioaccumulate and persist in protein-rich 

compartments of fish, birds, and marine mammals such as carcass, blood, and liver (Conder, 

2008). Studies have found fish bioconcentration factor (BCF) values for C8 to C14 PFAC 

ranging from 4 – 40,000 in rainbow trout (Martin, 2003). Fish BCF values for C8-C11 PFAS are 

relatively lower (4-4900). There are two BCF study results for long chain PFAC with BCF 

values from 4,7000 to 4,800 for perfluorohexadecanic acid (C16) in carp and BCF values from 

320 to 430 for perfluorooctadecanoic acid (C18) in carp (Martin, 2003). Available evidence 

shows the likely potential for bioaccumulation or biomagnifications in marine or terrestrial 

species. This is due to conformational changes into a helical structure in the molecule resulting in 

a smaller cross-sectional diameter as chain length increases which can lead to the ability to 

accumulate in organisms (NITE, 2002a, 2002b). Additional evidence that C14 and C15 PFAC 

bioaccumulate and are bioavailable is their presence in fish, invertebrates, and polar bears. The 

bioaccumulation of PFOS and PFAC (C8 through C14) in air-breathing animals (e.g., birds and 

mammals) is thought to represent biomagnification due to high gastrointestinal uptake and slow 

respiratory elimination (B. Kelly, MG Ikonomou, JD Blair, B Surridge, F Hoover, R Grace, APC 

Gobas 2009; B. C. Kelly, Ikonomou MG, Blair JD, Morin AE, Gobas APC, 2007). In addition, 

Conder et al. state that the bioaccumulation and bioconcentration potential of PFAC are directly 

related to the length of the perfluorinated chain, and PFAS are more bioaccumulative than PFAC 

of the same chain length(Conder, 2008). 

Within the PFAC and PFAS categories, the perfluorinated carboxylic and sulfonic acids 

(Rf from C5 to C20) are persistent chemicals that are resistant to degradation under 

environmental conditions. Even the reaction of PFAS/PFAC precursors with hydroxyl radicals in 

the atmosphere are considered to be so slow that long range transport is considered a viable 

exposure pathway (Hurley, 2004; G. W. Olsen, DC Mari, WK Reagen, ME Ellefson, DJ 

Ehresman, JL Butenhoff, LR Zobel, 2007). 

Toxicity in Humans

Until recently, epidemiological and medical surveillance studies have been conducted 

primarily in the United States on workers occupationally exposed to POSF-based 

fluorochemicals. These studies specifically examined PFOS or PFOA exposures and possible 

adverse outcomes. One occupational study of exposures to a PFNA surfactant blend was 

undertaken. The studies on PFOS and PFOA include mortality and cancer incidence studies, a 

study examining potential endocrine effects, an ‘‘episodes-of-care’’ study evaluating worker 

insurance claims data, and worker surveillance studies examining associations between primarily 

PFOS and/or PFOA serum concentrations and hematology, hormonal and clinical chemistry 

parameters. The PFNA study examined liver enzymes and blood lipid levels. In general, no 

consistent association between serum fluorochemical levels and adverse health effects has been 

observed. 
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Toxicity in Laboratory Animals

PFOA 

The toxicity of PFOA has been extensively studied. Repeated-dose studies in rats have 

shown reduced body weight, hepatotoxicity, reduced cholesterol, and a steep dose-response 

curve for mortality. Due to gender differences in elimination, adult male rats exhibit effects at 

lower administered doses than adult female rats. Thus, dietary exposure for 90 days resulted in 

significant increases in liver weight and hepatocellular hypertrophy in female rats at 1000 ppm 

(76.5 mg/kg-day) and in male rats at doses as low as 100 ppm (5 mg/kg-day). Studies in 

nonhuman primates have shown similar effects at doses as low as 3 mg/kg-day, although the 

reduction in cholesterol has not been observed. 

The carcinogenic potential of PFOA has been investigated in two dietary carcinogenicity 

studies in Sprague-Dawley rats, and has been shown to induce hepatocellular adenomas, Leydig 

cell tumors, and pancreatic acinar tumors. It has not been shown to be mutagenic in a variety of 

assays. There is sufficient evidence to indicate that PFOA is a PPARα-agonist and that the liver 

carcinogenicity (and toxicity) of PFOA is mediated by PPARα in the liver in rats. There is no 

evidence that the liver toxicity in nonhuman primates is due to PPARα-agonism. There is 

controversy over the relevance of this particular mode of action for humans. The mode of action 

for the Leydig cell tumors and pancreatic acinar tumors has not been established, and therefore 

these are assumed to be relevant for humans. 

Several studies have shown that PFOA is immunotoxic in mice. PFOA causes thymic 

and splenic atrophy, and has been shown to be immunosuppressive in both in vivo and ex vivo

systems. Studies using transgenic mice showed that the PPARα was involved in causing the 

adverse effects to the immune system. 

Standard prenatal developmental toxicity studies in rats and rabbits in which pregnant 

animals are exposed only during gestation and sacrificed prior to the birth of the pups have not 

shown many effects. Thus, there was no evidence of developmental toxicity after exposure to 

doses as high as 150 mg/kg-day in an oral prenatal developmental toxicity study in rats. In a rat 

inhalation prenatal developmental toxicity study, the NOAEL and LOAEL for developmental 

toxicity were 10 and 25 mg/m3, respectively. In a rabbit oral prenatal developmental toxicity 

study there was a significant increase in skeletal variations after exposure to 5 mg/kg-day, and 

the NOAEL was 1.5 mg/kg-day. 

However, the potential developmental toxicity of PFOA is evident when the pups are 

evaluated during the postnatal period. Thus, a two-generation reproductive toxicity study in rats 

showed a reduction in F1 pup mean body weight during lactation at 30 mg/kg-day group and 

during the post-weaning period at 10 mg/kg-day. In addition, there was a significant increase in 

mortality mainly during the first few days after weaning, and a significant delay in the timing of 

sexual maturation for F1 male and female pups at 30 mg/kg-day. 
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Due to the rapid elimination of PFOA in female rats, many researchers have examined 

the developmental toxicity of PFOA in mice. These studies have shown a pattern of 

developmental effects similar to those observed with PFOS. Full liter resorptions were noted at 

40 mg/kg-day and the percent of live fetuses and fetal body weight were reduced at 20 mg/kgday. The most notable effect of prenatal exposure to PFOA was the severe compromise of 

postnatal survival at doses as low as 5 mg/kg-day, and the postnatal growth impairment and 

developmental delays noted among the survivors; the BMD5 and BMDL5 for neonatal survival 

were estimated at 2.84 and 1.09 mg/kg-day, respectively. Additional studies in mice have shown 

that PFOA exposure causes a significant reduction in mammary glad differentiation in the dams 

and stunted mammary gland development in the female pups. 

Several studies have examined the mode of action for the developmental effects. These 

have shown that exposure to a dose of 20 mg/kg-day for 2 days late in gestation is sufficient to 

cause the neonatal mortality in mice. Studies with PPARα knockout mice have shown that the 

PPARα is required for the neonatal mortality and expression of one copy of this gene is 

sufficient. This is in contrast to the studies showing that PPARα is not involved in the neonatal 

mortality associated with PFOS exposure. Although there is controversy over the human 

relevance of the PPARα-agonist hepatotoxicity observed in rodents, the role of PPARα in 

development and particularly in the PFOA-induced neonatal mortality observed in mice is 

unknown; therefore this mode of action is assumed to be relevant for humans. 

Other PFAC Chemicals 

Although there is an extensive database for PFOA, few studies have examined the 

toxicity of the shorter or longer chained PFAC. However, the data suggest that the toxicity 

profile is quite similar to that of PFOA, albeit at different dose levels presumably due to the 

differences in elimination half-life. 

Although standard repeated-dose toxicity studies have not been conducted on the PFAC 

with chain lengths greater than PFOA, many studies have been conducted examining the 

potential for hepatomegaly and peroxisome proliferation (a marker for the activation of PPARα). 

Kudo et. al. found that PFOA, PFNA, and PFDA induced the activity of peroxisomal Boxidation in male rats (2000). Kudo et al. showed that all PFAC with six- to nine-carbon length 

chains induced hepatomegaly and peroxisomal B-oxidase activity in mice, and the potency was 

in the order of PFNA > PFOA > perfluoroheptanoic acid (2006). Permadi et al. also showed that 

PFDA induces hepatomegaly and hepatic peroxisomal palmitoyl-CoA oxidase (1993). Thus, 

these studies indicate that the PFAC with a carbon chain length of eight and greater activate 

PPARα. The differences in potency probably reflect the differences in the half-life of the varying 

chain lengths. Despite the lack of traditional toxicity studies, it is likely that these compounds 

would produce similar effects as those observed with PFOA. 

With respect to the potential developmental effects of PFAC with carbon chain lengths 

greater than C8, are completing a developmental toxicity study of PFNA in mice (C. Lau, 

personal communication, 2009). Maternal body weight gain was reduced at 3 mg/kg-day, and 

severe toxicity was observed at 10 mg/kg-day. Neonatal survival was compromised at 5 mg/kg-
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day, and significant lags in neonatal growth were observed at 3 mg/kg-day. Thus, this study 

shows a pattern of effects very similar to those observed with PFOA. It is likely that PFAC with 

carbon chain lengths greater than nine would also result in similar effects, and that the potency 

would be dependent on the half-life of the compound. 

PFOS 

The toxicity of PFOS has also been extensively studied and was summarized in OECD 

report (2002) and by Lau et al. (). Repeated-dose studies in rats and nonhuman primates have 

shown reduced body weight, hepatotoxicity, reduced cholesterol, and a steep dose-response 

curve for mortality. These effects occur in nonhuman primates at doses as low as 0.75 mg/kgday, and in rats at 2 mg/kg-day. 

The carcinogenic potential of PFOS has been investigated in a dietary carcinogenicity 

study in Sprague-Dawley rats, and has been shown to induce hepatocellular adenomas at 20 ppm. 

In addition, thyroid follicular cell adenomas were observed in male rats that had been allowed to 

“recover” for a year following treatment for one year; the reason for this is unclear. However, 

thyroid follicular tumors have also been observed in rats exposed to N-EtFOSE, a major 

precursor of PFOS. PFOS has not been shown to be mutagenic in a variety of assays. Although 

PFOS can activate PPARα, the data are not sufficient to establish a PPARα-agonist mode of 

action for the liver tumors. 

A standard prenatal developmental toxicity study in rats has shown a significant decrease 

in fetal body weight and significant increase in external and visceral anomalies, delayed 

ossification, and skeletal variations; a NOAEL of 1 mg/kg-day and a LOAEL of 5 mg/kg-day for 

developmental toxicity were indicated. In rabbits, significant reductions in fetal body weight and 

significant increases in delayed ossification were observed; a NOAEL of 1.0 mg/kg-day and a 

LOAEL of 2.5 mg/kg-day for developmental toxicity were indicated. 

A two-generation reproductive toxicity study in rats showed neonatal mortality. All F1 

pups at the highest dose of 3.2 mg/kg-day died within a day after birth, while close to 30% of the 

F1 pups at 1.6 mg/kg-day died within 4 days after birth. As a result of the pup mortality in the 

two top dose groups, only the two lowest dose groups, 0.1 and 0.4 mg/kg-day, were continued 

into the second generation. The NOAEL and LOAEL for the F2 pups were 0.1 mg/kg-day and 

0.4 mg/kg-day, respectively, based on reductions in pup body weight. 

The results of this study prompted additional research. Studies in which pregnant rats and 

mice were dosed during gestation and the pups were followed postnatally provided a BMD5 and 

BMDL5 for neonatal survival of 1.07 and 0.58 mg/kg-day in rats, respectively, and 7.02 and 3.88 

mg/kg-day in mice, respectively. Studies have shown that the critical period of exposure is 

during late gestation. Mode of action studies initially focused on the lung and found significant 

histological and morphometric differences in the lungs of pups treated with PFOS. However, 

subsequent studies did not find any effect on lung phospholipids and rescuing agents failed to 

mitigate the neonatal mortality. Thus, the mortality does not appear to be related to lung 

immaturity. In contrast to PFOA, studies with PPARα knockout mice have shown that the 
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PPARα is not involved in the neonatal mortality. Current research is focusing on the possibility 

that the physical properties of PFOS may interfere with the normal function of pulmonary 

surfactant, leading to neonatal mortality.

Other PFAS Chemicals 

A combined reproductive/developmental toxicity study of PFHxS has been conducted in 

rats. In the parental males there was a significant reduction in cholesterol at doses as low as 0.3 

mg/kg-day, and hepatotoxicity at doses as low as 3 mg/kg-day. There was no evidence of 

developmental or reproductive toxicity at doses as high as 10 mg/kg-day. 

Toxicity to Wildlife

Adverse effects on exposed populations of organisms have been observed with exposure 

to perfluorinated compounds in the parts per million range. Studies have shown a reduction in 

hatchability of chickens when they were exposed in ovo to PFOS, and a reduction in survival in 

14-day old Northern bobwhite quail from hens exposed to 10 ppm of PFOS in the diet. In 

addition, a delay in growth and metamorphosis in the Northern leopard frog exposed to 3 mg/L 

of PFOS has been reported, as well as reduced cumulative fecundity and fertility effects in 

fathead minnows exposed to 0.1 mg/L PFOS. Further evidence of potential reproductive effects 

has been observed with exposure to C9-C11 PFAC. A significant induction of vitellogenin in 

rainbow trout was observed in a dose-dependent manner at concentrations of C10 PFAC 0.0256-

2000 μg/g in the diet as well as a weak affinity demonstrated for the hepatic estrogen receptor 

from C9-C12 PFAC. 

Mortality in sediment dwelling organisms such as the nematode, Caenorhabditis elegans

has been observed with concentrations of C9 up to 0.66 mM and subsequent effects in offspring 

generations were found at concentrations up to 1nM as evidence by a 70 % decline in fecundity. 

VI. Fate Characterization Summary

The PFAS and PFAC acids are strong acids that exist in equilibrium between the neutral 

form and the anionic form. Both the anionic and neutral forms of PFOA are soluble in water. 

While the Henry’s law constant values suggests partitioning to air for the neutral, protonated 

form, predicting the amount that partitions into air is complicated because there is uncertainty 

over the degree to which carboxylic and sulfonic acids partition from the water to atmosphere. 

The uncertainty arises with regard to the value of the acid dissociation constant (i.e., pKa), or the 

fraction of the acid form present at environmentally relevant pH. PFAC and PFAS have been 

detected in air, water, and soil samples collected throughout the world. The oceans have been 

suggested as the final sink and route of transport for perfluorinated carboxylic and sulfonic acids, 

where they have been detected on the surface and at depths > 1,000 meters(Yamashita, 2005). 

Some PFAS/PFAC have the potential for long-range transport. They are transported over 

long distances (i.e., long-range transport) by a combination of dissolved-phase ocean and gasphase atmospheric transport; however, determining which is the predominant transport pathway 
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is complicated by the uncertainty over water to atmosphere partitioning. Furthermore, there is 

evidence that transport and subsequent oxidation of volatile alcohol PFAS/PFAC precursors may 

contribute to the levels of PFAS / PFAC in the environment. 

In addition to perfluoro carboxylic acids and perfluoro sulfonates, a number of other 

chemicals with perfluorinated moieties have been and continue to be used in a wide variety of 

industrial and consumer applications. When these chemicals are released intentionally or 

unintentionally through manufacturing, use, and disposal, they can be degraded in the 

environment or be metabolized in organisms to form perfluoro carboxylic acids and perfluoro 

sulfonates. Limiting exposure to PFAC and PFAS will require limiting both the exposure to 

these precursors and the release of precursors that will form PFAC and PFAS in the 

environment. 

Studies by industry and academic researchers have shown that fluorotelomer alcohols 

(FTOH) can be degraded by microorganisms and by abiotic processes. 8-2 FTOH and FTOH of 

other chain lengths, and related chemicals in mixed microbial cultures, activated sludge and soil 

systems have been shown to be easily degraded to form PFOA and related perfluorinated acids. 

Some studies have also shown that –CF2- groups can be mineralized, forming shorter chain 

perfluoro acids. If FTOH are absorbed from ingestion, inhalation, dermal or ocular exposure or 

formed in vivo by from other compounds they can be metabolized by mammals and other 

organisms to form perfluorinated acids and other fluorinated compounds. FTOH can be degraded 

by abiotic processes in water and air to produce PFAC and various intermediates. FTOH are 

fairly volatile. Based on atmospheric half-lives determined in chamber studies, FTOH can be 

transported globally. Deposition or degradation in areas far from the source can result in PFAC 

contamination in high latitudes and other remote locations and contribute to global background 

levels of PFAC and PFAS. 

Data submitted by industry and in the open literature show that perfluorooctane sulfonyl 

fluoride (POSF) and its derivatives can be degraded under environmental conditions to form 

perfluoroalkyl sulfonates and carboxylic acids. Reaction of POSF (CF3(CF2)n-SO2F) with methyl 

or ethyl amines is used to produce N-ethyl or N-methyl perfluorooctane sulfonamidoethanols 

(FOSE). Similar reactions are used to make shorter and longer chain analogs to POSF and POSF 

derivatives. FOSE compounds, (or CF3(CF2)n-SO2N(R1)(R2), where R1 and R2 can be 

hydrogen, methyl or longer alcohols or other organic chains), such as N-methyl and N-ethyl 

FOSEs can be degraded though a series of intermediates to form both perfluoro carboxylic acids 

and perfluoroalkyl sulfonates. Data on the degradation of individual intermediates has been used 

to identify these pathways and has confirmed that these compounds can be degraded by a 

number of microbial and abiotic mechanisms. Reaction with other chemical intermediates 

produces other FOSA derivatives, including phosphate esters, fatty acids esters, silanes, 

carboxylates, and polymers with acrylate, urethane and other linkages. Longer and shorter chain 

perfluoro sulfonyl derivatives have also been produced intentionally and as unintended reaction 

products. Based on existing data from the open literature and CBI data, it is expected that that 

most, if not all, of these POSF and other chain length sulfonyl fluorides and their derivatives will 

be degraded to carboxylic acids and/or sulfonate over time. Most of these compounds will have 

environmental and metabolism half-lives of week to months. Some will be degraded faster and 
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some will persist for longer, but all will eventually be degraded. 

Very little data is available on the behavior of other perfluorochemicals in the 

environment and in vivo but the existing data suggest that they will also be degraded to form 

PFAC. For example, recent studies have shown that ingested mono and di polyfluoroalkyl 

phosphates (PAPs) can be degraded in rats to form PFOA and other PFAC in the body. They can 

also be degraded by microbial processes in soil and wastewater to form perfluorinated 

acids(D'eon, 2007). 

A limited number of studies on the degradation of fluorotelomer-based polymers have 

been submitted in support of PMN submissions and existing chemicals, and published in the 

open literature. Based on studies conducted using rigorous methods that are believed to have 

yielded valid data, some fluorotelomer-based polymers are subject to hydrolysis, photolysis and 

biodegradation to some extent. Studies have shown half-lives of a few days to hundreds of years. 

In addition, preliminary research on degradation of fluorotelomers has shown that some 

urethanes and acrylates biodegrade; however, half-lives and kinetics of the fluorotelomers are 

not yet well-defined. The ongoing EPA’s Office of Research and Development (ORD) research 

is designed to generate high quality data that will help the Agency address some key 

uncertainties in pathways of exposure and potential risks from PFOA (Washington, 2009). 

These studies have shown that the perfluorinated portion of some polymers is released as 

the polymer is degraded by microbial or abiotic processes to form telomer alcohols or other 

intermediates and that they eventually form PFAC. Polymers based on POSF and other chain 

length chemistries show similar degradation rates and release intermediates which further 

degrade to form perfluorinated acids and sulfonates. Studies have shown that some polymers can 

undergo indirect photolysis in soil and in aquatic systems and be degraded with half-lives of days 

to several years. 

VII. Exposure Characterization Summary

The pattern of PFAS and PFAC contamination varies with location and among species, 

which suggests multiple sources of emission and patterns of migration into environmental media 

from the sources of emission. Major pathways that enable PFOA and PFOS to get into human 

blood in small quantities are not yet fully understood. Manufacturing releases are known to have 

contaminated local drinking water supplies in the immediate vicinity of some industrial plants, 

leading to localized elevated blood levels. The widespread presence of PFOA and PFOS 

precursors in human blood samples nationwide suggests other pathways of exposure, possibly 

including long range air transport, and the release of PFOA and PFOS from treated articles. 
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Summary of Exposure to Consumers and Children from PFCs in Indoor Environments

PFCs in Articles of Commerce 

EPA's ORD has conducted research on 116 articles of commerce documenting that PFCs 

contained in articles of commerce have the potential to be released from those articles. Articles 

tested and found to contain the highest levels of PFAC were carpet and carpet treatment 

products, various types of apparel, home textiles, thread sealant tape, floor wax and other 

sealants, and food contact paper and paper coatings. Carpet and carpet treatment products 

contained individual PFAC in levels from 0.04-14100 ng/g; food contact paper and paper 

coatings: 0.05-160,000 ng/g; thread sealant tape and apparel: ND (non-detect)-3488 ng/g and 

ND-4640ng/g respectively; floor wax and sealer: 0.03-3720 ng/g; and home textiles: ND-519 

ng/g. Some of the more commonly found PFAC measured in these articles were PFHxA, 

PFHpA, PFNA, PFDA, PFUnDA, PFOA and PFOS. Inhalation levels of PFOA and total PFCs 

measured in carpet were 5385 pg/cm3

 and 32500 pg/cm3 respectively (Guo, 2009).

Children are particularly susceptible to exposure from inhalation of PFC off-gassing from 

carpet and carpet protectants during their earliest years when they are lying, crawling and 

spending large amounts of time playing on the carpet. The significantly high levels of PFC found 

by ORD in carpet and carpet protectants pose an exposure concern for children through this 

pathway. Adults can also be exposed to PFCs in carpets through inhalation and dermal contact. 

Consumers and children may also be exposed to PFCs in apparel, home textiles, thread sealant 

tape, floor wax, contact paper and paper coatings. Some of these articles such as paper coatings 

for foods cannot be ruled out for the ingestion exposure pathways for children and adults 

depending upon how the PFCs in the paper contacts the food and subsequently humans. 

PFCs in Indoor Air 

Another source of PFCs to the indoor environment is dust containing not only PFAC and 

PFAS but also fluorotelomer alcohols. Maximum indoor dust air measurements of 6:2 FTOH 

were found at 804 ng/g in the eastern United States (Strynar, 2008). The PFAS (ET-FOSA, EtFOSE, MeFOSE) chemicals were measured at 646 ng/g, 75440 ng/g, and 8860 ng/g respectively 

in indoor air in Canada (Shoeib, 2005). PFOA was found at 3700 ng/g in Japanese household 

vacuum cleaner dust (Moriwaki, 2003). 

Summary of Exposure to the General Population

PFCs in Groundwater, Freshwater, Saltwater, and Rainwater 

PFAC and PFAS have been found in many countries as well as in Unites States in 

untreated groundwater, rivers, streams, bays, estuaries, oceans and rain water. Levels of PFAC in 

groundwater near the 3M Cottage Grove, MN industrial site have been measured as high as 

846,000 ng/l (PFOA) and in freshwater as high as 178,000 ng/l (PFBA) (Department of Health 

and Human Services, 2005). PFOS has been found near Cottage Grove, MN in groundwater at 
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levels of 371,000 ng/l and in freshwater at 18,200 ng/l. PFAC in rainwater has been measured in 

the United States between 0.1 and 1006 ng/l (PFHpA) (Scott BF, 2006). 

Saltwater levels of PFOS have been measured in the Pacific Ocean at 57,700 ng/l and in 

precipitation from snow and rain in China at 545 ng/l (Liu W, 2009; Yamashita, 2005). While 

the general population may not directly ingest these groundwater, freshwater and saltwater levels 

as drinking water, the ground water and freshwater containing PFCs may discharge to surface 

waters from which municipalities withdraw drinking water. The general population may also 

experience dermal, ingestion and inhalation exposures when coming into contact with freshwater 

containing PFCs. Rainwater containing PFCs may contribute PFCs to vegetables and fruits in 

home gardens, crops grown on commercial crop lands, drinking water reservoirs, and surface 

waters from which drinking water is withdrawn. 

PFCs in Freshwater and Saltwater Fish 

Freshwater fish have been found to contain levels of PFAS and PFAC. The highest levels 

of PFAS measured in the United States to date were near the 3M Cottage Grove, MN site (Oliaei 

F, 2006). Liver samples of bass, walleye and carp ranged from 130-6350 ng/g PFOS wet weight. 

Blood samples of these same fish ranged from PFOS levels of 136-29600 ng/ml in serum. Total 

PFCs for the blood of freshwater fish in the same area was measured at 32248 ng/ml serum. The 

highest levels of PFAC for freshwater fish were found near the 3M Cottage Grove, MN site and 

were measured for blood samples of bass, walleye, and carp in the range of 2.53-210 ng/ml 

serum. For comparison, saltwater fish in Danish seas had measured levels of PFOS up to 156 

ng/g and saltwater fish in Charleston Harbor South Carolina were found with PFOS levels up to 

101 ng/g (Bossi R, 2005; Houde M, 2006). 

VIII. Risk Management Considerations

Current Risk Management Summary

PFAS Chemicals 

Following the voluntary 3M phase-out of PFAS chemicals in the United States in 2002, 

EPA issued SNURs to control the reintroduction of these chemicals into the U.S. market. Final 

rules were published on March 11, 2002 (EPA, 2002b) and December 9, 2002 (EPA, 2002a), to 

limit any future manufacture or importation of 88 PFAS chemicals specifically included in that 

phase-out. Furthermore, on October 9, 2007, EPA published another SNUR on 183 additional 

PFAS chemicals (EPA, 2007). Those actions were necessary because data showed that certain 

alkyl chain lengths of the PFAS chemicals are toxic to human health, bioaccumulate, and are 

persistent in the environment. PFAS chemicals are no longer manufactured in United States. 

However a limited set of existing uses was excluded from the SNURs because alternatives are 

not yet available. 

Similar to the PFAS SNURs in United States, PFOS has also been restricted in the 

European Union, Canada, Australia and other countries, and has been nominated for inclusion in 
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the Stockholm Convention and the Convention on Long-Range Transboundary Air Pollution 

(LRTAP) Persistent Organic Pollutants (POPs) protocol. At the fourth Conference of the Parties 

(COP) to the Stockholm Convention on POPs, held in May 2009, delegates agreed to add PFOS, 

its salts, and perfluorooctane sulfonyl fluoride (PFOSF) to Annex B, subjecting it to restrictions 

on production and use. Parties agreed that while the ultimate goal is the elimination of PFOS, 

production of the chemical may continue for limited purposes, including coatings for 

semiconductors, firefighting foam, photo imaging, aviation hydraulic fluids, metal plating, and 

certain medical devices. Countries must notify the Convention Secretariat whether they intend to 

continue production for acceptable purposes. Countries can also ask for specific exemptions 

allowing the production of PFOS for use in the production of chemical substances used in goods 

such as carpets, leather and apparel, textiles, paper and packaging, coatings, and rubber and 

plastics(POPs, 2009). 

PFAC Chemicals 

OPPT’s core strategy for working towards the elimination of PFAC chemicals has been 

through the PFOA Stewardship Program. Under the program, eight major companies operating 

in the United States committed to reduce global facility emissions and product content of PFAC 

chemicals by 95 percent by 2010, and to work toward eliminating emissions and product content 

by 2015 (EPA, 2009a). Companies provide annual progress reports, and most companies have 

reported significant progress in meeting program goals. 

On March 7, 2006, EPA published a proposal to amend the polymer exemption rule to 

exclude from eligibility for the exemption polymers containing certain perfluoroalkyl moieties 

(EPA, 2006). Under this proposal, polymers containing these perfluoroalkyl moieties would need 

to go through the pre-manufacture notification (PMN) review process so that EPA can better 

evaluate these polymers for potential effects on human health and the environment. This change 

to the current regulation is necessary because, based on current information, EPA can no longer 

conclude that these polymers “will not present an unreasonable risk to human health or the 

environment” under the terms of the polymer exemption rule, which is the determination 

necessary to support an exemption under section 5(h)(4) of TSCA. This amendment to the 

polymer exemption rule is a necessary complement to the PFOA Stewardship Program and will 

give EPA the necessary tools to review and control risk of PFC-based and related polymers, 

including those PFAS/ and PFAC containing polymers. 

In January 2009, EPA’s Office of Water (OW) developed Provisional Health Advisory 

(PHA) values for PFOA and PFOS to mitigate potential risk from exposure to these chemicals 

through drinking water (EPA, 2009c). Due to limited information on the toxicity of PFCs other 

than PFOA and PFOS, no attempt was made by OW at that time to develop Provisional Health 

Advisory (PHA) values for the other PFCs. OPPT and OW are working together to determine 

whether revised health advisory values are needed for PFOA and PFOS. 

In October 2009, EPA’s Office of Solid Waste and Emergency Response (OSWER) used 

OW’s PHA’s to derive sub-chronic RfD values for PFOA and PFOS. These values may be used 
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in the Superfund program's risk-based equations to derive Removal Action Levels and/or 

Screening Levels for water and other media, as appropriate. 

EPA has taken the leadership role in raising the profile of PFCs at an international level 

stemming from Agency concerns about the role of long range transport in the environmental 

distribution of PFCs, and U.S. importation of products containing these chemicals (UNEP, 

2009b). As a result of these activities, in May 2009, during the International Conference on 

Chemicals Management (ICCM2), delegates to the Strategic Approach to International 

Chemicals Management (SAICM) agreed to consider the development of stewardship programs 

and regulatory approaches to reduce emissions and content of PFAC and PFAS chemicals in 

products and to work towards their elimination, where feasible (UNEP, 2009a). 

Remaining Issues and Concerns

PFAS Chemicals 

PFAS chemicals are no longer manufactured in United States but continue to be 

manufactured outside of United States. Although the PFAS SNURs are an important step toward 

controlling any future manufacture or import of PFAS chemicals, these chemicals may continue 

to be imported into United States in articles, such as carpets, leather and apparel, textiles, paper 

and packaging, coatings, and rubber and plastics. 

Possible scenarios of concern: 

o Direct releases to the environment from U.S. facilities as a result of few existing uses. 

o Direct releases to the environment from non-U.S. facilities, resulting in transboundary 

environmental transport to United States. 

o Articles containing PFAS chemicals. Recent research by EPA’s ORD has shown that 

consumer articles could release PFCs, significantly increasing the magnitude and duration of 

exposure to humans and the environment to these chemicals. 

PFAC Chemicals 

Although the 2010/15 PFOA Stewardship Program is expected to eliminate the 

production of C8-based fluorotelomers by the eight participating companies by 2015, the 

potential remains for continued environmental and human loading of PFAC in the United States. 

This is in part because companies not participating in the PFOA Stewardship Program are 

expected to seize the market opportunity presented when the eight PFOA Stewardship Program 

companies leave the PFAC market by 2015. This occurred with PFAS production in some Asian 

countries after the 3M 2002 phase-out of PFAS chemicals in United States (Wenya, 2008). 

Possible scenarios of concern: 

o Direct releases to the environment from U.S. facilities not participating in PFOA 

Stewardship Program. 

o Direct releases to the environment from non-U.S. facilities not participating in PFOA 

Stewardship Program, resulting in transboundary environmental transport to United States. 
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o Articles, including imports, containing PFAC chemicals. These articles could release PFAC 

as a result of their residual content in fluorotelomer-based products and/or as the 

fluorotelomers-based polymers in articles biodegrade. 

IX. Next Steps

To date, significant adverse effects have not been detected in humans. However, given 

the long half-life of these chemicals in humans (years), it can reasonably be anticipated that 

continued exposure could increase body burdens to levels that would result in adverse outcomes. 

Consequently, EPA intends to propose actions in 2012 under TSCA to address the potential risks 

from long-chain PFCs. 

EPA intends to initiate a TSCA § 6 rule for managing long-chain PFCs. If EPA can make 

certain findings with respect to these chemicals, TSCA section 6 provides authority for EPA to 

ban or restrict the manufacture (including import), processing, and use of these chemicals. A rule 

addressing the PFAS sub-category could expand the reach of three SNURs that the Agency has 

promulgated over the past decade. For example, the rule could address PFAS-containing articles. 

A rule addressing the PFAC category could expand the reach of the 2010/15 PFOA Stewardship 

Program beyond the eight participating companies and further address the concerns for potential 

PFAC exposure through the use of PFAC-containing articles. 

As part of the Agency's efforts to address PFCs, EPA also intends to evaluate the 

potential for disproportionate impact on children and other sub-populations. Given that 

NHANES and other data have demonstrated that humans are exposed to PFCs in utero, as 

babies, and during puberty, and that animal studies have shown that the fetus and neonate are 

sensitive life stages to PFC exposures, EPA will consider effects to the developing fetus and 

children. 

X. References

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sulfonate (PFOS) and other fluorochemicals in fish, birds, and marine mammals from Greenland and the Faroe 

Islands Environmental Pollution, 136(2), 323-329. 

Calafat AM, Wong LY, Kuklenyik Z, Reidy JA, Needham LL (2007). Polyfluoroalkyl chemicals in the U.S. 

Population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and 

comparisons with NHANES 1999-2000. . Environmental Health Perspective, 115(11), 1596-1602. 

Canada (2006). Ecological Screening Assessment Report on Perfluorooctane Sulfonate, Its Salts and Its Precursors 

that Contain C8F17SO2, C8F17SO3 or C8F17SO2N Moiety. From 

<http://www.ec.gc.ca/CEPARegistry/documents/subs_list/PFOS_SAR/PFOS_TOC.cfm> 

Conder JM., Hoke RA, de Wolf W, Russell MH, Buck, RC (2008). Are PFCAs bioaccumulative? A critical review 

and comparison with regulatory criteria and persistent lipophilic compounds. Environmental Science and 

Technology, 42, 995-1003. 

D'eon JC, Mabury SA (2007). Production of perfluorinated carboxylic acids (PFCAs) from the biotransformation of 

polyfluoroalkyl phosphate surfactants (PAPs): exploring routes of human contamination. Environmental Science 

and Technology, 41(13), 4799-4805. 
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De Silva AO (2008). Perfluorocarboxylate isomer analysis as a tool for source elucidation Unpublished 

Dissertation University of Toronto. 

Delinsky AD, Strynar MJ, Nakayama SF, Varns JL, Ye XB, McCann PJ, Lindstrom AB (2009). Determination of 

ten perfluorinated compounds in bluegill sunfish (Lepomis macrochirus) fillets Environmental Research, 109, 975-

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at the 3M-Cottage Grove Facility, City of Cottage Grove, Washington County, Minnesota. 

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perfluorooctanoate: relationships between serum levels and certain health parameters Journal of Occupational 

Environmental Medicine 48(8). 

EPA (2002a). Perfluoroalkyl Sulfonates; Significant New Use Rule. from <http://www.epa.gov/fedrgstr/EPATOX/2002/December/Day-09/t31011.htm> 

EPA (2002b). Perfluoroalkyl Sulfonates; Significant New Use Rule. . from <http://www.epa.gov/fedrgstr/EPATOX/2002/March/Day-11/t5746.htm> 

EPA (2006). Premanufacture Notification Exemption for Polymers; Amendment of Polymer Exemption Rule to 

Exclude Certain Perfluorinated Polymers. from <http://www.epa.gov/fedrgstr/EPA-TOX/2006/March/Day07/t2152.htm> 

EPA (2007). Perfluoroalkyl Sulfonates; Significant New Use Rule. from <http://www.epa.gov/fedrgstr/EPATOX/2007/October/Day-09/t19828.htm> 

EPA (2009a). 2010/2015 PFOA Stewardship Program from <http://epa.gov/oppt/pfoa/pubs/stewardship/index.html> 

EPA (2009b). New Chemical Review of Alternatives for PFOA and Related Chemicals from 

<http://epa.gov/oppt/pfoa/pubs/altnewchems.html> 

EPA (2009c). Perfluorooctanoic Acid (PFOA) and Perfluorooctance Sulfonate (PFOS): Provisional Health Advisory 

information, from: <http://www.epa.gov/waterscience/criteria/drinking/pha-PFOA_PFOS.pdf>

EPA (2009d). PFOA Risk Assessment from http://www.epa.gov/oppt/pfoa/pubs/pfoarisk.html

Guo Z, Liu X, Krebs K, Roache N (2009). Perfluorinated carboxylic acids (PFACs) in articles of commerce (AOCs) 

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