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EWG Assessment of EPA Draft Human Health Risk Assessment for the Teflon Chemical PFOA

EWG Assessment of EPA Draft Human Health Risk Assessment for the Teflon Chemical PFOA

Wednesday, November 7, 2007

Summary. An Environmental Working Group (EWG) analysis of the Environmental Protection Agency's (EPA's) newly released draft human health risk assessment for the Teflon chemical (C-8, APFO, or PFOA) shows that the Agency has dramatically underestimated human health risks from exposures to this ubiquitous, persistent toxic chemical (EPA 2005). The Agency substantially tilts the assessment in DuPont's favor first by summarily discounting and then by outright ignoring significant scientific studies pointing to increased risks for heart attack, stroke, breast cancer, testicular cancer, and numerous other health harms. For some of the most critical health risks, such as those on the immune system, studies have yet to find a safe dose, yet EPA has excluded these effects altogether in this new assessment without explanation.

If not substantially improved in the upcoming review by EPA's Science Advisory Board, slated for February 22, 2005, this tilted study will prove a shaky foundation for future EPA health protection policies for the more than 95 percent of the American public carrying the chemical in their bloodstream.

Heart attack and stroke. Six studies now point to risk for heart attack and stroke from exposures to the Teflon chemical, two of which have emerged in the last month (DuPont 2005, Shea 2004, Olsen et al. 2001, Goldenthal 1978, Alexander, 2001, Haughom and Spydevold 1992). Just yesterday (January 11 2005) DuPont released the latest in this series, a study showing elevated cholesterol levels in workers exposed to the Teflon chemical, a known risk factor for heart attack and stroke. EPA has ignored all six of these studies.

Cancer. EPA has ignored data linking the Teflon chemical to four types of cancer or tumors: mammary, testicular, pancreatic, and liver. According to the Agency's own standardized method for assessing the cancer potential of a chemical, the Teflon chemical falls squarely in the range of a "likely" human carcinogen. The chemical meets three of five EPA cancer criteria (see note 1), while a categorization of "likely carcinogen" requires that just one of these criteria is met. In this case, the Teflon chemical has been linked to multiple cancers in male and female mice, in more than one study, in tumors that are statistically significant and assumed to be relevant for humans (Sibinski 1987).

Nevertheless, in this new Teflon assessment the Agency ignores its own guidance, claiming that the evidence for carcinogenicity is "suggestive" but not "sufficient." The Agency does not assess human cancer risk from exposures to the Teflon chemical, and gives no rationale for this glaring exclusion that flouts its own cancer risk guidance.

Breast cancer. In 2002 EPA scientists concluded that exposures to the Teflon chemical may put humans at risk for breast cancer (EPA 2002, Sibinski 1987). EPA found that mammary tumor increases shown in animal studies were significant. Yet in their new assessment they have overturned that finding with shoddy reasoning. This finding was based on a DuPont-funded laboratory study showing that mammary tumor rates significantly increased in animals dosed with the Teflon chemical, with rates more than doubling in the high dose group. EPA has discounted this significant finding, using confused statistical reasoning that independent scientists found "violates the rationality of the statistical reasoning" (Yoshimura and Matsumoto, 1994). In EPA's new argument, breast cancer is discounted because control animals in other studies with other chemicals also show mammary tumors.

Testicular cancer. EPA has ignored testicular cancer risk in their new assessment, despite industry data showing statistically significant, elevated risk for testicular tumors from exposures to the Teflon chemical (Cook et al 1994, Sibinski 1987). EPA's own Science Advisory Panel instructed the Agency to consider testicular cancer from laboratory studies relevant to humans for chemicals like the Teflon chemical that are known to cause health harms through a mechanism called peroxisome proliferation: "chemicals [peroxisome proliferators] that induce pancreatic or Leydig cell [testicular] tumors may pose a carcinogenic hazard for humans." (SAP, 2003) EPA inexplicably chose to ignore their panel's advice.

Additionally, EPA discounts testicular cancer in humans based on unproven Agency hunches of potential mechanisms of action. EPA first guesses what might be the root cause, or mechanism, for the testicular tumors seen in laboratory studies, and then argues that since these particular mechanisms were not observed in a monkey study, testicular cancer should not be included in a human health risk assessment. The Agency did not allow for the fact that their guess might have been wrong.

Pancreatic cancer. EPA has also ignored pancreatic cancer, again despite industry data showing significantly increased occurrence of pancreatic tumors for animals dosed with the Teflon chemical (Cook et al. 1994). And again, the Agency is flouting the advice of their own Science Advisory Panel, which specifically instructed the Agency to consider pancreatic cancer from laboratory studies relevant to humans for chemicals like the Teflon chemical that fall into the category of "peroxisome proliferators" (SAP, 2003).

And yet again, EPA scientists guessed that Teflon's influence on a particular enzyme might be responsible for the pancreatic tumors seen in laboratory studies. When Agency scientists did not see elevated levels of that enzyme in an industry monkey study, they then argued that pancreatic cancer is not relevant to humans.

Immune system damage — no known safe dose. A series of industry studies show that the Teflon chemical suppresses the immune system, creating increased risks for developing and dying from infectious disease (Yang et al. 2002). Every dose of the Teflon chemical tested thus far has been shown to suppress the immune system; there is no known safe dose. Nevertheless, EPA fails to include this critical health endpoint of the Teflon chemical in its final calculations of human health risk.

Pituitary gland damage. EPA scientists determined that the Teflon chemical damages the pituitary gland — the master gland of the body controlling a host of critical life functions (EPA 2002; York 2002). In its new assessment EPA has chosen to ignore this important potential health impact, even as it admits that it is statistically significant, because scientists do not fully understand why the effects peak in the middle instead of the top end of the dosing range.


Note 1: The three EPA cancer criteria that are met by the Teflon chemical are below. Just one of these criteria is required according to Agency guidelines (EPA 2003) for a chemical to be classified as a "likely" human carcinogen.

  • an agent that has tested positive in more than one species, sex, strain, site, or exposure route, with or without evidence of carcinogenicity in humans;
  • a positive study that indicates a highly significant result, for example, an uncommon tumor, a high degree of malignancy, or an early age at onset;
  • a robust animal tumor response in a single experiment that is assumed to be relevant to humans.

References

Alexander, B. 2001. Mortality study of workers employed at the 3M Cottage Grove Facility. Final Report. Division of Environmental and Occupational Health, School of Public Health, University of Minnesota. AR 226-1136. Washington, DC: U.S. Environmental Protection Agency.

Cook JC, Hurtt ME, Frame SR, Biegel LB. 1994. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in Crl:CD BR(CD) rats. Toxicologist 14: 301.

DuPont. 2005. DuPont Reports First-Phase Results of Health Study Examining PFOA Exposure. Press Release, Jan 11, 2005 Link: http://www1.dupont.com/NASApp/dupontglobal
/corp/index.jsp?page=/content/US/en_US/news/releases/2005/nr01_11_05a.html

Goldenthal, E.I. 1978. Ninety Day Subacute Rhesus Monkey Toxicity Study. Final Report Prepared for 3M, St. Paul, Minnesota, by International Research and Development Corporation, St. Paul, Minnesota, November 10, 1978. AR226-1136. Washington, DC: U.S. Environmental Protection Agency.

Haughom B, Spydevold O. 1992. The Mechanism Underlying the Hypolipemic Effect of Perfluorooctanoic Acid (PFOA), Perfluorooctane Sulphonic Acid (PFOSA) and Clofibric Acid. Biochimica et biophysica acta. 1128(1): 65-72.

Olsen GW, Burlew MM, Burris JM, Mandel JH. 2001. A cross-sectional analysis of serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) in relation to clinical chemistry, thyroid hormone, hematology and urinalysis results from male and female employee participants of the 2000 Antwerp and Decatur fluorochemical medical surveillance program. Final report. 3M Medical Department.

SAP. 2003. FIFRA Scientific Advisory Panel Meeting Minutes on Proposed Science policy: PPAR- agonist-mediated hepatocarcinogenesis in rodents and relevance to human health risk assessment. SAP Minutes No 2003-05.

Shea EE. 2004. Report on the meeting held on Friday 20th and Saturday 21st 2004 at the Inn at Montchanin Village (Wilmington, USA) with 3M and DuPont delegations. OPPT TSCA 8(e) docket #8EHQ-0904-15663.

Sibinski, LJ. 1987. Two-Year oral (diet) toxicity/carcinogenicity study of fluorochemical FC-143 (perfluorooctane ammonium carboxylate) in rats. Report prepared for 3M, St. Paul, Minnesota by Riker Laboratories Inc. Study No. 0281CR0012; 8EHQ-1087-0394, October 16, 1987.

U.S. EPA. 2002. Revised draft hazard assessment of perfluorooctanoic acid and its salts. ANNEX 1, Robust summaries U.S. EPA Office of Pollution Prevention and Toxics. 4 November, 2002. AR226-1137. Washington, DC: U.S. Environmental Protection Agency.

U.S. EPA. 2003. Draft Final Guidelines for Carcinogen Risk Assessment.

U.S. EPA. 2005. Draft Risk Assessment of the potential human health effects associated with exposure to perfluorooctanoic acid and its salts. January 4, 2005. (Released January 12, 2005). Available online at www.epa.gov/oppt/pfoa.

Yang, Q, Abedi-Valugerdi, M, Xie, Y, Zhao, XY, Moller, G, Nelson, BD and DePierre, JW. 2002. Potent suppression of the adaptive immune response in mice upon dietary exposure to the potent peroxisome proliferator, perfluorooctanoic acid. Int Immunopharmacol 2(2-3): 389-97.

York, RG. 2002. Oral (gavage) two-generation (one litter per generation) reproduction study of ammonium perfluorooctanoate (APFO) in rats. Report prepared for 3M, St. Paul, MN by Argus Research (Horsham, PA). Sponsor's Study No. T-6889.6. AR226-1092. Washington, DC: U.S. Environmental Protection Agency.

Yoshimura I, Matsumoto K. 1994. Notes on the use of historical controls. Environ Health Perspect. 102 Suppl 1:19-23.