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Reductions in Serum Lipids with a 4-year Decline in Serum Perfluorooctanoic Acid and Perfluorooctanesulfonic Acid

Fitz-Simon, Nicola; Fletcher, Tony; Luster, Michael I.; Steenland, Kyle; Calafat, Antonia M.; Kato, Kayoko; Armstrong, Ben

doi: 10.1097/EDE.0b013e31829443ee
Pollutants

Background: Several epidemiological cross-sectional studies have found positive associations between serum concentrations of lipids and perfluorooctanoic acid (PFOA, or C8). A longitudinal study should be less susceptible to biases from uncontrolled confounding or reverse causality.

Methods: We investigated the association between within-individual changes in serum PFOA and perfluorooctanesulfonic acid (PFOS) and changes in serum lipid levels (low-density lipoprotein [LDL] cholesterol, high-density lipoprotein cholesterol, total cholesterol, and triglycerides) over a 4.4-year period. The study population consisted of 560 adults living in parts of Ohio and West Virginia where public drinking water had been contaminated with PFOA. They had participated in a cross-sectional study in 2005–2006, and were followed up in 2010, by which time exposure to PFOA had been substantially reduced.

Results: Overall serum concentrations of PFOA and PFOS fell by half from initial geometric means of 74.8 and 18.5 ng/mL, respectively, with little corresponding change in LDL cholesterol (mean increase 1.8%, standard deviation 26.6%). However, there was a tendency for people with greater declines in serum PFOA or PFOS to have greater LDL decrease. For a person whose serum PFOA fell by half, the predicted fall in LDL cholesterol was 3.6% (95% confidence interval = 1.5–5.7%). The association with a decline in PFOS was even stronger, with a 5% decrease in LDL (2.5–7.4%).

Conclusions: Our findings from this longitudinal study support previous evidence from cross-sectional studies of positive associations between PFOA and PFOS in serum and LDL cholesterol.

Supplemental Digital Content is available in the text.

From the aDepartment of Social and Environmental Health Research, London School of Hygiene and Tropical Medicine, London, United Kingdom; bDepartment of Community Medicine, West Virginia University, Morgantown, WV; cDepartment of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA; and dDivision of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA.

Supported by The C8 Class Action Settlement Agreement.

Supplemental digital content is available through direct URL citations in the HTML and PDF versions of this article (www.epidem.com). This content is not peer-reviewed or copy-edited; it is the sole responsibility of the author.

Editors’ note: Related papers appear on pages 577 and 580.

Correspondence: Nicola Fitz-Simon, Neonatal Medicine, Imperial College London, 4th Floor, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, United Kingdom. E-mail: n.fitz-simon@imperial.ac.uk.

Received May 1, 2012

Accepted March 4, 2013

Copyright © 2013 Wolters Kluwer Health, Inc. All rights reserved.