Richard Green and the Toxicology of Auschwitz

[friedrichjansson]

The amount of cyanide used in the alleged Auschwitz gassings are an important subject of controversy. They bear on several revisionist arguments, including the practicality of ventilation systems, the ability of the sonderkommando to enter the chamber after a certain time, the accumulation of cyanide in the walls, etc. Several factors influence estimates of this amount, including the amount of time the gassings are assumed to have taken and whether there are assumed to have been devices for removing the zyklon-B (which deserves a thread of its own). This thread is for a different factor: the amount of cyanide assumed to be necessary to kill people in a certain amount of time.

The major critic of revisionists on this point is Richard Green, primarily in his affidavit and his article Chemistry is not the Science, as well as in his article The Chemistry of Auschwitz. Other anti-revisionists seem mainly to have simply repeated his theses. Therefore I want to focus this thread especially on Green's assertions.

Green writes as a critic of Germar Rudolf, so we have to start by explaining Rudolf's position. Rudolf uses information on the times to death typically experienced in US gas chamber executions, and compares them to witness statements on time to death in Auschwitz gassings. He then infers a comparison of cyanide concentrations from the comparison of times to death, and using data on the evaporation rate of zyklon-B deduces the amount of cyanide used.

Richard Green attacks this argument on multiple fronts. He questions Rudolf's statements on time to death and cyanide concentrations in US gas chamber execution; these questions are dealt with in this thread. He questions Rudolf's interpretation of the Auschwitz witness statements with respect to gassing durations; that is addressed in this thread. The present thread is for dealing with Green's third line of attack, which builds on the first two by using them to bypass the question of US gas chamber executions entirely and attempt to establish the amount of cyanide used in Auschwitz by a completely different method, using information on the toxicity of hydrogen cyanide to estimate the HCN concentration needed for Auschwitz gassings. I aim both to show that Green is wrong, and to establish what can be said about cyanide concentrations at Auschwitz and related questions on the basis of toxicology.

Comments, contributions, and criticisms are encouraged.

[friedrichjansson]

Richard Green's assertions on cyanide toxicity begin with information from a Dupont data sheet. He writes:

According to Dupont the following thresholds apply:

2-5 ppm Odor threshold
4-7 ppm OSHA exposure limit, 15 minute time weighted average
20-40 ppm Slight symptoms after several hours
45-54 ppm Tolerated for 1/2 to 1 hour without significant immediate or delayed effects
100-200 ppm Fatal within 1/2 to 1 hour
300 ppm Rapidly fatal (if no treatment)

In his article The Chemistry of Auschwitz he also quotes the Merck index:

The Merck index warns, "Exposure to 150 ppm for 1/2 to 1 hr may endanger life. Death may result from a few min exposure to 300 ppm"

Here is the context from the Merck index:

A preliminary observation: even at first glance, it seems rather doubtful that such sources, aiming at industrial safety rather than toxicological rigor, can be taken seriously for the purpose of estimating HCN concentrations needed in a homicidal gas chamber. Germar Rudolf states as much, when after giving the DuPont source and another [F. Flury, F. Zernik, Schädliche Gase, Dämpfe, Nebel, Rauch- und Staubarten, Berlin 1931, p. 405] that offers similar numbers, he states:

These are not, of course, the results of experiments on human beings, but rather extrapolations, in which lower risk thresholds have been determined on the grounds of safety.

Rudolf then gives an important argument to substantiate this, which we defer considering until later.

But while the DuPont and Merck documents could be dismissed as merely concerned with safety, Rudolf's own citation of Flury and Zernik does not seem to belong to the same industrial-safety genre. In his affidavit Green cites some more sources which also raise concern, the first of which is this:

An article in Human Toxicology [J.L. Bonsall, Human Toxicol. (1984), 3, 57-60.] gives similar thresholds:

Response Concentration (ppm)

Immediately fatal 270

Fatal after 10 min 181

Fatal after 30 min 135

Fatal after 30-60 110-135
min or later, or
dangerous to life

Tolerated to 30-60 45-54
min without
immediate or late
effects

Slight symptoms after 18-30
several h

These citations would seem, at first glance, to provide a fairly authoritative case. They are from the proper scientific literature, rather than the industrial safety literature. A difficulty comes up, however, when we ask just what the basis of these numbers is. Do they have an empirical foundation? No. Are they based on some theoretical calculation? No.

So why do we find all these mentions of 300 ppm (or 270 ppm = 300 mg m^-3) and other similar figures?

The answer is very simple . People have simply been formulaically repeating more or less the same numbers since 1912 [!] without any empirical or theoretical foundation! The details can be found in a 1976 paper of McNamara, available here:
http://www.dtic.mil/dtic/tr/fulltext/u2/a028501.pdf

It's worth reading this in full; I'll reproduce the relevant part of the paper here. To quote just the key parts:

All of the above references on the toxicity of HCN in humans apparently originated with K. B. Lehmann prior to 1912 when first quoted by Kobert. 9 None of these references give the experimental basis for the human values. The publication is not cited by any of those who quote Lehmann. Our attempts to locate such an article have been fruitless.

And then when some work of Lehmann on HCN is tracked down, what does it say?

I have studied the effect of HCN vapors quantitatively with my students Hagschal and Ahlmann. Doses of 0.06 mg are tolerated well even after 5 hrs: 0.14 mg was tolerated by a rabbit with some increased respiration even for 2 hrs; others died even at 0.13 mg in 1 hr, and at 0.15 mg in 1/2 hr. At 0.2 mg even after 4 min, sudden collapse occurs: we saw an actual pulmonary hemorrhage in a rabbit poisoned with HCN vapor (until now published only in the dissertations of my students). As yet we have not conducted experiments on cats and dogs. I can make no quantitative statements about men.

Note that the book by Flury and Zernik that Rudolf cites is included among those who are relying on Lehmann.


In summary, there is absolutely no foundation for the number 300 ppm (or 270 ppm = 300 mg m^-3) or for the other numbers frequently mentioned along with it. None whatsoever. No experiments. No theoretical calculation. Zilch. Just repeating what the
other guy said, all the way back to the citation of Lehmann by Rudolf Kobert (whose work, incidentally, is cited on the corpse color thread). As noted in Acute Exposure Guideline Levels for Selected Airborne Chemicals, volume 2:

Several review sources, such as Dudley et al. (1942), Hartung (1994), and ATSDR (1997), report human toxicity data that appear to be based largely on pre-1920 animal data.

The work of destroying Green's structure complete, we can build afresh on new foundations, although we will return to Green's claims from time to time.

[friedrichjansson]

A bit of advice to people reading this: there are a lot of things to discuss, and I'm sure I won't do an optimal job at explaining them. So if you're interested, you should really read the literature yourself. These are the important things to read:

1. this paper by Barcroft
2. the paper by McNamara cited above
3. the paper by Moore and Gates
4. toxicological profile for cyanide
5. Acute Exposure Guideline Levels for Selected Airborne Chemicals, volume 2

[EtienneSC]

I understand that the toxic effect of hydrogen cyanide (HCN) arises (at least in part) from the cyanide combining with the molecule in red blood cells that draws in and releases oxygen. Would it not then be possible to do experiments on animal and human blood to see if the same effect occurred and to the same or a similar degree. It would then be possible to do back of the envelope calculations on body mass, blood quantities, respiration and circulation rates to estimate toxicity. This could then be compared with the actual data for animal and limited data for executed prisoners in the US.

German Rudolf's line of argument was then to use this data to come up with plausible figures (based on the extermination hypothesis) for the duration and level of exposure to HCN of the brickwork and plaster in the supposed gas chambers. Then he estimates the likely effects in formation of ferric cyanide compounds with that type of material. This can be corroborated with the actual figures from the delousing chambers. Then he compared that with the actual (trace) levels of ferric cyanide compounds found in the supposed homicidal gas chambers. It was a normal scientific procedure of making a hypothesis (extermination), drawing an inference using auxiliary hypotheses, then seeing if that inference was confirmed by observation. It wasn't, so at least one of the inputs into the inference was wrong.

Your line of argument then, seems to be that the figures for the presence of HCN in the homicidal gas chambers may need to be reworked for new data on HCN toxicity. I'm not sure how this is relevant to Green:
http://www.holocaust-history.org/irving ... affweb.pdf
Green seemed to argue that ferric cyanide compounds were visible to the naked eye (Prussian blue, p16 of linked document) so the knowledge of chemistry that he shared with Rudolf was not that important. He made some unconvincing speculations on densities of cyanide compounds and cited Rudolf's remark that chemistry was not the science that would prove or disprove the holocaust. As this remark of Rudolf's would have no particular authority on the basis of knowledge of chemistry alone - for it involves a comparison of that knowledge with knowledge of other areas in which he has no particular expertise - the citation struck me as inept [see p59 of the link above]. Green's disapproval of using chemistry to "trump historical evidence" (i.e. supposed eye-witness testimony - also p59) is also unconvincing.

Nonetheless, if it is possible to access more reliable information on cyanide toxicity, that would be relevant to the gas chamber argument.

[Horhug]

Re: the testing of Leuchter's samples and the Roth / Green position on the dilution of "surface" HCN by crushing the samples.

This is so obvious, I feel slightly embarrassed to have to ask about it but because I think I may be missing something.

Even if the 10 micron penetration argument does prove to be valid, surely the sample dilution argument offered by Roth would apply to all mortar / masonry samples ?

It seems to me the layman, unless I've missed something really obvious that, Roth is arguing because the HCN would only penetrate to 10 microns then crushing any sample would dilute the concentration of surface HCN in the sample because of mixing any HCN contaminated parts with the crushed up whole sample.

If I've got that correct, then, surely this arguement must be applied to both sets of samples, those that were taken from the alleged HGCs and those taken from other areas, including the delousing chambers.

If the measured scale of magnitude differences are correct then those saturations have been measured in all samples after their alleged dilution caused by crushing and mixing with non-contaminated material.

So, if the 10 micron pentration is correct then it's easy to see how the testing wasn't specific to the "surfaces" of those samples but other than that I still don't fully comprehend the force of argument being used here to render the method of testing invalid.

If "dilution" occurred then it occurred for all samples surely and given that the tests revealed magnitudinal differences in HCN concentration, what is in fact the problem ?

[friedrichjansson]

Re: the testing of Leuchter's samples and the Roth / Green position on the dilution of "surface" HCN by crushing the samples.

This is so obvious, I feel slightly embarrassed to have to ask about it but because I think I may be missing something.

Even if the 10 micron penetration argument does prove to be valid, surely the sample dilution argument offered by Roth would apply to all mortar / masonry samples ?

It seems to me the layman, unless I've missed something really obvious that, Roth is arguing because the HCN would only penetrate to 10 microns then crushing any sample would dilute the concentration of surface HCN in the sample because of mixing any HCN contaminated parts with the crushed up whole sample.

If I've got that correct, then, surely this arguement must be applied to both sets of samples, those that were taken from the alleged HGCs and those taken from other areas, including the delousing chambers.

If the measured scale of magnitude differences are correct then those saturations have been measured in all samples after their alleged dilution caused by crushing and mixing with non-contaminated material.

So, if the 10 micron pentration is correct then it's easy to see how the testing wasn't specific to the "surfaces" of those samples but other than that I still don't fully comprehend the force of argument being used here to render the method of testing invalid.

If "dilution" occurred then it occurred for all samples surely and given that the tests revealed magnitudinal differences in HCN concentration, what is in fact the problem ?

I completely agree with this line of thought. I've never been able to figure out what the dilution argument is supposed to show.

[friedrichjansson]

I understand that the toxic effect of hydrogen cyanide (HCN) arises (at least in part) from the cyanide combining with the molecule in red blood cells that draws in and releases oxygen. Would it not then be possible to do experiments on animal and human blood to see if the same effect occurred and to the same or a similar degree. It would then be possible to do back of the envelope calculations on body mass, blood quantities, respiration and circulation rates to estimate toxicity. This could then be compared with the actual data for animal and limited data for executed prisoners in the US.

Cyanide toxicity comes mainly from inhibiting the enzyme cytochrome c oxidase - an enzyme involved in the electron transport chain, in processing oxygen. It's not from bonding with haemoglobin as in the case of carbon monoxide, where CO bonds with haemoglobin to form carboxyhaemoglobin. With carbon monoxide, the problem is that oxygen can't bond with haemoglobin because CO is in the way, and CO is better at bonding with haemoglobin than oxygen is. With cyanide, the problem is the opposite: oxygen bonds with haemoglobin, but it can't get off. Normally you want to have oxyhaemoglobin in arterial blood coming from the heart, then to have the oxygen get off where it's needed, so you have deoxyhaemoglobin in venous blood going back to the heart. With cyanide poisoning the oxygen can't get off, so you have lots of oxyhaemoglobin in the venous blood; having venous blood the same color as arterial blood is a sign of cyanide poisoning. This is the reason that cyanide poisoning often causes redness, both during the poisoning and in the livor mortis. Here's how one source puts it:

Cyanide exerts its primary toxicological effects by binding to the metallic cofactor in metalloenzymes, thereby impairing enzyme and cell function. Cytochrome c oxidase (an enzyme in the mitochondrial respiratory chain) is the most significant target of cyanide exposure since its inhibition prevents tissues from using oxygen. The result is a reduction in oxygen sufficient to cause tissue damage (histiotoxic hypoxia) throughout the body, with the most vulnerable tissues being those with high oxygen demands and/or a deficiency in detoxifying enzymes such as rhodanese. The inhibition of oxygen use by cells causes oxygen tensions to rise in peripheral tissues; this results in a decrease in the unloading gradient for oxyhemoglobin. Thus, xyhemoglobin is carried in the venous blood, which is one biomarker of cyanide exposure. In addition to binding to cytochrome c oxidase, cyanide inhibits catalase, peroxidase, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, and succinic dehydrogenase activities, which may also contribute to the signs of cyanide toxicity.

That said, one can try to make cross species toxicity estimates, using factors like those you describe plus experimental data. It's tough to be very precise, though. The earlier studies are in some ways more useful than the more recent ones, because the more recent ones are all on rats, mice, and rabbits, while the earlier ones included larger animals such as cats, dogs, goats, and monkeys. There will be more about this to come.

German Rudolf's line of argument was then to use this data to come up with plausible figures (based on the extermination hypothesis) for the duration and level of exposure to HCN of the brickwork and plaster in the supposed gas chambers. Then he estimates the likely effects in formation of ferric cyanide compounds with that type of material. This can be corroborated with the actual figures from the delousing chambers. Then he compared that with the actual (trace) levels of ferric cyanide compounds found in the supposed homicidal gas chambers. It was a normal scientific procedure of making a hypothesis (extermination), drawing an inference using auxiliary hypotheses, then seeing if that inference was confirmed by observation. It wasn't, so at least one of the inputs into the inference was wrong.

Your line of argument then, seems to be that the figures for the presence of HCN in the homicidal gas chambers may need to be reworked for new data on HCN toxicity. I'm not sure how this is relevant to Green:
http://www.holocaust-history.org/irving ... affweb.pdf
Green seemed to argue that ferric cyanide compounds were visible to the naked eye (Prussian blue, p16 of linked document) so the knowledge of chemistry that he shared with Rudolf was not that important. He made some unconvincing speculations on densities of cyanide compounds and cited Rudolf's remark that chemistry was not the science that would prove or disprove the holocaust. As this remark of Rudolf's would have no particular authority on the basis of knowledge of chemistry alone - for it involves a comparison of that knowledge with knowledge of other areas in which he has no particular expertise - the citation struck me as inept [see p59 of the link above]. Green's disapproval of using chemistry to "trump historical evidence" (i.e. supposed eye-witness testimony - also p59) is also unconvincing.

It's not relevant to Green's main line of argument, the chemical one. It deals with his toxicological sideshow. The only bearing it has on the chemical issues is by influencing the concentrations of HCN that are supposed to be present. It also influences factors like the possibility of the gassings occurring as quickly as the witness accounts say, both with respect to killing time and ventilation. In the affidavit, I'm dealing only with section II under The Leuchter Report, titled Concentration of Cyanide Required for Killing Purposes, pp. 19-34. So just a quarter of the affidavit, page wise.

[friedrichjansson]

This post will be about actual data on humans under acute exposure to HCN. The data are quite sparse, so they can all be fit in a single post! Of course, I'm ignoring the data from the experience of operating execution gas chambers in the United States because there's another thread for that.

One data point was posted here recently here. It is a case report of an industrial worker who survived a six minute exposure to some 450 ppm of HCN without sequelae. He was not given treatment for a full hour after his exposure. This suggests that it's quite likely, although not certain, that he would have survived even without treatment. Usually when cyanide kills it does so quickly, and often (but definitely not always) people who survive for an hour recover completely.

I don't have a copy of the study, but Green quotes it as follows

This case is unusual in that survival without sequelae occurred despite exposure to HCN in the order of 500 mg/m for a 6 min exposure; especially as treatment was initiated until 1 h after exposure.

Even if the initial exposure was lower than 500 mg/m , experiments carried out subsequently have indicated that the build up of HCN in the circumstances described is rapid.

Acute Exposure Guideline Levels for Selected Airborne Chemicals, volume 2 contains the following summary of the case:

During inspection of a tank containing a thin layer of hydrazodiisobutyronitrile (HZDN), a worker collapsed after 3 min, was fitted with a breathing apparatus after another 3 min, and removed from the tank after 13 min, resulting in a 6-min exposure
(Bonsall 1984). At that time the worker was unconscious with imperceptible breathing and dilated pupils. He was covered with chemical residue. The tank had previously been washed with water; HZDN decomposes with water to give HCN and acetone. No HCN was measured prior to entry into the tank, but immediately after the incident, levels of HCN of about 500 mg/m3 (450 ppm) were measured. One hour after the exposure, the comatose individual was administered sodium thiosulfate, and following subsequent complications and treatment, he was discharged after 2 weeks (wk). No sequelae were apparent.

The other main data point on acute human exposures to HCN is contained in the outstanding paper of Barcroft cited above. Here's the summary given in Acute Exposure Guideline Levels for Selected Airborne Chemicals, volume 2:

Barcroft (1931) described the controlled exposure of a 45-year-old, 70-kg man and a 12-kg dog to a concentration of HCN at 500–625 ppm in an airtight chamber. The human volunteer attempted to maintain the same level of activity as the dog. The dog
became unsteady at 50 seconds (s), unconscious at 75 s, and convulsive at 90 s. One second later, the man walked out of the exposure chamber with no apparent effect. At 5 min after initiation of exposure, the man experienced a momentary feeling of nausea, and at 10 min from the start, his ability to concentrate in “close conversation” was altered. The dog at first appeared to be dead but recovered without adverse signs by the next day. Barcroft (1931) cites two other studies in which fumigation workers were exposed to a concentration of HCN at 250 ppm for 2 min or 350 ppm for 1.5 min without dizziness.

In fact, Barcroft was his own experimental subject. The actual concentration was 625 ppm, nominally - 500 ppm comes from Barcroft trying to give a lower bound after factoring in adsorption losses. Here's his account from his paper:

Now that's an experiment! If only we had more like that. It's worth noting that the experience of the dog in this study is another piece of evidence why you need a good margin of safety in a gas chamber, and waiting until apparent death is not sufficient.

[friedrichjansson]

Now it's necessary to explain some terminology. The LD50 of a substance is the lethal dose for 50% of the population; that is, it is a dose sufficient to kill 50% of the people exposed to it. Obviously the number 50 can be changed to other values, so you can have an LD75 or an LD90 or an LD1. These figures are generally expressed in mg kg^-1, milligrams per kilogram of body weight.

Since we're talking about inhalation rather than ingestion or injection, talking about doses can be kind of awkward. What we want to look at is the effect of a given concentration of HCN in the atmosphere. An LC50 is the lethal concentration of a substance sufficient to kill 50% of people exposed to it. An LC50 has to come with a time – e.g. a “10 minute LC50,” meaning a concentration such that a 10 minute exposure would be sufficient to cause death to 50% of those exposed. Again, 50 can be replaced by other values. The units for an LC50 are just units of concentration – generally they will be ppm, or mg m^-3, or sometimes mg/l.

Sometimes you want to combine the time and the concentration in a single figure; this is an LCt50 (again 50 can be replaced...). A 10 minute exposure to 500 mg m^-3 would be an LCt of 5000 mg min m^-3 – you get the idea.

Now, what are the LC50s for exposures to hydrogen cyanide?

Well, McNamara (in the paper linked above) estimated the 10 minute LC50 at 546 ppm. Toxicological Profile for Cyanide states the following:

Based on case report studies, the following acute median lethal exposure levels for humans were estimated: an LC50 of 524 ppm for a 10-minute inhalation exposure to hydrogen cyanide

Richard Green has rather different ideas about the LC50. There's one more reference that Green gives that hasn't been dealt with yet; it contains statements about LC50s:

One source [Marrs, Maynard and Sidell, Chemical Warfare Agents: Toxicology and Treatment, 1st edition, 1996] gives the following values for LC50:

Precise figures for the acute toxicity of HCN to humans are unknown. The acute lethality is, by analogy with animals and on theoretical grounds, likely to be time dependent and some guideline figures are available in table 2.

Time LC50 LCt50
(mg m^-3 ) (mg min m^-3 )
15s 2400 660
1 min 1000 1000
10 min 200 2000
15 min 133 4000

However it should be stated that these figures are extremely uncertain, and a higher figure of 4400 mg m^-3 was given by MacNamara based on an estimate of Moore and Gates.... MacNamara's own estimates for the toxicity of inhaled HCN in humans is based on the similarity in responses to HCN of humans and goats, and he gives a 1-min LC50 of 3404 mg m^-3 .

The value given for 10 minutes is equivalent to 181 ppm. Regardless of the absolute accuracy of these numbers, it would be ridiculous to suggest that 300 ppm is LC1 for ten minutes. The LC50 estimate for 15 seconds corresponds to 0.21%, which is smaller than Rudolf's claim of LC100 for 10 minutes. McNamara's LC50 value for 1 minute is 3080 ppm, which is Rudolf's minimum LC100 value for 10 minutes. The value of 4400 mg m^-3 is difficult to interpret without a timeframe. Perhaps it is an LCt value, but the units are wrong in that case.

(A reminder: 1 ppm = 1.1 mg m^-3.)

I do not have a copy of the first edition of Chemical Warfare Agents: Toxicology and Treatment, so I cannot assess how faithful Green's representation of its contents is. I have to wonder what is contained in Green's ellipsis. I do, however, have access to the second edition of the same book; you can find it here. It does not contain the table that Green quotes. It does contain the (much higher) estimates of McNamara and of Moore and Gates, as well as estimates by Hilado and Cumming, whose paper I have not been able to find. Apparently the authors realized the table Green quotes was wrong and removed it.

Green writes

The value of 4400 mg m^-3 is difficult to interpret without a timeframe. Perhaps it is an LCt value, but the units are wrong in that case.

Had he bothered to read Moore and Gates' paper, he would know that it's an estimated 1-minute LC50, based on a breathing rate of 25 l/m. I'll write more about the Moore Gates estimates soon.

Green writes:

The value given for 10 minutes is equivalent to 181 ppm. Regardless of the absolute accuracy of these numbers, it would be ridiculous to suggest that 300 ppm is LC1 for ten minutes

Indeed, if 181 ppm were the LC50 for 10 minutes, it would be ridiculous to suggest that 300 ppm is the 10 minute LC1. However, the real value of the 10 minute LC50 is much higher – I quoted 524 ppm as a modern estimate. Is it still ridiculous to say that 300 ppm might be an LC1? The following data from rat studies suggests not:

The LC1 for 5 minutes was 76.7% of the LC50, for 15 minutes it was 70.4%, for 30 minutes it was 73.4%. If we take 70% of the suggested human LC50 of 524 ppm we get 367 ppm – more than the 300 ppm which Green thought couldn't possibly be the LC1. I am not suggesting that this really is the human LC1, because different species can respond differently, but this does show that available data on the relative values of LC1 and LC50 figures suggests that what Green thinks is ridiculous is in fact entirely reasonable.

In his affidavit, Green also writes along these lines:

it is not unreasonable to assume that the claim that 300 ppm is "rapidly fatal" would apply to times of 10 minutes at most.

As modern estimates of the 10 minute LC50 are over 500 ppm, we can be quite sure that this is wrong.

Now going back to the quote from Marrs et al - Green writes

McNamara's LC50 value for 1 minute is 3080 ppm, which is Rudolf's minimum LC100 value for 10 minutes.

This brings up a very important point. Green does not understand what an LC figure is. Rudolf gave 3000 ppm as a minimum to kill 100% of people within 10 minutes - i.e. as the concentration needed to make sure that they were dead within ten minutes. That is not what an LC100 is. A k-minute LCx figure gives the concentration necessary such that a k minute exposure is fatal to x% of those who receive it. It does NOT mean the concentration such that x% are already dead within k minutes.

To give an example, suppose you have 20 goats and you expose them to some concentration of HCN for 10 minutes. Four of them die during the exposure, three die five minutes later, two die 20 minutes later, and one lingers an hour before dying. Altogether 10 of the 20 goats died, 4 of the 20 within the 10 minute exposure. You will say “half the animals died; this concentration must be around the 10 minute LC50.” You will not say “four out of 20 died within the exposure, so this must be the 10 minute LC20.” LCx and time to death studies are completely different. It's true that cyanide usually kills quickly, so a high percentage of those that die will probably do so within the exposure or shortly after it, but cyanide deaths can also be lingering (more on this later).

Just to restate the point: Green uses LC figures in a completely inadmissible way; in particular he interprets a 10 minute LC100 to mean that everyone is dead within 10 minutes. That is not what it means; it means everyone has absorbed a lethal dose within ten minutes. Some of them might take quite a bit longer to die. You can see this in animal studies. To quote from the summaries given of three studies on rats in Acute Exposure Guideline Levels for Selected Airborne Chemicals, volume 2

The animals were observed for 7 days (d) following exposure. [...] HCN concentrations were continuously monitored using specific ion electrodes. All deaths occurred during the exposure period or within 20 min after exposure.

For all exposure durations, deaths occurred during exposures or within 1 d postexposure.

Most deaths occurred during the exposures. The 30-min LC50, calculated from deaths during the exposure period plus any deaths occurring up to 24 h postexposure...

Many studies specify postexposure monitoring periods of 7, 10, or even 14 days. Cyanide usually kills faster than that, of course, but the point is that people doing LC studies are looking for all deaths caused by an exposure, not just those that occur within the exposure.

[friedrichjansson]

Now how would we calculate LC50s, short of actually exposing humans to HCN? There are two primary methods (which can of course be used in conjunction): based on studies with animals, and based on theoretical inference from experience with humans. I'll summarize the results of animal studies in this post.

The paper of Barcroft is the best starting point for looking at animal data, as it looks at many different species. Here are Barcroft's LC50 curves:

Here are the results specifically for goats and monkeys in tabular form:

Here is Barcroft's comparison of the species:

How do humans compare with other animal species? As Barcroft noted in his experiment with himself and the dog, humans appear to be one of the more tolerant species, especially with respect to short exposures. On the other hand, humans have nothing on the mighty guinea pig for tolerating cyanide over longer time periods.






Recent studies have dealt primarily with rats, mice, and rabbits. Here are some tables summarizing their findings:

[friedrichjansson]

Animal data doesn't translate very directly to human data, but it's worth noting one thing right away. Animal studies support the idea that time to death is much greater than time to inhale a lethal dose. For example, Acute Exposure Guideline Levels for
Selected Airborne Chemicals, volume 2 summarizes one study as follows:

According to Matijak-Schaper and Alarie (1982), the 30-min LC50 of male Swiss-Webster mice inhaling HCN is 166 ppm. Mortality ratio for the mice (four per exposure group) were 0/4, 2/4, 3/4 and 4/4 for exposure to concentrations of HCN at 100, 150,
220, and 330 ppm, respectively. The recovery period was 10 min, during which the surviving mice appreciably recovered. The LC50 was the same for cannulated mice. At exposure concentrations of 500 and 750 ppm, the mean times to death were 12 min and 2 min, respectively.

The 5-minute LC50 for mice has been given at 323 ppm; a reasonable estimate would make 500 ppm something like the 3-minute LC50 (a conservative estimate – it's probably even less than three minutes). Therefore when mice were exposed to a concentration that was the LC50 for a 3-minute (or less) exposure, the average time to death was 12 minutes! It's worth noting that in general large animals take longer to die than small ones, so this effect may be even more pronounced in humans.

[friedrichjansson]

Now I want to talk about how we might get an estimate of cyanide's inhalation toxicity on theoretical grounds. The thing to read in this connection is the paper of Moore and Gates, and in particular its derivation of LC50 estimates.

Germar Rudolf, in arguing against the idea that 300 ppm is rapidly fatal to all humans, has already hit on the fundamental idea of such a calculation. I'll start from his simplified version, and then indicate how it needs to be altered. Rudolf writes:

This [these numbers are primarily a safety threshold] will be demonstrated in the following. To kill an average person with a body weight of 100 kg, the victim must therefore ingest approximately 100 mg hydrogen cyanide (1 mg per kilo body weight). The respiration of a human being at rest amounts to approximately 15 liters of air per minute.441 With a hydrogen cyanide content of 0.02% (approximately 0.24 mg per liter) the victim must inhale approximately 416 liters of air before ingesting the fatal quantity of hydrogen cyanide. At 15 liters per minute, this will take about half an hour.

In other words, Rudolf realizes that there is a connection between LD50s and LC50s: if it takes a certain amount of cyanide to kill you, then you will need to inhale that amount of cyanide to die. That is to say, LD figures should equal LC figures times the time of the exposure times the respiratory volume per minute. If it takes 100 mg of HCN to kill you, then if you are breathing air with 1 mg/l (=1000 mg m^-3) of HCN, you should have to breathe around 100 liters of air to inhale a lethal dose. If your rate of breathing (respiratory minute volume) is 10 liters per minute, this will take 10 minutes. Or if the LD50 is 70 mg, and that the concentration is 700 mg m^-3. Then you need to breathe 1/10 of a cubic meter (=100 liters) to have inhaled the LD50. The time it takes you to do this will depend dramatically on your breathing rate; therefore the breathing rate will be an extremely important variable, to be discussed later.

This is the essential idea for performing a theoretical calculation of human susceptibility to HCN inhalation, but it needs to be polished somewhat.

Why is this analysis too simple? The first difficulty is that the lungs do not absorb all of the HCN that is breathed. Rudolf is incorrect when he writes

Due to the extremely high capability of the lungs to absorb HCN, the human lung acts like a perfect filter which absorbs all hydrogen cyanide out of the air.

A study on dogs found that they absorb 70% of inhaled HCN. This is the figure used by Moore and Gates. After the Moore/Gates paper was written, however, a study on humans was done. Toxicological Profile for Cyanide summarizes its results:

Cyanide as hydrogen cyanide is rapidly absorbed (within seconds) following inhalation exposure. Humans retained 58% of hydrogen cyanide in the lungs after inhaling the gas through normal breathing (Landahl and Herrmann 1950).

I don't have a copy of this study, but the abstract is available here, and offers some additional and useful information:

Measurements were made of the percentages of selected vapours and gases retained in the respiratory passages of human subjects under various experimental conditions. Alcohol and acetone vapours, and ammonia and hydrogen cyanide gases were used. By means of a somewhat complicated device a desired concentration of gas or vapour was drawn through the nose while the subject held his breath, or the vapour was inhaled at a breathing rate determined by a metronome through one valve and then expired through another valve. An illustration shows how the flow of the vapours and gases is directed. Various concentrations, flow rates and breathing patterns were employed. The results obtained are presented in tabular form; they indicate that the concentration of a vapour or gas plays only a secondary role in determining the percentage retained in either the nose or the lung during the first few minutes of respiration. In the case of alcohol vapour a twenty-fold change in concentration, from 0.7 to 13 mgm. per litre, had a negligible effect on the percentage of pulmonary retention. In the case of hydrogen cyanide gas, a forty-fold change in concentration, from 0.5 to 20 microgrammes per litre, caused no appreciable change in the percentage retained in the lung. Similarly, a ten-fold change in concentration, from 1.1 to 11 microgrammes per litre, showed no effect on the percentage of hydrogen cyanide gas retained in the nose. The results for acetone vapour and ammonia gas also substantiated this generalization. An instance may be quoted: for alcohol vapour, at 54 litres per minute, 1, 350 cc. of tidal air and standard breathing, the percentage exhaled was 38; for a flow rate of 18 litres per minute, 450 cc. of tidal air and the same breathing pattern, the concentrations just greater than and less than that for the rate of 54 litres per minute gave 35 and 40 per cent, exhaled, i.e., practically the same. The percentage retained in the nose was greatest for short samples of each of the materials tried; but in about half a minute the retention had become fairly stable. Some rather definite individual differences were found in the percentage penetrating the nose; but they were not excessive, and may depend upon nasal resistance to the passage of air. For both nose and lung, the percentage retention increased in the following order: acetone, hydrogen cyanide, alcohol and ammonia.

The upshot of all this is that the amount of HCN absorbed in a given inhalation exposure is only 58% of what Rudolf assumed.

The second thing that needs adjustment is that humans detoxify cyanide. If you breathed 10 ppm for ten days, you would not die, even though the total exposure is the same as 2400 ppm for an hour. Some term needs to be included to account for detoxification. This factor really doesn't matter if we're just talking about concentrations where a fatal dose is absorbed in a few minutes at the most, but if we stretch things out to 30-45 minutes as van Pelt likes to then it does play a role.


The approach Rudolf suggests amounts to, mathematically, saying that (volume of air breathed)*(concentration) = lethal dose. With the two corrective factors mentioned above – accounting for the fact that not all HCN breathed in is absorbed, and for the fact that the body detoxifies cyanide – one gets a different equation. Moore and Gates write:

It is suggested that the toxicity of agents like AC [hydrogen cyanide] and CK can be described as a first approximation by the formula

VaC - Dt = K

in which

V = total volume of air breathed in l/kg
a = the fraction of inhaled gas absorbed
C = concentration in mg/l
D = rate of detoxication in mg/kg/min
t = time in minutes from first entrance of the substance into the body (roughly, the exposure time)
K = the lethal dose in mg/kg

Here the term Dt accounts for the body's detoxification of cyanide, and the constant "a" accounts for the fact that the lungs do not absorb all of the HCN they inhale.

Assuming that one accepts this formula, then statements on toxicity can be read off for any exposure, assuming that one is given a figure for the lethal dose, the rate of detoxification, the rate of breathing, and the fraction of HCN absorbed by the lungs. The last of these has been given at 58%. Determining the others will be the key to estimating the toxicity of HCN.

Moore and Gates use values of K=1.1 mg/kg, D = 0.017 mg kg^-1 min^-1, an absorption rate of 70% as in dogs, and a breathing rate of 25 liters/minute to derive the following LC50 estimates for a man weighing 70 kg:

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[EtienneSC]

You should probably take account of the fact that gaseous and liquid (i.e. re-condensed) HCN is also absorbed through the skin, as evidenced by the use of gloves by those required to handle it.

[friedrichjansson]

You should probably take account of the fact that gaseous and liquid (i.e. re-condensed) HCN is also absorbed through the skin, as evidenced by the use of gloves by those required to handle it.

Yes, this is an important factor, but it's difficult to get definite numbers. I've never seen anyone factor percutaneous absorption into calculations of inhalation toxicity, because the inhalation route is much more significant, but it may play a too big a role to be completely ignored. For absorption of vapor, Moore and Gates state the following:

AC vapor is absorbed slowly through the skin. Experiments on body exposure during which the animals breathed uncontaminated air indicated that mice were killed at 10-minute Ct's of about 200,000 mg min/m^3, cats at 500,000, and dogs at 1,000,000. The order of the sensitivity in these tests is to be expected on the basis of an increase in the required Ct with decrease in the ratio of body surface to body weight. The results serve to indicate that for man the required Ct is of such a magnitude that it does have significance in the consideration of AC as chemical warfare agent.

I'm pretty sure that they meant to write "does not" rather than "does." These numbers indicate a percutaneous Ct of millions, in comparison with ~5,000 for inhalation exposure. On the other hand, this study suggests percutaneous LC50s for rabbits in full body (minus the head) exposure of around 5000 ppm for a 90 minute exposure, 8000 for a 30 minute exposure, and 20000 for a 10 minute exposure (these are just guesses based on their data - they didn't really measure LC50). For comparison, the 30-minute inhalation LC50 is some 200 ppm. This suggests that percutaneous absorption contributes something like 2.5% to the toxicity of an inhalation exposure - for rabbits.


This is the best information I've found from a survey article:

Contribution of percutaneous absorption to the lethal toxicity of HCN vapor
It is well known that cyanides applied to the skin as solids or in solutions can readily penetrate to the extent that percutaneous (pc) LD50 values can be calculated (Ballantyne, 1994a). Likewise, HCN vapor can be absorbed across the skin and additively contribute to the toxicity resulting from pulmonary absorption (Steffens, 2003). Fairley et al. (1934) demonstrated in guinea pigs and rabbits that exposure to HCN vapor resulted in the percutaneous absorption of the material sufficient to produce signs of toxicity, and with prolonged exposure to cause mortality. That there may be symptomatic percutaneous absorption of HCN vapor also comes from observations on occupationally exposed workers. Thus, employees working for 8 to 10 min in an atmosphere containing around 20 000 ppm HCN (22 400 mg m−3 ), but wearing respiratory protective equipment, developed dizziness, weakness and headache (Drinker, 1932). Two reports of percutaneous HCN vapor intoxication, one in a fire fighter wearing self-contained breathing equipment, were described by Steffens (2003). According to Dugard (1987), the rate of absorption of HCN across human skin is proportional to the concentration of CN in the atmosphere. His studies lead to a conclusion that total body surface contact (18 500 cm2 for a 70 kg individual) with 1 ppm (1.12 mg m−3 ) HCN (by volume) can result in the absorption of 32 μg CN h^−1.

I haven't found a copy of Drinker's article. One source summarizes it as follows

Drinker (1931) cites the case of three men protected with gas masks in an atmosphere of 2% (20,000 ppm) HCN. After 8 or 10 min the men felt symptoms of marked dizziness, weakness, and throbbing pulse. They left the chamber just before collapse. For several hours after the exposure they experienced weakness, high pulse rate, and headache. They were incapacitated for several days, followed by complete recovery.

This suggests that 20,000 ppm through the skin acts like ~200 ppm inhaled - suggesting percutaneous absorption is ~1% of inhalation absorption. However this was not a full body (naked) exposure - that could be several times higher.

Such higher numbers are suggested by the study of Dugard. His numbers indicate that percutaneous absorption is roughly the equivalent to inhaling 1 liter per minute - thus if we assume an inhalation rate of 20 l/min, percutaneous absorption would contribute 5% to HCN absorption. I have not been able to find a copy of Dugard's study.

The paper linked above also has some information on the effect of liquid HCN on the skin:

IV. NOTE ON THE EFFECTS OF LIQUID HYDROCYANIC ACID ON THE SKIN

On account of the statement by the International Labour Office (1930, 1, 995) that experiments by Lehman on chemists prove that severe symptoms may occur through dipping the fingers into a solution of HCN, a simple experiment to investigate the possible danger from spilling or splashing the liquid upon the skin was carried out. A 44 lb. rabbit was selected and amounts of liquid HCN (about 80 per cent. pure) up to 1 c.c. were dropped on to the clipped skin from a pipette, and allowed to evaporate in the open air on a winter day. No symptoms developed. Ten c.c. of the liquid was then splashed upon the skin. The rabbit developed convulsions in 30 sec. and collapsed within a minute, but had completely recovered in 4 hours.

As far as it is permissible to argue from the results on a single rabbit to a hypothetical case in man, this experiment suggests that an 11-stone man could spill 29 c.c. of pure HCN on his bare skin with impunity, and would still have a chance of recovery if he so spilled 290 c.c.-again of the pure compound without taking any precautionary measures other than allowing free evaporation in the open air. It is suggested that free facility for evaporation is the important factor, and that, in conditions such as those of Lehman's experiments, this factor would be absent. Again, in the case of clothed skin, danger might well occur from hindrance to evaporation.

No study has been made of the effects of dilute solutions of HCN on the skin. The solution of HCN vapour, from an atmospheric concentration, into sweat on the body surface might amount to the same thing, and constitute a greater risk than the strength of the vapour concentration in the atmosphere would suggest.

It's difficult to know what to assume about sweat, but it seems unlikely that all people being gassed at Auschwitz would have been sweaty. After all they had just come from a train ride on an unheated train; if the weather was cold they probably would not have been sweating. My guess is that condensation will be much more likely to form on the cold walls than on the warm dry people. But as humidity goes up from respiration there will definitely be HCN losses as the water condenses and takes HCN with it.

The same paper also has some interesting information on the influence of moisture:

Absorption of HCN by moisture: In another case, an initial concentration of 1 in 60 was obtained. Early in the experiment the animal passed urine, and an immediate fall to 1 in 90 occurred, and it was found impossible to increase this concentration by any reasonable addition of HCN. The same effect was produced by immersing animals in water and drying them roughly with a towel before placing them in the apparatus.

The rabbits took about 10% of the volume of their apparatus, which is less than the percentage of the Auschwitz gas chambers that would have been taken up by Jews if they really were packed in as the witnesses describe. Losses to moisture could have been considerable.

(Another point of comparison: Barcroft experienced 22% adsorption and inhalation losses in the course of a 38 minute gas chamber experiment - but didn't mention anything about moisture, or urine.)

[friedrichjansson]

For absorption through the skin, I should also mention Ballantyne's article in this volume, although the conditions he worked with are considerably different from the conditions we are interested in.