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It seems I shouldn’t have posted this without context

TL;DW

  • yes the video is (at least partially) about Teflon, hence the cynical title

  • no, Teflon (or generally big Fluoropolymers) are not the problem. Ingesting them does nothing to you, because as long, chemically inert polymers they just pass through you from one end to the other

  • The problem are perfluoroalkyl acids: C8 (PFOA) and later substitutes such as C6/GenX, PFOS, PFHA, PFHxS which are chemicals used to start the Teflon polymerization. They are short-chained carbon-fluorine molecules that coincidentally mimic the structure of fatty acids, thus can accumulate in our bodies without a way for our bodies to break them down.

  • These chemicals leach into the environment from factories and accumulate in everything, to the point that the whole water cycle has been contaminated (yes that shit comes down everywhere with the rain)

  • There is conclusive proof that PFOA exposure is linked to a number of organ damage and cancers, particularly testicular cancer and kidney cancer, with likely links to lung and pancreatic cancer not reflected in the study due to survivor bias (they died before the study was concluded)

  • pixxelkick@lemmy.world
    13·
    17 hours ago

    it states that the indirect genotoxic (and thus carcinogenic) potential of PFOA cannot be dismissed

    Its important to understand that “cannot be dismissed” is not the same as “we think it does do this”

    It’s a double negative, its “we dont not think it causes it”, but waaaaay more study is needed.

    Serum Concentrations of Per- and Polyfluoroalkyl Substances and Risk of Renal Cell Carcinoma Actually is a new one for me, I havent seen this one, and it does look much more compelling than the other smaller studies, this one is more concerning than the others.

    The Panel determined in 2012 there was a ‘probable link’ (i.e., more probable than not based on the weight of the available scientific evidence)

    Fourth link is a lot of nothing, why did you bother linking it? It just discusses other studies but doesnt add anything new of substance.

    Fifth link is pretty sketchy, theres many other variables that also associate, and they didnt even find a link between specifically PFOS anyways

    while no significant association was observed for PFOS (OR = 1.14; 95% CI 0.98-1.34; P = 0.09)

    Its important to note that every single one of these studies is empirical post exposure which means many other associated variables can also contribute.

    People with low PFAS vs high PFAS exposure almost undoubtedly are also exposed to many other things… like pollution in general

    It’s borderline impossible to actually separate out PFAS levels from these other entangled variables, people who are heavily exposed to 1 type of pollution will also be exposed to many others, and theres a heavy association between living situation and PFAS exposure.

    That is why its so damn hard to get any conclusive proof on this, the only way to truly figure it out would be to purposefully administer PFAS to people intentionally in a controlled environment, to try and separate out variables.

    The relationships that do show up are all very tenuous, and could easily be also explained by the dozens of other variables, so thats why you keep seeing the wording of “may contribute” or “requires further study” or “associated with”

    • pulsewidth@lemmy.world
      1·
      1 hour ago

      Your comment cherry picks the weakest language of the Wikipedia article and studies and ignores the rest. You’ll struggle to find any reputable study anywhere that says “our study proves that X does Y” like you’re asking, because thats not how studies language is conveyed and would be incorrect language to use in a medical study. When 20 studies all say “we have shown a strong correlation between cigarette consumption and cancer of the throat, mouth, and lungs” then you will hear scientists say “the link between cancer and cigarettes is known, and well studied” and news articles will say “cigarettes cause cancer”.

      Your suggestion that the only way we’d know for sure is human trials of intentional PFOA exposure is… I’m gonna be generous and say… naieve. Scientists are perfectly fine with using lab, mouse, and emprical cross-sectional studies - that’s all valid scientific evidence. They don’t actually need to take the final Dr Mengele step of subjecting people directly to suspected toxins before they can draw highly accurate conclusions, especially for something like PFOA that has large sections of the population with high dosages that they can compare against those with low dosages already.

      It’s borderline impossible to actually separate out PFAS levels from these other entangled variables, people who are heavily exposed to 1 type of pollution will also be exposed to many others, and theres a heavy association between living situation and PFAS exposure.

      Not true. Just one example, we have many population groups that live in areas where groundwater is used for drinking that also live near a firefighting training base/station that has released huge amounts of PFOAs into the aquifers. These populations are otherwise quite normally distributed for age/weight/health/occupation and exposure to other chemicals and perfect for study of PFOAs and have been shown in studies to have much higher levels in their blood serum.

      It’s fine though - if you wanna sprikle PFOA on your cereal or something until 100 more studies are done, I can’t stop you. But just know that your tendency to cherry pick data and your unconventional assessment methods of studies is giving you a very poorly informed choice.