Comment by jjoonathan | Hacker News Reader

Comment by jjoonathan | Hacker News Reader

I've heard a suspiciously large number of explanations for HF's toxicity.

1. It eats your bones (BS meter at 99.9% due to stoichiometry)

2. It poisons enzymes (as seen in TFA, passes the BS detector, but begs the question: which ones?). EDIT: "which ones?" answered by [2], but it's focus is on cell biology not toxicology, so it's possibly answering the question "what causes the local burns?" rather than "what kills you dead?".

3. It binds Ca++ in your blood, stopping the power stroke of your heart [1] (my own suspicion, although it's obvious enough that there is a 0% chance of it being "original"). EDIT: [3] pretty much confirms this.

I've lost convenient access to the academic literature, so if there's anyone on here who would be willing to do a quick (ha) dive on my behalf, I'd be much obliged. EDIT: I think I found the answers I wanted, but most of the top results were paywalled, so I'd still appreciate a second look by someone with access to institutional subscriptions.

[1] https://cnx.org/resources/cee66a1bf085ebac300c9c15805098f254...

[2] http://www.researchgate.net/profile/Luz_Maria_Del_Razo/publi...

[3] http://www.atsdr.cdc.gov/mhmi/mmg11.pdf

In safety training at a university, we were instructed that if we were exposed to aqueous HF, we were to immediately slather on calcium gluconate on the burn area, grab an HF MSDS, and demand that the ambulance take us to a specific Level 1 trauma center and insist that the physicians understand that we were exposed to HF and not some generic acid.

I don't know the precise mechanism for toxicity (I thought it was hypocalcemia), but if the tradionally safety-lax academia takes HF that seriously, you know it's the real deal.

Yep, I got the same lecture, I was specifically asking about mechanism because the explanation we were given was "eats your bones" which is patently ridiculous.

Your bones are constantly remodeled, as part of calcium regulation in the body. HF, interfering with that remodeling, may give the appearance of it "eating your bones".

As a mechanism for chronic toxicity? Sure. As a mechanism for acute toxicity? Not a chance.

The "slap on some calgonate and rush to the hospital" protocol (of which you were quick to remind us) was justified by way of the acute toxicity (to me, anyway), not prevention of chronic toxicity, so my remark stands.

The calcium ion depletion version is the correct one, at least from days handling fluorine chemistries. The poisoning risk covers a more diverse range of common fluorine compounds than just hydrofluoric acid. Skin exposure to these compounds is often sufficient for it to enter the bloodstream and there can be a significant delay to the effects as it moves through tissues.

Treatment for fluoride poisoning is intravenous calcium solution, which provides an ion buffer for the calcium ion depleting effects of the fluoride until all the fluoride binds to something that renders it inert.

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