Chemistry (including Biochemistry)/Question for a story.


This is perhaps a bit of a strange question.  I hope you can answer.  It is for a story I'm working on.

In short, there is a killer whose MO is injecting the victim with hydrofluoric acid, intravenously.

I have searched and searched and there is nothing relating to this anywhere that I can find.  The closest I can find is a scene from Breaking Bad where apparently someone attempts to dissolve a body in a bathtub with HF, ending up dissolving the whole room or something.  The other is a scene at the end of one of the various Saw movies, which I think involves injecting it with a bunch of needles into the person's back.  Either way, nothing in real life.  (That's good, actually.)

My questions I suppose are as follows:
- Supposing a high concentration (70% seems to be 'full strength' according to everything I've found) and an amount that could be injected into the bloodstream in less than 5 seconds.  ...  That's not a question.
- Could the acid burn through the walls of the blood vessels, causing a structural failure of the blood vessels?
- And if so, how quickly?
- I'm aware of its interaction with calcium and thus its toxicity, its ability to cause cardiac arrest.  But everything I've found relates to external HF exposure.  Injected directly into the blood, what would happen?
- I found one discussion semi-relating to this, someone mentioned the compound formed with the calcium in the body (ugh, I don't really remember much) would be solid - not liquid - and thus would slow or stop blood flow ... Would this be accurate?

- I suppose I can envision three main possible scenarios ... The first is that the HF burns through the walls of the veins quickly, causing massive blood loss (even if it's only into the body tissues).  The second would be similar, that death is caused by cardiac arrest and only later the acid remaining in the stagnant blood could corrode through the vessel walls.  The third I suppose is that the majority of the HF finds its calcium (and magnesium) right there in the bloodstream, creating calcium fluoride?, crystalline and insoluble, slowing/stopping blood flow, and/or directly interfering with the heart's calcium supply, causing cardiac arrest, but also leaving a lot less acid free to go corroding things.

I'm not sure any of these scenarios are close.

Hello Caren! (Sorry this is late. Thanksgiving and travel ate me.)

That's a nasty and painful way to die. Damn, that's creative.

Reading the materials safety data sheet for hydrofluoric acid tells me that concerted acid produces skin burns in seconds. So injected into a vein, I would imagine a good deal of the acid would burn the vein and surrounding tissues. The human heart recirculates all the blood through your body in about a minute. I would expect chemical burns throughout the circulatory system shortly thereafter, with many sites of deep-tissue burns.

I expect it would depend on how much volume of concentrated HF was injected whether or not the victim simply bled out the melting injection hole, or if the heart was sufficiently weakened by acid to fail, or if the acid-denatured blood cell proteins started a fatal blood clot that was then circulated to somewhere important. (Brain= stroke, heart supply =heart attack) Some combination of the three may still occur. The other question is if the killer has some medical knowledge. Where the injection is initially will have a lot to do with what organ system fails first. This can be utilized to mask the MO if the serial killer has a few victims prior to the story's beginning.

I'm not certain precipitation would be a major factor. In terms of timing, I'd worry more about blood clots. After the victim is dead then you might see some crystallization of precipitates. As to timing, I'd say you'd have structural tissue failure of anywhere that came into direct contact with the concentrated HF within the first 60 seconds, anticipating about a cm of major damage until the acid is neutralized for each succeeding minute.

Other things to think about. It shouldn't be difficult to get disposable plastic syringes that don't react to HF. Needles on the other hand will be corroded by the HF. Plungers and needles are readily available separately, and can be assembled onsite. Once the needle is affixed, however, the killer has a definite time limit on getting the injection accomplished before the needle corrodes too far, rendering it useless. Of course, the killer can always pack spares.

I hope this information helps guide your thinking. Here's the msds information, including advice to physicians on what to do in the advent of HF burns.

Happy Thanksgiving!

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Trista Robichaud, PhD


No homework questions, especially ones copied and pasted from textbooks. I will answer questions about principles or give hints, but I do not do other's homework. I'm comfortable answering basic biochemistry, chemistry, and biology questions up to and including an undergraduate level of understanding. This includes molecular biology, protein purification, and genetics. My training/inclination is primarily in structural biology, or how the shapes of things affect their function. Other interests include protein design, protein engineering, enzyme kinetics, and metabolic diseases such as cancer, atherosclerosis, and diabetes. My chemistry weaknesses are that I do not know organic or inorganic synthesis well, nor am I familiar with advanced inorganic reactions. I will attempt quantum mechanics and thermodynamics questions, but primarily as they relate to biological systems. Furthermore, I cannot tell you if a skin photograph is cancerous, or otherwise diagnose any disease. I can tell you how we currently understand the basic science behind a disease state, but I cannot recommend treatment in any way. Please direct such questions to your medical professional.


I hold a PhD in Biomedical Science from the University of Massachusetts Medical School in Worcester. I specialize in Biochemistry, with a focus on protein chemistry. My thesis work involved the structure and functions of the human glucose transporter 1. (hGLUT1) Currently I am a postdoc working in peptide (mini-protein) design and enzymology at the University of Texas Health Science Center in San Antonio, Texas. I am in Bjorn Steffensen's lab (PhD, DDS), studying gelatinase A and oral carcinoma.

2001 American Association for the Advancement of Science
2007 American Chemical Society
2007 Protein Society
2011 UTHSCSA Women’s Faculty Association

Levine KB, Robichaud TK, Hamill S, Sultzman LA, Carruthers A. Properties of the human erythrocyte glucose transport protein are determined by cellular context. Biochemistry 44(15):5606-16, 2005. (PMID 15823019)
Robichaud TK, Appleyard AN, Herbert RB, Henderson PJ, Carruthers A “Determinants of ligand binding affinity and cooperativity at the GLUT1 endofacial site” Biochemistry 50(15):3137-48, 2011. (PMID 21384913)
Xu X, Mikhailova M, Chen Z, Pal S, Robichaud TK, Lafer EM, Baber S, Steffensen B. “Peptide from the C-terminal domain of tissue inhibitor of matrix metalloproteinases-2 (TIMP-2) inhibits membrane activation of matrix metalloproteinase-2 (MMP-2)” Matrix Biol. 2011 Sep;30(7-8):404-12. (PMID: 21839835)
Robichaud TK, Steffensen B, Fields GB. Exosite interactions impact matrix metalloproteinase collagen specificities. J Biol Chem. 2011 Oct 28;286(43):37535-42 (PMID: 21896477)

Poster Abstracts:
Robichaud TK, Carruthers. A "Mutagenesis of the Human type 1 glucose transporter exit site: A functional study." ACS 234th Meeting, Boston MA. Division of Biological Chemistry, 2007
Robichaud TK, Bhowmick M, Tokmina-Roszyk D, Fields GB “Synthesis and Analysis of MT1-MMP Peptide Inhibitors” Biological Chemistry Division of the Protein Society Meeting, San Diego CA 2010
Robichaud TK; Tokmina-Roszyk D; Steffensen B and Fields GB “Catalytic Domain Exosites Contribute to Determining Matrix Metalloproteinase Triple Helical Collagen Specificities” Dental Science Symposium. UTHSCSA 2011
Robichaud TK; Tokmina-Roszyk D; Steffensen B and Fields GB “Exosite Interactions Determine Matrix Metalloproteinase Specificities” Gordon Research Conference on Matrix Metalloproteinase Biology, Bristol RI 2011

Oakland University, Auburn Hills MI BS, Biochemistry 1998
University of Massachusetts Medical School, Worcester MA PhD, Biochemistry & Molecular Pharmacology 2001-2008
University of Texas Health Science Center, San Antonio TX Postdoc, Biochemistry 2009-Present

Awards and Honors
1998 Honors College Graduate, Oakland University
2009 Institutional National Research Service Award, Pathobiology of Occlusive Vascular Disease T32 HL07446
2011 1st Place, Best Postdoctoral Poster, Dental Science Symposium, UTHSCSA, April 2011

Past/Present Clients
Invited Seminars:
Robichaud TK, Fields GB. “Synthesis and Analysis of MTI-MMP Triple Helical Peptide Inhibitors” Pathology Research Conference, University of Texas Health Science Center San Antonio Pathology Department (June 18th, 2010)
Robichaud TK & Hill, B “How To Give A Great Scientific Talk” Invited Lecture, Pathobiology of Occlusive Vascular Disease Seminars, UTHSCSA (Nov 11th 2010), Cardiology Seminar Series, Texas Research Park (Feb 21st, 2011)
Robichaud TK; Tokmina-Roszyk D; Steffensen B and Fields GB “Exosite Interactions Determine Matrix Metalloproteinase Specificities” Gordon-Keenan Research Seminar “Everything You Wanted to Know About Matrix Metalloproteinases But Were Afraid to Ask” Bristol, RI (Aug 6th, 2011)

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