Studies have found PFOS and PFOA in the blood samples of the U.S population, indicating that exposure to the chemicals is widespread (ATSDR 2009; EPA 2006a). In 2003-­‐2004, PFOS and PFOA were detected in 99–100% of blood samples collected from both pregnant and non-­‐pregnant women (Woodruff et al., 2011).

Current PFOS and PFOA levels can be found in the 2015 report: http://www.cdc.gov/biomonitoring/pdf/FourthReport_UpdatedTables_Feb2015.pdf.     Tables with breakdowns by age, ethnicity, and gender are available in the Appendix at the end of this factsheet.

While current evidence is compelling, causality has not been definitively established for a wide range of health effects. Many uncertainties and data gaps remain and will require further research.

The most consistent findings from epidemiology studies are elevated blood serum total cholesterol levels among exposed populations, with strong evidence for a causal relationship between PFOA exposure and elevations in serum lipids (C8 Science Panel, 2011c).

• General population cross-­‐sectional studies found associations with several health endpoints including increased serum cholesterol (Nelson et al., 2009) and uric acid (Shankar, et al., 2011 a), increased incidence of thyroid disease (Melzer et al., 2010), increased serum liver enzymes (Lin et al., 2010) and decreased renal glomerular filtration (Shankar et al, 2011 b).
• In May 2006, the EPA Science Advisory Board suggested that perflurooctanoic acid (PFOA) cancer data are consistent with the EPA guidelines for the Carcinogen Risk Assessment descriptor “likely to be carcinogenic to humans.” EPA is still evaluating this information and additional research pertaining to the carcinogenicity of PFOA (USEPA 2006, 2014). In 2011, the Institute of Medicine concluded that currently available data suggests the possibility of a link with breast cancer and PFOA
• Epidemiologic studies have also found associations between kidney, testicular, ovarian, prostate, and non-­‐Hodgkins lymphoma with PFOA exposure (Barry et al., 2013; Vieira et al., 2013).
• High levels of PFOA exposure in workers has been linked to high levels of uric acid and cholesterol (Nelson et al., 2010) risk factors for cardiovascular disease.
• PFOS-­‐exposed workers have demonstrated elevated incidence of bladder cancer mortality following at least one year of exposure (Lindtrom et al., 2011).
• Epidemiologic studies have shown an association between PFOS exposure and bladder cancer; however, further research and analysis are needed to understand this association (Alexander, 2003; Lau, 2007).
• Several population-­‐based reproductive outcome studies found statistically significant inverse relationships between birthweight or other measures of fetal growth and PFOA and/or other PFCs (Washino et al., 2009; Olsen et al., 2009; Apelberg et al., 2007). Fee et al. (2008) studying the Danish National Birth Cohort found associations between prenatal exposure to PFOS or PFOA and a range of adverse birth outcomes, such as low birth weight, decreased head circumference, reduced birth length, and smaller abdominal circumference.
• Exposure in infants (breast fed or formula fed) is higher than in adults using the same drinking water source due to PFOA’s presence in breast milk and the greater drinking water intake of infants on a body weight basis (Post et al., 2012).
• Elevated exposures to PFCs were associated with reduced vaccine-­‐induced immune protection in children (Grandjean et al., 2012).
• Increased risk of pre-­‐eclampsia was associated with PFOA exposure (Stein et al., 2009; C8 Science Panel 2011a,b).
• Exposure has been linked to endocrine disruption (Casal-­‐Casas et, 2011).

• Altered gene expression and testosterone synthesis (Shi et al., 2007)
• Behavioral (Ciu et al., 2009; (Onischenko et al., 2010),
• Reproductive, (Fuentes et al., 2006)
• Neonatal mortality (Luebker et al., 2005)
• Increased liver weight (ATSDR, 2009; Ciu et al., 2009)
• Reduced immunological function (Dewitt et al., 2012).
• Adverse effects on mammary gland development in mice (Post, 2012).