U.S. Environmental Protection Agency Draft, 12/ 2 9/2009 U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

Long-Chain Perfluorinated Chemicals (PFCs)

I. Overview

Long-chain perfluorinat ed 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 found in humans. the general human population; however, significant adverse effects have been iden tified in laboratory animals and wildlife. G However,

g iven the long half-life of these chemicals in humans (years), it can reas onably be anticipated that continued exposure could increase body burdens to levels that would result in adverse

outcomes.

Since 2000, the Agency has taken various actio ns to help minimize the potential impact of PFCs on human health and the environment, including the publication of three Significant New Use Rules on perfluoroalkyl sulfonate (PFAS) chemicals and the review of substitutes for

these long-chain chemicals PFCs as part of its review proces s for new chemicals under EPA's New Chemicals Program. Although such actions ar e important steps to reducing exposure to these chemicals, EPA continues to be concer ned with long-chain PFCs. Consequently, EPA intends to propose actions in 2012 under the Toxi c Substances Control Act (TSCA) to address the potential risks from long-chain PFCs.

EPA intends to consider initiat ing e a TSCA section § 6 rule making for managing longchain PFCs. If EPA can make certain fi ndings with respect to these chemicals (further analysis of the information will be performed as part of TSCA section§ 6 rulemaking) , TSCA section 6 provides authority for EPA to ban or restrict the manufacture (includi ng import), processing, and

use of these chemicals. A rule addre ssing the PFAS sub-category could expand beyond the reach

of the three SNURs that the Agency has promulgated over the past decade. For example, the rule could address PFAS-containing ar ticles. A rule addressing the perfluoroalkyl carboxylate ( PFAC ) sub- category could expand the reach of the 2010/15 PFOA Stewardship Program beyond the eight participating companies and furt her address the concerns for potential PFAC exposure through the use of PFAC-containing articles. EPA will develop more detailed assessments to support the TSCA section 6(a) "p resents or will present an unreasonable risk" findings. If these more detailed assessments i ndicate that a different approach to risk management is appropriate, EPA w ill consider additional approaches.

Long-chain PFCs are a concern for children’s he alth. Studies in laboratory animals have demonstrated developmental toxicity, includi ng neonatal mortality. Chil dren’s exposures are greater than adults due to increased intakes of food, water, and air per pound of body weight, as well as child-specific exposure pathways such as breast milk consumption, mouthing and ingestion of non-food items, and increased contac t with the floor. Biomonitoring studies have

1 The terms long-chain PFCs, long-chain perfluoroalkyl sulfonate ( PFAS ) , and long-chain perfluoroalkyl carboxylate ( PFAC ) chemicals in this document refer only to chemicals described in the chemical identity section

, including certain polymers that contain perfluorinated moie ties. They do not include other PFCs, particularly those having shorter chain lengths.U.S. Environmental Protection Agency Draft,
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2 found PFCs in cord blood and breast milk, and have reported that children have higher levels of some PFCs compared to adults. Thus, given the pervasive exposure to PFCs, the persistence of PFCs in the environment, and studies finding deleterious health effects, EPA will examine the potential risks to fetuses and children. As part of the Agency's efforts to addre ss PFCs, EPA also intends to evaluate the potential for disproportionate im pact 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 an imal studies have shown that the fet us and neonate are sensitive life stage s to PFC exposures , EPA will consider effects to the developing fetus and

children

.

II. Introduction

As part of EPA's efforts to enhance th e existing chemicals program under the Toxic Substances Control Act (TSCA) 2 , the Agency identified an ini tial list of widely recognized chemicals, including PFCs, for action plan deve lopment based on their pr esence in human blood; persistent, bioaccumulative, and toxic (PBT) 3 characteristics; use in consumer products; production volume; and other similar factors. This Action Plan is based on EPA’s initial review of readily available use, exposure, and hazard information 4 on PFCs. EPA considered which of the various authorities provided under TSCA and other statutes mi ght 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 plan s 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 indicate d by the Action Plan will include appropriate opportunities for public and stakeholder i nput, 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 Pre vention 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 Persis tent Organic Pollutants (POPs, 2009)

, and other sources. The summary of the toxici ty information is based on these previous assessments, and where appropriate, additional information on lower and higher chain lengths is provided.

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/

. 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 includi ng 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.U.S. Environmental Protection Agency Draft,
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3 III. Scope of Review

Continuing contributions of PFAS/PFAC to th e environmental/human reservoir are best addressed using a category approach because all the chemicals are PBT chemica ls or degrade to

PBT chemicals. A chemical

- by

- chemical analysis is not needed and would be imprac tical

.

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 sub

categories that comprise the PFC category are PFAS and PFAC chemicals

.

Conti nuing contributions of PFAS/PFAC to the environmental/human reservoir need to be addressed using a category approach because all the chemicals are PBT chemica ls or degrade

to PBT chemicals. A chemical

- by

- chemical analysis is not needed and would be impract ical.

The PFAS/PFAC precursors may be polymers that are coated on a specific substrate. This action is considering only the contribution of pr ecursors as a source of PFAS/PFAC, and not the inherent toxic effects of the polymer or exposur e to dust that contains fluorinated polymers.

Long-Chain Perfluoroalkyl Sulfonate ( PFAS ) Sub-Category

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

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

The similarities of the chemicals within th e PFAS sub-category can be established when reviewing representative structures of the different category member compounds:

5 CF 3 -(CF 2 ) 5 -SO 3 H; CAS RN: [355-46-4].

6 CF 3 -(CF 2 ) 7 -SO 3 H; CAS RN: [1763-23-1].U.S. Environmental Protection Agency Draft,
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4 a. CF 3 (CF 2 )

n -SO 3 - M where M = H + or any other group where a form al dissociation can be made;

and

b. CF 3 (CF 2 )

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

where n > 4.

Long-Chain Perfluoroalkyl Carboxylate ( PFAC ) Sub-Category

The PFAC sub-category includes perfluorooctanoic acid (PFOA) 7 and other higher homologues. The category also includ es the acid salts and precursors.

These similarities within the PFAC sub- category can be established by reviewing representative structur es of the different category member compounds:

a. CF 3 (CF 2 )

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

b. CF 3 (CF 2 )

n -CH=CH 2 ;

c. CF 3 (CF 2 )

n -C(=O)-X where X is any chemical moiety;

d. CF 3 (CF 2 )

m -CH 2 -X where X is any chemical moiety; and

e. CF 3 (CF 2 )

m -Y-X where Y = non-S, non-N hetero atom and where X is any chemical moiety.

where n > 5 or m > 6.

7 CF 3 -(CF 2 ) 5 -COOH; CAS RN: [335-67-1].U.S. Environmental Protection Agency Draft,
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5 IV. Uses and Substitutes Summary

Production Volume

PFAS Chemicals

Commercial production of PFA S 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, produc tion shifted to other c ountries. 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 a nnual production in 2004 of less th an 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 fl uorotelomers was estimated at 20 million pounds in 2006. The United States accounts for more than 50 pe rcent 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 diffe rent steps of manufacturing. Because each

intermediate contains the same R f moiety, the polymers also c ontain this moiety. The 2010/15 PFOA Stewardship Program encourages the elimin ation of PFAC precursors in product content. Companies reporting under PFOA Stewardship Program differen tiate between the amounts of PFAC precursors present in the final polymer produc t as residuals and the amount present in the polymer as R f 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, not just the small amounts of residual mono mers and other monomer raw material and

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

precursors.

UsesU.S. Environmental Protection Agency Draft,
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6 PFCs are substances with special properti es that have thousands of important manufacturing and industrial app lications. They impart valuable properties, including fire resistance and oil, stain, greas e, and water repellency. For exampl e, they are used to provide nonstick surfaces on cookware and wa terproof, breathable membranes for clothing, and are used in many industry segments, including the aerospace, automotive, building/construction, chemical processing, electronics, semiconduc tors, and textile industries.

PFAS Chemicals

PFOS is a PFAS are synthetic chemical chemicals that do es not occur naturally in the

environment. Long-chain 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 chem icals 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 – fo r example, PFOS-based fire fighting foams produced before the rules took effect in 2002 – can also still be used with out providing notice to the Agency. Because the PFAS SN URs exempt articles, PFOS may be imported or processed as part of an article without the Agency receiving prior notice.

PFAC Chemicals

PFOA is a PFAC are synthetic chemical chemicals that do es not occur naturally in the environment. PFOA is manufactured for use prim arily as an aqueous dispersion agent [as the ammonium salt] in the manuf acture of fluoropolymers, which are substances with special properties that have thousands of important manufacturing and industrial applications.

PFOA can 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 fluorotelom er based products are also used as high performance surfactants in products where an even flow is essential, such as paints, co atings, cleaning products, and firefighting foams for use on liquid fuel fires. Fl uorotelomer-based products can be applied to articles both at the factory and by consumers a nd commercial applicators in after-market uses such as carpet treatments and water repe llent sprays for apparel and footwear.

Fluoropolymers, such as polyt etrafluoroethylene (PTFE), which may contain some PFAC contamination, or that use PFOA as an emulsion st abilizer 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 reporte d production volume.U.S. Environmental Protection Agency Draft,
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7 Fluoropolymers are used in a wide variety of mechanical and i ndustrial components, such as plastic gears, gaskets and sealants, pipes a nd tubing, O-rings, and ma ny other products. Total U.S. demand for fluoropolymers in 2004 was between 50,000 and 100,000 metric tons. The 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 consumpti on of other fluoropolymers. PTFE is the most commonly used fluoropolymer, and the United Stat es 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 chemi cals new to the marketplace.

EPA's review of alternatives to long-ch ain 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 th e new substances against the range of toxicity, fate, and bioaccumulation issues that have caused past con cerns with perfluorinated substances, as well as any issues that may be raised by new chemistries (EPA, 2009b).

V. Hazard Identification Summary

The information used by EPA for this Action Plan includes the Organisation for Economic Co-operation and Development’s (OEC D) assessments of PF OS (OECD, 2002) and PFOA (OECD, 2006), EPA’s Office of Pollution Pr evention 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 toxi city information is based on these previous assessments, and where appropriate, additional information on short- and long-chain lengths is provided.

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 th e 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 in clude perfluorooctane sulfonamide (PFOSA), 2-(N-methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH), 2-(Nethylperfluorooctane sulfonamido) acet ic acid (Et-PFOSA-AcOH or PFOSAA),U.S. Environmental Protection Agency Draft,
12/ 2 9/2009 U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

8 perfluoroheptanoic acid (PFHpA), perfluorononanoate (PFNA), pe rfluorodecanoic acid (PFDeA or PFDA), perfluoroundecanoic acid (PFUA) , perfluorododecanoic acid (PFDoA), perfluoropentanoic acid (PFPeA) , perfluorohexanoic acid (P FHxA), and perfluorobutane sulfonate (PFBS).

National Health and Nutrition Examination Survey (NHANES) data show that mean levels of PFOS, PFOA and PFHxS in the genera l 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, Nobile tti JB, Rios JA, Butenhoff JL, Zobel LR 2008). The biggest drop reported in both survey s was in PFOS (~30% in NHANES and ~60% in 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 a nd 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 PF AC 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 ch ildren 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 i ndividuals who have been exposed to perfluorinated compounds at levels much higher than the majority of th e 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 ge neral population (Calaf at, 2007; Emmett, 2006).

Presence in the Environment and Wildlife

Water

Log K
ow values for PFOA, PFOS and other commercially available ammonium salts range from -0.52 to > 6.8 (De Silva, 2008; Tomli n, 2005) and have water so lubilities 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 Ar ctic (Northwest Territo ries 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 bl ood 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 ri vers in Minnesota and North Carolina (Delinsky,U.S. Environmental Protection Agency Draft,
12/ 2 9/2009 U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

9 2009). In general, the highest con centrations in wildlife have b een found in the livers of fisheating animals close to industrialized areas.

Soil and Sediment

PFOA and PFOS are considered to be resistan t to degradation in so il. Levels of C9-C11 PFAC have been found in remote Arctic regi on sediment ranging from 0.68 μg/kg – 2.58 μg/kg.

PFAC are known to increase over time in sedime nt as observed in a 22-year study (1980-2002) of the Niagara River discharge. Sediment dw elling 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 clam s ranged from 0.51 ng/g to 1.01 ng/g. Mussels and oysters in Tokyo Bay were found to contai n 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 eliminat ed; they are not metabol ized, and they undergo extensive uptake from enterohepatic circulat ion. Studies of PFOS and PFOA have shown that these compounds are distributed mainly to the seru m, kidney, and liver, with liver concentrations being several times higher than serum concentra tions; the distribution is mainly extracellular. Both compounds have a high affin ity for binding to B-li poproteins, albumin, a nd liver fatty acidbinding protein. Studies have re ported PFOS, PFOA, and several other PFAS and PFAC in umbilical cord blood indicating these chemicals cross the placenta.

The elimination half-lives of several PFA S and PFAC are summarized in Table 1. In general, the rate of eliminati on decreases with increasing chain length, although the half-life of PFHxS (C6) is longer than the ha lf-life of PFOS (C8) in humans. There is a tremendous species difference in elimination, and elimination is gr eatly 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 fo r the species and gender differences in

elimination are not well understood. These differen ces are hormonally controlled, and may also be due to the actions of orga nic 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 2 days 59 daysU.S. Environmental Protection Agency Draft,
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10 6-7 days 31 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 no te 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 bioaccu mulate in humans, and comparatively low exposures can result in large body burdens. The gender and species differe nces in elimination 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 mamma ls 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). Th ere 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 conformati onal changes into a helical structur e in the molecule resulting in a smaller cross-sectional diameter as chain lengt h increases which can le ad to the ability to accumulate in organisms (NITE, 2002a, 2002b). Additional evidence that C14 and C15 PFAC bioaccumulate and are bioavailable is their presen ce in fish, invertebrates, and polar bears. The bioaccumulation of PFOS and PFAC (C8 through C 14) in air-breathing animals (e.g., birds and mammals) is thought to represent biomagnification due to high gast rointestinal 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 bi oconcentration potential of PFAC are directly related to the length of the pe rfluorinated chain, and PFAS are more bioaccumulative than PFAC of the same chain length (Conder, 2008).

Within the PFAC and PFAS categories, the pe rfluorinated carboxylic and sulfonic acids (R f from C5 to C20) are pers istent chemicals that are re sistant to degradation under

environmental conditions. Even the reaction of PFAS/PFAC precursors with hydroxyl radicals in the atmosphere are considered to be so slow th at 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).U.S. Environmental Protection Agency Draft,
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11 Toxicity in Humans

Until recently, epidemiological and medical surveillance studies have been conducted primarily in the United States on worker s 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 st udies examining associa tions between primarily

PFOS and/or PFOA serum concentrations and hematology, hormonal and clinical chemistry parameters. The PFNA study examined liver enzy mes and blood lipid levels. In general, no

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

observed.

Toxicity in Laboratory Animals

PFOA

The toxicity of PFOA has been extensively st udied. Repeated-dose st udies in rats have shown reduced body weight, hepatotoxicity, redu ced 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 we ight and hepatocellular hypertr ophy 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 sh own 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 PPAR α -agonist and that the liver carcinogenicity (and toxicity) of PFOA is mediated by PPAR α in the liver in rats. There is no evidence that the liver toxicity in nonhuman primates is due to PPAR α -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 pa ncreatic 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 show n to be immunosuppressive in both in vivo and ex vivo systems. Studies using transgenic mice showed that the PPAR α was involved in causing the adverse effects to the immune system.

Standard prenatal developmental toxicity studi es in rats and rabbits in which pregnant animals are exposed only during gestation and sacrif iced prior to the birth of the pups have notU.S. Environmental Protection Agency Draft,
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12 shown many effects. Thus, there was no evidence of developmental toxici ty after exposure to doses as high as 150 mg/kg-day in an oral prenat al 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 increa se in skeletal variations af ter exposure to 5 mg/kg-day, and the NOAEL was 1.5 mg/kg-day.

However, the potential developmental toxic ity of PFOA is evident when the pups are evaluated during the postnatal pe riod. Thus, a two-generation repr oductive 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, ther e 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.

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 w ith 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 expo sure 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 BMD 5 and BMDL 5 for neonatal survival were estimated at 2.84 and 1.09 mg/kg-day, respec tively. Additional studies in mice have shown that PFOA exposure causes a sign ificant reduction in mammary glad gland 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-da y for 2 days late in gestation is sufficient to cause the neonatal mortality in mice. Studies with PPAR α knockout mice have shown that the

PPAR α 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 PPAR α is not involved in the neonatal mortality associated with PFOS exposure. A lthough there is contr oversy over the human

relevance of the PPAR α -agonist hepatotoxicity observed in rodents, th e role of PPAR α in development and particularly in the PFOA-indu ced 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 fo r PFOA, few studies have examined the toxicity of the shorter or longe r chained PFAC. However, the da ta suggest that the toxicity profile is quite similar to that of PFOA, albeit at different dos e levels presumably due to the

differences in elimination half-life.

Although standard repeated-dos e 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 pro liferation (a marker for the activation of PPAR α ).U.S. Environmental Protection Agency Draft,
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13 Kudo et. al. found that PFOA, PFNA, and PF DA 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 > perf luoroheptanoic acid (2006). Perm adi et al. also showed that PFDA induces hepatomegaly and hepatic per oxisomal palmitoyl-CoA oxidase (1993). Thus,

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

PPAR α . The differences in potency probably reflect th e differences in the half-life of the varying chain lengths. Despite the lack of traditional toxicity studies, it is likely reasonable to conclude that these compounds would likely produce similar effects as those observed with PFOA.

With respect to the potential developmenta l effects of PFAC with carbon chain lengths greater than C8, are EPA is completing a developmental toxic ity study of PFNA in mice (C. Lau, personal communication, 2009). Mate rnal 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/kgday, and significant lags in neonatal growth we re observed at 3 mg/kg- day. Thus, this study shows a pattern of effects very si milar to those observed with PFOA. It is likely that PFAC with carbon chain lengths greater than nine would also re sult 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 extens ively studied and was summarized in OECD report (2002) and by Lau et al. ( 2006 ). 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 di etary 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 PPAR α , the data are not suffici ent to establish a PPAR α -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 signifi cant increase in external and visceral anomalies, delayed ossification, and skeletal variations; a NOAEL of 1 mg/kg-day and a LOA EL of 5 mg/kg-day for developmental toxicity were indi cated. In rabbits, significant re ductions in fetal body weight and significant increases in delaye d 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 t oxicity study in rats showed neonatal mortality. All F1 pups at the highest dose of 3.2 mg/k g-day died within a day after bi rth, while close to 30% of theU.S. Environmental Protection Agency Draft,
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14 F1 pups at 1.6 mg/kg-day died w ithin 4 days after birth. As a re sult 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 LOA EL 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 BMD 5 and

BMDL 5 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 sh own 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 PPAR α knockout mice have shown that the

PPAR α is not involved in the neonatal mortality. Cu rrent research is focusing on the possibility that the physical properties of PFOS may interf ere with the normal function of pulmonary surfactant, leading to neonatal mortality.

Other PFAS Chemicals

A combined reproductive/developmental toxic ity 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 or ganisms have been observed with exposure to perfluorinated compounds in the parts per m illion 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. Furt her 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 or ganisms 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 concen trations up to 1nM as evidence by a 70 % decline in fecundity.

VI. Fate Characterization SummaryU.S. Environmental Protection Agency Draft,
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15 The PFAS and PFAC acids are stro ng acids that exist in equi librium between the neutral

form and the anionic form. Both the anionic a nd 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 aci ds partition from the water to atmosphere. The uncertainty arises with regard to the va lue of the acid dissociation constant (i.e., pK

a ), or the fraction of the acid form present at environmen tally relevant pH. PFAC and PFAS have been detected in air, water, and soil samples coll ected throughout the world. The oceans have been suggested as the final sink and route of transport for perfluorinated carbo xylic 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 tr ansport) by a combin ation of dissolved-phase ocean and gasphase atmospheric transport; howev er, determining which is the predominant transport pathway is complicated by the uncertainty over water to atmosphere partitioning. Furthermore, there is evidence that transport and subs equent oxidation of volatile al cohol 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 chemical s are released intentionally or unintentionally through manuf acturing, use, and disposal

, they can be degraded in the environment or be metabolized in organisms to form perfluoro carboxylic acids and perfluoro sulfonates. Limiting exposur e to PFAC and PFAS will require limiting both the exposure t o these precursors and the release of precurso rs 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 a nd by abiotic processes. 8-2 FTOH and FTOH of other chain lengths, and related chemicals in mixe d microbial cultures, activ ated sludge and soil systems have been shown to be easily degraded to form PFOA and related perfluorinated acids.

Some studies have al so shown that –CF 2 - groups can be mineralized, forming shorter chain perfluoro acids. If FTOH are absorbed from inge stion, 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 ot her fluorinated compounds. FTOH can be degraded by abiotic processes in water and air to produ ce 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 lite rature show that perfluorooctane sulfonyl fluoride (POSF) and its derivatives can be de graded under environmental conditions to form perfluoroalkyl sulfonates and carbox ylic acids. Reaction of POSF (CF 3 (CF 2 )

n -SO 2 F) with methyl or ethyl amines is used to produce N-ethyl or N-methyl perfluorooctane sulfonamidoethanolsU.S. Environmental Protection Agency Draft,
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16 (FOSE). Similar reactions are used to make shor ter and longer chain analogs to POSF and POSF derivatives. FOSE compounds, (or CF 3 (CF 2 )

n -SO 2 N(R1)(R2), where R1 and R2 can be hydrogen, methyl or longer alcohol s or other organic chains), su ch as N-methyl and N-ethyl FOSEs can be degraded though a series of interm ediates to form both perfluoro carboxylic acids and perfluoroalkyl sulfonates. Da ta on the degradation of individual intermediates has been used to identify these pathways and has confirme d that these compounds can be degraded by a

number of microbial and abiotic mechanisms. Reaction with other chemical intermediates produces other FOSA derivatives, including phos phate 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 an d as unintended reaction products. Based on existing data from the open litera ture and CBI data, it is expected that that most, if not all, of these POSF and other chain length sulfonyl fluorides a nd 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 weeks to months. Some will be degraded faster

and some will persist for longer degrade more slowly , but all will eventually be degraded.

Very little data is available on the beha vior of other perfluorochemicals in the environment and in vivo but the existing data sugg est that they will also be degraded to form PFAC. For example, recent studies have shown that ingested mono a nd 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 degradati on 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 ar e subject to hydrolys is, photolysis and biodegradation to some extent. Stud ies have shown half-liv es of a few days to hundreds of years.

In addition, preliminary research on degrada tion of fluorotelomers has shown that some urethanes and acrylates biodegrad e; however, half-lives and kinetics of the fluorotelomers are not yet well-defined. The ongoing Ongoing research by EPA’s Office of Research and Development (ORD) research is de signed to generate high quality da ta 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 so me 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 si milar degradation rates and release intermediates which that further degrade to form perfluorinated acids and sulfona tes. 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 SummaryU.S. Environmental Protection Agency Draft,
12/ 2 9/2009 U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

17 The pattern of PFAS and PFAC contaminati on varies with location and among species, which suggests multiple sources of emission and pa tterns of migration into environmental media from the sources of emission. Major pathways th at enable PFOA and PFOS to get into human blood in small quantities are not yet fully unders tood. 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 widesp read presence of PFOA and PFOS precursors in human blood samples nationwide s uggests other pathways of exposure, possibly including long range air transpor t, and the release of PFOA and PFOS from treated articles.U.S. Environmental Protection Agency Draft,
12/ 2 9/2009 U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release

18 Summary of Exposure to Consumers and Ch ildren from PFCs in Indoor Environments

PFCs in Articles of Commerce

EPA's ORD has conducted research on 116 arti cles of commerce documenting that PFCs contained in articles of commerce have the potentia l 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 textile s, thread sealant tape, floor wax and other sealants, and food contact pape r 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 a nd apparel: ND (non-detect)-3488 ng/g and ND-4640ng/g respectively; floor wax and seal er: 0.03-3720 ng/g; and home textiles: ND-519 ng/g. Some of the more commonly found PFAC m easured in these articles were PFHxA, PFHpA, PFNA, PFDA, PFUnDA, PFOA and PFOS. I nhalation levels of PFOA and total PFCs measured in carpet were 5385 pg/cm 3 and 32500 pg/cm 3 respectively (Guo, 2009).

Children are particularly sus ceptible to exposure from inha lation of PFC off-gassing from carpet and carpet protectants during their earl iest years when they are lying, crawling and spending large amounts of time playing on the carp et. 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 inhalatio n 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. So me of these articles such as paper coatings for foods cannot be ruled out for the ingesti on exposure pathways fo r 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 environm ent is dust containing not only PFAC and

PFAS but also fluorotelomer al cohols. Maximum indoor dust air measurements of 6:2 FTOH were found at 804 ng/g in the house dust of eastern United States (Strynar, 2008). The PFAS (ET-FOSA, Et-FOSE, 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 count ries as well as in Unites States in untreated groundwater, rivers, streams, bays, estuar ies, 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 atU.S. Environmental Protection Agency Draft,
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19 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 direc tly ingest these groundwater, fr eshwater 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 gene ral population may also experience dermal, ingestion and inhalation exposu res when coming into c ontact with freshwater containing PFCs. Rainwater containing PFCs may c ontribute PFCs to vegetables and fruits in home gardens, crops grown on commercial crop lands, drinking water reservoirs, and surface

waters from which drinki ng 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 we re 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 sa me area was measured at 32248 ng/ml serum. The highest levels of PFAC for freshw ater fish were found near the 3M Cottage Grove, MN site and were measured for blood samples of bass, wa lleye, 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 Char leston 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 On October 9, 2007, EPA published a nother 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 chemical s are no longer manufactur ed in United States. However a limited set of existing uses was ex cluded from the SNURs because alternatives

are were not yet available.

Similar to the PFAS SNURs in United States, PFOS has also been restricted in the European Union, Canada, Australi a and other countries, and has b een nominated for inclusion inU.S. Environmental Protection Agency Draft,
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20 the Stockholm Convention and the Convention on Long-Range Transboundary Air Pollution (LRTAP) Persistent Organic Pollutants (POPs) pr otocol. 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 sulf onyl 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 fo r limited purposes, including coatings for semiconductors, firefighting foam, photo imaging, aviation hydraulic fluids, metal plating, and certain medical devices. Countries must notify th e 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 p ackaging, coatings, and rubber and plastics (POPs, 2009).

PFAC Chemicals

OPPT’s core strategy for working towards th e elimination of PFAC chemicals has been through the PFOA Stewardship Pr ogram. 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 from eligibility for the exemption (EPA, 2006). Under this proposal, polymers containing these perfluoroalkyl moieties would need to go through the pre-ma nufacture 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 nece ssary because, based on current information, EPA can no longer conclude that these polymers “will not present an

unreasonable risk of injury to human health or the environment” under the terms of the polymer exemption rule, which is the determination ne cessary 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 th e necessary tools to review and control risk of PFC-based and related pol ymers, 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 pot ential risk from exposure to these chemicals through drinking water (EPA, 2009c). Due to limite d information on the toxi city of PFCs other than PFOA and PFOS, no attempt was ma de 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 valu es 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 R f D values for PFOA and PFOS. These values may be usedU.S. Environmental Protection Agency Draft,
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21 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 cont aining these chemicals (UNEP, 2009b). As a result of these activities, in May 2009, during the Inte rnational Conference on Chemicals Management (ICCM2), delegates to the Strategic Approach to International Chemicals Management (SAICM) ag reed to consider the devel opment of stewardship programs and regulatory approaches to reduce emissions and content of PFAC and PFAS chemicals in products and to work toward s their elimination, where feasible (UNEP, 2009a).

Remaining Issues and Concerns

PFAS Chemicals

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

manufactured outside of the 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 carpet s, leather and apparel, textiles, paper and packaging, coat ings, 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, significa ntly 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 a nd human loading of PFAC in the United States. This is in part because companies not pa rticipating in the PFOA Stewardship Program are expected to may seize follow 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 envi ronment from non-U.S. facilitie s not participating in PFOAU.S. Environmental Protection Agency Draft,
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22 Stewardship Program, resulting in transboundary environmental transport to United States.

o Articles, including imports, containing PFAC chem icals. These articles could release PFAC

as a result of their residual content in fl uorotelomer-based products and/or as the fluorotelomers-based polymers in articles biodegrade.

IX. Next Steps

To date, significant adverse effects have not been detected found in humans. general human population; however, signif icant adverse effects have b een identified in laboratory

animals and wildlife.. G However, g iven the long half-life of these chemicals in humans (years), it can reasonably be anticipated that continued exposure could in crease body burdens to levels

that would result in adverse outcomes. Conse quently, EPA intends to propose actions in 2012 under TSCA to address the potenti al risks from long-chain PFCs.

EPA intends to consider initiat ing e a TSCA section § 6 rule making for managing longchain PFCs. If EPA can make certain fi ndings with respect to these chemicals (further analysis of the information will be performed as part of TSCA section§ 6 rulemaking) , TSCA section 6 provides authority for EPA to ban or restrict the manufacture (includi ng import), processing, and

use of these chemicals. A rule addre ssing the PFAS sub-category could expand beyond the reach

of the three SNURs that the Agency has promulgated over the past decade. For example, the rule could address PFAS-containing arti cles. A rule addressing the PFAC sub- category could expand the reach of the 2010/15 PFOA Stewardship Prog ram beyond the eight participating companies and further address the concerns for poten tial PFAC exposure through the use of PFACcontaining articles. EPA will develop more detailed assessments to support the TSCA section 6(a) "presents or will present an unreasonable risk" findings. If these more detailed assessments indicate that a different approach to risk management is appropriate, EPA will consider additional approaches.

EPA will continue with the 2010/15 PFOA Stewar dship Program to work with companies toward the elimination of long-chain PFCs from emissions and products. EPA will also continue

to evaluate alternatives under EPA's New Chemicals Program and collaborate with other countries on managing PFCs.

As part of the Agency's efforts to addre ss PFCs, EPA also intends to evaluate the potential for disproportionate im pact 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 an imal studies have shown that the fet us and neonate are sensitive life stage s to PFC exposures , EPA will consider effects to th e developing fetus and

children

. As part of the Agency’s efforts to address these chemicals, EPA also intends to evaluate the potential for disproportionate impact on children and other sub-populations. The Agency will also continue to analyze the science as it pertains to making any necessary findings for the rulemakings indicated above

.U.S. Environmental Protection Agency Draft,
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23 X. References

Bossi R, R. F., Dietz R, Sonne C, Fauser P, Dam M, Vorkamp K (2005). Preliminary screening of perfluorooctane 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, Needha m LL (2007). Polyfluoroalky l chemicals in the U.S. Population: data from the National Health and Nu trition 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 C 8 F

17

SO 2 , C 8 F

17

SO 3 or C 8 F

17

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