Credibility Gap: Toxic Chemicals in Food Packaging

How Green is DuPont's Alternative?

Study authors: Olga Naidenko, PhD, Senior Scientist; Renee Sharp, MS, Senior Scientist; Jane Houlihan, MSCE, Vice President for Research; Bill Walker, Vice President West Coast

In 2006, under pressure from the U.S. EPA, DuPont and 7 other companies promised to phase out by 2015 a cancer-causing chemical called PFOA, used to make Teflon and also found in grease-resistant coatings for food packaging. In its place, the chemical industry is pushing new, supposedly “green” food package coatings.

But an investigation by Environmental Working Group (EWG) finds no evidence that the industry-touted replacement chemicals being rushed to market are safer -- and plenty of evidence that DuPont and other manufacturers are continuing a decades-long pattern of deception about the health risks of PFOA and related chemicals.

View EWG's guide to PFCs

Like PFOA-based coatings, the new compounds are also made from, contaminated with, or break down into perfluorochemicals (PFCs), including new coatings for household products like stain-resistant fabrics and carpet, waterproof clothing, and food packaging. Like PFOA, they persist in the environment and can cross the placenta to contaminate babies before birth. But unlike PFOA – for which there are dozens of peer-reviewed studies showing links to cancer, reproductive problems and immune disorders – for the replacement chemicals there are almost no publicly available data on their health risks, leaving in question whether food packaging and other PFC-containing products are any safer.

EWG’s investigation is the first review of health data and industry greenwashing since the phaseout agreement was announced. We examined federal reports on food packaging toxicity; industry-funded health studies in Environmental Protection Agency files; and company e-mails unearthed in a lawsuit over PFOA pollution of drinking water near a DuPont facility in West Virginia, and found:

  • Despite agreeing to phase out PFOA, DuPont and other makers of perfluorinated chemicals continue to maintain that it is safe. A DuPont press release from March 2008 said “. . . PFOA exposure does not pose a health risk to the general public. To date, there are no human health effects known to be caused by PFOA.” This is not only contradicted by the EPA Science Advisory Board’s 2005 finding that PFOA is a likely human carcinogen, but by DuPont’s own scientific advisors. In 2005, in response to a similar statement by the company, an ethics advisor on DuPont's Epidemiology Review Board wrote: “The claim of no health effects is not supported by available facts (factual inappropriateness) … Such a statement is misleading, whether intentionally or not, and it is unacceptable to mislead in this way (moral inappropriateness).” In fact, to date at least 10 studies of people show significant health risks of PFOA, including elevated risk for obesity, heart disease, endocrine disorders, and infectious diseases in a study of 4538 children younger than 10 years of age living near a DuPont plant in West Virginia.

  • From January 2007 to April 2008, chemical manufacturers reported to the EPA 19 studies on PFC chemicals that showed “substantial risk” to human health or the environment under section 8(e) of the Toxic Substance Control Act (TSCA). The health effects reported in these studies of anonymous PFCs include the deaths of laboratory animals as well as damage to the liver, thyroid and prostate. Yet under EPA regulations shielding confidential business information, in 17 of 19 cases the exact name of the chemical is not identified and in 13 of 19 cases the manufacturer is not identified. This information is secret not only from the public, but from health officials in states, like California, that are considering laws to ban PFCs in food packaging. These reports are doubly troubling: Not only is information being hidden that is important to public health, but by their own admission companies are finding substantial health risks for chemicals they may well be using as PFOA replacements.

  • From 2005 through November 2007 FDA approved 8 new food packaging fluorochemicals that may replace older, PFOA-contaminated or C8-based PFCs. These approvals were granted with no public record of any health risk assessment from exposures to the contaminant residues and breakdown products of greatest concern, according to documents EWG obtained from the Food and Drug Administration. Since that time FDA has approved 2 additional substitute chemicals, and DuPont has announced that its new PFOA replacement, the CapstoneTM grease-proofing chemicals, will be available for packaging products beginning in 2009. This dramatic shift in the market and in human exposures has occurred with no public assessment of the safety of the replacements.

  • A similar pattern of unproven claims and secrecy is found in reports filed by chemical makers on the progress of the PFOA phaseout. Since the phaseout is voluntary, EPA has no authority to verify claims of reduced PFOA use or releases. Some companies report little or no progress. Others claim significant reductions, but again hide the details as confidential business information. Worse, the industry’s claims that the phaseout will eliminate PFOA by 2015 are shattered by the fact that no company from China, the third-largest producer of packaging in the world, is a party to the agreement.


The industry’s contention that its PFOA replacements are safer rests on two atoms of carbon. PFOA is sometimes called C8 because it has 8 carbon atoms. A key replacement chemical, perfluorohexanoic acid (PFHxA), contains 6 carbon atoms and is often called C6. The chemical industry would have us believe that the removal of two carbon atoms removes human health risks.

On April 23, 2008, a scientist representing the Telomer Research Program, a chemical industry group that includes DuPont and other PFC makers, testified before the Health Committee of the California State Senate against a bill to ban both PFOA/C8 and PFHxA/C6 in food packaging. He repeated the claim that PFOA is not harmful to humans, and that a ban is not needed because of the voluntary phaseout program. He also repeatedly described C6 as an example of the “green chemistry” approach the state is developing to encourage the production of safer alternative chemicals:

[The bill] would derail a promising example of green chemistry at work . . . [B]y targeting perflourinated compounds with chain links of 6 or higher in this legislation, the bill would frustrate the conversion from the C8 based products, that are the source of the PFOA, to a set of effective C6 based compounds whose breakdown products are much, much less toxic and don’t have the same persistence issues that PFOA and some of the C8s have. . . . [O]ur companies are addressing the concerns about PFOA; we’re aggressively doing so. And we believe the proposed legislation would actually do harm to an effective green chemistry strategy for reducing the concerns about this chemical. (Lawyer 2008)

This is greenwashing – claiming environmental benefits for a product that's little better than its replacement – at its worst. PFOA is so remarkably persistent in the environment and broadly toxic to living organisms that using it as a bar against which to judge "green chemistry" is like calling anything under 200 miles per hour a safe speed limit. For C6 replacements, the full extent of the public record on their safety consists of a PowerPoint presentation delivered by Asahi Glass Company to the Environmental Protection Agency. Public records show that DuPont, Asahi, and Clariant are all shifting from PFOA to C6 chemistries despite an absolute dearth of public safety data, and despite the fact that on 3 critical counts, C6 may be as great a concern as PFOA:

  • C6, like all the other PFCs, is extraordinarily persistent in the environment (NAS 1972).
  • C6 is potentially 3 to 5 times more toxic than C8 to aquatic organisms (Asahi 2006).
  • C6 crosses the placenta to contaminate children before birth, according to an EWG study of umbilical cord blood from 10 newborn babies (EWG 2005). While many studies of thousands of people by CDC, industry, and academic university researchers show that PFOA contaminates nearly the entire U.S. population, industry has failed to publish even a single study of C6 in people. EWG's tests of cord blood show it to be potentially as great a concern as PFOA.

Truly green chemistry is sustainable chemistry with products and processes that reduce or eliminate the use and generation of hazardous substances. Much remains unknown about C6, but what is known – that it is bioaccumulative, persistent and crosses the placenta to pollute human blood – is enough to disqualify it as green chemistry. Promoting a PFOA replacement that raises such serious safety concerns while simultaneously withholding critical toxicity data violates the spirit of the PFOA phaseout agreement and undermines the credibility of the entire industry.

New Food Packaging Chemicals: No Health Data

In March 2008 EWG received from the FDA Center for Food Safety and Applied Nutrition FDA's safety assessments for all 8 new fluorochemical-based food packaging chemicals approved by the agency between 2005 and November 2007, including four based on C6 chemistry. A substantial amount of information in these documents was redacted by FDA as alleged confidential business information, but EWG's review of the remaining information finds no evidence that FDA adequately assessed the safety of people's exposures to C6 from these coatings. In particular, the information provided to EWG demonstrates that:

FDA failed to assess how quickly these food coatings would break down into C6, and no mention is made in the FDA documents of companies submitting such data.

  • FDA failed to require industry to submit any safety studies on C6 itself (perfluorohexanoic acid or PFHxA). Of the 4 C6-based chemicals approved by the FDA for food packaging and reviewed by EWG, only Asahi Glass submitted a C6 toxicity study. Even though Asahi research showed smaller than normal growth, lower cholesterol and calcium in PFHxA-exposed test animals (Asahi 2006), FDA did not take into consideration the C6 health effect data when approving the chemical for food packaging.
  • FDA approved the C6-based and other fluorochemical replacements for C8- and larger PFC-based food packaging based on its assessment that since C6 is not C8 (PFOA), there would be little chance of C8 residues in the food package coatings.
  • In all of its new approvals of fluorochemicals for food packaging, FDA failed to consider the long-term health and environmental consequences of the continued use of vast amounts of PFC-based food packaging chemicals that are extraordinarily persistent in the environment and that can cross the human placenta.

In addition to the food packaging chemicals FDA has already approved, DuPont marketing materials indicate that another new, grease-proof paper coating will be available in 2009, made from C6 and related chemicals (see DuPont's CapstoneTM "Paper packaging" factsheet available for download at DuPont 2008a). If the last 3 years of FDA approvals are any indication, DuPont could likely win FDA approval of this product for food packaging with no assessment of the safety of C6.

Although FDA and industry chemists know that food packaging chemicals are not without hazard and can migrate into food, most consumers are surprised to learn that the inner lining of their favorite fast food wrapper may expose them to chemicals linked to potential health consequences ranging from developmental problems to heart disease, stroke and cancer. This includes a wide variety of food packaging that for decades has been treated with fluorochemicals to increase its resistance to oil and water stains (Begley 2005).

Federal records for food packaging fluorochemicals go back to 1969 when a Scotchban paper coating manufactured by 3M was approved as "safe" by the FDA (FDA 1969). Since that time, FDA continued to sanction various kinds of fluorochemicals to be used directly in contact with food. However, much has changed since 1969. We now know that perfluorochemicals (PFCs) contaminate the bodies of 98% of Americans (Calafat, Wong 2007). These are long-lasting, toxic chemicals that, once ingested with food or water, will linger in human bodies for years (Conder 2008). And - unknown to consumers - these chemicals can and do migrate from food packaging into food and then into human bodies (Begley 2005; Deon and Mabury 2007; Sinclair 2007; Tittlemier 2007). One could argue that the time has come for close public and regulatory scrutiny of fluorochemicals in food packaging. Are the purported convenience (however slight) and manufacturers' profits (however big) worth the dangers of getting an extra helping of PFCs into our bodies, already assailed with so many other toxic industrial chemicals from other sources?

Fortunately, the tide is changing as more and more people clearly state that they don't want PFCs on their food packaging. And companies are listening: Burger King, for instance, stopped using PFC-coated take-out boxes in 2002. However, food packaging PFCs are still on the market and are still covered by summary approvals from the FDA, even though their effects, in an assessment by the FDA's own scientists, "may only become apparent many years later" (Begley 2005). Indeed, we are not talking about doses that are immediately harmful after a single helping of microwaved popcorn. Instead, we need to be concerned about on-going, continuous ingestion of small quantities of these chemicals, their documented build up in the human body over the years - and the subsequent health effects with which these chemicals are unambiguously associated.

Of particular concern is the fact that there are no publicly available market surveys quantifying PFC use in packaging. As a result, consumers are unfairly deprived of their essential right to know and to make informed, independent decisions. Meanwhile, two studies detected PFCs leaching out of food packaging under normal cooking temperatures (Begley 2005; Sinclair 2007). However, a consumer going to the store would not know which brands to avoid because manufacturers are conveniently withholding this crucial information. And it is not only the consumers who are in the dark. When the FDA scientists conducted their small-scale survey, they noted that the "paper products [tested by the FDA] were not necessarily treated with perfluoro paper coatings" (Begley 2005). As a result of the secrecy about PFC content in packaging, consumers don't know what to buy and what to avoid, while FDA does not know what market products to test. Manufacturers know but they will not tell anyone.

Following the EPA scrutiny of PFOA (perfluorinated chemical with an 8-carbon backbone, thus also known as C8) and general public outrage over the widespread contamination with this noxious chemical, fluorochemical manufacturers are shifting to smaller PFCs, especially C6 PFC replacements. Clariant Corporation, for example, states in its Annual Report that its “new generation of fluorocarbons [is] based on C6 Chemistry” (Clariant 2008) and will be used for food packaging as well as other end uses (Clariant 2008, Sanitized AG 2008, Nanowerk 2008). Similarly, DuPont has just introduced a new generation of PFC products intended to be used in various applications including paper packaging “where the fluorochemical portion is made up of six or fewer perfluorinated carbons” (DuPont 2008a). And Asahi Glass company has also developed a series of C6-based PFCs for food packaging paper and textile applications (Asahi Glass Co 2007). In fact, of the 10 fluorochemicals that FDA has approved for food contact uses since 2005, 6 of them were based on C6 PFC building blocks (Food Contact Substance Notifications (FCNs) 542, 599, 604, 628, 746, 783) (FDA 2008).

Since the voluntary PFOA phaseout was announced, FDA and the PFC manufacturers seem most interested in claiming that the replacement products are not PFOA, while failing to make public even the most basic health and safety data on the C6 replacements. Unfortunately, DuPont’s statements about the glowing promise C6 (CapstoneTM) chemistry being the answer to PFC contamination of consumer products and the environment are sorely lacking in credibility. We know that PFCs as a class undergo hardly any natural degradation (NAS 1972), so claims about their not being persistent in the environment are likely not true. We know that while the shorter-chain length PFCs may be less bioaccumulative (Martin 2003), they are better able to cross the placenta and transfer from the mother’s body to the fetus (Midasch 2007). We know that these chemicals are already found in people and babies: biomonitoring studies have already found C6 chemicals in adult and cord blood, proving that they do indeed cross the placenta (EWG 2005; Frisbee 2008). We know that the FDA has concerns about the biopersistence of PFCs, including C6-based PFCs (FDA 2006). And we know that shorter-chain PFCs have been already been detected as contaminants in drinking water due to emissions from fluorochemical manufacturing facilities (MDH 2008).

And what we certainly don’t know is that these C6 chemicals are safe. With the exception of one presentation from the Asahi Glass Company delivered at the EPA's PFOA Information Forum (Asahi 2006), there are no published studies on the toxicity of C6 compounds. The FDA’s toxicology reviews of approved C6 food contact substances are cursory. For example, they typically consider only the toxicity of the coating compounds and not the chemicals they break down into over time. Furthermore, companies’ claims of negligible PFOA contamination in their new C6 PFC products are taken as evidence of safety – in the absence of any substantiating data that would look at the toxicity of C6 itself.

Meanwhile, industry is aggressively promoting the C6 replacements for every imaginable application. On April 23, 2008, a scientist representing the Telomer Research Program, a chemical industry group that includes DuPont and other PFC makers, testified before the Health Committee of the California State Senate against a bill to ban both perfluorooctanoic acid (PFOA/C8) and perfluorohexanoic acid (PFHxA/C6) in food packaging. He repeated the claim that PFOA is not harmful to humans, and that an outright ban would be unnecessary in the presence of the voluntary phaseout program. He also repeatedly described C6 as an example of the “green chemistry” approach the state is developing to encourage the production of safer alternative chemicals:

[The bill] would derail a promising example of green chemistry at work . . . [B]y targeting perflourinated compounds with chain links of 6 or higher in this legislation, the bill would frustrate the conversion from the C8 based products, that are the source of the PFOA, to a set of effective C6 based compounds whose breakdown products are much, much less toxic and don’t have the same persistence issues that PFOA and some of the C8s have. . . . [O]ur companies are addressing the concerns about PFOA; we’re aggressively doing so. And we believe the proposed legislation would actually do harm to an effective green chemistry strategy for reducing the concerns about this chemical. (Lawyer 2008)

Green chemistry is sustainable chemistry with products and processes that reduce or eliminate the use and generation of hazardous substances. In the absence of transparent, independently conducted toxicity studies, replacement PFC chemicals in food packaging may very well become new, emergent contaminants whose health consequences will be directly tested on people. And while much remains unknown about C6, what is known – it is bioaccumulative, persistent and crosses the placenta to pollute human blood – is enough to disqualify it as green chemistry.

New Chemicals & Risks are Confidential

In the wake of the voluntary PFOA phaseout agreement, US industries are shifting the kinds of chemicals they are using in consumer products, including in food packaging. But when it comes to the new fluorochemicals manufacturers are developing at a breakneck speed, the only available data on toxicity come not from published scientific studies but from “substantial risk” notifications that federal law requires companies to submit to the Environmental Protection Agency (EPA). Though the submissions are publicly available, an EWG review shows that companies are claiming as confidential the chemical name in 90% of the studies and the company name in 70% of the studies. Redacted studies that conceal the chemical name and the company name and that contain no information on the range of consumer products the chemicals might be used in are of little use to the public. This lack of transparency means, in effect, that DuPont, 3M and other companies are either already manufacturing or gearing up to produce millions of pounds of chemicals for application to food packaging in place of PFOA but that have no openly accessible and scientifically supported safety data. A key section of the federal Toxic Substances Control Act (TSCA), known as section 8(e), requires U.S. chemical manufacturers, importers, processors and distributors to notify the EPA within 30 calendar days of any new, unpublished information on their chemicals that may lead to a conclusion of substantial risk to human health or to the environment (US EPA 2008). These TSCA 8(e) notices are the only glimpse that anyone outside of the EPA and the chemical industry may have into the potential toxicity of the replacement fluorochemicals. But when EWG analyzed the industry studies submitted to EPA's 8(e) docket between January 2007 and April 2008, what we found was startling. During this eighteen-month period, EPA received at least nineteen notices from chemical manufacturers that reported toxicity of fluorochemicals (US EPA 2008). All of these notices report at least one health effect seen in test animals, and the health endpoints themselves were often quite serious. Deaths of exposed animals were reported in five studies. In one 2007 study submitted by 3M, every single female animal tested died after 4-5 exposures to the chemical. [PDF file] Overall, these 19 studies found a staggering array of different health effects, including irregular breathing, muscle incoordination, lowered fertility, birth defects, increased numbers of stillborn pups, absence of pupilary light reflex in the eye, lack of normal startle response, dermal sensitization, and changes in the weights and/or size of vital organs such as the heart, kidney, liver, spleen, thymus, prostate, ovaries, and adrenal glands. Yet, despite these reams of troubling health data, 90% of the time the public has no way of knowing what compound was responsible: EWG found that for 17 of the 19 notices submitted to the EPA from January 2007 to April 2008 the name of the chemical has been redacted from the text under the claim of confidential business information. For example, while we know that there is a fluorochemical that was associated with death of a dam, reduced pup weight per litter, increased percentage of dams with all pups dying, reduced live-born pups per litter, and increased number of stillborn pups per litter, but all we know about the chemical’s identity is that it is a “fluorinated surfactant salt." [PDF file submitted by 3M on December 14, 2007] Similarly, a different study found that gestational exposure to a fluorochemical was associated with abnormal/difficult birth, lower fertility, reduced offspring body weights, skeletal abnormalities in offspring (effects on teeth, appearance of bent rib and 7th cervical rib), and lower maternal and offspring viability during lactation, but all we know is that the chemical was a “hydrofluorocarbon.” [PDF file 1 and PDF file 2 submitted by an unnamed manufacturer on 15 August 2007]

Table. Manufacturers’ submissions to TSCA 8(3) docket

Date Submitter Chemical Description Health effects reported
25-Feb-08 Unknown Hydrofluorocarbon Increased kidney weight Increased liver weight Increased spleen weight Increased cardiomyopathy
15-Jan-08 Unknown Perfluorinated aliphatic carboxylic acid, Ammonium salt Decreased body weight gain Decreases in red blood cells Increased liver weight Decreased heart weight Increased kidney weight
15-Jan-08 Unknown Perfluorinated aliphatic carboxylic acid Decreases in red blood cells Decreases in serum lipids (triglycerides and/or cholesterol) Increased liver weight Increased liver b-oxidation Hepatocellular hypertrophy
14-Dec-07 3M [Fluorinated surfactant salt] Death of dam Reduced pup weight per litter Increased percentage of dams with all pups dying Reduced live-born pups per litter Increased stillborn pups per litter
20-Nov-07 3M [Fluorinated surfactant salt] Dermal sensitization
30-Oct-07 Unknown Perfluorinated aliphatic carboxylic acid, Ammonium salt Ulceration Erythema
30-Oct-07 Unknown Polyfluorosulfonic acid Substantial cytotoxicity Reduced body weight
18-Oct-07 Unknown Ammonium salt of fluoroalkyl
carboxylic acid
Substantial cytotoxicity
17-Oct-07 DuPont Poly[oxy[trifluoro(trifluoromethyl)-1,2-ethanediyl]],
Dermal sensitization
10-Oct-07 Unknown Ammonium salt of fluoroalkyl carboxylic acid Death Ataxia
15-Aug-07 Unknown Hydrofluorocarbon Reduced motor activity Reduced forelimb grip strength Reduced hindlimb grip strength Reduction in live born index Lower food efficiency
15-Aug-07 Unknown Hydrofluorocarbon Dystocia (abnormal or difficult birth) Lower fertility Lower maternal and offspring viability during lactation Effects on teeth Reduced offspring body weights
15-Aug-07 Unknown Hydrofluorocarbon Decreased maternal body weight gain Increased occurrence of skeletal malformations in offspring (bent rib and 7th cervical rib)
7-Aug-07 Unknown Ammonium salt of fluoroalkyl carboxylic acid Death
26-Jul-07 Unknown Fluorinated aliphatic alcohol Death Ataxia (nervous dysfunction and incoordination of muscle movements)
11-Jul-07 3M [Fluorochemical intermediate] Reduced prostate and seminal vesicle size Reduced absolute epididymes weight Reduced absolute adrenal weight Reduced absolute ovary weight Reduced absolute thymus weight Reduced absolute spleen weight Reduced relative thymus weight
12-Mar-07 Unknown Fluorocarbon "Became anesthetized" Irregular breathing No startle response Body weight losses
26-Feb-07 3M [Fluorinated surfactant salt] Death (six out of six female rats died after 4-5 doses; no mortality in male rats)
5-Jan-07 3M Ammonia perfluorobutanoate (PFBA) Absence of pupillary light reflex in both eyes Increase in hepatocellular hypertrophy Increased incidence and/or severity of hypertrophy/hyperplasia of follicular epithelium of the thyroid glands Increased liver weight

It should also be noted that in the vast majority (70%) of cases, the public also doesn’t even know what company sponsored the study and submitted to the EPA: in 13 of 19 submissions, this information has been redacted under claims of confidential business information. Essentially, the only piece of information that the general public is usually allowed to know is how hazardous an anonymous chemical may be. But what the identity of that chemical is, which company manufactures it, how much is being produced, and what consumer products it might be used in, remains a secret. This is hardly an assurance for safety. While we obviously don’t know the identities of the fluorinated compounds that were tested in these studies, we can be reasonably certain that they are not PFOA, PFOS, or their higher homologues, which are the chemicals subject to the voluntary phaseout DuPont, 3M, and other manufacturers have agreed to under pressure from EPA. Animal testing is expensive, and chemical companies would have no incentive to pay for testing of compounds that had few remaining uses. And since TSCA requires companies to report the results of new studies indicating significant health concern within 30 days, there is also little chance of these being old PFOA or PFOS studies that are only now being submitted to the EPA. What this means is that these studies showing dramatic adverse health effects are probably PFCs designed to be replacements for PFOA, PFOS and/or their higher homologues. And there is a decent chance that they are C6 fluorinated chemicals since market trends and FDA records indicate that many fluorochemical producers and secondary business users are shifting to the C6 PFC chemistry (Asahi Glass Co 2007; Clariant 2008; DuPont 2008a; DuPont 2008b; FDA 2006; FDA 2008; Nanowerk 2008; Sanitized AG 2008). But we will likely never know. Because the identity of the compounds found toxic in these 8(e) TSCA studies are held secret, not only from the general public, but even from regulators in state agencies that may be making decisions about these same compounds.

DuPont Claims at Odds with Science

No matter how strong the evidence that PFOA may be harming human health, DuPont spokespeople refute it, year after year: "…PFOA does not harm human health or the environment." (See DuPont press quotes) Normally, this might be dismissed as a typical corporate interpretation of study results or just another example of a company over-zealously defending a profitable chemical. But in this case DuPont has gone beyond spin, to a much higher level of deception.

Documents obtained from litigation against DuPont for PFOA contamination of water supplies in West Virginia and Ohio show that DuPont’s own ethicists and medical experts found the company’s spin on PFOA science to be “misleading”, "disingenuous", "unacceptable", and "not supported by the available facts" (DuPont's Epidemiology Review Board 2005-2006).

DuPont’s mischaracterizations of the science have long raised concerns from environmental advocates and communities affected directly by their pollution and neglect. But in 2005 and 2006, this misinformation campaign ran into a serious buzzsaw in the form of DuPont’s own Epidemiology Review Board (ERB), a group of independent scientists, medical doctors, and ethicists from Harvard, Yale, Georgetown, Johns Hopkins and other prestigious universities, chosen by DuPont to review PFOA epidemiology studies, including several studies of workers at their Parkersburg, West Virginia fluorochemical plant.

DuPont’s own Epidemiology Review Board (ERB)

Thomas Beauchamp PhD
Professor of Philosophy and Senior Research Scholar,
Georgetown University's Kennedy Institute of Ethics

Mark Cullen MD
Director, Section of Occupational and Environmental Medicine,
Yale University School of Medicine

Ellen Eisen PhD
Adjunct Professor,
Department of Environmental Health,
Harvard University

Jonathan Samet MD
Chairman of the Department of Epidemiology,
Johns Hopkins Bloomberg School of Public Health

Noah Seixas PhD
Professor, Department of Environmental and Occupational Health Sciences,
University of Washington ERB Chair

David Wegman MD
Dean, School of Health and Environment,
University of Massachusetts Lowell

Beginning in 2005, ERB members raised serious ethical and scientific concerns about the manner in which DuPont was deliberately mischaracterizing the results of studies of workers in Parkersburg. Over the course of the next two years the committee was extremely critical of DuPont’s public presentation of this and other scientific information.

For example, DuPont's presentation of the results a worker study to plant workers and the press in 2005, concluded, among other things, that:

Based on an evaluation of human health and toxicology studies, DuPont believes that the weight of evidence suggests that PFOA exposure does not cause cancer in humans and does not pose a health risk to the general public... To date, no human health effects are known to be caused by PFOA, even in workers who have significantly higher exposure levels than the general population.

-- Washington Post, June 29, 2005

This interpretation was far from an objective reading of the study results, and in response, DuPont's Epidemiology Review Board (ERB) member, Thomas Beauchamp PhD, of Georgetown University called DuPont's conclusion:

"Somewhere between ‘misleading' and ‘disingenuous' has red-flag written all over it;"

The entire committee shared this opinion, as expressed by David Wegman, MD, and chair of the ERB:

"We were unanimous in believing that, contrary to the statement at the start of the [employee] letter, we believe that the results do show a health effect"…"it is certainly not appropriate to say ‘… no human health effects;'"

Beauchamp, commenting on the specific nature of DuPont's ethical lapses, further stated:

"The claim of no health effects is not supported by available facts (factual inappropriateness)... such a statement is misleading, whether intentionally or not, and it is unacceptable to mislead in this way (moral inappropriateness)."

Overall, the ERB concluded that DuPont's presentation of the study results:

"Was considered by us all to be misleading;"

(See PDF file for ERB February 2005)

This was not the last time that the ERB would catch DuPont ignoring or twisting the facts for their own benefit. Throughout 2005 and 2006, things got worse for PFOA manufacturers. In December 2005 EPA settled its PFOA case against DuPont for the largest environmental administrative penalty under the Toxic Substances Control Act in agency history (US EPA 2005).

The charge against the company was that for 20 years it had failed to disclose important study results, as required by law, showing that PFOA crossed the placenta, as demonstrated in a study showing that two out of seven female DuPont workers tested for PFOA during pregnancy gave birth to babies with severe facial birth defects (US EPA 2004). In DuPont's view, these findings, which were reported by company scientists in 1981, did not indicate a substantial risk to human health, even though they represented the first evidence ever that PFOA could make its way to the fetus and potentially cause serious birth defects. In the end, DuPont was forced to pay a record $16.5 million fine for failing to report these findings to the EPA (US EPA 2005). But despite this record fine for concealing critical data in a study showing severe birth defects in babies exposed to PFOA, the company did not change in any way its claim that no human health effects are known to be caused by PFOA.

One month later, in January 2006, the PFOA Review Panel of EPA's Science Advisory Board (SAB) issued its draft report recommending that, based on its review of available PFOA carcinogenicity data, PFOA should be considered a "likely human carcinogen" (SAB 2006). DuPont responded with their stock claim that "to date no human health effects are known to be caused by PFOA" (DuPont 2006a).

In February 2006, members of DuPont's ERB, who were apparently becoming increasingly fed up with DuPont spin, submitted two consecutive memoranda to DuPont, stating: "Given the many gaps in understanding of population exposures to PFOA and of possible health consequences, we strongly advise against any public statements asserting that PFOA does not pose any risk to health… We also question the evidential basis of DuPont's public expression asserting, with what appears to be great confidence, that PFOA does not pose a risk to health" (DuPont's Epidemiology Review Board 2005-2006). (See PDF file for ERB February 2006)

In March 2006 eight fluorochemical manufacturers, including DuPont, agreed to participate in EPA's PFOA Stewardship Program aimed at reducing facility emissions and product content of PFOA and related chemicals on a global basis (US EPA 2006a).

In July 2006 members of the ERB panel stated again that DuPont's ongoing reports continue "to avoid or downplay the significant findings" (DuPont's Epidemiology Review Board 2005-2006) (See PDF file for ERB July 2006).

Later that year, in October 2006, DuPont publicly announced preliminary results of its own study of death rates among PFOA-exposed workers at the Washington Works plant, indicating increased rates of death for heart disease, kidney cancer and diabetes (DuPont 2006b). Members of the ERB panel were very concerned about DuPont's press release that "appears written to leave the impression ‘don't worry'" (DuPont's Epidemiology Review Board 2005-2006). (See PDF file for ERB October 2006)

In November 2006 DuPont entered into a Consent Order with EPA for additional tests on PFOA under which EPA noted that new PFOA studies have raised a "concern for public health" and that PFOA "may present an imminent and substantial endangerment to the health of persons" (US EPA 2006b).

The company's response continued in the same vein, "So DuPont's position on this is, to date, there are no known health effects from exposure to PFOA." Fort Worth Star Telegram, December 5, 2006

One month later, DuPont Spokesman David Booth offered this riff on the same propaganda, adding that PFOA is "essentially a high-tech detergent" that has been used for 50 years in manufacturing plastic and "as there are no known health effects from PFOA."" Biloxi Sun Herald, January 26, 2007

Throughout 2007, a series of human studies were released unambiguously demonstrating adverse health effects linked to PFOA exposure. These include two studies that observed association between PFOA blood levels and smaller birth weight and size in newborn babies (Apelberg, Witter 2007; Fei 2007); two DuPont worker studies showing increased levels of cholesterol and liver damage related to PFOA exposure (Sakr, Kreckmann 2007; Sakr, Leonard 2007); a DuPont study demonstrating increased mortality from diabetes, cancers of kidney and bladder, all cardiovascular disease and ischemic heart disease in fluorochemical plant workers (Leonard 2007); and two 3M studies indicating abnormal thyroid hormones, elevated cholesterol and increased blood levels of liver enzymes as well as increased risk of mortality due to stroke and prostate cancer for PFOA-exposed employees (Lundin 2007; Olsen 2007).

One of the studies, carried out by researchers at the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, found the chemical in every single one of the 299 umbilical cords analyzed, suggesting that every baby is born in the US already contaminated with PFOA. Similar levels have been found in babies in Europe and Japan. It also found that the babies whose cords had the highest concentrations of PFOA were born lighter, thinner and with smaller head circumferences than others. The second study - carried out in the US and Denmark, with babies drawn from the Danish National Birth Cohort - came up with similar findings for birth weight, the only measurement the scientists made.

Not surprisingly this new science has not swayed the DuPont public relations machine. Commenting on this wave of new science that has repeatedly shown adverse health effects of PFOA exposure in newborn babies, DuPont once again stated that "there are no human health effects known to be caused by PFOA", adding that "Our position is that the studies have not changed our position." The Independent, August 26, 2007

Voluntary Phaseout Not Working

In May 2000, the Environmental Protection Agency (EPA) announced it was “examining its options” regarding the toxic and persistent chemical PFOA. In reality a toothless, 30-year-old federal law left EPA with few options to examine. The Agency could not even ban asbestos, a known human carcinogen, under the 1976 Toxic Substances Control Act. For PFOA, EPA settled on a voluntary phase-out agreement in lieu of an enforceable ban. In January 2006 DuPont, 3M and six other chemical companies entered into the EPA-brokered Voluntary Stewardship Program, in which companies committed to phasing out by 2015 the use of the Teflon chemical PFOA and other closely related chemicals (“higher homologues”) (US EPA 2006a). These companies have pointed to this agreement to argue against actions proposed since that would further reduce the public’s exposures to PFCs. But unlike an enforceable ban, which would have been the ideal outcome for a chemical as hazardous and persistent as PFOA, the voluntary phase-out agreement leaves open the possibility that consumers will continue to be exposed to PFOA for decades to come. Because of significant gaps in the agreement, it failed to obviate the need for additional actions to reduce the public’s exposures to PFOA and other perfluorochemicals. First and foremost is the simple fact that the stewardship program is voluntary. Under the EPA agreement, companies only "commit to working toward the elimination" of the targeted perfluorochemicals by 2015 with no EPA enforcement mechanism in place and no penalties if deadlines are not met. This means that consumers and EPA essentially have to trust chemical companies to do the right thing. When one considers the track record of the industry for complying with legally enforceable statutes with steep penalties – take DuPont and their record-setting fine, for failing to report pollution data to EPA as required by federal law (US EPA 2005), for example – this is not a particularly encouraging option. That the stewardship program is voluntary also means that companies can choose whether they want to opt in at all – and not a single company from China is participating. Biomonitoring data from China where production of PFOS and other PFCs continues indicate that the levels of these chemicals are increasing in the bodies of Chinese citizens (Jin 2007; Olsen 2008). These disconcerting findings are evidence that a US-only voluntary program will likely not be sufficient to protect American consumers from PFC contamination of everyday products given the massive quantity of goods the US imports from China. This is especially a concern when it comes to food packaging, for China is the third largest producer of packaging in the world (Packaging Expo 2008), and food packaging is considered to be an important source of exposure to PFCs (Begley 2005; Tittlemier 2007). The voluntary nature of the program also means that companies face no penalties for failing to comply with the agreement, and that the EPA has no authority to require companies to submit to independent verification of the data and claims they are providing to EPA to document their efforts. EWG’s analysis of the first year of progress reports from companies participating in the stewardship program revealed mixed results. A number of companies have reduced their use of PFOA only minimally or not at all. The submitted data are neither clear nor transparent, and thus fail to provide the information needed to assess companies’ progress. For example, many companies list a 10-fold range for emissions, making it impossible to determine if there has been any progress. Some companies report PFOA and higher homologues separately, obscuring the true state of the industry.

Table I. Summary data on emissions from fluoropolymer (FP) and fluorotelomer manufacturing facilities and PFOA product content1

  Emissions from FP and telomer manufacturing facilities, kg PFOA (and higher homologues) product content
Dispersions (ppm wet weight) Other fluoropolymers (ppm dry-weight)
Company and chemical Baseline2 2006 Claimed % reduction Baseline 2006 Claimed % reduction Baseline 2006 Claimed % reduction
Arkema, PFOA+HH3 >10,000-
22% >500-
0% >70 -150 >70 - 150 30%
Asahi PFOA+HH 5,230 4,922 6% 1,364 500-1,570 12% CBI 0.12 NA
Ciba4 Baseline PFOA total for emissions and product content reported at 30 kg; 2006 reported as 0.05 kg
Daikin PFOA CBI CBI 92-94% 420 280 34% 14 Plastics: 2 Elastomers: 300 0%
DuPont PFOA 49,400 1,100 98% 970 547 44% 340 69 80%
3M/ Dyneon PFOA 1,700 0 100% 4,300 0 100% not reported not reported not reported
Solvay Solexis PFOA, 1000-
higher homologues, 1000-10,000
PFOA+HH >1000-10,000 28% 1,500-1,700 PFOA + HH 600-700 PFOA +HH 59% 140-170 PFOA + HH 170-200 PFOA + HH Increased by 17%

1. Data from the US EPA website Eight companies signed up to participate in the stewardship program; One signer, Clariant declared both baseline and follow up data as “Not applicable”. 2. Baseline values were collected around 2000 (Arkema 1999; Asahi Glass Co 2000; Ciba 2002; Daikin 2000; Dupont 2000; 3M/Dyneon 1999; Solvay Solexis 2000). 3. Higher homologues (HH) of PFOA. 4. Ciba reported emissions and product content in the same category, making it impossible to determine the extent of progress in decreasing of PFOA product content or PFOA emissions.

For example, Daikin claims its PFOA emissions have been reduced by 92-93% but then lists their actual emission numbers as confidential business information (CBI), calling into question the reliability of their claims. Similarly, Arkema reports its emissions as a 10-fold range, making it impossible to estimate change between baseline and reporting years. Arkema also reported unchanged PFOA content in dry-weight fluoropolymers, which raises questions about its claim of 30% product content reduction. Furthermore, for at least four different companies, no significant progress has been observed so far. Asahi Glass Co. only reduced its emissions by 6%, and the company’s product content for wet fluoropolymer dispersions was only reduced by 12%. Arkema did not report any reduction in PFOA content in wet dispersions, while Daikin reported no reduction in PFOA content in dry-weight fluoropolymers. Meanwhile, Solvay Solexis reported a 17% increase in PFOA content in dry-weight fluoropolymers. The Year 1 summary does, of course, report some positive steps. Dupont, for example, reported a 98% reduction of emissions and 80% PFOA reduction in dry-weight fluoropolymers. Reductions in PFOA content in wet dispersions were reported by Daikin, Dupont, and Solvay Solexis. But when talking about toxic chemicals that will never break down in the environment, such piecemeal positive steps are not enough to call a program successful. Especially when it is hampered by unreliable data and no possibility of enforcement.

New scientific research shows PFC-related health effects in people

For decades, health surveys of workers at DuPont and 3M fluorochemical plants indicated that exposure to PFCs poses serious health dangers. In 1992, employee surveillance data at the DuPont Washington Works fluorochemical plant revealed a statistically significant excess of cancers of the buccal cavity and pharynx, kidney and other urinary cancers, and leukemia among the workers (DuPont 1992). The next year, a retrospective cohort mortality study was conducted by 3M at the Cottage Grove, Minnesota plant that produced PFOA, reviewing the employee records for the 1947-1983 period. The study found that occupational exposure to PFOA was associated with two-fold higher rate of death from prostate cancer (Gilliland 1993). And in 1998, Cottage Grove workers occupationally exposed to PFOA were found to have abnormal levels of reproductive hormones (higher levels of estradiol in workers with highest PFOA blood levels) (Olsen 1998). In addition DuPont has known since the 1980s that PFOA can cross the placenta and cause developmental abnormalities in children of women exposed to this toxic chemical at work (US EPA 2004; reviewed in EWG 2004). Despite this evidence of health problems in fluorochemical plant workers, industry did not take any precautionary action to protect public health. For decades, data on human health effects of PFOA was suppressed and not submitted to the EPA (US EPA 2004). This is especially egregious considering that animal studies have long linked PFCs with a striking and diverse array of health problems. This incredibly long list includes: a broad range of developmental effects, from smaller birth weight, developmental delays, and organ abnormalities, to stillborn pups and whole litter loss (Andersen 2008; Lau 2007; Lau, Butenhoff 2004); severe liver toxicity (Guruge 2006; Martin 2007; Rosen 2007; Yeung 2007); suppression of the immune system and predisposition to allergies (DeWitt 2008; Fairley 2007; Peden-Adams 2008; Yang 2002; Yang 2000); behavioral changes (Johansson 2008); altered hormonal function, especially thyroid and sex hormones (Lau 2007; Biegel 1995; Bookstaff 1990; Cook 1992; Liu 1996); as well as liver, pancreatic, testicular, and mammary cancers (Sibinski 1987). Everything changed, however, when the studies by both industry and academic researchers revealed that PFOA, PFOS, and other PFCs had become widespread, global contaminants that polluted bodies of humans and wildlife world-wide (Houde 2006; Kannan 2002; Kannan 2004; Prevedouros 2006; Sinclair 2006). Now, not only occupationally exposed workers were at risk from PFCs (Olsen 2004; Joyce 2007), but every American (Calafat, Wong 2007). Especially worrisome, children, the most vulnerable population, appeared to have higher levels of PFCs in their bodies compared to adults (Emmett 2006; Olsen 2004). While the scientific evidence linking PFCs to a wide range of health effects was more than strong enough in 2006 for the EPA to elicit a phaseout of many of these compounds, new studies published in the last two years show even greater cause for concern. Of particular note are three epidemiological studies, all conducted by independent scientists looking at people exposed to PFCs through consumer products and/or through contaminated drinking water, and all showing that exposure to these chemicals may be particularly dangerous for the developing fetus and children. Previous studies from the US, Canada, Germany and Japan have shown that PFCs can cross the placenta and transfer from mother’s body to the fetus (Apelberg, Goldman 2007; Inoue 2004; Midasch 2007; Tittlemier 2004), and are also found in breast milk (Karrman 2007; Kuklenyik 2004; So 2006; Tao 2008; Volkel 2007). Since there have been numerous animal studies demonstrating developmental toxicity of PFCs (Lau 2007; Lau, Butenhoff 2004; Andersen 2008; Fenton 2007) and the links between early developmental problems and health consequences later in life (Lau and Rogers 2004; Needham 2008), the next obvious question was whether any of these same health effects might be seen in human populations. Two sets of researchers set out to answer this question. Unfortunately, both found that the answer was ‘yes.’ The first study, conducted by researchers from Johns Hopkins University and the Centers for Disease control, looked at PFOS and PFOA levels in 293 randomly collected samples of fetal cord blood from babies born in Baltimore, Maryland. The scientists found a statistically significant relationship between the levels of these two compounds and low birth weight and size – even though the blood levels of PFOS and PFOA were within the range found in general population (Apelberg, Witter 2007). These results were featured in the November 2007 issue of the prestigious journal Environmental Health Perspectives (EHP), published by the National Institute of Environmental Health Sciences. The second paper, published in the same issue of EHP, was an even larger study conducted by scientists from University of California, Los Angeles in conjunction with the Institute of Public Health at Aarhus University in Denmark (Fei 2007). The researchers enrolled a randomly selected group of 1,400 Danish women and followed them throughout their pregnancy and birth. They found that levels of PFOA in the mothers’ blood were correlated with their baby having a higher chance of being born with low birth weight. While the term “low birth weight” sounds relatively innocuous, it is a well known harbinger of more serious medical problems. For example, in 2001 a study published in the British Medical Journal (Matte 2001) found that there was a proportional relationship between birth weight and average IQ by age 7, with low birth weight babies scoring lower on IQ tests during development. Another study found a statistically significant link between low birth weight and adverse developmental effects including learning disabilities (Sauve 1998). And a 1999 study found much higher risks of mortality for infants born far underweight (Chye 1999). The most troubling aspect of these two new PFOA studies is that the negative effects of PFOA were seen at levels present in the general population. The participating mothers in these studies were exposed through simple, every-day activities: through contact with PFC-containing products, food, and food packaging that is coated with fluorochemicals. With research conducted by the Centers for Disease Control and chemical manufacturers alike showing that the blood of more than 98% of Americans are contaminated with PFCs (Calafat 2006; Calafat, Kuklenyik 2007; Calafat, Wong 2007; Olsen 2004), these two studies show that there is real reason to be concerned about the ubiquity of PFC exposure. The C8 Health Project: largest PFC study to date The third key epidemiological study would be important if for no other reason because of its sheer size. With 69,000 study subjects, and known as the C8 Health Project, it is by far the largest study ever of PFC health effects in people. But the story of how it came about and its striking findings may make it the most important PFC study to date. In 1981 two of seven children born to PFOA-exposed female workers in DuPont’s Washington Works plant chemical plant in Parkersburg, West Virginia were found to have birth defects involving the eye. But DuPont never told the EPA, even after it learned from 3M that PFOA had been linked to birth defects of the eye in studies of laboratory animals (reviewed in EWG 2004). Three years later, between March and June 1984, DuPont tested for, and found, PFOA in tap water taken from a store in Little Hocking, Ohio, not far from the Washington Works plant. Again, DuPont failed to inform U.S. EPA of the finding. Nor did it inform the Little Hocking Water Association of this finding until seventeen years later in 2001, when it was revealed during the course of establishing a consent order between DuPont and the West Virginia Department of Environmental Protection (reviewed in EWG 2004). These two events were just the beginning of a several decade long cover-up that eventually landed DuPont with a $16.5 million fine, by far the largest in EPA’s history (US EPA 2005). But due to the company’s negligence, unsafe chemical disposal practices, and decades of deception and cover-ups, tens of thousands of people living in Ohio and West Virginia communities near the DuPont plant have been exposed to contaminated drinking water. The C8 Health Project was created to determine what, if any, health effects these community members might be suffering from as the result of this PFC exposure. A number of worrisome trends emerged from the initial analysis of the C8 Health Project data first presented to the public in May of this year (Frisbee 2008; West Virginia University School of Medicine 2008):

  • Children in the study had higher median levels of PFOA in their blood. Among the 69,000 enrolled participants, serum PFOA levels ranged between 0.5 ppb and 22,412 ppb, with a median concentration of 28 ppb (West Virginia University School of Medicine 2008). Among the enrolled children under 10, serum PFOA concentrations ranged between 0.7 ppb and 2,070 ppb, with median concentration of 34 ppb.

  • Higher PFOA concentrations in study children were correlated with higher total cholesterol levels, predisposing these children to future weight problems and accompanying risks of heart disease as well as other illnesses. Similarly, in industry studies elevated cholesterol was one of the hallmark health findings observed in PFC-exposed workers (Olsen 2003; Sakr, Kreckmann 2007; Sakr, Leonard 2007). The problem of obesity in children has now become so severe so as be considered an epidemic. Several prior biomonitoring studies indicated that children tend to have higher serum levels of PFCs compared to adults (Emmett 2006; Olsen, Church 2004). A link between PFCs and elevated lipids thus presents an especial danger to children's health.

  • Higher PFOA levels in study participants were correlated with lower levels of serum immunoglobulin, the key protein that helps the body fight bacteria, viruses, and other pathogenic microorganisms. Similarly, EPA researchers reported PFOA-exposed mice had low immunoglobulin levels (DeWitt 2008). And in animal studies PFC exposure has been linked with death of immune cells and weakening of the body’s ability to protect itself from infection (DeWitt 2008; Peden-Adams 2008; Yang 2002; Yang 2000).

  • Higher PFOA concentration in study participants was also correlated with elevated levels of alanine transaminase (ALT) and aspartate transaminase (AST), two key enzymes used in clinical blood assays to detect liver problems. When the liver is damaged, hepatocytes (liver cells) leak these enzymes into the blood, where higher levels of ALT and AST are then detected. Similar to findings of the C8 project, workers occupationally exposed to PFOA have increased levels of ALT (Olsen and Zobel 2007) and AST (Sakr, Leonard 2007). In addition, serum concentrations of the liver-secreted C-reactive protein, an important element early defense system against infections, decreased with higher PFOA levels in the C8 Health Project cohort.

  • Finally, thyroid function was affected in PFOA-exposed cohort participants. There are two types of thyroid hormones easily measurable in the blood, thyroxine (T4) and triiodothyronine (T3). In the study, researchers analyzed free thyroxine index (FTI), which indicates how much thyroid hormone is free in the blood stream to work on the body. Unlike the T4 alone, FTI is not affected by estrogen levels and can thus be used to assess thyroid function in both genders. FTI is elevated in hyperthyroidism and depressed in hypothyroidism. In the study, FTI response followed an inverted U curve (higher at moderate-high PFOA levels and decreasing again at the highest PFOA levels). This trend is in agreement with worker studies that demonstrate negative association between PFOA serum concentration and free T4 and positive association between PFOA and T3 (Olsen and Zobel 2007).

In summary, C8 Health Project scientists concluded that this pilot analysis of C8 health data points to the association between PFOA and a wide range of adverse health effects including immune function, liver function, cholesterol (especially in children), and thyroid (Frisbee 2008). Results of studies of this size and complexity often take years to make their way into the scientific literature, and the researchers have cautioned that they are preliminary. The trends, however, are so clear and so consistent with previous worker and animal studies that they are deeply worrisome.

DuPont Press Quotes

In public statements, press releases, and on its website, DuPont continuously reiterated the same statement that “there are no human health effects known to be caused by PFOA.” (DuPont 2007a, 2008a). DuPont’s persistence in holding on to these statements is especially disingenuous in light of the extensive body of scientific literature that demonstrates toxicity of PFOA and other PFCs both in humans and in all other mammals tested to date. However, all of these findings have been hushed up, disregarded or minimized by DuPont for years.

DuPont has repeatedly said there is no evidence that PFOA causes adverse health effects and that data recently generated by the company will show that the chemical has a higher margin of safety than was determined in EPA's draft assessment.

-- Pesticide & Toxic Chemical News. April 14, 2003

"One reason is that C-8 persists in the environment for a long time; blood samples from around the country have found it in measurable quantities in more than 80 percent of the population. Some 3M tests showed toxicity in rats; DuPont dismisses those tests as not applicable to humans… DuPont apparently is too dependent on C-8 for Teflon manufacture to phase it out quickly, so its Web site explains, "There is no evidence or data that demonstrates PFOA causes adverse human health effects" at low levels of exposure."

-- News Journal, April 17, 2003

"DuPont defends its actions in not disclosing the test results because it said it "acted with the absolute confidence that the low or nondetectable levels of C8 found in the Little Hocking water samples in the mid-1980s posed no risk to the health of Little Hocking residents or our own employees in the area."

-- Plastics News, June 16, 2003

"By 1991, DuPont had information that C-8 was in the water supplies, according to company documents. But the EPA said DuPont did not inform federal regulators. DuPont asserts that there is no legal basis for the EPA's allegations. The company contends that it has fully complied with statutory reporting requirements and disputes any association between C-8 and harmful effects on human health or the environment."

-- News Journal, July 9, 2004

DuPont General Counsel Stacey J. Mobley said the company would "vigorously defend our position" that no laws were broken and that the chemical was safe. "The evidence from over 50 years of experience and extensive scientific studies supports our conclusion that PFOA does not harm human health or the environment," Mobley said.""

-- LA Times, July 9, 2004

"DuPont is contesting the accusations, and insists that neither PFOA nor Teflon poses risks to humans. ''The evidence from over 50 years of experience and extensive scientific studies supports our conclusion that PFOA does not harm human health or the environment,'' said Stacey J. Mobley, general counsel of DuPont, in a statement responding to the E.P.A. ruling."

-- NY Times, August 8, 2004

The company (DuPont) says it has broken no laws and has sharply reduced emissions of PFOA. And studies on plant workers have shown PFOA to be safe, said Don Duncan, president of the Society of the Plastics Industry, and industry group. "It's not as if we've got people dropping in the streets out there," he said.

In a study awaiting publication, DuPont scientists say they find no risk associated with the everyday use of coated clothing, carpets and cookware, among other products. "We can say unequivocally that those articles are safe," said Robert C. Buck, a Ph.D chemists and senior research scientist with the company.

-- Philadelphia Inquirer, September 27, 2004

Although to date, no human health effects are known to be caused by PFOA, the company recognizes that the presence of PFOA in human blood raises questions that should be addressed," the company (Dupont) said in a statement. Dupont has said that 50 years of use and study support its conclusion that the chemical poses no danger to people.

-- Los Angeles Times, January 13, 2005

"DuPont remains confident that based on over 50 years of use and experience with PFOA there is no evidence to indicate that it harms human health or the environment," [stated] company spokesman R. Clifton Webb.

DuPont documents, though, show company officials were worried the public would learn the PFOA had contaminated local water supplies... "Biggest potential downside: plant contamination issues surface, case becomes class action," DuPont attorney concluded in a March 2000 e-mail.

-- Chicago Tribune, January 18, 2005

"Based on an evaluation of human health and toxicology studies, DuPont believes that the weight of evidence suggests that PFOA exposure does not cause cancer in humans and does not pose a health risk to the general public," DuPont spokesman R. Clifton Webb said. "To date, no human health effects are known to be caused by PFOA, even in workers who have significantly higher exposure levels than the general population."

-- Washington Post, June 29, 2005

The information demonstrating that PFOA moves across the placenta "should have been reported immediately to EPA," Nakayama says. DuPont also allegedly failed to report the results of blood tests, done at the company's request, of plaintiffs in a class-action lawsuit who live near the West Virginia plant. Those people drank water drawn from wells near the plant and had blood levels of PFOA that were significantly higher than that of the U.S. population. Other data DuPont allegedly did not turn over to EPA as promptly as required by law include three studies showing that an unidentified perfluorochemical was "significantly lethal" when inhaled by laboratory rats.

-- Chemical and Engineering News, December 19, 2005

DuPont, which manufactures Teflon and has used the chemical for more than 50 years, says there is no evidence that PFOA is harmful to humans. "The chemical does have an effect on animals that are fed high doses of it. But animals respond differently to PFOA than people, and there is no evidence that there are any health effects in people," said David Boothe, a DuPont manager.

-- Baltimore Sun, February 6, 2006

"We think the weight of evidence and science says, look, the things that are happening in rats don't happen in people," Boothe said. He also said the EPA has ignored company studies that did not find health problems in workers "exposed to thousands of times higher levels than in the general population." "So DuPont's position on this is, to date, there are no known health effects from exposure to PFOA," Boothe said."

-- Fort Worth Star Telegram, December 5, 2006

DuPont Spokesman David Booth testified PFOA is "essentially a high-tech detergent" that has been used for 50 years in manufacturing plastic and "as there are no known health effects from PFOA.""

-- Biloxi Sun Herald, January 26, 2007

"Dan Turner, a spokesman for DuPont, which uses PFOA in the production of Teflon, said the company is convinced its products pose no threat to human health. "DuPont believes and maintains that consumer products sold with trace levels of PFOA are safe for their intended use," he said. He added that he was familiar with the Johns Hopkins research. "To date, there are no known human health effects known to be caused by PFOA," he said."

-- Cox News Service, Atlanta Journal-Constitution, May 26, 2007

One of the studies, carried out by researchers at the blue-chip Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, found the chemical in every single one of the 299 umbilical cords analyzed, suggesting that every baby is born already contaminated by it. Similar levels have been found in babies in Europe and Japan. It also found that the babies whose cords had the highest concentrations of PFOA were born lighter, thinner and with smaller head circumferences than others. The second study - carried out in the US and Denmark, with babies drawn from the Danish National Birth Cohort - came up with similar findings for birth weight, the only measurement it made. "DuPont has long insisted that "there are no human health effects known to be caused by PFOA", and now adds: "Our position is that the studies have not changed our position."

-- The Independent, August 26, 2007

Dupont statements on its website (2007)

DuPont Position on PFOA: "To date, there are no human health effects known to be caused by PFOA. Based on health and toxicological studies conducted by DuPont and other researchers, DuPont believes the weight of evidence indicates that PFOA exposure does not pose a health risk to the general public" (DuPont 2007a).

PFOA Facts: "Occupational exposure to PFOA has been associated with small increases in some lipids (e.g. cholesterol). It is not known whether these are causal associations. These associations were not observed in a community study. Based on health and toxicological studies, DuPont believes the weight of evidence indicates that PFOA exposure does not pose a health risk to the general public. To date, there are no human health effects known to be caused by PFOA, although study of the chemical continues" (DuPont 2007b).

PFOA - Safety: "PFOA has been used safely by DuPont and others for more than 50 years with no known human health effects to date" (DuPont 2007b).

"Still, DuPont -- which paid a heavy fine to the EPA for failing to report internal studies on the health risks of PFOA and settled a lawsuit that alleged PFOA-contaminated drinking water near a DuPont plant -- insists that PFOA does not pose a health risk to the general public."

-- Chicago Tribune, March 11, 2008

"DuPont has stated that there is no evidence of health threats from PFOA, but a federal advisory panel recommended classifying it as a probable carcinogen."

-- AP, May 7 2008

Dupont website and press releases (2008)

"DuPont believes the weight of evidence indicates that PFOA exposure does not pose a health risk to the general public. To date, there are no human health effects known to be caused by PFOA" (DuPont 2008a, 2008b).

"Based on health and toxicological studies, DuPont believes the weight of evidence indicates that PFOA exposure does not pose a health risk to the general public. To date, there are no human health effects known to be caused by PFOA, although study of the chemical continues" (DuPont 2008c).

Notably, the same stance is adopted by other fluorochemical manufacturers:

3M website, 2008

"In more than 25 years of medical surveillance we have observed no adverse health effects in our employees resulting from their exposure to PFOS or PFOA. This is very important since the level of exposure in the general population is much lower than that of production employees who worked directly with these materials." "The extensive research to date shows no adverse human health effects resulting from exposure to PFOS or PFOA. This is supported by observational research involving thousands of 3M production employees" (3M 2008).


For more than 50 years DuPont, 3M and other companies produced PFOA for a stunning range of consumer products and dumped it into the environment in amounts that have left a long-term legacy of pollution. PFOA contaminates 98% of the American population, taints drinking water supplies in at least 11 states around the country, and pollutes people and wildlife the world over, including polar bears in the Arctic. It crosses the placenta to contaminate nearly every baby before the moment of birth, and is now linked to a broad range of health problems in ten studies of the general public and workers at fluorochemical plants.

Since this tragedy was uncovered beginning in 2000, public pressure forced 8 companies, including DuPont and 3M, to sign a voluntary agreement with EPA to phase out the use of PFOA by 2015. Outcomes in the government and courts have not been voluntary, and include DuPont's obligation to fund health studies of people with contaminated drinking water, and to pay to EPA the largest administrative fine of its type in the Agency's history for failing to divulge, as required by federal law, that PFOA crosses the placenta to pose significant risks to the health of the child developing in the womb.

Yet despite the embarrassment that DuPont's public thrashing must have brought, all indications are that the company and their competitors are launching a repeat performance, replacing PFOA with a chemical called C6 that, like PFOA, is extraordinarily persistent in the environment and crosses the placenta to pose risks to babies during development. DuPont is calling this "green chemistry." And the fluorochemical industry is engineering this wholesale shift in the market without publishing a single study on the safety of this alternative.

Companies place human health and the environment at risk when they expose the population to chemicals that haven't been proven safe, that get into people's bodies, and that pollute the environment indefinitely. To remedy this situation, we recommend the following:

  • The California legislature should pass SB1313, a bill that would prohibit the use of food packaging chemicals that are contaminated with or break down into C6, PFOA, PFOS, and/or related chemicals. This bill would have national and potentially global benefits as market changes filter out from California. And when passed, it will be the only enforceable ban of PFOA and related chemicals in the country. Eight companies are phasing out their use of PFOA by 2015, but chemical companies in China and many other parts of the world have expressed no such intention. As a result, the United States could still import PFOA-containing food packaging for years to come. SB1313 would keep these toxic food packaging products out of the state. C6, a key PFOA replacement chemical, has not been proven safe. Instead, it has already been shown to cross the placenta to contaminate babies in utero. Its inclusion in the final SB1313 bill is critical.
  • The U.S. Congress should close the loophole that allows EPA and other federal public health agencies to deny states access to critical public health data on industrial chemicals, and that allows chemical companies near carte blanche to claim as confidential business information any health and safety data submitted to the government, including even the identity of the chemical. This lack of transparency severely hampers the ability of states to set policies that protect public health when the federal government fails to do so. This gap must be closed.

As well established by science and acknowledged by the FDA, food packaging chemicals can migrate into food. People ingest them, and can be exposed to significant amounts that pose risks. Persistent chemicals that pollute human blood have no place in food packaging.

The health risks from food packaging chemicals add to the risks from hundreds of other industrial chemicals that contaminate the human body. EWG studies show an average of 200 industrial chemicals, pollutants and pesticides in newborn babies. Federal law fails to require that companies test industrial chemicals for safety before they are sold and does not mandate that FDA, EPA or any other public health agency consider the totality of human exposures to toxic chemicals when assessing potential health risks, including risks from food packaging chemicals like PFOA and C6-based chemicals. Ultimately, it will take broad reform of public health protections at the federal level to fix this badly broken system; such reform must require that companies test chemicals for safety before they are sold in order to protect the health of children and others who are most vulnerable to the harmful effects of chemical exposures.

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3M. 2008. Information about PFOS and PFOA. Available: [accessed June 4 2008].

Andersen ME, Butenhoff JL, Chang SC, Farrar DG, Kennedy GL, Jr., Lau C, et al. 2008. Perfluoroalkyl Acids and Related Chemistries Toxicokinetics and Modes of Action. Toxicol Sci 102(1): 3-14.

Apelberg BJ, Goldman LR, Calafat AM, Herbstman JB, Kuklenyik Z, Heidler J, et al. 2007. Determinants of fetal exposure to polyfluoroalkyl compounds in Baltimore, Maryland. Environ Sci Technol 41(11): 3891-7.

Apelberg BJ, Witter FR, Herbstman JB, Calafat AM, Halden RU, Needham L, et al. 2007. Cord Serum Concentrations of Perfluorooctane Sulfonate (PFOS) and Perfluorooctanoate (PFOA) in Relation to Weight and Size at Birth. Environ Health Perspect 115(11): 1670-6.

Asahi. 2006. Slide presentation by AGC Chemicals, Asahi Glass Co., Ltd., entitled "Non-ECA PFOA Information Forum" at the PFOA Information Forum on June 8, 2006. Document EPA-HQ-OPPT-2003-0012-1094.4.

Asahi Glass Co. 2007. AsahiGuard E-SERIES. Available: [accessed June 4 2008].

Begley TH, White K, Honigfort P, Twaroski ML, Neches R, Walker RA. 2005. Perfluorochemicals: potential sources of and migration from food packaging. Food Addit Contam 22(10): 1023-31.

Biegel LB, Hurtt ME, Frame SR, O'Connor JC, Cook JC. 2001. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Toxicol Sci 60(1): 44-55.

Biegel LB, Liu RC, Hurtt ME, Cook JC. 1995. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro, in vivo, and ex vivo studies. Toxicol Appl Pharmacol 134(1): 18-25.

Bookstaff RC, Moore RW, Ingall GB, Peterson RE. 1990. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Toxicol Appl Pharmacol 104(2): 322-33.

Calafat AM, Kuklenyik Z, Reidy JA, Caudill SP, Tully JS, Needham LL. 2007. Serum concentrations of 11 polyfluoroalkyl compounds in the u.s. population: data from the national health and nutrition examination survey (NHANES). Environ Sci Technol 41(7): 2237-42.

Calafat AM, Needham LL, Kuklenyik Z, Reidy JA, Tully JS, Aguilar-Villalobos M, et al. 2006. Perfluorinated chemicals in selected residents of the American continent. Chemosphere 63(3): 490-6.

Calafat AM, Wong LY, Kuklenyik Z, Reidy JA, Needham LL. 2007. Polyfluoroalkyl chemicals in the U.S. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Environ Health Perspect 115(11): 1596-602.

Chye JK, Lim CT. 1999. Very low birth weight infants--mortality and predictive risk factors. Singapore Med J 40(9): 565-70.

Clariant. 2008. Annual Report "Clariant_AR07_e_12_3.pdf" updated 14 April 2008. Available: [accessed June 2 2008].

Conder JM, Hoke RA, De Wolf W, Russell MH, Buck RC. 2008. Are PFCAs bioaccumulative? A critical review and comparison with regulatory criteria and persistent lipophilic compounds. Environ Sci Technol 42(4): 995-1003.

Cook JC, Murray SM, Frame SR, Hurtt ME. 1992. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Toxicol Appl Pharmacol 113(2): 209-17.

Deon JC, Mabury SA. 2007. Production of perfluorinated carboxylic acids (PFCAs) from the biotransformation of polyfluoroalkyl phosphate surfactants (PAPS): exploring routes of human contamination. Environ Sci Technol 41(13): 4799-805.

DeWitt JC, Copeland CB, Strynar MJ, Luebke RW. 2008. Perfluorooctanoic Acid–Induced Immunomodulation in Adult C57BL/6J or C57BL/6N Female Mice. Environ Health Perspect 116(5): 644-50.

DuPont. 1992. Washington Works - surveillance data. Mortality and cancer incidence. US EPA Administrative Record AR226-1546.

DuPont. 2006a. DuPont Participation in Voluntary EPA PFOA Stewardship Program. Available: [accessed June 5 2008].

DuPont. 2006b. DuPont Concludes Washington Works Employee PFOA Study. DuPont Media Center News Releases: October 17, 2006.

DuPont. 2007a. DuPont Position on PFOA/The Facts about PFOA/Health/Health Effects. Available: [accessed February 27 2008].

DuPont. 2007b. PFOA Facts. Available: [accessed February 27 2008].

DuPont. 2008a. Fact Sheet: DuPontTM CapstoneTM Products for the Paper Packaging Industry. Available: [accessed June 4 2008].

DuPont. 2008b. DuPontTM CapstoneTM Press Release. Available: [accessed June 4 2008].

DuPont. 2008c. PFOA: Occupational & Public Health. Available: [accessed June 8 2008].

DuPont's Epidemiology Review Board (ERB). 2005-2006. E-mail communications and memoranda prepared by members of the DuPont's ERB. Filed in the United States District Court - Southern District of West Virginia, Civil Action No. 6:06-cv-00530 (Rhodes, et al. v. E.I.DuPont de Nemours and Company).

Emmett EA, Shofer FS, Zhang H, Freeman D, Desai C, Shaw LM. 2006. Community exposure to perfluorooctanoate: relationships between serum concentrations and exposure sources. J Occup Environ Med 48(8): 759-70.

Environmental Working Group (EWG). 2004. Update to EWG petition to EPA concerning DuPont's response to EPA's inquiry of possible TSCA Section 8(e) substantial risk reporting violations. Available: [accessed June 6 2008].

EWG. 2005. Environmental Working Group Human Toxome Project: PFHxA (Perfluorohexanoic acid). Available: [accessed May 26 2008].

Fairley KJ, Purdy R, Kearns S, Anderson SE, Meade B. 2007. Exposure to the Immunosuppresant, Perfluorooctanoic Acid, Enhances the Murine IgE and Airway Hyperreactivity Response to Ovalbumin. Toxicol Sci 97(2): 375-83.

FDA. 1969. Division of Pharmacology and Toxicology. Memorandum. Food Additive Petition No. 0B2434 (Evaluation of 7/1/69 submission) 3M Company.

FDA. 2006. Division of Food Contact Notifications Toxicology Group. Memorandum. FCN 599. Final Toxicology memorandum: Use of copolymer of polyfluorooctyl methacrylate, 2-N,N-diethylaminoethylmethacrylate, 2-hydroxyethylmethacrylate, and 2,2’-ethylenedioxydiethyldimethacrylate as an oil, grease, and water resistant treatment for paper and paperboard employed either prior to the sheet forming operation or at the size press.


FDA. 2008. Food and Drug Administration Center for Food Safety and Applied Nutrition Office of Food Additive Safety: Inventory of Effective Food Contact Substance (FCS) Notifications. Available: [accessed June 4 2008].

Fei C, McLaughlin JK, Tarone RE, Olsen J. 2007. Perfluorinated Chemicals and Fetal Growth: A Study within the Danish National Birth Cohort. Environmental Health Perspectives 115(11): 1677-82.

Fenton SE, Lau C, Hines EP, Thibodeaux JR, White SS. 2007. Long-term health effects of PFOA after prenatal and lactational exposure in mice. Toxicologist 96: 12.

Frisbee S. 2008. The C8 Health Project: How a Class Action Lawsuit Can Interact with Public Health - History of Events. Available: [accessed May 12 2008].

Gilliland FD, Mandel JS. 1993. Mortality among employees of a perfluorooctanoic acid production plant. J Occup Med 35(9): 950-4.

Guruge KS, Yeung LW, Yamanaka N, Miyazaki S, Lam PK, Giesy JP, et al. 2006. Gene expression profiles in rat liver treated with perfluorooctanoic acid (PFOA). Toxicol Sci 89(1): 93-107.

Houde M, Martin JW, Letcher RJ, Solomon KR, Muir DC. 2006. Biological monitoring of polyfluoroalkyl substances: A review. Environ Sci Technol 40(11): 3463-73.

Inoue K, Okada F, Ito R, Kawaguchi M, Okanouchi N, Nakazawa H. 2004. Determination of perfluorooctane sulfonate, perfluorooctanoate and perfluorooctane sulfonylamide in human plasma by column-switching liquid chromatography-electrospray mass spectrometry coupled with solid-phase extraction. J Chromatogr B Analyt Technol Biomed Life Sci 810(1): 49-56.

Jin Y, Saito N, Harada KH, Inoue K, Koizumi A. 2007. Historical trends in human serum levels of perfluorooctanoate and perfluorooctane sulfonate in Shenyang, China. Tohoku J Exp Med 212(1): 63-70.

Johansson N, Fredriksson A, Eriksson P. 2008. Neonatal exposure to perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) causes neurobehavioural defects in adult mice. Neurotoxicology 29(1): 160-9.

Joyce JM. 2007. Ahlstrom Windsor Locks LLC FYI-0407-01539B TSCA 8(e) submittal to US EPA Office of Pollution Prevention and Toxics. Available: [accessed May 12 2008].

Kannan K, Corsolini S, Falandysz J, Fillmann G, Kumar KS, Loganathan BG, et al. 2004. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Environ Sci Technol 38(17): 4489-95.

Kannan K, Corsolini S, Falandysz J, Oehme G, Focardi S, Giesy JP. 2002. Perfluorooctanesulfonate and related fluorinated hydrocarbons in marine mammals, fishes, and birds from coasts of the Baltic and the Mediterranean Seas. Environ Sci Technol 36(15): 3210-6.

Karrman A, Ericson I, van Bavel B, Darnerud PO, Aune M, Glynn A, et al. 2007. Exposure of perfluorinated chemicals through lactation: levels of matched human milk and serum and a temporal trend, 1996-2004, in Sweden. Environ Health Perspect 115(2): 226-30.

Keil DE, Mehlmann T, Butterworth L, Peden-Adams MM. 2008. Gestational exposure to perfluorooctane sulfonate suppresses immune function in B6C3F1 mice. Toxicol Sci 103(1): 77-85.

Kuklenyik Z, Reich JA, Tully JS, Needham LL, Calafat AM. 2004. Automated solid-phase extraction and measurement of perfluorinated organic acids and amides in human serum and milk. Environ Sci Technol 38(13): 3698-704.

Lau C, Anitole K, Hodes C, Lai D, Pfahles-Hutchens A, Seed J. 2007. Perfluoroalkyl acids: a review of monitoring and toxicological findings. Toxicol Sci 99(2): 366-94.

Lau C, Butenhoff JL, Rogers JM. 2004. The developmental toxicity of perfluoroalkyl acids and their derivatives. Toxicol Appl Pharmacol 198(2): 231-41.

Lau C, Rogers JM. 2004. Embryonic and fetal programming of physiological disorders in adulthood. Birth Defects Res C Embryo Today 72(4): 300-12.

Lau C, Thibodeaux JR, Hanson RG, Rogers JM, Grey BE, Stanton ME, et al. 2003. Exposure to Perfluorooctane Sulfonate During Pregnancy in Rat and Mouse. II. Postnatal Evaluation. Toxicol Sci 4(2): 382-92.

Lawyer AL. 2008. Testimony by Arthur L. Lawyer, Vice President, Technology Sciences Group, Inc.. April 23, 2008. California State Senate Health Committee. Available: [accessed May 2 2008]

Leonard RC, Kreckmann KH, Sakr CJ, Symons JM. 2007. Retrospective Cohort Mortality Study of Workers in a Polymer Production Plant Including a Reference Population of Regional Workers. Ann Epidemiol 18(1): 15-22.

Liu RC, Hurtt ME, Cook JC, Biegel LB. 1996. Effect of the peroxisome proliferator, ammonium perfluorooctanoate (C8), on hepatic aromatase activity in adult male Crl:CD BR (CD) rats. Fundam Appl Toxicol 30(2): 220-8.

Lundin JI, Alexander BH. 2007. Mortality of Employees of an Ammonium Perfluorooctanoate Production facility. Final Report to US EPA Office of Pollution Prevention and Toxics (OPPT) Docket No AR-226.

Martin JW, Mabury SA, Solomon KR, Muir DC. 2003. Bioconcentration and tissue distribution of perfluorinated acids in rainbow trout (Oncorhynchus mykiss). Environ Toxicol Chem 22(1): 196-204.

Martin MT, Brennan RJ, Hu W, Ayanoglu E, Lau C, Ren H, et al. 2007. Toxicogenomic study of triazole fungicides and perfluoroalkyl acids in rat livers predicts toxicity and categorizes chemicals based on mechanisms of toxicity. Toxicol Sci 97(2): 595-613.

Matte TD, Bresnahan M, Begg MD, Susser E. 2001. Influence of variation in birth weight within normal range and within sibships on IQ at age 7 years: cohort study. British Medical Journal (BMJ) 323(7308): 310-4.

MDH. 2008. Minnesota Department of Health: Perfluorochemicals in Minnesota. Available: [accessed May 20 2008].

Midasch O, Drexler H, Hart N, Beckmann MW, Angerer J. 2007. Transplacental exposure of neonates to perfluorooctanesulfonate and perfluorooctanoate: a pilot study. Int Arch Occup Environ Health 80(7): 643-8.

Nanowerk. 2008. NanoSphere At The Cutting Edge. Available: [accessed June 2 2008].

NAS. 1972. National Academy of Sciences: Degradation of synthetic organic molecules in the biosphere.

Needham LL, Calafat AM, Barr DB. 2008. Assessing developmental toxicant exposures via biomonitoring. Basic Clin Pharmacol Toxicol 102(2): 100-8.

Olsen GW, Gilliland FD, Burlew MM, Burris JM, Mandel JS, Mandel JH. 1998. An epidemiologic investigation of reproductive hormones in men with occupational exposure to perfluorooctanoic acid. J Occup Environ Med 40(7): 614-22.

Olsen GW, Burlew MM, Marshall JC, Burris JM, Mandel JH. 2004. Analysis of episodes of care in a perfluorooctanesulfonyl fluoride production facility. J Occup Environ Med 46(8): 837-46.

Olsen GW, Burris JM, Burlew MM, Mandel JH. 2003. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. J Occup Environ Med 45(3): 260-70.

Olsen GW, Burris JM, Ehresman DJ, Froehlich JW, Seacat AM, Butenhoff JL, et al. 2007. Half-life of serum elimination of perfluorooctanesulfonate, perfluorohexanesulfonate, and perfluorooctanoate in retired fluorochemical production workers. Environ Health Perspect 115(9): 1298-305.

Olsen GW, Church TR, Hansen KJ, Burris JM, Butenhoff JL, Mandel JH, et al. 2004. Quantitative Evaluation of Perfluorooctanesulfonate (PFOS) and Other Fluorochemicals in the Serum of Children. Journal of Children's Health 2(1): 53-76.

Olsen GW, Mair DC, Church TR, Ellefso ME, Reagen WK, Boyd TM, et al. 2008. Decline in Perfluorooctanesulfonate and Other Polyfluoroalkyl Chemicals in American Red Cross Adult Blood Donors, 2000?2006. Environ Sci Technol: in press.

Olsen GW, Zobel LR. 2007. Assessment of lipid, hepatic, and thyroid parameters with serum perfluorooctanoate (PFOA) concentrations in fluorochemical production workers. Int Arch Occup Environ Health 81(2): 231-46.

Packaging Expo. 2008. About Packaging - The Market. Available: [accessed June 6 2008].

Peden-Adams MM, Keller JM, Eudaly JG, Berger J, Gilkeson GS, Keil DE. 2008. Suppression of Humoral Immunity in Mice Following Exposure to Perfluorooctane Sulfonate (PFOS). Toxicol Sci: in press.

Prevedouros K, Cousins IT, Buck RC, Korzeniowski SH. 2006. Sources, fate and transport of perfluorocarboxylates. Environ Sci Technol 40(1): 32-44.

Rosen MB, Thibodeaux JR, Wood CR, Zehr RD, Schmid JE, Lau C. 2007. Gene expression profiling in the lung and liver of PFOA-exposed mouse fetuses. Toxicology 239(1-2): 15-33.

SAB. 2006. US EPA Science Advisory Board Review of EPA's Draft Risk Assessment of Potential Human Health Effects Associated with PFOA and Its Salts. EPA-SAB-06-006; Washington, DC, 2006.

Sakr CJ, Kreckmann KH, Green JW, Gillies PJ, Reynolds JL, Leonard RC. 2007. Cross-sectional study of lipids and liver enzymes related to a serum biomarker of exposure (ammonium perfluorooctanoate or APFO) as part of a general health survey in a cohort of occupationally exposed workers. J Occup Environ Med 49(10): 1086-96.

Sakr CJ, Leonard RC, Kreckmann KH, Slade MD, Cullen MR. 2007. Longitudinal study of serum lipids and liver enzymes in workers with occupational exposure to ammonium perfluorooctanoate. J Occup Environ Med 49(8): 872-9.

Sanitized AG. 2008. New generation of fluorocarbons based on C6 chemistry. Available: [accessed June 2 2008].

Sauve RS, Robertson C, Etches P, Byrne PJ, Dayer-Zamora V. 1998. Before viability: a geographically based outcome study of infants weighing 500 grams or less at birth. Pediatrics 101(3 Pt 1): 438-45.

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 Reviewed in US EPA "Revised Draft PFOA Hazard Assessment-Robust Study Annex" AR226-1137, (pp. 260-267; PDF pp 157-164).

Sinclair E, Kim SK, Akinleye HB, Kannan K. 2007. Quantitation of Gas-Phase Perfluoroalkyl Surfactants and Fluorotelomer Alcohols Released from Nonstick Cookware and Microwave Popcorn Bags. Environ Sci Technol 41(4): 1180-5.

Sinclair E, Mayack DT, Roblee K, Yamashita N, Kannan K. 2006. Occurrence of perfluoroalkyl surfactants in water, fish, and birds from New York State. Arch Environ Contam Toxicol 50(3): 398-410.

So MK, Yamashita N, Taniyasu S, Jiang Q, Giesy JP, Chen K, et al. 2006. Health risks in infants associated with exposure to perfluorinated compounds in human breast milk from Zhoushan, China. Environ Sci Technol 40(9): 2924-9.

Son HY, Kim SH, Shin HI, Bae HI, Yang JH. 2007. Perfluorooctanoic acid-induced hepatic toxicity following 21-day oral exposure in mice. Arch Toxicol 82(4): 239-46.

Tao L, Kannan K, Wong CM, Arcard KF, Butenhoff JL. 2008. Perfluorinated Compounds in Human Milk from Massachusetts, U.S.A. Environ Sci Technol 42: 3096-101.

Tittlemier SA, Pepper K, Seymour C, Moisey J, Bronson R, Cao XL, et al. 2007. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat, fish, fast foods, and food items prepared in their packaging. J Agric Food Chem 55(8): 3203-10.

Tittlemier SA, Ryan JJ, Van Oostdam J. 2004. Presence of anionic organic compounds in serum collected from northern Canadian populations. In: Organohalogen Compounds, 4009-14.

US Environmental Protection Agency (US EPA). 2004. EPA Takes Enforcement Action against DuPont for Toxic Substances Reporting Violations [Press Release]. Available:!OpenDocument [accessed 27 December 2007].

US EPA. 2005. EPA Settles PFOA Case Against DuPont for Largest Environmental Administrative Penalty in Agency History. Available:!OpenDocument [accessed June 5 2008].

US EPA. 2006a. 2010/15 PFOA Stewardship Program. Available: [accessed 27 December 2007].

US EPA. 2006b. Fact Sheet: EPA, DuPont Agree on Measures to Protect Drinking Water Near the DuPont Washington Works. Available: [accessed December 28 2007].

US EPA. 2008. Toxic Substance Control Act (TSCA) Section 8(e) Notices. Available: [accessed June 3 2008].

Volkel W, Genzel-Boroviczeny O, Demmelmair H, Gebauer C, Koletzko B, Twardella D, et al. 2007. Perfluorooctane sulphonate (PFOS) and perfluorooctanoic acid (PFOA) in human breast milk: Results of a pilot study. Int J Hyg Environ Health: in press.

West Virginia University School of Medicine. 2008. The C8 Health Project: WVU Data Housing Website. Available: [accessed May 12 2008].

White SS, Calafat AM, Kuklenyik Z, Villanueva L, Zehr RD, Helfant L, et al. 2007. Gestational PFOA exposure of mice is associated with altered mammary gland development in dams and female offspring. Toxicol Sci 96(1): 133-44.

Wolf CJ, Fenton SE, Schmid JE, Calafat AM, Kuklenyik Z, Bryant XA, et al. 2007. Developmental toxicity of perfluorooctanoic acid in the CD-1 mouse after cross-foster and restricted gestational exposures. Toxicol Sci 95(2): 462-73.

Yang Q, Abedi-Valugerdi M, Xie Y, Zhao XY, Moller G, Nelson BD, et al. 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.

Yang Q, Xie Y, Depierre JW. 2000. Effects of peroxisome proliferators on the thymus and spleen of mice. Clin Exp Immunol 122(2): 219-26.

Yeung LW, Guruge KS, Yamanaka N, Miyazaki S, Lam PK. 2007. Differential expression of chicken hepatic genes responsive to PFOA and PFOS. Toxicology 237(1-3): 111-25.

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