Perfluorooctanoic acid (PFOA) is a manmade chemical with a variety of uses, including coatings for nonstick cookware and food packaging, waterproof fabrics, and fire-fighting foam (Agency for Toxic Substances and Disease Registry [ATSDR], 2018; Organisation for Economic Co-operation and Development, 2002; U.S. Environmental Protection Agency [U.S. EPA], 2009). PFOA is highly persistent in most environments, particularly in drinking water (ATSDR, 2018). Exposure to PFOA is so widespread that it is present in the blood of most people (ATSDR, 2018; Kannan et al., 2004; Perfluoroalkyl Sulfonates Significant New Use Rule, 2007). National Health and Nutrition Examination Survey data indicate that the geometric mean level of serum PFOA in people in the U.S. is 1.9 [micro]g/L (Centers for Disease Control and Prevention [CDC], 2017).
The persistence of PFOA in the environment is a concern because exposure to PFOA has been associated with adverse health outcomes (Post, Cohn, & Cooper, 2012; Steenland, Fletcher, & Savitz, 2010). Among adults exposed to PFOA through ingestion of contaminated drinking water, higher serum PFOA concentrations are strongly associated with high cholesterol (Emmett et al., 2006; Steenland, Tinker, Frisbee, Ducatman, & Vaccarino, 2009; Winquist & Steenland, 2014), altered lipid profiles (Steenland, Fletcher, et al., 2010; Steenland, Tinker, et al., 2009), elevated uric acid levels (Steenland, Tinker, Shankar, & Ducatman, 2010), and pregnancy-induced hypertension (Darrow, Stein, & Steenland, 2013). Studies have shown associations between exposure to PFOA and ulcerative colitis (Steenland, Zhao, Winquist, & Parks, 2013), altered liver enzyme levels (Frisbee et al., 2009; Gallo et al., 2012), thyroid disease (Melzer, Rice, Depledge, Henley, & Galloway, 2010), and kidney and testicular cancer (Barry, Winquist, & Steenland, 2013; Vieira et al., 2013). While studies have demonstrated these relationships, further research might help to refine our understanding of the impact of PFOA on these outcomes.
Despite the voluntary phaseout of PFOA beginning in 2000, new discoveries of local PFOA contaminations continue to emerge (Hu et al., 2016). In 2014, PFOA was discovered in drinking water near a CHEMFAB manufacturing facility in Hoosick Falls, New York. Following this discovery, residents in nearby Bennington, Vermont, raised concerns about a former CHEMFAB/SaintGobain manufacturing facility in their community, which had applied nonstick coatings to fiberglass fabrics from 1969-2002.
In 2016, the Vermont Department of Environmental Conservation (DEC) began testing private drinking water wells for PFOA near the former manufacturing facility. At the time this exposure assessment was conducted, 304 of the 365 tested wells exceeded the advisory limit of 20 ppt for PFOA and perfluorooctanesulfonic acid (PFOS) combined, as set by the Vermont Department of Health (Health Department) in 2016. PFOA levels ranged from nondetectable to almost 3,000 ppt. This discovery prompted a public health investigation by the Health Department beginning in April 2016.
The goal of this investigation was to assess potential PFOA exposure pathways for people in the Bennington community, and to inform study participants of their PFOA blood concentrations and how those concentrations compared with background levels in the U.S. population. While it was not a primary goal of the investigation, information about health outcomes that have been associated with PFOA exposure was collected from study participants. This information was used to evaluate potential associations between exposure to PFOA in Bennington and health outcomes.
Participants were considered for inclusion in the study if 1) DEC tested the well of their current home or their previous home (within the past 8 years) in Bennington or 2) they worked or previously or currently live at the former CHEMFAB/Saint-Gobain facility in Bennington. Each participant was asked to complete a questionnaire and to provide a blood sample. Water monitoring was conducted by DEC in private drinking water wells surrounding the former manufacturing facility. Water monitoring in the area continues (see supplemental map at www.neha.org/jeh/supplemental). Water monitoring data for 365 private drinking water wells were linked to participants based on their home address. Overall, 477 participants initially enrolled in the study, with 475 completing the questionnaire and having blood drawn. An additional 3 individuals were excluded due to missing exposure data, leaving a final analytic sample size of 472.
Prior to study participation, each adult participant provided written consent. For children, a parent provided consent. This exposure assessment study was deemed to be public health practice and was therefore exempt from Vermont Agency of Human Services Institutional Review Board approval.
All participants were asked to answer questions about sex, age (years), race (White, other), education level (
PFOA Sampling: Serum and Drinking Water
Serum samples were collected from participants and shipped on dry ice to the Centers for Disease Control and Prevention (CDC) for analysis. Given the ubiquity of PFOA in the environment, sample collection was conducted following CDC guidelines (2013-2014) to prevent potential contamination. Serum concentrations of linear PFOA (n-PFOA) and branched isomers of PFOA (Sb-PFOA) were quantified using a modification of the on-line solid-phase extraction coupled with isotope dilution high-performance liquid chromatography tandem mass spectrometry approach (Kato, Basden, Needham, & Calafat, 2011). Low and high concentration quality-control materials, prepared from a calf serum pool, were analyzed with the study samples, analytical standards, and with reagent and matrix blanks to ensure the accuracy and precision of the data as described in CDC Laboratory Method 6304.06 (CDC, 2013-2014). The limits of detection (LOD) for n-PFOA and Sb-PFOA were 0.1 ng/mL. We assessed PFOA as total concentrations (sum of n-PFOA and Sb-PFOA); for values
Drinking water samples were collected following a standard operating procedure for the laboratory analysis of PFOA as described in the U.S. Environmental Protection Agency (U.S. EPA) Laboratory Method 537 version 1.1 (Shoemaker, Grimmett, & Boutin, 2008). Briefly, sample containers were filled with water from the water supply at each site (generally, from the spigot at the bottom of the water supply pressure tank) after running the water for 10 min. A field blank was included for each site. Samples were stored in coolers filled with ice for shipment to Northern Lake Services in Wisconsin for analysis. Water samples were analyzed using a liquid chromatography linked to tandem mass spectrometry method. The detection limit for PFOA ranged from 2.1-6.7 ppt.
Exposure Assessment and Health Outcomes
Questionnaires were used to collect self-reported information about water consumption and dietary habits, as well as residential and occupational information related to the CHEMFAB/Saint-Gobain...