DuPont C8 and Health

As early as 1961, DuPont scientists issued internal warnings about the health risks of PFOA (Perfluorooctonoic Acid), also known as C8. Following these warnings, DuPont and 3M, the chief supplier of the chemical, began studying the health outcomes associated with PFOA. These studies demonstrated that PFOA accumulates in human blood and does not break down in the environment and therefore may cause serious health problems, including liver damage. In 1978, DuPont began a testing program to understand the health effects of PFOA and by 1980 had found elevated levels of the chemical in workers at the DuPont Washington Works plant in Wood County, West Virginia.
Based on its findings, the company recommended that workers with potential exposure to PFOA wear special protective clothing and equipment, including breathing devices. A company memo, dated July 1980, concluded that, "continued exposure (to C8) is not tolerable." Between 1979 and 1981, two of seven children born to female plant workers at the Washington Works plant had birth defects, which led DuPont to reassign 50 women who worked in the plant's Teflon production division to other areas of the plant. 3-M sent Dupont results from a study demonstrating that PFOA causes birth defects in rats prompting Dupont to conduct additional occupational studies. In addition to these occupational studies (which are still ongoing), DuPont conducted tests, between 1981 and 1984, for PFOA contamination in tap water in Little Hocking, Ohio, which lies on the Ohio River opposite the Washington Works plant in West Virginia. A DuPont memo stamped "personal and confidential" stated that these tests found evidence of C8 contamination in drinking water on both the Ohio and West Virginia sides of the river. None of this information was reported to EPA.

The U.S. Environmental Protection Agency's (EPA) Office of Pollution Prevention and Toxics has been studying perfluorooctanoic acid (PFOA) in order to understand the health and environmental impact of perfluorochemicals. The EPA has completed its draft Risk Assessment of Potential Human Health Effects Associated with PFOA and Its Salts, and the EPA Science Advisory Board (SAB) has been asked to review and comment on the scientific soundness of this assessment. http://www.epa.gov/sab/panels/pfoa_rev_panel.htm 
In response to a request from EPA’s Office of Pollution Prevention and Toxics (OPPT), the Science Advisory Board (SAB) convened an expert panel to conduct a peer review of EPA's Draft Risk Assessment of Potential Human Health Effects Associated with Perfluorooctonoic Acid (PFOA) and Its Salts (dated January 4, 2005). PFOA is a synthetic (man-made) chemical used in the manufacture of several commercially important products. PFOA has been detected in the blood of the general U.S. population. In certain areas, exposure is much higher due to the location of facilities involved with the use or manufacture of the substance, known also as C8. To determine whether environmental exposure to PFOA might pose a risk to human health, EPA’s draft assessment provided an evaluation of available information on the health effects and human exposure to PFOA. The draft assessment also compared measured human blood levels with the estimated PFOA blood levels that are not anticipated to produce (or can produce minimal) toxicities based on data in tested laboratory animals.
The SAB was asked to comment on: (a) EPA’s analysis of how PFOA causes tumors in
rats and its relevance for human health and the weight-of- evidence conclusion about the potential for PFOA to cause cancer in humans; (b) the selection of health effects endpoints for risk assessment; (c) the adequacy of available data to provide information on exposure of the general population to PFOA; and (d) EPA’s risk assessment approach including the use of kinetic models to estimate PFOA blood levels in available laboratory animals studies.
In general, the SAB Panel endorsed EPA’s risk assessment approach, particularly, the inclusion of multiple non-cancer health endpoints for risk assessment, and the use of PFOA blood levels as a measure of estimated dose in place of the administered dose in toxicologic studies. The Panel recommended the inclusion of additional non-cancer health endpoints for risk assessment, and the use of the Benchmark Dose method to better estimate the lowest observed effect levels and no observed effect levels for risk assessment. Three-quarters of the Panel judged that the weight-of-evidence conclusion for the potential of PFOA to cause cancer in humans was more aligned and consistent with the hazard descriptor of “likely to be carcinogenic” as described in the Agency’s cancer guidelines (i.e., 2003 EPA Guidelines for Carcinogen Risk Assessment). They also recommended that a risk assessment be conducted for carcinogenic effects. About one-quarter of the Panel agreed with EPA’s conclusion regarding the potential cancer hazard of PFOA to humans and the designation of the cancer descriptor of “suggestive evidence of carcinogenicity”. Three quarters of the Panel considered the available human biomonitoring studies adequate to characterize environmental risk to PFOA for the general population. However, about one-quarter of the Panel believed that the available studies are inadequate for risk assessment of subpopulations possibly more highly exposed to PFOA. The scientific rationales for these viewpoints along with specific recommendations on these issues are detailed in the Panel’s report

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