Epidemiologic Evidence on the Health Effects of Perfluorooctanoic Acid (PFOA)

• Type of Material: Article
• Authors: Kyle Steenland, Emory University; Tony Fletcher, London School of Hygiene and Tropical Medicine; David A. Savitz, Mount Sinai School of Medicine
• Language: English
• Date: 2010-04-27
• Publisher: National Institute of Environmental Health Sciences (NIEHS)
• Publication Version: Final Published Version
• Copyright Statement: Publication of EHP lies in the public domain and is therefore without copyright. All text from EHP may be reprinted freely.
• Final Published Version (URL): http://ehp.niehs.nih.gov/0901827/
• Title of Journal or Parent Work: Environmental Health Perspectives
• ISSN: 0091-6765
• Volume: 118
• Issue: 8
• Start Page: 1100
• End Page: 1108
• Grant/Funding Information: This research was funded by the C8 Class Action Settlement Agreement (Circuit Court of Wood County, West Virginia) between DuPont and Plaintiffs, which resulted from releases of the chemical perfluorooctanoic acid (PFOA, or C8).; Funds are administered by an agency that reports to the Court.
• Keywords: epidemiology; health effects; PFOA
• Research Categories: Health Sciences, Public Health; Health Sciences, Epidemiology

Abstract

Objective and sources We reviewed the epidemiologic literature for PFOA. Data synthesis Perfluorooctanoic acid (PFOA) does not occur naturally but is present in the serum of most residents of industrialized countries (U.S. median, 4 ng/mL). Drinking water is the primary route of exposure in some populations, but exposure sources are not well understood. PFOA has been used to manufacture such products as Gore-Tex and Teflon. PFOA does not break down in the environment; the human half-life is estimated at about 3 years. PFOA is not metabolized in the body; it is not lipophilic. PFOA is not directly genotoxic; animal data indicate that it can cause several types of tumors and neonatal death and may have toxic effects on the immune, liver, and endocrine systems. Data on the human health effects of PFOA are sparse. There is relatively consistent evidence of modest positive associations with cholesterol and uric acid, although the magnitude of the cholesterol effect is inconsistent across different exposure levels. There is some but much less consistent evidence of a modest positive correlation with liver enzymes. Most findings come from cross-sectional studies, limiting conclusions. Two occupational cohort studies do not provide consistent evidence for chronic disease; both are limited by sample size and reliance on mortality data. Reproductive data have increased recently but are inconsistent, and any observed adverse effects are modest. Conclusions Epidemiologic evidence remains limited, and to date data are insufficient to draw firm conclusions regarding the role of PFOA for any of the diseases of concern.