I feel like I must be saying the wrong things on facebook, because the stuff that gets served up to me is… well, maybe it’s because I click it out of curiosity that it might be material for debunking. See what I do for you folks? You should appreciate me. This week’s #SkepticalTuesday post is about a story on Teflon, perfluorooctanoic acid (PFOA, or “C8”), and the DuPont corporation. It’s a little long, but I hope you’ll enjoy it. Read on, fellow skeptics.
Because I click on links to things which are certain to bother me, I ended up reading this piece the other morning over at The Intercept by one Sharon Lerner entitled (sigh) “The Teflon Toxin: DuPont and the Chemistry of Deception.” It’s long, it’s detailed, it’s accusatory, and I’m just not sure it’s very scientifically valid. It’s a story about a chemical, PFOA, that was used until a few years ago in the making of Teflon-coated pots and pans (among other things). The gist is that Lerner is trying to claim that (a) PFOA exposure is toxic and (b) that DuPont knew this and is somehow criminally negligent.
The long and short of it is, she doesn’t really do a convincing job of either, even if both might be true.
So ever since I read it, I’ve been digging into studies, talking to friends in the sciences, and generally trying to wrap my head around it. Here’s what I’ve found out.
For me, this was what set me off. Even if we forgive the title — which relies on currently-existing and unfounded fears of the safety of Teflon-coated cookware, even though the article is really about a chemical used in the making of Teflon — there’s a lot more to question. It begins with a victim — a former DuPont employee who no longer has a rectum, because he had cancer, because he had ulcerative colitis, because he was exposed to C8/PFOA — and a question: ““Who knew?” he asked. “When did they know? Did they lie?”
It starts with begging the question: taking for a fact that the dust in his workplace was PFOA, and that it ultimately caused his cancer, and moves on to “did they know it would give me cancer?” It’s like McCarthy asking someone “when did you become a communist?” instead of “are you a communist?” So from page one I could tell the rhetoric was going to be a problem.
As I read on, there were a lot of what appeared to be scientific studies referred to in the piece, lending it an air of credibility, but even so there were occasional slips that made it fairly clear the author either wasn’t aware of the science behind toxicity or simply didn’t care. Take the following passages:
“The harder question was to determine a maximum safe dosage. How much could an animal — or a person — be exposed to without having any effects at all? The 1965 DuPont study of rats suggested that even a single dose of a similar surfactant could have a prolonged effect. Nearly two months after being exposed, the rats’ livers were still three times larger than normal.”
“To get a sense of exactly how extensive that exposure was, in March 1984 an employee was sent out to collect samples, according to a memo by a DuPont staffer named Doughty. The employee went into general stores, markets, and gas stations, in local communities as far as 79 miles downriver from the Parkersburg plant, asking to fill plastic jugs with water, which he then took back for testing. The results of those tests confirmed C8’s presence at elevated levels.“ [emphases mine]
If you’re like me, the first thing you think when you read those statements is “how much is a dose?” and “what’s elevated compared with normal?” because, like me, you know that the dose makes the poison.
What about this quote:
“In 1989, DuPont employees found an elevated number of leukemia deaths at the West Virginia plant. Several months later, they measured an unexpectedly high number of kidney cancers among male workers. Both elevations were plant-wide and not specific to workers who handled C8. But, the following year, the scientists clarified how C8 might cause at least one form of cancer in humans. In 1991, it became clear not just that C8-exposed rats had elevated chances of developing testicular tumors — something 3M had also recently observed — but, worse still, that the mechanism by which they developed the tumors could apply to humans.“
This is just shoddy, from start to finish: People at the plant had more leukemia. Then they had more kidney cancer. More than who? How much more? We don’t know. But wait, they weren’t even related to exposure to PFOA? Let’s just tuck that in there before saying that scientists found a pathway that might allow PFOA to cause testicular cancer in humans — because all cancers are the same disease, amirite?
The story moves on, trying to put together a case against DuPont, mostly with circumstantial evidence that really reaches at times.
“Not long after the decision was made not to alert the EPA, in 1981, another study of DuPont workers by a staff epidemiologist declared that liver test data collected in Parkersburg lacked “conclusive evidence of an occupationally related health problem among workers exposed to C-8.” Yet the research might have reasonably led to more testing. An assistant medical director named Vann Brewster suggested that an early draft of the study be edited to state that DuPont should conduct further liver test monitoring. Years later, a proposal for a follow-up study was rejected.”
With the lacking causal links and cagey use of “might,” the argument seems to be that the studies they did didn’t find any evidence linking C8 exposure to negative effects, but it’s the company’s fault nevertheless for not looking harder. I’ll admit, I’d like to live in a world where companies exhaustively test the safety of all the chemical compounds that are in use, but the fact that they were doing any testing at all on a compound that had been in use since the 1930s without any obvious health effects is actually quite informative. Lerner even admits that DuPont passed on to their employees a study on the compound done by 3M which said that PFOA built up over time in their bodies. (And remember, a lot of the employees of DuPont are chemists. If they’d had any worries at all about PFOA, finding out it builds up in your body would, one presumes, have been of rather great concern.)
Next she moves on to animal studies, ignores dose dependency once again, and then we get this paragraph:
“Of course, enough of anything can be deadly. Even a certain amount of table salt would kill a lab animal, a DuPont employee named C. E. Steiner noted in a confidential 1980 communications meeting. For C8, the lethal oral dose was listed as one ounce per 150 pounds, although the document stated that the chemical was most toxic when inhaled. The harder question was to determine a maximum safe dosage. How much could an animal — or a person — be exposed to without having any effects at all? The 1965 DuPont study of rats suggested that even a single dose of a similar surfactant could have a prolonged effect. Nearly two months after being exposed, the rats’ livers were still three times larger than normal.”
Why attribute the fact about salt to someone else? Pointing out that the dose makes the poison is not suspicious, but she seems to treat it that way — and then completely ignores the truth of the statement in favour of more scaremongering. “Surfactants” aren’t scary; soap is a surfactant. Meanwhile this is a major missed opportunity — this would have been a great point to look at the studies and see: how much were they being exposed to? What is a safe exposure level? But no, instead we get the claim that “one dose” of not even the same compound could have a lasting effect on rodents’ livers. At this point I almost rage-quit, but for you, dear readers, I went the extra mile and finished it (and god, it’s only part 1).
From the rhetoric you can tell one thing: this article isn’t going to actually answer the important questions: is PFOA actually bad for you? Was it bad for the employees? And what, if anything, does any of this have to do with your frying pan?
The EPA has a ton of information on PFOA. It has an exhaustive FAQ on the stuff, if you’re interested. Long story short, PFOA is a surfactant. It makes liquids flow more evenly, and when it was used in making Teflon (the goal is to largely eliminate PFOA use by the end of this year) that’s what it was used for. Most of the PFOA that was added to the Teflon evaporated out during heat treatment, so even if PFOA is bad for you, you have nothing to worry about from your frying pan (unless you heat it up on high, empty, and breathe in the fumes. That’s probably not great for you).
PFOA is ubiquitous in your bloodstream and in the environment, in very, very small amounts. How small? There are two ways to measure this. If you go by blood serum levels, we have fairly reliable data that the average member of “the general population has about 5 parts per billion (ppb) of PFOA in their blood, with high values at about 20-30 ppb […] Some workers in factories that use or manufacture PFOA have levels much higher than those found in the general population, averaging about 1-10 parts per million (ppm) (equivalent to 1,000 to 10,000 ppb).“(p.7) If you go by levels in the water supply, there are fewer data, but, “in areas surrounding plants in West Virginia and in Alabama, the levels of PFOA in drinking water have averaged about one part per billion (ppb), ranging up to about 10 parts per billion. In a six-city survey, drinking water levels of PFOA were much lower, ranging from non-detectable to 0.029 ppb.” (p.8)
Plus, there’s good news from the CDC: PFOA levels in the general population have dropped to 3.07ppb in 2009-2010. (p. 236) That doesn’t mean it’s necessarily bad for you, but congratulations, you have less of it than you used to in your blood. This actually tracks fairly well with studies that seem to show an elimination [“peeing it out”] half-life in the human body (at least, in women) of 3.8 years. (p.376)
So is it bad for you? That’s a much, much harder question to answer. Animal studies have shown that if given enough of it, rats will develop enlarged livers, and sometimes testicular and kidney cancers. (p.86)
In 2005, as a result of a class action lawsuit against the DuPont company by people living around DuPont’s West Virginia Washington Works Plant, DuPont agreed to fund a research into PFOA, and to determine “whether there is a probable link between C8 and any human disease.” They also paid tens of millions of dollars to the community as a part of the settlement (without, as is usual for settlements, legally admitting to any wrongdoing). So far, the panel’s many reports have concluded the following:
There is not “a probable link between exposure to C8 (also known as PFOA)” and: diagnosed hypertension or coronary artery disease; chronic kidney disease; liver disease; osteoarthritis; Parkinson’s disease; rheumatoid arthritis, lupus, Type I diabetes, Crohn’s disease, or multiple sclerosis; common infections, including influenza, in children or adults; neurodevelopmental disorders in children, including attention deficit disorders and learning disabilities; asthma or chronic obstructive airways disease (COPD); stroke; Type II (adult-onset) diabetes; birth defects; miscarriage or stillbirth; and preterm birth or low birth weight.
There is “a probable link between exposure to C8” and: diagnosed high cholesterol; ulcerative colitis; thyroid disease; testicular cancer and kidney cancer; and pregnancy-induced hypertension.
This sounds bad for DuPont, and it might well be, but when you dig into it, there are some almost tangible lingering uncertainties.
The high cholesterol data seems to my admittedly amateur eyes the strongest. This study indicates that there’s a dose-dependent response to levels in blood serum, which seems to come down as the levels of PFOA in the blood drop over time. But of course correlation isn’t necessarily causation.
This study of environmental exposure seems to show a dose-dependent correlation of ulcerative colitis incidence, however according to the findings of the panel, “there are no toxicological data specifically regarding PFOA and autoimmune disease,” (p.5) which is to say we don’t know how it would cause ulcerative colitis, only that people who have been highly exposed seem to have more cases of it than the general populous. This lack of causal data leaves open the possibility of third-party causality — that is, the possibility that something else is causing the ulcerative colitis that’s correlative with both the disease and PFOA — which is why they can only say there’s a “probable link.”
The link with testicular cancer is much more tenuous. According to their conclusions, there was “evidence of a positive trend in risk across exposure groups, in some analyses […] On the other hand there was little or no evidence of increasing risk in analyses from the same cohort compared with the US population, and in the period after 2005, there were no new cases compared to about five expected).” As well, “the high exposure group, where the higher risk was observed, comprises only six cases therefore there remains some uncertainty.” That is, their numbers are very small, don’t seem to be any different from incidence rates in the general population, and since 2005 there haven’t been any new cases in the region so it’s hard to draw any conclusions. And so they fall back on animal models, which are at the least imperfect in this case because of the high doses given to the rats (mg/kg/day) which may or may not be offset by the apparently slower elimination speed in humans vs. mice.
The kidney cancer the story is pretty similar: “For kidney cancer, the worker mortality study conducted by the Science Panel showed a higher risk in the most highly exposed group compared to lower exposure groups among the workforce, but the risks were not elevated compared to the US population. In the cohort study, there was a gradient of increasing risk with increasing exposure but most strongly in the analyses that included exposure up to the time of diagnosis. When the 10 years of exposure prior to diagnosis was excluded, the association was less evident. No association was seen in the prospective analysis of cohort data, although the latter is limited by small numbers. In the geographic study some results suggested an increasing risk of kidney cancer with increasing exposure and others did not.”
A 2014 review in The Lancet Oncology described the data on the topic similarly: “On the basis of limited evidence in humans that PFOA causes testicular and renal cancer, and limited evidence in experimental animals, the working group classified PFOA as possibly carcinogenic to humans.” [That’s category 2B, if you’re wondering.]
Possibly and probably sit uncomfortably within the realm of the dose making the poison. Take the WHO classification of glyphosate as (2A) “probably carcinogenic to humans,” which, again, relies on dosage to be relevant. Now, remembering that we’re talking about people exposed at much higher levels than the general population, it’s definitely possible based on their reported data that these links exist and are causal. But the science is really limited and, because with every passing year the amount of PFOA in the blood of the highly-exposed population decreases, I’m guessing that it’s going to become increasingly challenging to prove causal links going forward.
Is PFOA something you need to worry about? Given that the possible health effects are difficult to detect even in a highly-exposed population like the communities surrounding the plants, and that even now the average level in the general population’s bodies is decreasing every year, probably not. Thanks to the EPA’s 2010/2015 PFOA Stewardship Program, they’ve phased PFOA out of most of their operations, so environmental contamination is decreasing. You won’t get any from your Teflon pans (even though you still shouldn’t burn them and inhale deeply over them as that would be bad for you and worse for your pet birds), but it might persist in the environment for a long time.
Did PFOA exposure cause the man at the start of Lerner’s piece to get cancer as a secondary effect of getting ulcerative colitis? It’s certainly possible, perhaps even probable, but right now the link is correlative (if dose-dependent) and not necessarily causal.
Finally, did DuPont know that exposure to PFOA was harmful? From my perspective, it’s hard to think they could have known, given that even now it’s not certain, but they might well have strongly suspected. Will that be enough to win a court case? That’s even more up in the air. As OSHA has claimed as recently as last year, every year workers in America are exposed to levels of harmful chemicals that are legal, but not safe. DuPont hasn’t always followed the letter of the law in reporting data, either. The EPA fined the company over ten million dollars in 2006 for failure to report the potential hazards of PFOA exposure, which may well come into play in future lawsuits. DuPont’s liability, I suspect, will simply have to come out in court.
As a final caveat, I’d like to say, once again, that I’m a layman. I’ve got a couple of years of practice writing science stories as a skeptic, but most of my training has been in spotting BS rhetoric when it arises, so while I’m very confident in my appraisal of The Intercept article’s prose, I’m only mostly sure about my analysis of the science. If you’re someone who works on these things for a living, and you think I’ve made some glaring errors, please contact me. I’d love to sit down and learn more. As a skeptic, I have to change my opinions when confronted with convincing evidence. Thanks again for reading, and, as ever, your mileage may vary.
Richard Ford Burley is a writer, library worker, and doctoral candidate in English at Boston College, where he’s studying remix culture and the processes that generate texts. In his spare time he writes about science, skepticism, and feminism (and potential carcinogens, apparently) here at This Week In Tomorrow.
One thought on “Teflon, PSOA, and DuPont | Vol. 2 / No. 42.2”
Comments are closed.