Perfluoroalkyl compounds (PFCs) in the Village of Hoosick Falls, Rensselaer County, New York: health risks and successive approximation toward enforceable national regulation

Perfluoroalkyl Compounds (PFCs) in the Village

of Hoosick Falls, Rensselaer County, New York Health Risks and Successive Approximation Toward Enforceable

National Regulation By Robert A. Michaels, Ph.D, CEP

Introduction

Perfluoroalkyl compounds (PFCs) include perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), which have been subjects of recent revelations about public health consequences arising from industrial releases in the manufacture of widely used commercial products of modern society. Common examples are Teflon used in cookware and fire retardants used in consumer fire extinguishers. The revelations, newsworthy for their human interest and exposé values, are of special scientific and regulatory significance because they suggest the need to regulate environmental residues of some substances down to the parts-pertrillion’ range, which usually has been dismissed as insignificant for public health.

Routine monitoring of PFCs in environmental media such as air and water, and in biological media such as blood serum and milk, in the ppt concentration range only recently has become feasible. To illustrate, EPA’s standard Method 537 for measurement of PFCs in water was published in 2009, whereas PFOA was introduced into commerce decades earlier, in the 1940s. Analysis for PFCs in drinking water can be performed by only a small number of laboratories in the U. S., certified by the U. S. EPA Environmental Laboratory Accreditation Program (ELAP), and still remains time-consuming and expensive. Monitoring in serum and milk has become possible, but still is not routine.”

In the U. S. PFCs are regulated mainly via unenforceable, provisional health “advisories.” PFCs with such advisories include PFOA and PFOS, issued by the U.S. EPA and the states of New Jersey and Vermont, and perfluorononanoic acid (PFNA), by New Jersey. Such advisories, however, apply to only some PFCs. This weak regulatory status raises two issues: whether more PFCs should be regulated more stringently and, if so, determination of safe PFC levels in environmental media that might suggest appropriate regulatory enforcement targets.

Recent findings enhance the relevance to New York: PFOA and perfluorobutanoic acid (PFBA) now have been detected in Hudson River water; which is a drinking water source. PFOA was detected in 15 of 24 samples, and PFBA in 11 of 24 samples, together taken at eight Hudson River locations, from the confluence with the Mohawk River to the Tappan Zee Bridge.

Accordingly, the present investigation assesses public health risks potentially posed by PFCs, and evaluates their possible management via regulation and implementation technologies. Assessment of PFC risks includes documenting environmental residues of PFCs and elucidating physical, chemical, and biological properties that give rise to their environmental and clinical dynamics. These “pharmacokinetic” and “pharmacodynamic” properties result in potential risks being posed to public and environmental health. A related issue is historical: how did environmental regulation fail to prevent PFOA and PFOS from attaining ubiquity as residues detectable in human blood serum globally?

Some substances placed in commerce before regulation under modern national and international environmental statutes have been disseminated globally, and some of these exhibit essentially infinite persistence in the environment. Most of the latter are heavy metals such as lead (Pb), until recent decades widely used in gasoline; and (the metalloid) arsenic (As), until recent decades widely used in (arsenical) pesticides. Several of the persistent substances are organic, including DDT, PAHs, PCBs, PFCs, and chlorinated dibenzo-p-dioxins, many of which also tend to bioconcentrate, meaning that they may attain concentrations in organisms that are higher, possibly orders of magnitude higher, than the concentrations in environmental media from which they originated.

Modern regulation of chemicals in U.S. commerce was codified under the Toxic Substances Control Act* enacted in 1976 and updated in 2016. TSCA required testing to demonstrate the safety of substances for their commercial uses. Under TSCA, EPA inventoried nearly 100,000 chemicals in U.S. commerce, but many were “grandfathered” because of longstanding usage, notwithstanding potential risks that substances such as PFOA and PFOS might pose to public and environmental health. Most grandfathered substances were exempt from safety testing requirements.

Some substances that were safety tested and found to be too toxic for use were replaced by structural analogs that had not been tested. Structural analogs often exhibit similar properties (structure-activity relationships; SARs), making them useful commercially, and likewise often exert similar toxic effects, making them dangerous to

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introduce into commerce without prior safety testing. Modernization of TSCA may improve this situation, but the U.S. and other societies must grapple with the legacy of multiple substances such as PFCs (including PFOA, PFOS, and PFNA) having been introduced into commerce in recent decades.

Methods

This assessment is based upon critical examination of available scientific, technical, and regulatory literature. It is meant to be general, not encyclopedic. Accordingly, it highlights concepts via examples, most notably relating to PFOA and PFOS rather than to an exhaustive list of all PFCs. Methods applied are generally those of scientific peer review and synthesis of published findings to draw new conclusions. The main example from which more broadly applicable conclusions may be drawn is the Village of Hoosick Falls.

Findings PFC Levels in Drinking Water

Perfluorinated compounds, most notably including PFOA and PFOS, have been detected in water in multiple locations, including widely publicized events in West Virginia and Ohio. Post, et al. (2013)° report PFC levels detected in public water supplies (PWSs) at multiple locations in New Jersey. Sampling in New Jersey occurred over multiple studies and years; results, presented in detail in the report, are too complex to present in similar detail here. The authors concluded that: “PFCs were frequently found at greater than or equal to 5 ng/L in raw water from NJ PWSs. At least 1 PFC was detected at 21 (70%) of 30 intakes (18 groundwater and 12 surface water) from 29 NJ PWSs. Multiple PFCs (up to 8 at one site) were found in 13 of these 21 samples. Although PFOA was the most commonly detected PFC (57% of samples) and was found at the highest maximum concentration (100 ng/L), relatively high levels of other PFCs were found in some samples with little or no PFOA.”

Additional locations of PFC contamination have emerged recently in New York and New England States. Concentrations of PFOA and other PFCs in water sampled from drinking water supply wells in

Honeywell International, which sold the site to SaintGobain, S. A. in 1996, as well as former Oak Industries and Dodge Industries. In view of the PFOA detections and holistic consideration of available evidence, the New York State Department of Environmental Conservation (NYS DEC) instructed SGPP and Honeywell to enter into a consent agreement to fund site investigation and remediation.”

PFOA first was detected in the Village of Hoosick Falls in August 2014,5 though the Village’s 2014 Water Quality Report? included neither PFOA nor other PFCs. PFOA is the predominant PFC that has been detected, though two water samples also contained perfluoroheptanoic acid (PFHPA, Supply Well 7, Table 2). The issue was addressed the Village Newsletter in 2015.1 Results of public water supply sampling on 2014.10.02 and 2014.11.04 are presented for all three Village supply wells (Well 3, Well 6, and Well 7), and for post-treatment finished-water with respect to PFOA (Table 1) and all sampled PFCs (Table 2).

Water samples were analyzed via EPA Method 537 (U.S. EPA 2009)," consisting of solid-phase extraction with sample concentration, followed by liquid chromatography and tandem mass spectroscopy for sensitivity in the ppt range. The geographic relationship of SGPP to the Village’s water treatment plant on Waterworks Road is depicted in Figure 1. Results of ongoing private well sampling current to 18 May 2016 are depicted graphically in Figure 2, showing 1006 sample results as follows: less than 2 ppt, 500 samples (49.7 percent); less than 70 ppt, 384 samples (38.2 percent); and more than 70 ppt, 122 samples (12.1 percent).

Physical and Chemical Properties

PFOA and PFOS are structurally similar (Figure 3). PFOA, used in manufacture of other PFCs, has a carboxylic (organic) acid group (COOH or O=C-OH) at the terminal carbon, with all other hydrogen atoms substituted by fluorine (F), producing the formula F3C-(CF2)6-COOH. PFC manufacture may involve the ammonium salt of PFOA (O=C-O- NHg' instead of O=COH), ammonium perfluorooctanoate (APFO),! rather than PFOA itself.

the Village of Hoosick Falls in Rensselaer County, New York

Table 1. Perfluorooctanoic Acid (PFOA) in the Village of Hoosick Falls, New York *

were reported by Attorney

: f . Well 3 Well 6 Well 7 pai Sewwadl (aw “ae (nanograms per liter, ng/L = parts per trillion, ppt) of Keller and Heckman, ;

Washington, DC) on behalf of Sample 1 pre-treated 230 280 540

client Saint-Gobain Performance

Plastics Corporation (SGPP;

Saint-Gobain, 2014).6 SGPP is a Sample 2 pre-treated 170 280 450 subsidiary of Saint-Gobain, S.A.,

a historic French multinational Sample 1 treated 440 corporation founded in 1665 and Sample 2 treated to be determined

headquartered in Paris. Prior owners of the SGPP site include

* Servadi letter, supra note 6, at appended laboratory reports

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Table 2. Perfluorinated Compounds in Water: Village of Hoosick Falls, New York*

Minimum . Reporting sample | date in|] Supply | Supply | Supply CAS No. | perfluorinated akyl compound Level (MRL)** no. 2014 Well 3 Well6 | Well7 (ng/L = pptr) (ng/L = pptr) pre-treatment 1 2-Oct <90 <90 <90 375-73-5 | perfluorobutanesulfonic acid (PFBS) 90 2 4-Nov <90 <90 <90 1 2-Oct <10 <10 10 375-85-9 | perfluoroheptanoic acid (PFHPA) 10 2 4-Nov <10 <10 10 1 2-Oct <30 <30 <30 355-46-4 | perfluorohexanesulionic acid (PFHxS) 30 2 4-Nov <30 <30 <30 1 2-Oct <20 <20 <20 375-95-1 | perfluorononanoic acid (PFNA) 20 2 4-Nov <20 <20 <20 1 2-Oct <40 <40 <40 1763-23-1 | perfluorooctane sulfonate (PFOS) 40 2 4-Nov <40 <40 <40 1 2-Oct 230 280 540 335-67-1 | perfluorooctanoic acid (PFOA) 20 2 4-Nov 170 280 450 post-treatment (water plant finished water) 375-73-5 | perfluorobutanesulfonic acid (PFBS) 90 we 4-Nov we we <90 375-85-9 | perfluoroheptanoic acid (PFHPA) 10 we 4-Nov we 10 355-46-4 | perfluorohexanesulionic acid (PFHxS) 30 we 4-Nov we “ <30 375-95-1 | perfluorononanoic acid (PFNA) 20 we 4-Nov we we <20 1763-23-1 | perfluorooctane sulfonate (PFOS) 40 we 4-Nov we we <40 335-67-1 | perfluorooctanoic acid (PFOA) 20 we 4-Nov we we 440

*Saint-Gobain. Submission of information concerning allegations of environmental contamination. Letter from Attorney David G. Servadi, law firm of Keller and Heckman, LLC (Washington, DC) to TSCA Confidential Business Information Center (Washington, DC) on behalf of Saint-Gobain Performance Plastics Corporation (SGPPC; Village of Hoosick Falls, New York), 2 pages plus attachments (8 pages), 30 December 2014

** US EPA: Shoemaker, J.A.; P.E. Grimmett, and B.K. Boutin. Method 537. Determination of selected perfluorinated alkyl acids in drinking water by solid phase extraction and liquid chromatography/tandem mass spectrometry (LC/MS/MS). Cincinatti, Ohio; U.S. Environmental Protection Agency, National Exposure Research Laboratory Office of Research And Development; Document No. EPA/600/R-08/092; Version 1.1, 50 pages, September 2009;

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Figure 1: Geographic Relationship of Saint Gobain Performance Plastics and the Water Treatment Plant on Water Works Road, Village of Hoosick Falls, New York

NCH 4 Saint-Gobain

Berformance Plastic:

Figure 2: PFOA Results for Private Wells in the Village and the Town of Hoosick Falls*

Village of Hoosick Falls and Town of Hoosick Private Well Sampling Perfluorooctanoic Acid (PFOA) Results Map - Updated May 18, 2016

‘Total Well Water Results (1006 total) [Eiconcentrations not detected (less than 2 ppt PFOA) (500 results) EiiiConcentrations detected below 70 ppt PFOA (84 results) Mil Concentrations detected at or above 70 ppt PFOA (122 results)

as | lene cee earn

* N.Y.S. Dept’ of Health, Village of Hoosick Falls and Town of Hoosick Falls Private Well Sampling, Perfluorooctanoic Acid (PFOA) Results Map,

https:/;www.health.ny.gov/environmental/investigations/hoosick/images/results_dist.jpg, updated May 18, 2016.

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Figure 3: Chemical Structure of Perfluorooctanoic Acid (PFOA) and Perfluorooctane Sulfonate (PFOS)*

F F

i

F

PN AN AN AN

OH eT I IK PFOA - perfluorooctanoic acid Rear FoF \d \E Ve Me Za OR aN “7 NA7 so,

= aN

PFOS - perfluorooctanesulfonic acid

F io} Nd

A.

F

*Image Source: http://charlestonwaterkeeper.org/watershed-facts/toxic-pollutants- 1-in-general-and-sources/pfoa-pfos-285x300/.

PFOA has Chemical Abstract Service Registration Number (CASRN) 335-67-1. Selected physical and chemical properties of PFOA are set forth in Table 3.

Acomprehensive but general explication of physical and chemical properties of PFCs, including PFOA, serves as a preamble justifying subsequent recommendations for comprehensive international action in the “Madrid Statement” (Blum, et al., 2015).!° The Madrid Statement highlights several environmental and toxicologically significant properties of PFCs, including the following:

¢ man-made, ubiquitous, globally distributed, and highly persistent;

¢ residues, which are found everywhere, eventually enter groundwater, surface water, and drinking water; and

¢ with high bioaccumulation potential, PFCs are listed by the UN Environment Programme Stockholm Convention as persistent organic pollutants.

Pharmacokinetics

“Pharmacokinetics” and “pharmacodynamics” (next section) are, respectively (and very generally), the effects of the body on substances, and the effects of substances on the body. Pharmacokinetics includes intake

(absorption), distribution, metabolism, and excretion (subsections below).

Principal routes of exposure to substances generally include inhalation, ingestion (“oral exposure”), and dermal contact. Routes are subdivided into pathways, for example, food vs. drinking water, for oral exposure.

Thus, body burdens depend upon the intensity and duration of exposure, the efficiency of absorption via all routes and pathways, the targets of substance distribution and possible storage, the efficiency and nature of metabolic breakdown and substance transformation, and the efficiency and time course of excretion.

Most generally, therefore, body burdens of substances depend upon the net result of processes of increase and processes of decrease, as well as the nature of storage and possible accumulation. Storage may include organs that metabolize and/or sequester substances out of harm’s way.

Substances may be stored in fat, for example, where they may be metabolically inactive; this may change in the event of fat metabolism, for example, as a result of metabolic challenges such as starvation or migration in which fat stores may be metabolized and fat-sequestered

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Table 3: Physical and Chemical Properties of Perfluorooctanoic Acid (PFOA)*

Property Perfluorooctanoic Acid Chemical Abstracts Registry 335-67-1

(CAS) No.

Synonyms PFOA; Hexanoy] fluoride;

3,3,4,4,5,5,6,6,6-nonafluoro-2-0xo; Pentadecafluoro-1-octanoic acid; Pentadecafluoro-n-octanoic acid; Octanoic acid, pentadecafluoro-; Perfluorocaprylic acid; Pentadecafluoroocanoic acid; Perfluoroheptanecarboxylic acid;

Chemical Formula CsHF,502 Molecular Weight 414.09 Color/Physical State White powder Boiling Point 189°C Melting Point 45-50°C Density (at 20°C) 1.7921 g/cm? Vapor Pressure 4.2 (25°C)

2.3 (20°C)

128 (59.3°C) pKa 25

1.5-2.8 pH value 2.6, 1 g/L (20°C) Koc 27,000 estimated Solubility in water (g-L*!) 9.5 (25°C)

4.1 (22°C)

Solubility in organic solvents

Conversion Factors for vapor phase

1 ppm = 17.21 mg/m?

Sources: HSDB (2006); SIAR (2006), EFSA (2008); RTECS (2008)

*Derived from: U.S. EPA, EPA 822R14001, Health Effects Document for Perfluorooctanoic Acid (PFOA) (Feb. 2014).

substances mobilized. These concepts are addressed in the subsections below.

Absorption. “Perfluoroalkyls... are readily absorbed following inhalation or oral exposure” (ATSDR, 2015).'4

Distribution. PFOA is highly cumulative once assimilated into the body. PFOA and PFOS tend to concentrate in the liver of animals.!> “Absorbed perfluoroalkyls distribute from plasma to soft tissues, with the highest extravascular concentrations achieved in liver” (ATSDR, 2015).!° In pregnant women PFCs are distributed to the fetus via the placenta and, after birth, to the breastfeeding infant via milk.!”

Metabolism. “Perfluoroalkyls... are not metabolized in the body” ATSDR (2015).18

Excretion. “Elimination half-times in humans of 3.8 years, 5.4 years, 8.5 years, 665 hours, and 72 hours have been estimated for PFOA, PFOS, PFHxS, PFBuS, and PFBA, respectively” (ATSDR, 2015;!° acronyms defined in Table 2 above).

Biomarkers, Serum Levels, and Body Burdens

Biomarkers are indicators of signal events in biologic systems or samples. They include markers of exposure, markers of effect, and markers of susceptibility.”° In the case of PFCs, the compounds themselves, detected in blood serum, are accepted markers of exposure. Specific biomarkers of effect, however, are unavailable, as are specific biomarkers of susceptibility.

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Virtually all people have been exposed to PFOA and PFOS, resulting in non-zero background body burdens and the absence of a strictly unexposed control group for use in epidemiology studies (Kerger, Copeland, and DeCaprio 2011).?! Ingelido, et al. (2010)? determined serum concentrations of PFOA and PFOS in 230 members of the Italian general population, in three age ranges: 2035 years, 36-50 years, and 51-65 years.

Median concentrations of all participants were 6.31 ng/g for PFOS and 3.59 ng/g for PFOA. The 90th percentiles were 12.38 and 6.92 ng/g, respectively. Men had higher concentrations of PFOS and PFOA than women, regardless of age. PFOS and PFOA concentrations in serum also increased with age.

The strong correlation between PFOS and PFOA concentrations, according to the authors, suggests the same or similar exposure routes.

The New York State Department of Health (NYS DOH) offered residents and former residents of the Village and the Town of Hoosick Falls blood tests at no charge to determine PFOA levels in their serum.” Results from 2081 participants tested from February to April 2016 are reported in Table 4. Results are placed in the context of the general U. S. population and other affected populations in Table 5.

The median (50th-percentile) serum level of PFOA was 28.3 ug/L (ppb) in Hoosick Falls (Table 4), about 11.3 times higher than the 50th percentile nationally, which was 2.08 ug/L (ppb, Table 5). In Hoosick Falls and nationally, PFOA levels were higher in males than in females, and higher in adults than in children. NYS DOH blood tests can quantify other PFCs besides PFOA, but other PFCs in serum were not reported.

Pharmacodynamics

Acute Toxicity. Acute toxicity refers to toxic effects resulting from short-term exposure of up to one day (24 hours). Acute toxicity of PFCs including PFOA may occur in special circumstances such as accidental exposures in industrial settings where PFCs may be manufactured, packaged, and stored. In contrast, environmental levels of PFCs including PFOA typically have been reported in the ppt to parts-per-billion (ppb) range. Acute toxicity typically is unassociated with such environmentally realistic concentrations.

Mutagenicity. Studies of PFC genotoxicity to humans were absent from available literature (ATSDR 2015).”4 ATSDR, summarizing mutagenicity studies, concluded that “in vitro studies provide evidence that PFOA and PFOS are not mutagenic at non-cytotoxic concentrations.”

At cytotoxic concentrations, greatly exceeding typical environmental levels, PFOA has been reported to cause DNA damage including DNA strand breaks, induction of micronuclei (small cell nuclei visible after extrusion of the main cell nucleus, relevant to potential carcinogenicity), and increases in reactive oxygen species.

Carcinogenicity: Animal studies. In rats PFOA has been associated causally with liver, testicular, and pancreatic tumors.?5

Carcinogenicity: Epidemiology studies. Studies of PFOA have involved the general population, populations exposed residentially to PFOA from an industrial source, and populations exposed to PFOA occupationally. Eriksen, ef al. (2009) investigated potential association between plasma levels of PFOA and PFOS and cancer risk within a prospective Danish cohort of 57,053 participants 50-65 years of age with no previous cancer diagnosis at enrollment.” They found no association of PFOA or PFOS

Table 4. Serum PFOA in Hoosick Falls Residents Tested Voluntarily, to April 2016*

es

FOR boas tee psols bY expees nd mem ate

Number of PFOA level in ug/L participants | Geometric mean 50" percentile Total 2081 23.5 28.3 By gender Females 1146 21:3 26.7 Males 935 26.6 30.7 By age group 0-17 353 16.3 19.8 18-39 458 18.7 22.6 | 40-59 700 25.7 32.8 60 and older 570 31.7 43.4

* Source: N.Y.S. Dep‘t of Health, Information Sheet, PFOA Biomonitoring Group-Level Results, Table 1, 1 (June 2, 2016), https://www.health. ny.gov/environmental/investigations/hoosick/docs/infosheetshortgroupresults. pdf (last visited Aug. 15, 2016).

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Table 5. Serum PFOA in Hoosick Falls Residents Tested Voluntarily, To April 2016*

PFOA RESULTS FOR eon wa.

_ PFOA Levels in Blood from Other Studies:

Other communities with PFOA in drinking water:

Little Hocking, Ohio

Lubeck, West Virginia

Tuppers Plains, Ohio

3M workers, Decatur, Alabama

DuPont workers, Parkersburg, West Virginia

| General U.S. population:

Middle level (50" percentile)

High level (95"" percentile)

E U.S. population age 12 and up A Males only 2.38 Females only 1.78 |

Young people age 12-19

NOTES FOR TABLE 2:

g/L = micrograms per titer: A microgram per titer equals one part per billion; about one drop of liquid in an Olympic-

size swimming pool.

Middle level (50" percentile): Half the people had a result below and half had a result above this level. High level (95" percentile): 95 of every 100 people had results below this level. Average level: The average is usually very similar to the middle level. In the published community studies, the average

level is used.

N.A.: These levels are not available in the published studies about these communities.

References:

1. General U.S. population: National Health and Nutrition Examination Survey (NHANES), National Report on Human Exposure to Environmental Chemicals, U.S. Centers for Disease Control and Prevention (CDC), 2011-12.218.

2. Ohio/West Virginia communities: Paustenbach DJ, Panko JM, Scott PK et al (2007). A methodology for estimating human exposure to perfluorooctanoic acid (PFOA): a retrospective exposure assessment of a community (1951-

2003). J Toxicol Environ Health 70:28-57.

3. Workers: Olsen GW (2015) “PFAS biomonitoring in higher exposed populations,” in DeWitt JC (ed.) Toxicological effects of perfluoroalkyl and polyfluoroalkyl substances. Humana Press, Springer.

FOR MORE INFORMATION: NYS DOH, Center for Environmental Health, Bureau of Environmental and Occupational Epidemiology, Corning Tower, Albany NY 12237 518-402-7950 or BEOE@health.ny.gov

* Source: N.Y.S. Dep‘t of Health, Information Sheet, PFOA Biomonitoring Group-Level Results, Table 1, 2 (June 2, 2016), https://www.health. ny.gov/environmental/investigations/hoosick/docs/infosheetshortgroupresults. pdf (last visited Aug. 15, 2016).

plasma concentrations in the general Danish population apparently with risk of prostate, bladder, pancreatic, or liver cancer.

In contrast, Barry, Winquist, and Steenland (2013)*” reported that PFOA exposure of 32,254 residents of the mid-Ohio Valley, exhibiting 2,507 validated cases of cancer of 21 different types, was causally associated

with renal (kidney) and testicular cancers. They also concluded that: “Because this is largely a survivor cohort, findings must be interpreted with caution, especially for highly fatal cancers such as pancreatic and lung cancer.” That is, these cancers might be caused by PFOA but not represented in the “survivor cohort” because of the brief time people have them before dying.

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Vieira, et al. (2013)°8 studied the relationship between exposure to PFOA and cancer among residents living near the duPont Teflon-manufacturing plant in Parkersburg, West Virginia. The authors analyzed incidence data on 18 cancers diagnosed from 1996 through 2005, including 7,869 cases in five Ohio counties and 17,238 in eight West Virginia counties. They concluded that their “results suggest that higher PFOA serum levels may be associated with testicular, kidney, prostate, and ovarian cancers and non-Hodgkin lymphoma. Strengths of this study include near-complete case ascertainment for state residents and well-characterized contrasts in predicted PFOA serum levels from six contaminated water supplies.”

The United Nations International Agency for Research on Cancer (UN IARC, 2014)? convened a Working Group on PFOA. Based upon consideration of available animal and human data the Working Group concluded that “[o]n the basis of limited evidence in humans that PFOA causes testicular and renal cancer, and limited evidence in experimental animals, the working group classified PFOA as possibly carcinogenic to humans (Group 2B).”

Teratogenicity. Available data on possible PFOA teratogenicity is limited but negative. ATSDR (2015) addressed this issue in its holistic review of PFOA toxicology. With respect to oral exposure ATSDR reported that “no fetal toxicity or teratogenicity was reported in offspring of rabbits exposed to up to 50 mg/kg d) PFOA on GDs [gestation days] 6-18...” No data on teratogenicity was presented in connection with either inhalation or dermal exposure.

Reproductive Effects. Studies of potential reproductive effects of PFOA and PFOS in people have been motivated by laboratory bioassays reporting reduced birth weight, increased postnatal mortality, and decreased postnatal growth in rats and mice (Olsen, Butenhoff, and Zobel, 2009).3! Olsen, Butenhoff, and Zobel reviewed eight epidemiological studies, together involving six general (non-occupational) populations and two occupational populations. In the five general population studies that measured PFOA and PFOS, inconsistent associations were obtained with respect to birth outcomes including birth weight, birth length, head circumference, and “ponderal index” (a measure of leanness, relating body length and body mass).

Infertility. Infertility attributable to endocrine disruptors including PFOA was studied epidemiologically via comparison of serum PFOA levels of fertile vs. infertile women,” but the authors concluded that “no significant difference was found between the groups with regard to perfluorooctane sulfonate (PFOS) [and] perfluorooctanoic acid (PFOA)...” In contrast, La Rocca, et al. (2011)** reported that PFOS levels were associated positively with infertility among a group including fertile and infertile couples in an unspecified metropolitan community in Italy.

Fecundity. A study by Fei, et al. (2009) involving 1,240 women from the Danish National Birth Cohort focused on fecundity based upon women’s reported time to pregnancy. The study revealed that high plasma levels of PFOA and/or of PFOS were associated with longer times to pregnancy. The authors concluded that their “findings suggest that PFOA and PFOS exposure at plasma levels seen in the general population may reduce fecundity; such exposure levels are common in developed countries.”

Birth outcomes. A study of birth outcomes of women exposed to PFOA and PFOS in the mid-Ohio Valley revealed that both were associated positively with pregnancy-induced hypertension (preeclampsia).°° Apelberg, et al. (2007) studied women living near a chemical plant; they quantified fetal exposure via PFOA concentrations measured in maternal blood serum sampled from umbilical cords. PFOA concentrations in cord serum were found to be negatively correlated with size and weight of infants at birth.* Fei, et al. (2007) conducted a general population study involving the national cohort of women in Denmark. Despite being a general population study, it likewise revealed a negative association of PFOA (though not of PFOS) levels in blood plasma with infant birth weight.”

In contrast, Hamm, et al. (2010) studied a cohort of 252 pregnant women,* and reported that maternal exposure to perfluorinated acids including PFOA and PFOS exerted “no substantial effect on fetal weight and length of gestation at the concentrations observed in this population.” Likewise, Savitz, et al. (2013) studied 11,737 pregnancies in a community highly exposed to PFOA. They reported “no associations between estimated serum PFOA levels and adverse pregnancy outcomes other than possibly preeclampsia.”

Onset of puberty and mammary gland development. Tucker, et al. (2015)*° investigated the effects of PFOA on female mouse pubertal development at doses <1 mg/kg. Female offspring from CD-1 and C57B1/6 dams were exposed to PFOA prenatally, creating serum concentrations similar to serum concentrations in people. The onset of puberty, including mammary gland development, was delayed in both mouse strains, in a dose-dependent manner.

Other reproductive effects. Hines, et al. (2009)*" reported that PFOA “is a proven developmental toxicant in mice, causing pregnancy loss, increased neonatal mortality, delayed eye opening, and abnormal mammary gland growth in animals exposed during fetal life.” They investigated fetal exposure of CD-1 mice to PFOA, and possible PFOA effects on birth weight, serum insulin, and leptin, a protein produced by fat that evidently is involved in fat storage. Their investigation revealed increased body weight, serum insulin, and leptin in mid-life of mice exposed developmentally. They concluded that their

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research revealed “an important window of exposure for low-dose effects of PFOA on body weight [BW] gain, as well as leptin and insulin concentrations in mid-life, at a lowest observed effect level of 0.01mg PFOA/kg BW.”

Other Chronic Effects. The presence of PFOA in water has been recognized as a potential chronic exposure risk to human health, not only in the scientific literature, but in litigation.” In the scientific arena, ATSDR undertook a “health consultation” relating to populations exposed to releases of PFCs including PFOA from an industrial facility in Cottage Grove, Minnesota.% As early as 2005 ATSDR concluded that “PFCs have a long half-life in humans and animal studies indicate a potential for toxicity to the liver and effects on reproduction and development.”

Cholesterol. Eriksen, et al. (2013) reported that PFOA and PFOS may affect serum cholesterol levels, mainly in highly exposed populations. They conducted a cross-sectional study of the plasma PFOA and PFOS vs. total cholesterol in a general middle-aged Danish population. They found positive associations of total cholesterol with both substances but, as in many epidemiology studies, theirs was unable to determine clearly whether the association was causal. Likewise, Kerger, Copeland, and DeCaprio (2011)* reported a trend of increasing blood cholesterol with increasing PFOA concentrations among 46,294 adult West Virginia residents who lived, worked, or went to school for at least one year in a C8 (PFOA and PFOS) contaminated drinking-water district.

Liver function. PFOA and PFOS tend to concentrate in the liver of animals.” As studies involving human exposure to PFOA have reported associations with liver function enzymes only inconsistently, Gallo, et al. (2012) undertook a massive study involving 69,030 persons (47,092 adults) to examine possible association of PFOA and PFOS with alanine transaminase (ALT), glutamyltransferase (GGT), and direct bilirubin (blood levels of bilirubin, a component of bile). Statistical analysis revealed associations of PFOA and PFOS with the liver function enzyme ALT, and inconsistent evidence of association with GGT and bilirubin.

Endocrine disruption. A recent concern is that low environmental levels of substances including PFOA and other PFCs have been found to affect the endocrine system. The effects may include causing obesity and the autoimmune disease ulcerative colitis. Such substances may act by mimicking or blocking endogenous hormones (ATSDR 2015).47

Ulcerative colitis. Ulcerative colitis was strongly associated with exposure to PFOA measured via concentrations in blood serum (Steenland, et al., 2013).48 Ulcerative colitis is an autoimmune disease, in which the immune system of affected individuals has been

compromised in a manner that reduces its ability to distinguish “self” from “non-self” targets of action.

The Steenland study involved interviews with 32,254 adults highly exposed to PFOA as community members and occupationally exposed individuals living near a chemical plant in the mid-Ohio valley. Interviewees were people with high serum PFOA levels (median 28 ng/

mL = 28 ug/L). The authors found that “the incidence of ulcerative colitis was significantly increased in association with PFOA exposure, with adjusted rate ratios by quartile

of exposure of 1.00 (referent) [‘referent’ was first quartile, against which the three higher quartiles were compared], 1.76 (95% CI: 1.04, 2.99), 2.63 (95% CI: 1.56, 4.43), and 2.86 (95% CI: 1.65, 4.96) (ptrend < 0.0001).”

Obesity. As reported above, exposure of developing embryonic mice to low doses of PFOA via their mothers (dams) has been associated with increased weight and with increased fat (“adiposity”) in postpubertal females.” This finding has been replicated in humans. Halldorsson, et al. (2012) undertook a prospective study of Danish women, and found that PFOA levels in blood serum sampled at pregnancy week 30 were correlated with obesity indicators in their daughters at 20 years of age.

PFOA has been identified as an endocrine disruptor capable of producing obesity via maternal exposure as described above. Skinner, et al. (2013), studying the pesticide DDT, reported that this endocrine disruption effect may occur, not only within a single generation, but extending into future generations.” Indeed, citing Newbold (2008), Halldorsson, et al. (2013), reported that endocrine disruptors “may lead to permanent changes in metabolic pathways that regulate body weight.”>! Grens (2015) outlined the history of the broadening of this observation involving DDT and animal studies to other endocrine disruptors (“obesogens”), associating (speculatively) the current human epidemic of obesity with increased environmental dissemination of endocrine disruptors in recent decades.

Immunosuppression. Immunosuppression by PFCs at low serum levels has been reported in multiple studies revealing reduced antibody response in adults, and in children following routine administration of childhood vaccines (US EPA 2016)*: “...three studies have reported decreases in response to one or more vaccines (e.g., measured by antibody titer) in relation to higher exposure to PFOA in children (Grandjean et al. 2012; Granum et al. 2013) and adults (Looker et al. 2014). In the two studies examining exposures in the background range (i.e., general population exposures, <0.010 g/m), the associations with PFOA also were seen with other correlated PFCs. This limitation was not present in the study in adults in the high-exposure C8 community population. Serum PFOA levels in this study population were approximately 0.014-0.090 g/mL” (pages 3-24 to 3-25).

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Sen e Subpopulations

Sensitive subpopulations are groups sharing distinctive characteristics. Individuals may belong to a sensitive subpopulation, but the designation usually excludes individuals considered alone, whose individual vulnerability to stressors depends upon his or her unique medical condition. Eventually each individual must die and, as the transition between life and death approaches, vulnerability to stressors may become arbitrarily great, and the presence or absence of the stressor arbitrarily insignificant in extending the dwindling life.

Examples of sensitive subpopulation commonly include the elderly, infants, and pregnant women. In the case of PFCs, individuals with specific pre-existing conditions may be unusually sensitive (ATSDR 2015, pages 313-4).™4 These include people with elevated serum cholesterol, a risk factor for cardiovascular disease, and people with elevated serum uric acid, a risk factor for hypertension (high blood pressure). People with compromised liver function also may be unusually sensitive to PFCs, because the liver may be a target of PFC toxic activity.

Chemical Interactions

According to ATSDR (2015, page 311)°5: “No relevant studies were located regarding interactions

Table 6a. Human Health Effects and Associated PFOA in Blood Serum, By System Affected*

of perfluoroalkyl compounds with other chemicals in children or adults.”

Serum Levels vs. Health Effects

Serum levels of PFOA associated with numerous human health conditions as reported in US EPA (2016)°° are set forth in Table 6. Table 6 is divided into two parts. Table 6a reports serum PFOA levels associated with specific human health conditions. Table 6b ranks serum PFOA levels from lowest to highest, and for comparison shows the Town of Hoosick and Village of Hoosick Falls 50th-percentile serum level. As Table 6b illustrates, many health conditions have been reported associated with serum PFOA levels below those commonly occurring among Hoosick residents and former residents.

Regulation-Based Risk Management

Much information is available about the unusually low concentrations of PFCs, especially PFOA, that have been shown to be toxic to people. This information has been used to form the basis for promulgating health advisories (Table 7), but not legally enforceable regulations such as Maximum Contaminant Levels (MCLs) under the 1974 Safe Drinking Water Act (Public Law 93-523). Data on PFCs are less detailed for cancer than non-cancer effects. Accordingly, health advisories primarily have been based upon extrapolating to

Table 6a, Human Health Effects and Associated PFOA in Blood Serum, By System Affected*

Tean or median EPA = health effect ener Mew ated aid mean or median (ug/mt = ppm) - ‘ oe — pera Pron. ; table lserum lipids, uric acid, from US EPA(2016)* Table B40 {ug/ml = ppm), 1.03 t01.90 (Olsen et al, 20016, 2003 B-4 |reproductive and developmental outcomes, from US EPA (2016)* Table B-8 i 1.36 to 1.77 Olsen et al. 200ic, 2003 8-4 0.428 Sakr et al. 2007a B4 breastfeeding duration reduced 0.0056 fala 200% 2008, 20085 1 1.04 to 1.16 Saker et al, 20075 Lea Fei et al. 2007, 2008a, 2009, 22 ‘Olsen and Zobel 2007 7) 0.0056 Fa oto 2007, 20088, 2008, |g 4.02 Costa ef af. 2009 Bs ase Fei et al. 2007, 20088, 2009, 0.08 Steenland et al, 2009 Ba 20108 | 6686 teteariand star 200 ee jecundity/fertility: me to pregnancy UtEE Fei et al 2007, 2008a, 2009, | 5 9 0.0261 Winquist and Steenland 20i4a/ 8-4 2010a i 0.0777 to 0.0618 Frisbee et al. 2010 B-4 infertility 0.0056 eee BS 010048. Nelson er al. 2010 B4 jecundity/fertility: time to pregnancy 0.00166 \Vélez et al. 2015 Bs 007i iErikgen, et al, 2013 [Ea infertility 000166” Vélez ef af 20188 lendocrine disruption, from US EPA (2016)* Table B-5 i preanency induced hyperencien 0,031 to 0.0337 Darrow et al, 2013, 2014 B-8 i + Kpreeclampsia) aie i liver enzymes, elevation of GGT 0.428 ‘Sala; eal 20070 6s eight, head circumference, ponderal index 0.0016 (cord) Apelberg et al. 2007 B-8 1,04 to 1.16 Sake, et al, 20076 Bs ALP, ALT, GGT 221 ‘Olsen and Zobel 2007 5 reduced 0.0037 Maisonet etal 2012s «BB ALP, ALT, GGT 4102 ‘Costa, et al, 2008 Bs reduced normal sperm count males: ALT, GGT 0,00505__ Lin, et al, 2010 Bs s) a Postisest eb at P00] ES aati 0.00406 Lin, et al. 2010 BS altered sperm quality PFOA, 6) 9 99479 to 0.00509 Buck Louis et al. 2015 8-8 (aoe a oe ee aaa ed PFCs (perfiuoroalkyl compounds) hronic kidney disease, eGFR decrease 0.0283 [Watkins, ef al. 2013 Bs FEUER InefesseceetAl 0.00456 Liew et al, 2014 88 palsy in boys ;hyroid disease, hormone levels, from US EPA (2016)* Table B-6 : 0:0014. Heyer et al. 20150 BS thyroid hormone elevati per ‘Gisen and Zobel 2007 Cee lneurodevelopmental: executive function; f ~~ ree TA thyroid hormone decline 2.21 ‘Olsen and Zobel 2007 BS DHD. aes paietial 2018 ES - —[Uo0s Shrestha et al. 2015-6 jneurodevelopmental: increased ADHD 0.0044 Hoffman et af. 2010 BS 9.0104 Shrestha et al 2015 Bs Eostratal dvel-s rethied wi, EMT in Bois 3 med om ee in girls 01000943 (cord) de Cock et al, 2014 cee fh mos, 0.0052 Andersen et al. 2010 58 hyroid disease in women elevated (0.019 (women) Melzer et al. 2010 86 rast ; i + ihyroid disease In children elevated 010293 Lopee-Espindsa et af 2012” "6-6 rea ah ae i 0.0037 Halldorsson, et al. 2012 8-8 from US EPA (2016)* Table B-7 Poststal devslopents: Incrasced 0.001 to 0.0018 Hoyer et al. 2015b B88 O.ii3 {Bz 0.02 t00.026 —Lopez-Espinosa et al. 2011 | B-8 0.113 8.7 rs. 7 a a oto bes ee ae 0.0032 57 postnatal development delayed puberty | “0.0036 (maternal) ” Kristensen ef al! 207 Be 0.00406 37 7 Toots i bey Havelbariant pee cit 0.0038 (maternal) Vested et al. 2013 B-8 afi nezeennd pevalenca pore 0.0010 Dong, et al. 2013 87 es 8-4 trough ESM . i t lWS EPA. Health Effects Support Document for Perfluorooctanoic Acid (PFOA). “Washington, DC; U.S. tha, increased prevalence 16648 Humblet, ef af, 3014 By g Acid ( SE eee ee ay ite ues Hurelet a Eo Environmental Protection Agency, Office of Water, EPA 822-R-16-003, 322 pages, May 2016.

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Table 6b. Human Health Effects and Associated PFOA in Blood Serum, By Serum Level*

Table 6b. Human Health Effects and Associated PFOA in Blood Serum, By Serum Level*

EPA jhealth effect iz ealth effe source table mean ormedian ooo EPA (ug/ml = pom} =a = sere lhe peewee ld i NYS DOH 2016; data to (ug/mi = ppm), Dede ula MS moze April 2016 ye 3 thyroid hormone elevation 0.0104 Shrestha et al. 2015 B-6 4 thyroid hormone elevation in gris | 0.000943 (cord) [de Cock et af 2014" B-6 4 thyroid hormone elevation 0.0104 Shrestha et ai. 2015 8-6 pi tote [ASD TE 0.0010 ‘Dong, et al. 2013 | 87 hyroid disease in women elevated 0.019 (women) Melzer et al. 2010 B-6 ——— 0.001 to 0,0018 Hoyer et al, 2015b Be postnatal development: delayed puberty'n | 9.07 00.026 Lopez-Espinosaet al, 2011 B-8 She Ee increased 0.0014 ‘Hoyer et al. 2015a BB lincreased total cholesterol 0.0261 \Winquist and Steenland 20144, B-4 ir, bis oaaed pravelatos eimai ates 8.0048 Bong et af, 3013 med hronic kidney disease, eGFR decrease 0.0283 Watkins, et al. 2013 85 jeight, head circumference, ponderal index 5 t 0.0016 (cord) Apelberg et a/. 2007 88 Hoosick Falls 50th percentile 0.0283 be) sel area gata ee 0.00166 Vélez et al. 2015 B-8 wl 0.00166 \Vélez et al. 2015 Bk hyroid aa ee! elevated 0.0293 Lopez-Espinosa et al. 2012 B-6 O005T ‘Grandjean, et al, 2012 Ez ie a pypecvansion 0.031 to 0.0337 Darrow et al. 2013, 2014 B-8 ‘6.0036 (maternal) Kristensen et al, 2013 ree ecramps! a an oe par ee laccine response, reduced antibody titer 0.0337 Looker, et al. 2014 B-7 falldorsson, et a - aa on a soem ae ae Z | Ineurodevelopmental: executive function; 0.0037 Maisonet et al, 2012 1 BS DHD auasl psnstal 2018 ES 0.0038 (maternal) Vested et al. 2013 3-8 ner total chol., LDL, triglycerides in children,| 9 0618 to 0.0777 Frisbee et al 2010 Pr jaccine response, reduced antibody titer ~0:00406"~ Grandjean, et af 012 BF i liver enzymes, elevation of ALT, GGT in magia ip) atl td ops 0.08 Steenland et al. 2009 84 altered sperm quality PFOA, 6) 0.00429 to 0.00509 ‘Buck Louis et a/. 2015 B-8 0.086 Steenland et al. 2010 B-4 PFCs (perfiuoroalky! compounds) i | 0.113 Steenland, et al. 2015 8-7 isthmna, increased prevalence | 0.0043 Hurmblety et aff 201487 a Creches oe deve 0.0048 Hoffman et al. 2010 Cee 0.113 Steenland, et al. 2015 B-7 jreurodevelopmental (100456 Liew et at 2014 Be jncreased total cholestercl, VBL, 0428 Gakr et al. 20072 Bd palsy in boys, i riglyoerides, uric acid A increased total cholecterol, non-HOL aly Z 0.0046 Nelson et a/. 2010 8-4 liver enzymes, elevation of GGT 0.428 Sakr, et al. 20072 B-5. tlh re ae OTT ReeraMTiooaTt 0.0049, ‘Doensen et al. 2009 Be triglycerides 1.03 to 1.90 ‘Olsen et ai, 2001b, 2003 B-4 al cholesterol 1.04 to 1-16 Sakr et ai. 2007 Ba fivarcenzymes; elevationtin.malest ALTGT 0050s eae ANS das liver enzymes, elevation of AST {04to 1.16 Sakr, etal 2007 B-5 Prost e EME s Feeney BMT IT ES. 0.0052 ‘Andersen et al. 2010 B-8 lincreased total cholesterol, triglycerides 136to1.77 Olsenet al 2001c, 2003 B-4 ‘Fei et af. 2007, 20080, 2009, | 221 (Olsen and Zobel 2007 8-6 0.0056 Bae 8-8 : ‘i 5 sear HO a9 s08i8 3008" increased triglycerides, reduced HDL 221 ‘Olsen and Zobel 200: 8 0.0056 20108 8-8 liver enzymes, elevation of ALP, ALT, GGT 2.21 (Olsen and Zobel 2007 B-S mugeE Fel et al-2007, 2008e, 2008, | 3 thyroid hormone elevation 221 (Olsen and Zobel 2007 56 sal ars ea) et al. 3607; 26088, 3609; Fe lincreased total cholesterol, uric acid 4.02 Costa et al. 2009 B-4 20102 { liver enzymes, elevation of ALP, ALT, GGT 4.02 ‘Costa, et al. 2009 BS 0.0056 i emaege meal Ro, I*Derived from Tables B-4 through B-8 in: disease, enzymes increase 0.0059 __Shanker, et al, 2011 8s lUS EPA. Health Effects Support Document for Perfluorooctanoic Acid (PFOA). Washington, DC; U.S. _ }ncreased total cholesterol 0.0071 Eriksen, et al 2013 5-4 Environmental Protection Agency, Office of Water, EPA 822-R-16-003, 322 pages, May 2016.

drinking water the PFC concentrations in blood serum at which non-cancer effects have been observed to occur.

Cancer. PFOA has been associated causally with testicular and renal (kidney) cancer based upon limited evidence in people (US EPA 2014).°” The United Nations International Agency for Research on Cancer (UN IARC) Working Group classified PFOA in Group 2B, “possibly carcinogenic to humans.” Evidently, limited quantitative data on human exposure and on subsequent cancer incidence together have precluded elucidation of the

dose-response curve in the low-dose range in sufficient detail for use in quantitative health risk assessment. Accordingly, regulation based upon carcinogenicity may be forthcoming with more detailed quantification of needed dose-response parameters.

Non-Cancer effects. ATSDR (2015)°* “has derived an intermediate-duration oral MRL [Minimal Risk Level] of 2x10° mg/kg/day [mg/kg d] for PFOA based on a BMDL [benchmark dose level] of 1.54x10° mg/kg/day [mg/kg d] for increased absolute liver weight in monkeys administered

Table 7. Health Advisories and Related Benchmarks for Perfluoroalkyl Compounds*

New Jersey** 40 ppt PFOA “chronic (lifetime)”

New Jersey 10 ppt PFNA interim specific groundwater criterion Vermont 20 ppt PFOA chronic

US EPA, national 400 ppt PFOA short-term

US EPA, Region 2 100 ppt PFOA chronic

US EPA, national 70 ppt PFOA + PFOS lifetime

US EPA, national 20 ppt PFOA Minimum Reporting Level (MRL)

*PFNA: perfluorononanoic acid; PFOA: perfluorooctanoic acid; PFOS: perfluorooctane sulfonate.

**N.J. Dep't of Health, Environmental and Occupational Health Surveillance Program, Drinking Water Facts: Perfluorinated Chemicals (PFCs) in Public Water Systems, http:/www.nj.gov/health/eohs/pfc_in_drinkingwater.shtml.

***Vermont Dep't of Health, PFOA (Perfluorooctanoic Acid), http:/healthvermont.gov/enviro/pfoa.aspx (June 7, 2016).

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PFOA via a capsule for 26 weeks (Butenhoff et al. 2002). The BMDL was estimated using serum PFOA levels as a dose metric; a HED [human equivalent dose] was estimated using an empirical clearance model. The BMDHED was divided by an uncertainty factor of 90 (3 for animal-to-human extrapolation with dosimetric adjustment, 10 for human variability, and 3 for database deficiencies, particularly the lack of developmental and immunological studies in monkeys.”

ATSDR (2015, page 435) also reported: “EPA has not derived reference dose (RfD) or reference concentration (RfC) values of perfluoroalkyl compounds.” The RfD and RfC are limits placed upon exposure via ingestion and inhalation, respectively. They differ significantly, in that the RfD is expressed in units of daily intake per unit of body weight [for example, mg/(kg d)], whereas the RfC is expressed as an airborne concentration (for example, mg/M”).

Both units are derived based upon many assumptions, critically including absorption efficiency (via the digestive or respiratory tract) and the relative source contribution of each exposure route.

In 2009 the U. S. EPA established a Provisional Health Advisory of 0.4 ppb (400 ng/L = 400 ppt) for short-term exposure (up to about two weeks) to PFOA in drinking water. As a concentration rather than an intake dose, the health advisory value is analogous to an RfC. As with RfC derivations, a critical parameter for derivation of the health advisory value was the relative source contribution, which is the share of total PFOA exposure assumed to be attributable to drinking water. EPA, in accordance with policy, assumed that 80 percent of total exposure to PFOA originates from non-drinking water pathways, and that 20 percent of total exposure is attributable to drinking water. In the Village of Hoosick Falls, other sources have been reported, including PFOA containers disseminated to the community and airborne sources of PFOA emitted from manufacturing processes. Such widespread dissemination, combined with the stability of PFOA in the environment, gives rise to the likelihood of biomagnification in the food chain, affecting garden vegetables, fish, and (hunted) birds consumed by residents. Children playing in soil contaminated with PFOA might consume it via hand-to-mouth contact, which tends to be exacerbated among people (children and adults) who habitually mouth non-food items, in a condition known as “pica.” Other exposure pathways of potential significance in the Village and elsewhere include cooking, bathing, and showering.

Inasmuch as most residential exposure to substances via drinking water occurs for years rather than weeks, EPA Region 2 in January 2016 augmented EPA’s 400-ppt short-term exposure advisory for PFOA by issuing an interim chronic health advisory value of 0.1 ug/L (100 ng/L = 100 ppt).°? Chronic exposure refers to an exposure period from a year, more or less, to a period of years, up to exposure for a lifetime, in health risk assessment typically assumed to be 70 years. This interim value

was effective during deliberations over a “final” health advisory value for chronic exposure to PFOA. In April 2016 EPA promulgated its final “lifetime” health advisory value, 70 ppt as the sum of the concentrations of PFOA and PFOS.

Superfund designation. The SGPP McCaffrey Street site acquired New York State Superfund status in 2016 and, via letter of 11 February,” potentially responsible parties (SGPP and Honeywell) were ordered to enter into a consent agreement for site remediation. As of this writing, U.S. EPA classification of PFOA as a hazardous substance has not occurred, but would qualify the site for inclusion on the Federal Superfund’s National Priority List (NPL).

Technology-Based Risk Management

Technology-based risk management includes mitigation and remediation technologies. Remediation of groundwater contamination emanating from a particular source is likely to include pumping to create a “cone of depression,” thereby reversing outward flow of groundwater from the source. Instead, groundwater flow in the vicinity would converge toward the source, at which continued pumping gradually would abate the contamination, eventually all the way to the cleanup goal. Treatment of pumped groundwater could include use of granular activated carbon (GAC) filtration for removal of PFCs and other substances.

When drinking water is contaminated with PFCs, the main mitigation technology used to remove them has been GAC filtration. Filtration units marketed for homes that are supplied by individual private wells, however, may include both GAC and reverse osmosis modules connected in series. GAC treatment has been used for municipal water treatment systems such as the system serving the Village of Hoosick Falls.

The GAC system for the Village consists of two carbon beds operating in series. A performance standard of 20 ng/L (20 ppt) initially was proposed for the Village, on the premise that a more stringent performance standard would be unnecessary and/or infeasible. This claim is false based upon abundant experience in the operation of GAC filters for removal of PFOA, both in the U.S. and abroad. For example, PFOA routinely is removed from water supplied by the Little Hocking Water Association, a rural user-owned water system in Washington County, Ohio. This facility’s GAC system is especially notable because, like the Village’s, the Little Hocking system is configured with two carbon bed units operating in series.

Dual units of two in-series carbon beds operate in the Little Hocking system. PFOA generally is undetected in finished water produced by each of the two units.

The method detection limit (MDL) for PFOA is indicated with each reported sample value, and most commonly it is the nominal MDL of 1.7 ppt for U.S. EPA analytical

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Method 537, which is used widely, including in the Village of Hoosick Falls.

EPA Method 537 invites procedural alterations to reduce its MDL if desired. That is, a lower MDL than 1.7 ppt may be applicable to routine PFOA analysis in finished drinking water. The Little Hocking database, for example, includes multiple samples in which PFOA was undetected at an MDL of 1.0 ppt. If performance at that more sensitive level can be achieved in the Little Hocking system, it unquestionably can be achieved in the Village of Hoosick Falls.

GAC technology is highly effective. Even so it requires close monitoring to quantify the rate at which PFC removal efficiency declines as the adsorptive surface area of the constituent carbon particles gradually but inevitably is exhausted. This raises the inter-related issues of performance standards to which treatment systems must be designed, drinking water sampling frequency, and PFC detection and Minimum Reporting Levels (MRLs). U.S. EPA MRLs for unregulated substances in drinking water are set forth in a document known as UCMR 3° and MRLs for six PFCs are listed in Table 3. EPA’s MRL for PFOA, for example, is < 20 ppt.

Discussion, Conclusions, and Recommendations

PFC Levels in Drinking Water and Blood Serum

PFCs, most notably PFOA and PFOS found in drinking water in the ppt range at which they are toxic, reveal the need for routine monitoring, aggressive cleanup, and promulgation of enforceable regulation to control human exposure, prevent disease, and help to clarify accountability, thereby preventing similar incidents elsewhere. PFOA was introduced into commerce in the 1940s when stringent environmental regulation was nonexistent and routine monitoring of ppt-range residues in environmental media infeasible. Historical data on PFC concentrations typically are unavailable. In view of its long industrial history, however, the Village of Hoosick Falls appears to have experienced unabated exposure to PFOA over a period of years at least, and more likely decades to a century. The time profile of exposure might be inferred from sampling for PFCs emitted to the atmosphere and deposited to the ground, from hydrogeological investigations to quantify PFC entry into groundwater, from data on groundwater direction and flow by depth, and from studies of PFC concentrations at increasing distance downstream (and downwind) of the Saint-Gobain Performance Plastics facility.

By comparison with the Village’s apparently long exposure history, the time required to reach a steadystate level of PFOA in the blood plasma was <17 days in the Lau, et al. (2006) high-exposure mouse study used to derive EPA’s initial (400-ppt) Provisional Health Advisory. The time to achieve steady-state serum concentrations in people exposed to environmental PFOA levels prevailing in the Village is unknown, but

likely to be a small fraction of exposure duration. Once

a steady state is attained, however, concentrations in serum will not decline unless and until exposure ceases or substantially abates. In the absence of exposure, the half-time for human elimination of PFOA, which is not metabolized appreciably, is approximately four years (as documented earlier; see Results section). That means that exposure via drinking water and other sources is subject to a multiplier effect, in which mechanisms of substance toxicity may continue acting for multiples of the exposure duration, for much or all of a lifetime, even after exposure is terminated completely.

In short, PFOA exhibits a “perfect storm” of troubling properties: essentially infinite lifetime in the environment, resistance to human metabolism, bioconcentration in the food chain, transmissibility to infants via breastfeeding, years-long excretion half-time in the human body, and causation of human cancer and non-cancer effects. These properties, along with widespread use in manufacturing Teflon and other widely used products of modern society, have resulted in PFCs becoming ubiquitous contaminants in the global environment. As a result they also have been detected ubiquitously in blood serum in the U.S. sampled around 2000, with median concentrations of 5 ng/mL (ppb) for PFOA and 30 ppb for PFOS. Concentrations in the serum of children have been reported generally to be higher than in adults.

Table 6 lists PFOA concentrations in blood serum that EPA reports as “associated” with specific adverse health effects in people. The concept of “association” encompasses relationships running the full gamut of the degree of certainty of causality, from causal to noncausal (“casual”), for example: “proven cause,” “known cause,” “presumptive cause,” “probable cause,” “likely cause,” and “possible cause.” Many if not most of the studies included in Table 6 are supported by animal bioassays or other data and, accordingly, were included based upon credible public comments or peer review

recommendations.

All of the studies included in Table 6 report on health effects that fall into one or more of five well-documented categories of PFOA adverse health effects. These health effect categories were explicated earlier (in the Results section):

¢ serum lipids, uric acid;

* immunotoxicity,

¢ thyroid disease,

¢ endocrine disruption, and

reproductive and developmental outcomes.

The health effects are grouped within their relevant health effect categories in Table 6a, and form a strong basis for using Table 6b as a basis for comparisons of indi-

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viduals’ PFOA serum levels with the (presumptive) causative serum levels reported in the table.

Aconcept in science generally, and in epidemiology specifically, is that of the default assumption which, in experiments, also may be termed the “null hypothesis.” The weight of evidence subtly shifts the default assumption, which is the assumption that is most likely to be true based upon available evidence. Progress in science occurs when a null hypothesis is tested, whether or not it is refuted, but usually more so if it is refuted. In short, with respect to the studies included in Table 6, PFOA must be regarded as at least the presumptive cause of the reported “associated” adverse health effects.

In public health policy, substances differ from people in our vaunted legal system: as a precaution, substances must be shown, not presumed, to be innocent. A corollary is that health effects cannot scientifically, and should not be dismissed as mere associations with high PFOA levels, without ominous implications for the affected individuals, notwithstanding a recent fact sheet issued by NYS DOH (2016) regarding its biomonitoring (serum PFOA) program.

The NYS DOH (2016) fact sheet regarding its biomonitoring program in the Village of Hoosick Falls fails to acknowledge the high probability that individuals with elevated serum PFOA probably have elevated risk of experiencing adverse health effects with which PFOA is associated, such as those reported in Table 6.” The fact sheet diligently explicates the meaning of “association,” most notably distinguishing it from “causation.” Regarding future risk, however, the fact sheet includes excessively disarming statements, such as:

Individual results only provide exposure information and are not cannot [sic] be used to determine of [sic] whether a person’s current illness is due to PFOA or if a future illness is likely to result from PFOA...

Future studies of PFOA exposure by scientists, public health experts, and government agencies may provide

more definitive information on health effects. Knowledge of an individual’s exposure may be helpful in applying this information in the future.

The NYS DOH fact sheet likewise is excessively disarming in presenting a comparison of “Average PFOA Levels in Blood” in eight populations, where the lowest is the U. S. population: 2 ug/L (ppb). The highest average PFOA level is reported in 3M workers in Decatur, Alabama: 1125 ug/L (ppb). By misleading comparison, “Hoosick Falls area, NY (all participants)” are reported to have an average PFOA level of 23.5 ug/L. Although this is still nearly 12 times the U.S. average, it understates the

magnitude of the serum PFOA elevation caused by PFOA contamination of groundwater emanating from the SaintGobain facility. To capture the magnitude of the resulting serum PFOA elevation, NYS DOH should report the average serum PFOA level in current residents until recently consuming the PFOA-contaminated public water supply, which is drawn from groundwater adjacent to the SaintGobain facility. Instead, the reported average is diluted via inclusion of the relatively low serum PFOA levels

of biomonitoring program participants who are former residents, and people who have private wells, most of which are located at relatively great distance from the Saint-Gobain facility.

Though PFCs persist in the environment, their concentrations in human blood serum declined significantly in the years since 2000,” possibly reflecting their gradual phaseout from U.S. commerce, completed in 2015. Thus, the public health benefit of phasing out PFCs appears to be evident based upon blood serum as an exposure marker, but this benefit clearly is unavailable to communities such as the Village of Hoosick Falls that are situated near a continuing source of PFC contamination. Yet, having been phased out of commerce, PFCs are regulated only by unenforceable health “advisories,” whereas persistent environmental contamination with PFCs would suggest the need for enforceable limits, especially in surface water and groundwater used for direct human consumption, gardening, and agriculture.

As a further concern, NYS DOH’s blood sampling program for Hoosick residents and former residents has resulted in disclosure to participants of their personal PFOA serum levels, and in public disclosure of the range of PFOA serum concentrations found. NYS DOH, however, has failed to disclose to individuals or to the public the range of serum concentrations of other PFCs. Although PFOA has been the predominant PFC detected in water in the Village of Hoosick Falls, only empirical data can reveal whether PFOA likewise is the predominant PFC in blood serum. Residents and former residents may have been exposed to PFCs environmentally, possibly via airborne sources emanating from manufacturing processes at the Saint-Gobain Performance Plastics facility. PFOA levels in serum, therefore, should be viewed in the context of related compounds that are likely also to be present. Moreover, distribution of PFCs in serum is a valuable marker of overall PFC exposure. Finally, SGPP employees might have occupational exposure to other PFCs, not just more exposure to PFOA than non-occupational residents. NYS DOH therefore should expand the scope of its disclosures to individuals and to the public regarding PFCs other than PFOA.

PFC Regulation via Advisories

The 2009 EPA health advisory value of 400 ppt for PFOA in drinking water, though legally unenforceable, nonetheless was influential in guiding the advice provided by some officials on the issue of whether or

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not residents of the Village of Hoosick Falls should consume their PFC-tainted drinking water. Indeed, the unenforceability of the health advisory seems to have precipitated official reversion to a far less stringent, but enforceable, standard of 50,000 ppt. Specifically, in 2015 the Village Newsletter”? reported on advice sought by the Village from the New York State Department of Health. The response, received from the Rensselaer County Department of Health on 12 January 2015, read in part: “Samples taken from the water supply wells on October 2 and November 4, 2014 were found to contain PFOA at levels ranging from 0.17 micrograms per liter (ug/L) to 0.54 ug/L... These levels are below the New York State unspecified organic contaminant public drinking water standard of 50 ug/L” (50,000 ng/L = 50,000 ppt; emphasis added).

The EPA health advisory was essentially irrelevant because it was intended to apply only to shortterm exposure durations of up to about two weeks, commensurate with the 17-day exposure duration used in the Lau, et al. (2006) study on which the advisory was based.”! This exposure duration might be commensurate

Recently the U.S. EPA replaced the Region 2 advisory value of 100 ppt by promulgating a new advisory of 70 ppt for “lifetime” exposure to the sum of PFOA and PFOS concentrations in drinking water nationally. Substitution of the term “lifetime,” which usually refers to 70 years in health risk assessment parlance, for the previously used “chronic,” referring to one year or more, is troubling because it suggests that EPA might regard a (70-times) higher value acceptable for chronic exposure for, say, just one year. Thus, the new 70-ppt “lifetime” advisory for PFOA + PFOS may be interpreted as being less stringent than the Region 2 “chronic” 100-ppt advisory for PFOA alone.

The latest (PFOA + PFOS) EPA national advisory is supported by description of, at best, a lengthy and uncertain pathway toward enforceable regulation.” EPA also has failed to show that its new advisory, even if enforced, is sufficiently stringent to protect public and environmental health. Several support documents” were found on EPA’s website, but none was linked to the advisory. Failure to link the support documents to

“Recently the U.S. EPA replaced the Region 2 advisory value of 100 ppt by promulgating a new advisory of 70 ppt for ‘lifetime’ exposure to the sum of PFOA and PFOS concentrations in drinking water nationally.”

with a typical vacation, but not with residential exposure, which typically is chronic (a year or, more often, multiple years). Accordingly, by the end of January 2016, EPA Region 2 promulgated a health advisory of 100 ppt for chronic exposure to PFOA in drinking water in Region 2.

The 2009 Health Advisory also was challenged by Grandjean and Budtz-Jorgensen (2013) based upon concentrations of PFCs in blood serum vs. immunological effects in children as the critical toxicological end point.” Their conclusion suggests that an appropriate PFOA limit in drinking water would be in the range of just 1 ppt: “when the results are converted to approximate exposure limits for drinking water, current limits appear to be several hundred fold too high. Current drinking water limits therefore need to be reconsidered.”

Similarly, Grandjean and Clapp (2015) found that “carcinogenicity and immunotoxicity now appear to be relevant risks at prevalent exposure levels. Existing drinking water limits are based on less complete evidence than was available before 2008 and may be more than 100-fold too high.””> A confirmatory study also was published, following up previous work in the Faroe Islands, involving children age 13 years.”4 At least one publication has suggested the possible need for a PFOA drinking water acceptability concentration that is even below 1 ppt.”

the health advisory document has the effect of obscuring EPA’s technical justification, and critical comments by peer reviewers and members of the public.

EPA’s support document” for the 2016 PFOA (and PFOS) drinking water advisory indicates that it is based upon “a reference dose (RfD) derived from a developmental toxicity study in mice; the critical effects included reduced ossification in proximal phalanges and accelerated puberty in male pups following exposure during gestation and lactation” (page 9). The mathematics of the derivation are set forth in EPA’s support document, including adjustment of animal dosing to equivalent human dosing. Setting aside the issue of the technical merit of the derivation, the choice of the animal study over available human studies, most notably Grandjean, et al. (2013),”? to derive the advisory is questionable and, indeed, was criticized in peer review.®°

The essential issue is that the Grandjean, et al. (2013) study would produce a lower health advisory value, which is undisputed by EPA. EPA’s basis for the decision to reject the study deserves scrutiny. The study showed that routinely administered childhood vaccinations produced a weaker antibody response among children whose PFC levels in serum were elevated compared with children with lower serum PFC levels. EPA rejected the study because it (and related studies) were confounded

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by multiple PFCs, and because the incidence of disease among children with weaker antibody response to vaccination was not observed to be elevated.*!

EPA often addresses multiple substances together. Examples include chlorinated dioxins, PAHs, and PCBs, even though nearly all studies of the toxicological effects of each of these groups may be confounded by the presence of multiple members of the group in a particular study. Indeed, EPA’s latest health advisory combines PFOA and PFOS. Clearly, an advisory could focus on the sum of all PFCs in addition to the sum of just the two specific PFCs.

EPA interpreted the Grandjean (and related) studies as if they primarily raised the narrow issue of childhood vaccine effectiveness. EPA ignored the broader significance of the Grandjean, et al. (and related) studies: that immunosuppression is a serious clinical outcome for anyone, and especially for children. Immunosuppression signifies that the effectiveness of immunosurveillance is reduced. Immunosurveillance is the essential bodily function of maintaining vigilance to detect invading foreign pathogens, and of mounting an antibody attack against foreign cells or against cancer cells, which a healthy immune system would interpret as “foreign.” Most essentially, immunosurveillance protects children against childhood cancers and against pathogens, whether or not vaccines against them were administered.

EPA did not cite evidence that PFOA (or PFOS, or any PFC) reduces the titer of only a particular vaccination disease target. The reasonable default assumption must be made, therefore, that PFOA-induced (and PFCinduced) immunosuppression is general, not diseasespecific. That is, the assumption must be made that failure to observe elevated incidence of the single vaccine disease target among low-antibody titer children is not probative, and therefore not reassuring, regarding PFOA (or PFC) risk of adverse effects on children.

EPA’s decision to construe Grandjean, et al. (and related studies) narrowly, at the expense of stringency in protecting children’s health, must be viewed in the context of EPA’s longstanding special mandate regarding children’s health, embodied by EPA’s Children’s Health Risk Initiative.*? In 1997 the Office of Children’s Health Protection was instituted within EPA. Its mission was and remains “to make children’s health protection a fundamental goal of public health and environmental protection... [by] ensuring strong standards that protect children’s health...”

PFC Performance Standards for Water Treatment Facilities

The performance standard of 20 ppt that initially was proposed for the GAC system serving the Village of Hoosick Falls water treatment facility was excessive. Given evidence of a long history of PFOA release in the

Village, public health protection requires that the GAC filter performance standard be set at a value that reflects the lowest feasible exposure going forward, with the tandem goals of reducing serum PFOA levels as quickly as possible and preventing disease. These goals are

best met by specifically establishing the most stringent feasible performance standard for PFOA in the water

supply.

Four primary conclusions are drawn below regarding the performance standard that is appropriate for the GAC filter for the Village of Hoosick Falls:

1. All routine analysis for PFOA should be conducted via EPA Method 537 and adhere to its nominal method detection level of 1.7 ppt or better; likewise for other PFCs;

2. All data produced by such analysis should be placed in the public domain,

3. The initially proposed performance standard of 20 ppt for PFOA in finished water is unacceptably high, as is the MRL published in UCMR 3; and

4. The GAC unit should be designed to reduce PFOA in finished water to the minimum concentration found to be feasible for routine sampling, which evidently is in the range of 1.0 to 1.7 ppt based upon experience of the Little Hocking water system in Ohio.

NYS DOH Cancer Cluster Analysis in the Village of Hoosick Falls

Reports of rare cancers and clusters of more common cancers in the Village of Hoosick Falls roughly coincided with discovery of PFOA in drinking water. The New York State Department of Health (NYS DOH) therefore is undertaking a health study to investigate possible cancer clustering, termed “unusual elevations.”*° The scope of the NYS DOH community health study should be expanded to include non-cancer effects. The cancer study also should include the following features:

¢ Adopt a health-protective criterion of statistical significance to trigger further investigation of cancer clusters, rather than 95-percent confidence, to assure that real clusters will not be interpreted as statistical flukes;

¢ Consider rare cancers, whose incidence is expected to be zero in the small population of Hoosick Falls (about 5,000), not just more common cancers in the Cancer Registry. Reports of multiple types of rare cancers are even more unlikely statistically, unless caused by stressors, and should be considered probabilistically together, not just individually, in isolation;

¢ Conduct a prospective health risk assessment to supplement retrospective assessment of cancer

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cases. Elevations of cancer incidence might be statistically insignificant, even in the presence of real cancer causes;

¢ Incorporate the time dimension into cancer incidence analysis. The time period of the NYS DOH study, 1995 through 2012, should be expanded using ancillary data. The longer period should be subdivided into time windows to examine possible trends in the appearance of cancer cases, such as individual years as illustrated in Kulldorff, et al. 1998);54

* Conduct detailed investigations aimed at attributing cancers to specific causes. NYS DOH fails to state the objective of elucidating the cause(s) of “unusual elevations” that might be found; and

¢ Consider anecdotal and other ancillary data, such as documented cancers among coworkers or among pets living in the same household. Animals may be more intimately associated than people with the water, soil, and biota in their outdoor environment. NYS DOH fails to explicate that such potentially probative data will be sought and used.

The standard of 95-percent confidence typically adopted in academic scientific publications, including for cancer cluster identification (Kulldorff, et al. 1998), may be inappropriate where human health and human lives are at stake, because it might result in rejection of real cancer clusters that might be, say, only 90 percent certain not to have occurred by chance alone. Classifying a cancer cluster as real may be required to justify measures, such as health monitoring, to protect life and health. Such protective measures should be taken if a cluster probably is real (a common legal standard: more probable than not), not just when it is 95-percent certain to be real.

The small size of the population of the Village of Hoosick Falls limits sample sizes, and thereby increases the degree of cancer incidence elevation needed to attain statistical significance and recognize cancer clusters. The small size of the study population, however, can be and should be used to advantage statistically with respect to rare cancers, whose incidence in a small population would be expected to be zero. The occurrence of unusual or rare cancers among Village residents should be accorded due weight. NYS DOH plans to study “total cancers and specific types of cancer,” but fails to assure that the specific types will include rare cancers, even if absent from the Cancer Registry, or to describe how rare cancers might be evaluated, specifically, the statistical significance that they might be accorded if found in a small population in which they might be unexpected. Finally, NYS DOH fails to describe how the Agency might interpret multiple types of rare cancers occurring in the Village, where each individually might be unexpected in such a small population, but all of which considered together might be expected to co-occur so rarely as to

demand explanation as a real cancer cluster rather than an inevitable statistical deviation from randomness.

All effects have causes and, specifically, all cancer cases have causes. Investigation of particular populations, such as Village residents and Saint-Gobain Performance Plastics Corporation employees, might reveal active cancer causes, and possibly might rule out inactive causes, even in the absence of any statistical elevation of cancer incidence at all. For example, the occurrence of related cancers among all members of a work team might be attributable to occupational exposure to PFOA, even in the absence of a statistical signal when cases among these coworkers are diluted into the larger population of SaintGobain employees, or into the even larger population of Village residents.

Public health professionals, like scientists generally, are accustomed to applying the 95-percent confidence criterion of statistical significance (P <0.05). The goal is to be conservative, that is, to protect the body of scientific knowledge from corruption by errors introduced by inadequate stringency. Public health professionals, however, simultaneously are responsible for being conservative in protecting human health and human life. Indeed, the American Statistical Association recently issued a statement to combat pervasive misunderstanding in the scientific, business, and public policy communities of the 95-percent confidence limit and its routine, often inappropriate, application.®

Being conservative requires giving serious consideration to observed associations that probably are causal rather than casual, or even to associations that only might be causal rather than casual. Public health professionals cannot overlook a cancer cluster, for example, because it is only 90 percent likely to be real rather than a statistical fluke. In statistics terms, the conflict is between Type 1 vs. Type 2 errors: rejecting a true null hypothesis (for example, a real cancer cluster is not recognized) vs. accepting a false null hypothesis (for example, a statistical fluke is interpreted as a real cancer cluster).

The conflict between conservatism in the interest of academic science vs. public health protection has not always been resolved in favor of the latter. Investigating brain cancers in Los Alamos, New Mexico, Kuldorff, et al. (1998),5° using a widely accepted statistical program called SaTScan, found that perceived clusters actually were statistical flukes: “The community was informed that such a finding could easily have resulted from random fluctuation in the incidence of a rare disease within a small population... With adjustment for age, sex, and race, the most likely cluster is in the Albuquerque-Santa Fe area during 1985 through 1989... With a P value of 0.074 [92.6 percent confidence limit], the cluster is not statistically significant” (pages 1378-9). Even so, it might have been real; it might have been caused by an environmental stressor, such as radioactivity of recent vintage, or radioactive residues

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dating back to the era of the Manhattan Project at Los Alamos.

In the case of the Village of Hoosick Falls, a strictly statistical approach narrowly focusing on incidence data seems fraught with the peril of overlooking possible clusters that are worthy of further, detailed investigation. The challenge after recognizing a cluster is attributing a cause or probable cause to it, if possible. This is another function of further, detailed investigation. In short, suggestive data should be investigated further, in detail, to avoid overlooking cancer clusters and cancer cluster causes.

Setting Enforceable PFC Regulations for the Nation

Revise Reporting Limits for PFCs. Reporting limits for unregulated substances are set forth in a U.S. EPA publication nicknamed UCMR-3.*” Determination of safe levels of PFCs in water, however, is underway, not completed. Until completion, a conservative approach to PFC reporting is appropriate. UCMR-3 therefore should be updated to specify reporting limits for PFCs that are identical to EPA Method 537 detection limits for PFCs. Higher reporting limits eventually might be justified but, until then, they are unjustified and potentially harmful because they can hide PFCs detected in water at concentrations below the current reporting limit that still might be found to be unsafe as a result of deliberations that are under way.

Revise basis for PFOA drinking water health advisory. The PFOA component of the most recent U.S. EPA advisory is based upon animal bioassay data rather than human immunosuppression studies as previously described, most notably in children. EPA’s justification fails, as also described earlier. If more persuasive reasoning were available, presumably EPA would have applied it. Accordingly, EPA should derive its drinking water advisory based upon the human immunosuppression studies, unless the Agency indeed can justify its contrary approach using more persuasive reasoning.

Issue drinking water health advisories for more PFCs. EPA’s most recent advisory addresses PFOA and PFOS, but not the suite of four additional PFCs that are measured routinely via Method 537, and not the numerous additional PFCs to which people might be exposed in their drinking water and/or environmentally. Accordingly, EPA should expand the scope of advisories for PFCs to include at least those that are routinely measured via Method 537, and possibly additional PFCs as well. Toward this goal, EPA should consider structureactivity relationships (SARs) to the maximum extent justifiable given the available data.

SARs may be discerned qualitatively and possibly also quantified, producing either qualitative or

quantitative SARs for PFCs, as exemplified by Hagenaars, et al. (2011). In either case SARs are derived based upon the premise that substances exhibiting similar chemical structure (structural analogs) often also

exhibit similarities in other properties. This may make them useful commercially, resulting in substitutions

of structural analogs when regulations preclude use

of an analog that is in use, but then is banned for use. Structural analogs, however, also may exert similar toxic effects, which makes them dangerous to introduce into commerce without prior safety testing. Accordingly, EPA’s approach to expanding the scope of its PFC health advisories should be pro-active, with maximum justifiable use of SARs.

Promulgate enforceable regulations for PFCs. PFOA and other PFC risks may be managed, retrospectively, via PFC classification as hazardous substances, and PFC site inclusion among State and Federal Superfund sites. Available data also support creation of enforceable regulations for PFOA and other PFCs to manage risks prospectively. EPA’s most recent health advisory for “lifetime” exposure to the sum of PFOA and PFOS in drinking water, however, is supported by description of, at best, an uncertain and lengthy pathway toward enforceable regulation. Such regulations potentially should include promulgating primary drinking water standards for PFCs under the Safe Drinking Water Act, and establishing cleanup targets under Superfund and other laws.

Summary. The present investigation reveals that EPA has issued three successive health advisories for PFOA in drinking water, moving from a “sub-chronic” exposure value of 400 ng/L to a “chronic” value of 100 ng/L and, most recently, to a (PFOA + PFOS) “lifetime” value of 70 ng/L. The present investigation also concludes that EPA has failed to show that its latest advisory, even if enforced, is sufficiently stringent to protect public and environmental health. The process of successive approximation toward an enforceable national standard must be concluded, and a more appropriate, enforceable value identified and promulgated forthwith. Available data explicated in Findings support the following U. S. EPA actions:

¢ Update UCMR-3 to incorporate Method 537 MDLs for PFCs;

¢ Revise the PFOA drinking water health advisory by basing it on immunosuppression, most notably as documented in children;

¢ Issue drinking water health advisories for more PFCs;

¢ Designate PFCs as hazardous substances and PFCcontaminated sites as eligible for inclusion in the Federal Superfund’s NPL; and

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¢ Promulgate enforceable national regulations / standards for PFOA and other PFCs in environmental media such as water and soil.

Endnotes

1.

10.

1.

12.

13.

14.

Units used:

parts per trillion (ppt) = nanograms per liter (ng/L) = 107; parts per billion (ppb) = micrograms per liter(ug/L) = 10°; parts per million (ppm) = milligrams per liter (mg/L) = 10°; Conversion: ug/mL = mg/L = ppm.

U.S. Dep’t of HEALTH & HUMAN SERVICE, PuB. HEALTH SERV., AGENCY FOR Toxic SUBSTANCES & DISEASE REGISTRY, DRAFT ToxICOLOGICAL PROFILE FOR PERFLUOROALKYLS (Aug. 2015) [hereinafter ATSDR], http: //www.atsdr.cde.gov /ToxProfiles/ tp200.pdf (last visited Aug. 15, 2016).

Amy PocHopyLo & DEMIAN E. HELBLING, TARGET SCREENING FOR MICROPOLLUTANTS IN THE HuDSON RIVER EsTuARY DURING THE 2015 RECREATIONAL SEASON (Cornell University, College of Agriculture & Life Sciences, New York State Water Resources Institute), http:// www.riverkeeper.org/wp-content /uploads/2016/07/AppendixA-2015-progress-report.pdf (last visited Aug. 15, 2016).

Toxic Substances Control Act of 1976, 15 U.S.C. §§ 2601-2697 (West, Westlaw through PL. 114-200 (also includes PL. 114-202 to 114-219).

Gloria B. Post et al., Occurrence of Perfluorinated Compounds in Raw Water from New Jersey Public Drinking Water Systems, 47 ENVL. Sct. & TEcu. 266-75 (2013).

Letter from Attorney David G. Servadi, Keller and Heckman, LLC (Washington, D.C.) to TSCA Confidential Business Information Center (Washington, DC) on behalf of Saint-Gobain Performance Plastics Corporation (SGPP; Village of Hoosick Falls, Rensselaer County, New York) (Dec. 30, 2014), http:// www.villageofhoosickfalls.com /Water /Documents/SaintGobainLetterToEPA_Re_TSCA.pdf (last visited Aug. 15, 2016).

Marie J. French, New York State: Saint-Gobain, Honeywell International responsible for Hoosick Falls water contamination, ALBANY Bus. Rev., Feb. 11, 2016, http:/ / www.bizjournals.com/albany / news/2016/02/11/new-york-state-says-saint-gobain-honeywell. html (“The agency did not rule out holding other companies liable as the investigation moves forward.”) (last visited Aug. 15, 2016).

Village of Hoosick Falls, Municipal Water, Overview, http://www. villageofhoosickfalls.com/Water/ (last visited Aug. 15, 2016).

Village of Hoosick Falls, Annual Drinking Water Quality Report for 2014, http:/ /www.villageofhoosickfalls.com/Media/PDE/ WaterQualityReport2014.pdf (last visited Aug. 15, 2016).

Village of Hoosick Falls. Village Water Quality Update, page 3 of 14 pages; 14 September 2015.

J. A. SHOEMAKER, P. E. GRIMMETT & B.K. Boutin, DocuMENT No. EPA/600/R-08/092, METHOD 537. DETERMINATION OF SELECTED PERFLUORINATED ALKYL ACIDS IN DRINKING WATER BY SOLID PHASE EXTRACTION AND LIQUID CHROMATOGRAPHY / TANDEM Mass SPECTROMETRY (LC/MS/MS), U. S. ENVIRONMENTAL PROTECTION AcENcY, Nat’L Exposure RESEARCH Las. OFFICE OF RESEARCH AND Dev. (Sept. 2009).

U.S. EPA, OFFICE OF WaTER, EPA 822-R-16-003, HEALTH EFFECTS Support DOCUMENT FOR PERFLUOROOCTANOIC AcID (PFOA) (May 2016) [hereinafter EPA PFOA Health Effects], https:/ / www.epa. gov/sites /production/files/2016-05 /documents/pfoa_hesd_ final_508.pdf (last visited Aug. 15, 2016).

Arlene Blum et al., The Madrid Statement on Poly- and Perfluoroalkyl Substances (PFCs), 123 ENVL. HEALTH Persp. A107, A107-11 (May 2015), http: //ehp.niehs.nih.gov /wp-content/uploads/123/5/ ehp.1509934.alt.pdf (last visited Aug. 15, 2016).

ATSDR, supra note 2, at 11.

15.

16. 17.

18. 19. 20. 21.

23.

24.

25.

26.

27. 28.

Valentina Gallo et al., Serum Perfluorooctanoate (PFOA) and Perfluorooctane Sulfonate (PFOS) Concentrations and Liver Function Biomarkers in a Population with Elevated PFOA Exposure, 120 ENVL. HEALTH Persp. 655, 655-60 (May 2012).

ATSDR, supra note 2, at 295.

L. L. Needham; P. Grandjean, B. Heinzow, et al., Partition of Environmental Chemicals Between Maternal and Fetal Blood and Tissues, 45 ENVL. Sct. & TECH. 1121, 1121-26 (2011); A. E. Loccisano, M. P. Longnecker, J. L. Campbell, Jr, et al., Development of PBPK models for PFOA and PFOS for Human Pregnancy and Lactation Life Stages. 76 J. oF ToxicoLocy & ENVL. HEALTH A. 25, 25-57 (2013).

ATSDR, supra note 2, at 11. Id. Id.

B. D. Kerger; T. L. Copeland & A. P. DeCaprio. Tenuous Doseresponse Correlations for Common Disease States: Case Study of Cholesterol and Perfluorooctanoate/Sulfonate (PFOA/PFOS) in the C8 Health Project, 34 DRUG CHEMISTRY & TOXICOLOGY 396, 396-404 (Oct. 2011).

A.M. Ingelido et al., Perfluorooctanesulfonate and Perfluorooctanoic Acid Axposures of the Italian GeneralPpopulation, 80 CHEMOSPHERE 1125, 1125-30 (Aug. 2010).

NYS DOH. Hoosick Falls and Town of Hoosick Questions and Answers About PFOA Blood Testing Program, Albany, New York; New York State Department of Health, 6 pages, http:// www.villageofhoosickfalls.com /Water /Documents/ HealthMonitoringFactSheet-06022016.pdf, June 2016;

ATSDR, supra note 2, at 240-41. (Regarding possible PFOA mutagenicity ATSDR also found:

A significant increase in mutation frequencies was observed in hamster-human hybrid cells exposed

to 200 pM PFOA for 1-16 days; a 79% decrease in cell viability was also observed at this concentration (Zhao et al. 2011). Concurrent treatment with

a ROS inhibitor significantly decreased the mutagenic potential, indicating that ROS may play an important role in mediating the genotoxic effects of PFOA. PFOA induced DNA damage in Paramecium caudatum following exposure to 100 pM for 12 and 24 hours (Kawamoto et al. 2010). Intracellular ROS was significantly increased and DNA damage was not reversed by the application of glutathione, a ROS-inhibitor, indicating that intracellular ROS may not be the cause of PFOA-induced DNA damage. PFOS did not induce DNA damage in this study. In contrast, no increases in DNA damage or micronuclei formation were found in human hepatoma HepG2 cells following a 24-hour exposure to PFOA concentrations as high as 800 pM (Florentin et al. 2011); cytotoxicity was observed at >200 pM. Eriksen et al. (2010) also found no evidence of DNA damage in HepG2 cells incubated with 100 or 400 »M PFOA for 24 hours.).

Vaughn Barry, Andrea Winquist & Kyle Steenland, Perfluorooctanoic Acid (PFOA) Exposures and Incident Cancers among Adults Living Near a Chemical Plant, 121 ENVL. HEALTH PERsP. 1313, 1313-18, http: / / dx.doi.org /10.1289 /ehp.1306615 (Nov.-Dec. 2013).

Kirsten T. Eriksen et al., Perfluorooctanoate and Perfluorooctanesulfonate Plasma Levels and Risk of Cancer in the General Danish Population, 101 J. of THE Nat’L CANCER INST. 605, 605-609, doi: 10.1093 /jnci/djp041, jnci.oxfordjournals.org, first published online April 7, 2009;

Barry, supra note 25, at 1313.

Verénica M. Vieira et al., Perfluorooctanoic Acid Exposure and Cancer Outcomes in a Contaminated Community: A Geographic Analysis,

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121 ENVL. HEALTH Pers. 1, 1-7 (Mar. 2013) http://ehp.niehs.nih. 44. Kirsten T. Eriksen et al., Association Between Plasma PFOA and gov/1205829/ (last visited Aug. 15, 2016). PFOS Levels and Total Cholesterol in a Middle-Aged Danish Population, 29. Lamia Benbrahim-Tallaa, Carcinogenicity of Perfluorooctanoic Acid, PLOS ONE (Feb. 18, 2013), http://journals.plos.org/plosone/ Tetrafl Uoroethylene, Dichloromethane, 1,2-Dichloropropane, and arielerid= 10.1571 /journal.pone.0056969 (last visited Aug. 15, 1,3-Propane Sultone (July 10, 2014) 15 THe Lancet 924~25, www. )- thelancet.com/oncology (last visited Aug. 15, 2016). 45. B.D. Kerger, T. L. Copeland & A.P. DeCaprio, Tenuous Dose30. ATSDR, supra note 2, at 18. Response Correlations for Common Disease States: Case Study of Cholesterol and Perfluorooctanoate/sulfonate (PFOA/PFOS) in the C8 31. G.W. Olsen, J. L. Butenhoff & L. R. Zobel, Perfluoroalkyl Chemicals Health Project, 34 DRUG CHEMIsTRY & ToxICOLoGy 396, 396-404 (Oct. and Human Fetal Development: An Epidemiologic Review with Clinical 2011). and Toxicological Perspectives, 27 REPRODUCTIVE TOXICOLOGY 212, 212-30 (June 2009). 46. Gallo, supra note 15, at 655. 32. D. Caserta et al., The Influence of Endocrine Disruptors in a Selected 47. ATSDR, supra note 2, at 304. (“The available data from Population of Infertile Women, 29 GYNECOLOGICAL ENDOCRINOLOGY epidemiology and animal studies are inconclusive to evaluate , 7 (May 2013). whether the toxicity of perfluoroalkyls is mediated through the 444, 444-4 'y neuroendocrine axis or whether they have the ability to mimic or 33. C. La Rocca et al., Exposure and Effective Dose Biomarkers for block endogenous hormone. . . The effects observed in humans Perfluorooctane Sulfonic Acid (PFOS) and Perfluorooctanoic Acid and/or animals exposed to perfluoroalkyls that may be related (PFOA) in Infertile Subjects: Preliminary Results of the PREVIENI to a disruption of the endocrine system include alterations in Project, 215 INT'L J. OF HYGIENE AND ENVL. HEALTH 206, 206-11 (Feb. reproductive hormone levels, infertility, development of the 2012). reproductive system, alterations of the endometrium or mammary 34. Chunyuan Fei et al., Maternal Levels of Perfluorinated Chemicals and gland, and alterations in the function of endocrine glands such as Subfecundity, HUMAN REPRODUCTION, 212-30 (May 2009). the thyroid.”). 35. Lyndsey A. Darrow, Chery R. Stein & Kyle Steenland, Serum 48. Kyle Steenland, Liping Zhao, Andrea Winquist & Christine Parks, Perfluorooctanoic Acid and Perfluorooctane Sulfonate Concentrations Ulcerative Colitis and Perfluorooctanoic Acid (PFOA) in a Highly in relation to birth outcomes in the mid-Ohio Valley, 2005-2010, 121 Exposed Population of Community Residents and Workers in the MidEnvi. HEALTH Persp. 1207, 1207-13, http:/ /dx.doi.org/10.1289/ Ohio Valley, 121 ENVL. HEALTH Persp. 900, 900-05 (2013), http:// ehp.1206372 (last visited Aug, 15, 2016). dx.doi.org/10.1289 /ehp.1206449 (last visisted Aug. 15, 2016). 36. Benjamin J. Apelberg et al., Cord Serum Concentrations of 49. Hines, supra note 41, at 97. Perfluorooctane Sulfonate (PFOS) and Perfluorooctanoate (PFOA) 50. MK. Skinner et al., Ancestral Dichlorodiphenyltrichloroethane (DDT) in Relation to Weight and Size at Birth, 115 ENVL. HEacrH Persp. Exposure Promotes Epigenetic Transgenerational Inheritance of Obesity, 1670, 1670-76, http:/ / www.ncbi.nlm.nih.gov/pmc/articles/ 11 BMC Mep. 228 (2013). PMC2072847/ (last visited Aug. 15, 2016). 51. Thorhallur I. Halldorsson et al., Prenatal Exposure to 37. C. Fei et al., Perfluorinated Chemicals and Fetal Growth: A Study Perfluorooctanoate and Risk of Overweight at 20 Years of Age: A Within the Danish National Birth Cohort, 115 ENVL. HEALTH Persp. Prospective Cohort Study, 120 ENVL. HEALTH Persp. 668, 668-73 (May 1677, 1677-82 (Nov. 2007). 2012); R.R. Newbold et al., Effects of Endocrine Disruptors on Obesity, 38. M.P. Hamm et al., Maternal Exposure to Perfluorinated Acids and 31 INT'L J. oF ANDROLOGY 201, 201-08 (2008). Fetal Growth, J. or Exposure Sct. & ENVL. EPIDEMIOLOGY 589, 589-97 52. Kerry Grens, Obesogens—Low doses of environmental chemicals (Nov. 2010). can make animals gain weight. Whether they do the same to humans 39. David A. Savitz et al., Perfluorooctanoic Acid Exposure and Pregnancy isa thorny issue, Te Screntist (Nov. 1, 2015), http://www.theOutcome in a Highly Exposed Community, 23 EPtDEMIOLOGY 386 (May scientist.com/?articles.view /articleNo/44278 /title/Obesogens 2012). (last visited Aug. 15, 2016). 40. Deirdre K. Tucker et al., The Mammary Gland is a Sensitive Pubertal 53. EPA PFOA Health Effects, supra note 12, at 3-24. (“Antibody Target in CD-1 and C57Bl/6mice Following Perinatal Perfluorooctanoic responses to diphtheria and tetanus toxoids following Acid (PFOA) Exposure, 54 REPRODUCTIVE ToxICoLocy 26, 26-36 childhood vaccinations were assessed in context of exposure (2015). to five perfluorinated compounds (Grandjean et al. 2012). The . — A rospective study included a birth cohort of 587 singleton births 41. EP Hines et al., Phenotypic Dichotomy Following Developmental during 1999-2001 from the National Hospital in the Faroe Islands. Exposure to Perfluorooctanoic Acid (PFOA) in Female CD-1 Mice: Low Serum antibody concentrations were measured in children at age Doses Induce Elevated Serum Leptin and Insulin, and Overweight in 5 boost imately 4 weeks after the boost. d a years prebooster, approximately 4 weeks after the booster, an Mid-life, 25 MOLECULAR & CELLULAR ENDOCRINOLOGY 97, 97-105 at age 7 years. Prenatal exposures to perfluorinated compounds (May 2009). were assessed by analysis of serum collected from the mother 42. A DuPont LeGAcy: PFOA PoLLution (Delaware Riverkeeper, May during week 32 of pregnancy (PFOA geometric mean 0.0032 2009), http:/ / www.delawareriverkeeper.org /sites /default/files/ ng/mL; IQR 0.00256~0.00401); postnatal exposure was assessed resources /Factsheets /fact%20sheet.pfoa.final%205.09.pdf (last from serum collected from the child at 5 years of age (PFOA visited Aug. 15, 2016); Andrew Welsh-Huggins, Woman Awarded geometric mean 0.00406 pg/mL; IQR 0.00333-0.00496). Multiple $1.6 Million Over DuPont Chemical in Water, AssoctaTED Press (Oct. regression analyses with covariate adjustments were used to 7, 2015); Tiffany Kary & Denise Trowbridge, Dupont, Chemours estimate the percent difference in specific antibody concentrations handed another loss in Teflon chemical case, BLOOMBERG News, July 6, per twofold increase in PFOA concentration in both maternal 2016, http: / /www.bloomberg.com/news/articles/2016-07-06/ and 5-year serum. Maternal PFOA serum concentration was dupont-loses-third-case-over-teflon-toxin-chemours-to-pay (last negatively associated with antidiphtheria antibody concentration visited Aug. 15, 2016). (-16.2%) at age 5 before booster. The biggest effect was found 43. U.S. Dep’t or HEALTH & HUMAN SERVICE, Pus. HEALTH SERV., in comparison of antibody concentrations at age 7 with serum AGENCY FOR Toxic SUBSTANCES & DISEASE REGISTRY, HEALTH PFOA concentrations at age 5 where a twofold increase mn PFOA ConsuLTATION: 3M CHEMOLITE, PERFLUOROCHEMICAL RELEASES was assoc iated with differences of 36 %o (95% CI, -52%~14%) and AT THE 3M—Corrace Grove FAcILtty, Crty oF Corrace -25' % (95! % CI, -43%—2%) for tetanus and diphtheria, respectively. Grove, WASHINGTON County, MINNESOTA; EPA Facitity ID: Additionally at age 7, asmall percentage of children had MND006172969 (Feb. 18, 2005), 27. antibody concentrations below the clinically protective level of 0.1 108 NYSBA The New York Environmental Lawyer | Fall 2016 | Vol. 36 | No.2

54. 55. 56. 57. 58. 59.

61.

62.

63.

65.

international unit (IU) /mL. The ORs of antibody concentrations falling below this level were 4.20 (95% CI, 1.54~11.44) for tetanus and 3.27 (95% CI, 1.43-7.51) for diphtheria when age 7 antibody levels were correlated with age 5 PFOA serum concentrations. Maternal and child PFOS levels also were negatively associated with antibody titers...”).

ATSDR, supra note2, at 313-14.

Id.

EPA PFOA Health Effects, supra note 12, at B-6-B-14. Id.

ATSDR, supra note 2, at 435.

U.S. ENVL. PRot. AGENCY, STATEMENT ON PRIVATE WELLS IN THE Town oF Hoosick AND VILLAGE OF Hoosick FALts, N.Y. (Jan. 28, 2016) (“The EPA is developing a lifetime health advisory level for PFOA. While this work continues, the EPA recommends that people in the Town of Hoosick and the Village of Hoosick Falls who have private wells at which PFOA has been found to be present at a level greater than 100 parts per trillion not use that water for drinking or cooking...”).

Letter from Thomas Berkman (New York State Dep’t of Envl. Conservation, Deputy Commissioner) to Edward Canning (Global Environmental Health and Safety Manager, Saint-Gobain Performance Plastics) and D. Evan Van Hook (Corporate Vice President, Honeywell International, Inc.) (Feb. 11, 2016), http:// www.dec.ny.gov /docs/administration_pdf/pfoa.pdf (last visited Aug. 15, 2016).

USS. ENVL. PRor. AGENCY, OFFICE OF WATER, EPA 815-F-12-003, THE THIRD UNREGULATED CONTAMINANT MONITORING RULE (UCMR3)— FACT SHEET FOR ASSESSMENT MONnrIrTORING OF List 1 CONTAMINANTS (May 2012), https:/ / www.epa.gov /dwucmr/third-unregulatedcontaminant-monitoring-rule (last visited Aug. 16, 2016).

A. M. Calafat, Z. Kuklenyik, J. A. Reidy, et al., Serum Concentrations of 11 Polyfluoroalkyl Compounds in the U.S. Population: Data From the National Health and Nutrition Examination Survey (NHANES), 41 Envl. Sci. & Tech. 2237, 2237-42 (2007).

Philippe Grandjean & Richard Clapp, Perfluorinated Alkyl Substances: Emerging Insights Into Health Risks, 25 NEw SOLUTIONS: AJ. or ENvL. & OccupaTIONAL HEALTH Poticy 147, 147-63 (2015); K. Kato, A. M. Calafat, L. Y. Wong, et al., Polyfluoroalkyl Compounds in Pooled Sera From Children Participating in the National Health and Nutrition Examination Survey 2001-2002, 43 ENVL. Sct. & TECH. 2641, 2641-47 (2009).

USS. ENVL. PRor. AGENCY, OFFICE OF WATER, EPA 822-R-16-005, DRINKING WATER HEALTH ADVISORY FOR PERFLUOROOCTANOIC ACID (PFOA) (May 2016), https://www.epa.gov /sites /production/ files /2016-05/ documents /pfoa_health_advisory_final_508.pdf (last visited Aug. 15, 2016), Appendix B: Studies Evaluated Since August 2014.

5. The study elucidates the mode of action for any toxicity endpoint or toxicokinetic property associated with PFOA exposure.

6. The effects observed differ from those in other studies with comparable protocols.

A.B. Hill, The Environment and Disease: Association or Causation? 58 PROCEEDINGS OF THE Royat Soc. OF MED. 295, 295-300 (1965).

N.Y.S. Dep’t of Health, PFOA Biomonitoring (Blood Sampling) Program, https://www.health.ny.gov /environmental/ investigations /hoosick/docs/pfoa_blood_sampling_q_ and_a_8-1-16.pdf (last visited Aug. 15, 2016):

5. What do the studies show about health effects, cancer, and PFOA exposure? Some human health studies have found associations between PFOA exposure and health effects. Others have not. The studies that found associations were not able to

67.

69.

70.

71.

72.

73.

determine with certainty if the health effects were

caused by PFOA or some other factors. These studies

did not show that PFOA caused diseases...

An association does not mean that one thing caused the other. For example, people with blue eyes

tend to be taller than people with other eye colors. This is an association. However, eye color does

not cause people to be taller and height does not cause people to have blue eyes. Northern European ancestry is known to be associated with blue eyes, and Northern European ancestry is associated with being relatively tall. But genetics alone do not cause increased height. Other factors, such as nutrition, are important as well.

[emphasis added]. Id.

What do the studies show about health effects, cancer, and PFOA exposure?

Some human health studies have found associations between PFOA exposure and health effects. Others have not. The studies that found associations were not able to

determine with certainty if the health effects were caused

by PFOA or some other factors. These studies did not

show that PFOA caused diseases...

An association does not mean that one thing caused the other. For example, people with blue eyes tend to be taller than people with other eye colors. This is an association. However, eye color does not cause people to be taller and height does not cause people to have blue eyes. Northern European ancestry is known to be associated with blue eyes, and Northern European ancestry is associated with being relatively tall. But genetics alone do not cause increased height. Other factors, such as nutrition, are important as well” [emphasis added].

“The level shown for PFOA in blood for the Hoosick Falls area is the geometric mean and is based on test results for 2,081 participants including people using Village water, people using private wells, people who work in the area, and former residents.” N.Y.S. Dep't of Health, PFOA Biomonitoring (Blood Sampling) Program, https://www. health.ny.gov /environmental/ investigations /hoosick/docs/ pfoa_blood_sampling_q_and_a_8-1-16.pdf (last visited Aug. 15, 2016).

K. Kato, L. Y. Wong, L. T. Jia, et al., Trends in Exposure to Polyfluoroalkyl Chemicals in the U.S. Population: 1999-2008, 45 ENVL. Sct. & TEcu. 8037, 8037-45 (2011); G. W. Olsen, C. C. Lange, M. E. Ellefson, et al., Temporal Trends of Perfluoroalkyl Concentrations in American Red Cross Adult Blood Donors, 2000-2010, 46 Envl. Sci. & Tech. 6330, 6330-38 (2012).

Village of Hoosick Falls, Village Water Quality Update, page 3 of 14 pages; 14 September 2015.

C. Lau, J.R. Thibodeaux, R.G. Hanson, et al., Effects of Perfluorooctanoic Acid Exposure During Pregnancy in the Mouse, 90 ToxicoLocicat Scr. 510, 510-08 (2006). On Jan. 14, 2015, a public meeting was held in the Village of Hoosick Falls, at which I alerted attending EPA Region 2 officials of the irrelevance of the EPA Provisional Health Advisory.

Philippe Grandjean & Esben Budtz-Jorgensen, Immunotoxicity of Perfluorinated Alkylates: Calculation of Benchmark Doses Based on Serum Concentrations in Children, 12 ENVL. HEALTH 1, 1-7 (2013), http: / /www.ehjournal.net/content/12/1/35 (last visited Aug. 15, 2016).

Philippe Grandjean & Richard Clapp, Perfluorinated Alkyl Substances: Emerging Insights Into Health Risks, 25 NEw SOLUTIONS: AJ. or ENvL. & OccupaTIONAL HEALTH Poticy 147, 147-63 (2015).

NYSBA The New York Environmental Lawyer | Fall 2016 | Vol.

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74.

Philippe Grandjean, Carsten Heilmann, Pal Weihe, Flemming

Nielsen, Ulla B. Mogensen & Esben Budtz-Jorgensen, Serum 81

Vaccine Antibody Concentrations in Adolescents Exposed to Perfluorinated Compounds, ENvL. HEALTH Persp., Advance Publication, (Aug. 9, 2016) http:/ /dx.doi.org/10.1289 /EHP275 (last visited Aug. 15, 2016).

15, 2016). DeWitt Comment and EPA Response:

B. Granum, L. S. Haug, E. Namork, et al., Pre-natal Exposure to Perfluoroalkyl Substances May be Associated with Altered Vaccine Antibody Levels and Immune-Related Health Outcomes in Early Childhood, 10 J. of IMMUNOTOXICOLOGY 373, 373-79 (2013).

75. Bill Walker & David Andrews, Teflon Chemical Unsafe at Smallest Doses—EPA’s “Safe” Level is Hundreds or Thousands of Times Too C. Looker, M.I. Luster, A.M. Calafat, et al., Influenza Vaccine Weak, ENVIRONMENTAL WorkKING Grovr, http://www.ewg.org/ Response in Adults Exposed to Perfluorooctanoate and Perfluorooctane research/teflon-chemical-harmful-at-smallest-doses (Aug. 2015). Sulfonate, 138 ToxtcoLocicat Scr. 76, 76-88 (2014).

76. U.S. ENVL. Prot. AGENcy, Fact SHEET: PFOA AND PFOS Any time the Grandjean et al. (2012) findings related DRINKING WaTER HEALTH ADvisorigs (May 2016), https:// to PFCS and vaccine responses are discussed, these www.epa.gov/sites/production/files/2016-05/documents/ references could /should be discussed as well as drinkingwaterhealthadvisories_pfoa_pfos_5_19_16.final_.1.pdf they report related findings in human populations.

(last visited Aug. 15, 2016). Although they also are confounded by multiple . . aye PFCs (as was the Grandjean et al. study), the’ EAs evaluating PFOAand PROS a drinking iend additional supporto immunotoxiity a an required by the Safe Drinking Water Act (SDWA)... se ete tion eee es « . . published after [and] In accordance with SDWA, EPA will consider the cutoff date for consideration for inclusion in the the occurrence data from UCMR 3, along with the document. peer reviewed health effects assessments supporting the PFOA and PFOS Health Advisories, to make EPA Response. “Both the Granum et al. 2013 and Looker et al. a regulatory determination on whether to initiate 2014 studies were added to both HESDs [Health Effect Support the process to develop a national primary drinking Documents]. A summary and conclusions write-up was added to water regulation. the epidemiology section, which discusses the immune function-

77. U.S. ENVL. PRot. AGENCY, OFFICE OF WATER, EPA 822-R-16-003, related findings together.

HEALTH EFFECTS SUPPORT DOCUMENT FOR PERFLUOROOCTANOIC Statement in EPA Health Effects Assessment Support Document Acip (PFOA) (May 2016), https://www.epa.gov/sites/ for PFOA. “None of the studies demonstrated a clinically production/ files /2016-05/documents/pfoa_hesd_final-plain. recognizable increased risk of infectious diseases as a consequence pdf (last visited Aug. 15, 2016); U.S. ENvL. Prot. AGENCY, OFFICE of a diminished vaccine response. Overall, although these results oF Water, EPA 822-R-16-005, DRINKING WATER HEALTH ADVISORY are not sufficient to establish a causal effect of PFOA exposure on FOR PERFLUOROOCTANOIC AciD (PFOA) (May 2016), https:// an impaired serological vaccine response, some of the positive www.eepa.gov/sites/production/files/2016-05/documents/ associations are striking in magnitude and require replication in pfoa_health_advisory_final_508.pdf (last visited Aug. 15, 2016); independent studies.”

U.S. Envi. Prot. AGENCY, OFFICE of WaTER, EPA 822-R-16-002, 82. U.S. Envl. Prot. Agency, Office of Inspector General Audit Heattu Errects SupPoRT DOCUMENT FOR PERFLUOROOCTANE Report, Grant Management, Report No. 2001-P-00002, Region Sutronare (PFOS), (May 2016), https://www.epa.gov/sites/ 2’s Management of Children’s Health Risk Initiative and Related production /files/2016-05 /documents/pfos_hesd_final_508.pdf Projects (Jan. 30, 2001), https:/ /www.epa.gov/sites/production/ (last visited Aug. 15, 2016); U.S. ENVL. PRot. AGENCY, OFFICE OF files /2015-12/documents/kidshealth.pdf (last visited Aug. 15, WarER, DRINKING WATER HEALTH ADVISORY FOR PERFLUOROOCTANE 2016).

SULFONATE (PFOS), EPA 822-R-16-004 (May 2016), https://www. , . a . . epa.gov/sites/ production /files/2016-05 /documents/pfos_ 83. N.YS. Dep't of Health, PFOA in Drinking Water in the Village of health_advisory_final-plain.pdf (last visited Aug. 15, 2016); U.S. Hoosick Falls and Town of Hoosick, https://www.health.ny.gov/ ENVL. Prot. AGENCY, OFFICE OF SCIENCE AND TECHNOLOGY, HEALTH environmental /investigations/hoosick/ (last accessed Aug. 15, AND ECOLOGICAL CRITERIA Division, EPA RESPONSE TO EXTERNAL 2016).

PEER Review COMMENTS ON EPA Drarr DocuMENTSs: HEALTH The State Health Department is conducting an

EFFECTS SUPPORT DOCUMENT FOR PERFLUOROOCTANOIC AcID (PFOA) investigation to see if there are unusual elevations

AND HEALTH EFFECTS SUPPORT DOCUMENT FOR PERFLUOROOCTANE of cancer among Village residents. The investigation SULFONATE (PFOS) (May 2016), https: //www.epa.gov/sites/ will include total cancers and specific types of cancer production/ files /2016-05 /documents/response_to_pfoa_pfos_ diagnosed from 1995 through 2012. To accomplish peer_review_comments_508.pdf (last visited Aug. 15, 2016); Joel this, the State Health Department will use data from Beauvais, U.S. ENVL. PRor. AGENCY, Science Guides Public Health the New York State Department of Health Cancer Protection for Drinking Water (May 2016), https:/ /blog.epa.gov / Registry, which receives reports on all cases of blog/2016/05 /protection-for-drinking-water/ (last visited Aug. cancer occurring in New York State. The planned

15, 2016). start date is 1995 because street address at the date

78. U.S. Env. Prot. AGENCY, OFFICE OF WATER, EPA 822-R-16-005, of diagnosis 1s available in computerized form for DrtnxkING WaTER HEALTH ADVISORY FOR PERFLUOROOCTANOIC ACID all cases starting with that year. The planned end (PFOA) (May 2016), https: / /www-epa gov /sites /production/ date is 2012 because 2012 is currently the most recent files /2016-05 /documents/ pfoa_health_advisory_final_508.pdf year for which data are available. The State Health (last visited Aug. 15, 2016). Department will produce a report on the findings of

. the investigation. Id.

79. Grandjean & Budtz-Jorgensen, supra note 72.

80. U.S. ENvL. PRot. AGENCY, OFFICE OF SCIENCE AND TECHNOLOGY, 84. Martin Kulldorff, William F Athas, Eric J. Feuer, Barry A. Miller

HEALTH AND ECOLOGICAL CRITERIA Diviston, EPA RESPONSE TO & Charles R. Key, Eoaluatis ing Cluster Alarms: A Space-Time Scan EXTERNAL PEER REVIEW COMMENTS ON EPA DRAFT DOCUMENTS: Statistic and Brain Cancer in Los Alamos, New Mexico, 88 AMERICAN HEALTH EFFECTS SUPPORT DOCUMENT FOR PERFLUOROOCTANOIC Journat oF Pustic HeattH 1377, 1377-80 (Sept. 1998). Acrp (PFOA) AND HEALTH EFFEcTs SupPporT DOCUMENT FOR 85. Steven N. Goodman, Aligning statistical and scientific reasoning, PERFLUOROOCTANE SULFONATE (PFOS) (May 2016), https://www. ScIENCE, 1180-81 (June 3, 2016); Ronald L. Wasserstein & Nicole epa.gov/sites / production files /2016-05/documents/response_ A. Lazar, The ASA’s Statement on p-Values: Context, Process, and to_pfoa_pfos_peer_review_comments_508.pdf (last visited Aug. Purpose, 70 THE AMERICAN STATISTICIAN 129-33, (June 25, 2016).

110 NYSBA The New York Environmental Lawyer | Fall 2016 | Vol. 36 | No.2

86. 87. 88.

Scientific conclusions and business or policy decisions should not be based only on whether a p-value passes a specific threshold.

Practices that reduce data analysis or scientific inference to mechanical “bright-line” rules (such

as “p < 0.05”) for justifying scientific claims or conclusions can lead to erroneous beliefs and poor decision making. A conclusion does not immediately become “true” on one side of the divide and “false” on the other. Researchers should bring many contextual factors into play to derive scientific inferences, including the design of a study, the quality of the measurements, the external evidence for the phenomenon under study, and the validity of assumptions that underlie the data analysis. Pragmatic considerations often require binary, “yes-no” decisions, but this does not mean that p-values alone can ensure that a decision is correct or incorrect. The widespread use of “statistical significance” (generally interpreted as “p < 0.05”) as a license for making a claim of a scientific finding (or implied truth) leads to considerable distortion of the scientific process. Id.

Kulldorff et al., supra note 84, at 1378. EPA, supra note 61, at 3.

A. Hagenaars, L. Vergauwen, W. De Coen & D. Knapen, StructureActivity Relationship Assessment of Four Perfluorinated Chemicals

Using a Prolonged Zebrafish Early Life Stage Test, 82 CHEMOSPHERE 764, 764-72 (JAN. 2011).

Robert Michaels (ram@ramtrac.com) is President of the Schenectady-based RAM TRAC Corporation, and a toxicologist focusing on assessment and management of risks to public health potentially posed by environmental contaminants. He has served numerous corporate clients, the U.S. Congressional Office of Technology Assessment, and public interest organizations such as the Natural Resources Defense Council (NRDC). Dr. Michaels chaired the State of Maine Scientific Advisory Panel, and for 20 years chaired the Certification Review Board of the Academy of Board Certified Environmental Professionals. He has been Secretary of the NFPA Committee on Classification and Properties of Hazardous Chemicals, Board Member of the National Association of Environmental Professionals, and Member of the Editorial Advisory Boards of Springer-Verlag and Cambridge University Press journals. He earned his doctorate at SUNY at Stony Brook in 1979, and in 2004 was awarded ABCEP’s Kramer Medal recognizing his professional contributions.

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Publication citation

Michaels, RA. Perfluoroalkyl compounds (PFCs) in the Village of Hoosick Falls, Rensselaer County, New York: health risks and successive approximation toward enforceable national regulation. Albany, New York State Bar Association, NYSBA New York Environmental Lawyer, 36(2):88-111, Fall 2016;

Robert A. Michaels on ResearchGate