Comments

1. #1 Trevor Butterworth

   August 21, 2007

   Interesting paper — but extremely limited due to methods and the subject population, as the authors point out:

   “Finally, our study population represented a group of individuals with more risk factors for adverse birth outcomes than the United States as a whole. Compared to national
   estimates, the subjects in our population were more likely to be Black, teenagers,
   unmarried, and cigarette smokers (Hoyert et al. 2006). This is perhaps not surprising
   given the location of the hospital in an urban and economically disadvantaged
   community. Although not quantified, these subjects may also have higher rates of other risk factors for poor outcomes, such as substance abuse and infections. It is not clear what, if any, impact the presence of concomitant risk factors would have on the results reported here, but future studies should be conducted in other settings to confirm these findings.”

   Key questions here are: did the mothers take vitamins prior to conception as well as after (OBGYNs routinely point to the former as the most significant health intervention routinely missed), did the mothers smoke, abuse drugs, suffer from poor diet, or drink alcohol (which is increasingly being tied to numerous negative health impacts). There’s a lot to confound here.

   That aside, the paper is one of those studies that raises interesting questions; but, there’s enough missing context and data from your post that I think I’m going to start calling you “alarmist toxicologist.” PFOA production will be eliminated by 2015. Annual emissions worldwide have already been reduced by 95- 98 percent, so this, thus far hypothetical, risk is in the process of being eliminated.

   So when you say DuPont ramped up production after 3M got out of the market, you need to note that while production has increased, environmental emissions have decreased. And, as a study in the Feb 2005 Environmental Health Perspectives noted, the levels of PFOA in German blood samples decreased during this time period, from approximately 12ppb to 6ppb, and stayed roughly the same in the U.S.(5ppb). Doesn’t that count as a bit of good news, worth noting?

   On a more technical point, you write that

   “PFOA isn’t in the clothes necessarily, but coating used in the clothes or food wrappers or carpet can break down into PFOA once it gets into the body;”

   Any evidence that this actually happens? Seriously, I’d love to know of a study showing this, other than the one that shows 1 percent of a precursor chemical to a flurotelomer coating — flurotelomer alcohol — was metabolized into PFOA in rats.

   Begley et al in Food Additives and Contaminants 22 (10) 2005 found that flurotelomer compound migration from coated paper “occurs in the form of telomer-based compounds themselves and should not be equated with PFOA exposure.”

   And, when you think about it, this makes sense. PFOA in blood serum is found everywhere from Sri Lankan tea workers to Polar bears, so industrial emissions are a more plausible culprit than popcorn bags or carpets.

   Finally, your conclusion — the trespass scenario — amounts to a banality: industry should never have polluted or pollute. Nothing wrong with that, but conceiving this as a form of trespass makes defining what constitutes “pollution” crucial. Should you ask permission of your neighbors before painting your house or choosing the color of the paint? We have all manner of implicit contractual agreements as agents who live in a society.

   If, in good faith, and supported by the evidence of the time, an industry, releases chemical x into the environment, at what point does the evolving evidence make them guilty of trespass? And, as you seem to be in favor of the precautionary principle, what would be a *workable* system of regulation for industrial processes and products to prevent such “trespass?”

   Regards

   Trevor

2. #2 angrytoxicologist

   August 21, 2007

   The main returning point is that world wide PFOA pollution is coming from the telomers (any search of pubmed will turn up dozens of papers confirming this fact. Not sure how you missed them). So the reduction in PFOA emissions alone doesn’t mean a whole lot and the general population values world wide aren’t going down.

   You note that products don’t actually have much or any PFOA in them. If they don’t and PFOA isn’t volatile, how does it get deposited in the artic and all the other places from the handful of factories? Also, human distribution is rather even as well discounting workers; this would not be the case if environmental effulent were to blame (you saying that environmental pollution of PFOA makes sense makes no sense it has no methods of long term transport). Also, the pattern of PFCs in the blood sugges that they are from precursors (the 6 and 8 chains being the highest). In fact, multiple studies have been done to show that the degradation also happens in the atmosphere (speaking of leaving things out, you seem to have forgot a lot!). Similarly PFOA is higher in waste water effluant than intake suggesting that precursors are the source in water as well.

   You ask to see a study then quote one showing 1% of the precursor chemical yields PFOA. I’m not sure if you thought the math through, but if you can’t get rid of the chemical very well (~3.8 yr half life) a tiny bit over time builds up, 1% isn’t small.

   All that being said, yes the study need confirmation, but it is good enough to make one put faith in the conclusions. As to the tresspass, it seems odd to me that chemical companies can be liable for polluting the water or air, but it’s okay if it’s in my blood. I didn’t say industry should pollute me. They shouldn’t pollute ME or my kids. The question is, how can you think that the PFOA situation is a fine state of affairs?

   The answer to your quesion about a workable system is actually rather simple. First, chemicals that persist like this one shouldn’t be allowed to be used unless in contained systems (intermediates, that sort of thing) or they have tox testing done upfront. Two, chemicals that sliped through the cracks (and some will) need to be tested comprehensively as they show up in people.

   The precautionary principle as it is done in REACH and supported by a lot of enviros is stupid. It targets chemicals not on risk but on hazard, and takes on too large a task. There are too many chemicals out there. An approach that is based on testing chemicals that show up in human blood make sense becuase it asks what we really want to know. Don’t tell me we shouln’t know the risks of what is floating around in our blood. And yes, I do think that if a company knows that this compound has problems and it isn’t excreted they are liable. How could they not be?

3. #3 Trevor Butterworth

   August 21, 2007

   Tsk, tsk, tsk. You’ve completely misconstrued my post: YOU originally claimed that PFOA gets into the body by telomer ingestion and breakdown. Which would be news to the FDA – and DuPont and 3M. I responded by saying that PFOA exposure is more likely through pollution (i.e. emissions from telomer manufacturing), indeed, the levels of pfoa in water near the manufacturing plants bear this out. But the fact is, we don’t really know how it has spread so widely (albeit at very low levels).

   Flurotelomers are extremely non-reactive due to the carbon fluorine bonds, that’s why PFOA doesn’t break down from the ingestion of telomer compounds. And flurotelomer alcohol, if ingested by humans (no evidence that it is), would be rapidly excreted from the body due to its low metabolic rate. So far, the only telomer breakdown into PFOA has occurred via flurotelomer alcohol in rats.

   If you’ve solved the problem of why PFOA is persistent in the environment at very low levels, I think a lot of people at the EPA and FDA would be interested in hearing about your theory.

4. #4 angrytoxicologist

   August 21, 2007

   as usual trevor you know a little but not enough to come to the right conclusions. First, you said it was PFOA emissions. It’s not. You now concede that and the fact that the PFOA ban will not stop the amount of PFOA in the atmosphere.

   Second, I didn’t say that it doesn’t come from ingestion. And it’s not news to the FDA (or the EPA for that matter – all this stuff is in their docket). In a presentation the FDA made to european authorities that is now public they note that telomers do transfer to food (popcorn was tested) and as you note, there is a study showing that transformation does happen. I never said that it has to be the whole source, but it is likely a source.

   Third, the telomer environmental source may not be industrial but comercial products anyway. A canadian study found that levels of the telomers (the precursors) are higher indoors than outdoors suggesting that items inside the house are a source (my guess – stain resistant carpet)

   Fourth, your chemistry sucks. That’s the best way to describe it with out curising. The fluro-carbon back bone isn’t hard to break, it’s near impossible under natural conditions, however, that’s not where the telomers break down into PFOA, it’s at the carboxy acid end. This isn’t some that anyone argues about anyway. In fact, most of the stuff you bring up isn’t even contested by Dupont. Which leads me to one conclusion after your couple of days of posts:….

   You have no idea what your are talking about. You are a hack with an ideology that can’t accept the science, and a brain that can’t understand it. From now on, if you don’t have some non-skewed beyond reasonable sciene, I’m not responding to ‘em; because frankly I don’t have the time to respond to your BS posts.

5. #5 Trevor Butterworth

   August 24, 2007

   You wrote in your original post:

   “PFOA isn’t in the clothes necessarily, but coating used in the clothes or food wrappers or carpet can break down into PFOA once it gets into the body; that’s probably how it got into me, and also you.”

   I pointed out that the FDA (whose officials I spent a long time talking with on this matter) said that they have not found this to be the case. Migration of telomer coatings is in the form of telomer compounds, but these have not been shown to — or rather had not been shown (at the time of the interview) — to break down in the body into PFOA. That is the point I was trying to make. Perhaps they were lying, or mistaken or whatever, but to trash me for raising this point (while citing the key paper on this matter) is excessive.

   Well, perhaps I am a hack who shouldn’t have the temerity to question your unverifiable authority. But it seems, if one takes your comment in a previous post that the Japanese had removed BPA from packaging — something which isn’t supported by any evidence — that you are not exactly rigorous in terms of the research you put into these posts. So there’s plenty of hackery to go around here.

   The terrible grammar and spelling also raises questions about whether, in a rush to post, you miss stuff, take other comments out of context, and make mistakes; either way, the prose does nothing to add to your credibility, although it certainly goes along with the whole “angry” m.o.

   And finally, the devolving of argument into schoolyard invective (viz, I don’t have the kind of brain that understands this stuff) detracts rather than adds to your intellectual cachet.

   I have taken quite a number of insults from you and other posters on this site — some of them driven by appeals to demonstrably false sources and information –
   and I tried to respond to them in good faith, and with appeals to evidence and logic. I may have been aggressive in responding to these, but I was never insulting in a manner that seems to come so easily to bloggers when shielded by anonymity.

   Anyway, even though we disagree on many things, I wish you the best with your site.

   Trevor

6. #6 Mark Powell

   August 25, 2007

   I like the way you think. I agree with the chemical trespass scenario, it’s a crime. What do we do to make that real?

7. #7 JLowe

   August 25, 2007

   I dunno. The way I see it, dumping a box of Krispy Kremes over my fence would still constitute chemical trespass.

8. #8 mdhatter

   August 27, 2007

   Trevor, you do come across as a not as a hack, but a bit of a crank. That isn’t an attack, as I happen to like cranks, but it’s darned hard to claim you’re being set upon after throwing rocks at people. (“tsk, tsk…” , telling people what they meant rather than what you heard, bothering to tell someone else what is wrong with them) (hehehe)

   Maybe you are not aware of it?

   As for the post, I was trying to explain to someone what makes me nerfous about Teflon. AngryT, you’ve saved me some hassle. Now I can link! Thanks!

9. #9 angrytoxicologist

   August 28, 2007

   JLowe,
   I suppose it is still trespass. If someone happens to dump some Krispy Kremes over your fence, however, and you don’t want them, send those cholesterol bombs over my way. I’ll even pay postage.

10. #10 angrytoxicologist

    August 28, 2007

    I forgot to post this paper earlier (on food wrapping as an exposure route to humans): http://pubs.acs.org/cgi-bin/abstract.cgi/esthag/2007/41/i13/abs/es070126x.html

    Somebody asked me about telomers so here’s a quick rundown.

    PFOA is like the back bone (think of this like a tree trunk, some are branched some are not.) Companies put some groups on the end that function as roots, these are telomers. Whent they want to put it on your clothes/wrapper, a surface is attached to the clothes/wrapper and the roots attach to those surface. It’s when the roots break off that the telomer can move into the food, air, you, etc.

    That’s kinds of technically off but gets the general idea across correctly.

11. #11 F

    September 4, 2007

    Anytime someone reports that chemical X has been detected in humans, I get really irritated. This means nothing unless you know something about detection limits and expected toxicity.

    For instance, in the paper you cite, the PFOA concentrations range from 0.3-7.1 ng/mL (which is not too different from parts per billion). In the text, the authors cite that “The toxicology literature provides evidence of developmental effects among animals dosed with PFOS and PFOA, albeit at substantially higher levels than observed here.” In both previous studies they discuss, effects on birth weight weren’t observed until the concentration reached 20,000 ng/mL.

    And the 95% confidence intervals for their birth weight effects included zero, indicating that they are not statistically significant at that level.

    Don’t get me wrong, there are probably significant health effect for PFOA levels in the ppm range (>1000 ng/mL). It’s just that even employees in PFOA factories don’t have levels that high.

12. #12 Insistent Chemist

    September 4, 2007

    It seems like not only the academics mentioned in this article (Lynn Goldman at Johns Hopkins), but now an industry study (sponsored by 3M) have found correlated dose-dependent effects at low ppb PFOA in serum in newborn humans. Bummer for the babies.
    We could debate round and round about the limitations of the papers, but we’ve moved from:
    1. Safe for people and critters (until about 2000)
    2. Bad for critters (too many to list, the list just keeps getting longer)
    3. Bad for workers at ppm doses (August 2007)
    4. Bad for babies at low ppb doses (July and August 2007)

    I’d say it is not looking positive for PFOA.

13. #13 Hank Roberts

    September 5, 2007

    I’d be very curious to know your read on this paper:

    Toxicology and Applied Pharmacology
    Volume 218, Issue 3, 1 February 2007, Pages 280-288
    doi:10.1016/j.taap.2006.11.029

    Analysis of the interaction of phytoestrogens and synthetic chemicals: An in vitro/in vivo comparison

    Grantley D. Charlesa, Corresponding Author Contact Information, E-mail The Corresponding Author, Chris Genningsb, Belen Tornesia, H. Lynn Kana, Timothy R. Zacharewskic, B. Bhaskar Gollapudia and Edward W. Carneya
    aToxicology and Environmental Research and Consulting, The Dow Chemical Company, Midland, MI 48674, USA
    bDepartment of Biostatistics, Virginia Commonwealth University, Richmond, VA 23298, USA
    cDepartment of Biochemistry and The National Food Safety and Toxicology Center, Michigan State University, East Lansing, MI 48824, USA
    Received 16 September 2006; revised 26 November 2006; accepted 27 November 2006. Available online 5 December 2006.

    Abstract

    In the evaluation of chemical mixture toxicity, it is desirable to develop an evaluation paradigm which incorporates some critical attributes of real world exposures, particularly low dose levels, larger numbers of chemicals, and chemicals from synthetic and natural sources. This study evaluated the impact of low level exposure to a mixture of six synthetic chemicals (SC) under conditions of co-exposure to various levels of plant-derived phytoestrogen (PE) compounds. Estrogenic activity was evaluated using an in vitro human estrogen receptor (ER) transcriptional activation assay and an in vivo immature rat uterotrophic assay. Initially, dose–response curves were characterized for each of the six SCs (methoxyclor, o,p-DDT, octylphenol, bisphenol A, ?-hexachlorocyclohexane, 2,3-bis(4-hydroxyphenyl)-propionitrile) in each of the assays. The six SCs were then combined at equipotent ratios and tested at 5–6 dose levels spanning from very low, sub-threshold levels, to a dose in which every chemical in the mixture was at its individual estrogenic response threshold. The SC mixtures also were tested in the absence or presence of 5–6 different levels of PEs, for a total of 36 (in vitro) or 25 (in vivo) treatment groups. Both in vitro and in vivo, low concentrations of the SC mixture failed to increase estrogenic responses relative to those induced by PEs alone. However, significant increases in response occurred when each chemical in the SC mixture was near or above its individual response threshold. In vitro, interactions between high-doses of SCs and PEs were greater than additive, whereas mixtures of SCs in the absence of PEs interacted in a less than additive fashion. In vivo, the SC and PE mixture responses were consistent with additivity. These data illustrate a novel approach for incorporating key attributes of real world exposures in chemical mixture toxicity assessments, and suggest that chemical mixture toxicity is likely to be of concern only when the mixture components are near or above their individual response thresholds. However, these data suggest that extrapolation from in vitro assays to in vivo mixture effects should be approached with caution.

14. #14 Aussie

    December 18, 2008

    Are Cast Iron Pans safe to use?
    Regards,
    Aussie.

15. #15 spor haberleri

    January 1, 2009

    thanks..best regards..

16. #16 bebek resimleri

    January 18, 2009

    The idea of creating a useful documentation for such projects is quite good, but should not permit to forget that you should also create a technical documentation, referring to all the classes, functions, etc..

17. #17 muhabbet

    March 26, 2009

    thanks..

18. #18 exe and ocx

    April 1, 2009

    I really like your blog, always something good to read.

19. #19 sohbet

    July 25, 2009

    I suppose it is still trespass. If someone happens to dump some Krispy Kremes over your fence, however, and you don’t want them, send those cholesterol bombs over my way. I’ll even pay postage.

20. #20 yonja

    July 25, 2009

    I like the way you think. I agree with the chemical trespass scenario, it’s a crime. What do we do to make that real?

21. #21 Abercrombie

    November 30, 2009

    Don’t get me wrong, there are probably significant health effect for PFOA levels in the ppm range (>1000 ng/mL). It’s just that even employees in PFOA factories don’t have levels that high.

22. #22 Payday Loans

    January 18, 2010

    I don’t think that trespassing can cause so many problems that are given here. But still I found your blog very interesting.

23. #23 jump higher

    August 16, 2010

    Flurotelomers are extremely non-reactive due to the carbon fluorine bonds, that’s why PFOA doesn’t break down from the ingestion of telomer compounds. And flurotelomer alcohol, if ingested by humans (no evidence that it is), would be rapidly excreted from the body due to its low metabolic rate. So far, the only telomer breakdown into PFOA has occurred via flurotelomer alcohol in rats.

    If you’ve solved the problem of why PFOA is persistent in the environment at very low levels, I think a lot of people at the EPA and FDA would be interested in hearing about your theory.

24. #24 jump higher

    March 28, 2011

    Flurotelomers are extremely non-reactive due to the carbon fluorine bonds, that’s why PFOA doesn’t break down from the ingestion of telomer compounds. And flurotelomer alcohol, if ingested by humans (no evidence that it is), would be rapidly excreted from the body due to its low metabolic rate. So far, the only telomer breakdown into PFOA has occurred via flurotelomer alcohol in rats.