The cause of death in exhaust gas chambers

Traditionally, the killing at the Reinhardt camps is said to have been done with steam electricity chlorine ether quicklime shooting vacuum chambers carbon monoxide from a diesel motor. Today, 30 years after the publication of F.P. Berg’s work on the technical absurdity of such a means of killing, some anti-revisionists have started to move the camps over to gasoline engines, which unlike diesels do emit high levels of carbon monoxide.

This move, however, does nothing to solve another exterminationist dilemma, that of corpse color. People killed by carbon monoxide are red, but the witnesses describe the bodies at the Reinhardt camps as blue or yellow. Because of this problem, anti-revisionists have attempted to argue that the cause of death in the Reinhardt gas chambers was not CO poisoning but something else – carbon dioxide and lack of oxygen being the leading candidates. I do not know where this argument originated, but a form of it is found on Nizkor, so it’s quite old. In recent years, this argument has been put forth by Roberto Muehlenkamp.

Muehlenkamp’s Claims

even with gasoline exhaust the people in the gas chambers may simply have suffocated from lack of oxygen before they could die of carbon monoxide poisoning, which would explain the “blue” color mentioned by some eyewitnesses,

Dalton: if some 70% of poisonings show red/pink discoloration, it could not have been missed by the witnesses. And yet not a single one is recorded as having seen pink or red corpses — which argues against any form of CO gassing.

Muehlenkamp: No, it only argues for the cause of death not having necessarily been CO poisoning and/or the victims having belonged in the 30 % non-discoloration category.

[Note that the figure of 70% for the proportion of cases of fatal CO poisoning showing red lividity, which Muehlenkamp has advanced, is wrong.]

You have to rule out the possibility that the victims, or at least a considerable part of them, succumbed to suffocation rather than to carbon monoxide poisoning. It stands to reason that the rapid introduction of gasoline fumes into a closed space where oxygen was sparse and CO2 was high anyway, due to the breathing of people packed in there like sardines in a can, might bring the oxygen and CO2 concentration to such levels that all or most of the victims would die before carbon monoxide poisoning could take effect

A necessary preliminary

Clearly it is possible for death in an exhaust gas chamber to come from a cause other than CO. All you need to do is reduce the amount of exhaust introduced to the tiniest trickle. For instance, if the chambers are adequately sealed and one liter of exhaust is introduced into gas chambers with a total volume of 1000 m^3, the people inside will not die from CO poisoning. But this setup is completely absurd and contradicted by all the testimonies. I will therefore assume a certain minimum flow rate of exhaust – say, 1 complete air change per hour.

Reminder on the conditions for cherry-red lividity

Cherry red lividity is characteristic of cases of carbon monoxide poisoning with COHb > 30% – see references given in this thread. Cases of CO poisoning from exhaust gas generally have COHb levels of ~70% – see references in the same thread.

Formulation of the Problem

The question we are faced with is this: would carboxyhaemoglobin levels in people killed in a gas chamber with the exhaust from a gasoline engine exceed 30%?

There are potential toxic effects from the following causes: CO, CO2 (from the exhaust and from exhaled air), and reduced O2 (from the effects of respiration and from the displacement of the original air by exhaust). Which will prevail?

The Answer

Consider this study on goats as described in the book Carbon Monoxide and Human Lethality:


COHb saturation was 86% in a simple exposure to 2.7% CO, and rose to 90% in the exposure to 2.7% CO and 3% oxygen. Adding 7% CO2 only raised that to 91%.

The same book also points out that

Studies with rats show that low oxygen (14%) and elevated CO2 (to 5.4%) decrease the mean survival time but do not change the final COHb at death.

Here is a pertinent human case from the same book (p. 194):

Female suicide victim connected oxygen mask hose to car exhaust and put on mask. Complete autopsy showed no signs of other contributing factors.

Her carboxyhaemoglobin level was 70%. Recall that the threshold for the appearance of prominent cherry-red coloration is 30% carboxyhaemoglobin.

By breathing pure exhaust from a gasoline engine she exposed herself to a lower oxygen environment than would have existed in an exhaust gas chamber, and to a higher level of CO2.

That pretty much wraps this up. I could say more about CO2 (*) and low oxygen toxicity (see for instance this paper; for CO2 specifically see Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 2) and perhaps I will at some point, but the above is already enough to show that carboxyhaemoglobin levels in people killed in a gasoline engine exhaust chamber would indeed be well over 30%.

(*) It should be noted that chapter 4.7 of Mattogno and Graf’s Treblinka overstates the lethality of CO2.

A Reformulation

How fast do COHb levels rise? CO is >200 times more able than O2 to bond with haemoglobin – so, quite fast.


Anti-revisionists have often emphasized the presumably rapid respiration of the Reinhardt victims as a result of their run through the tube, so they may not object to the high respiration rate used here, but if we want to use a more modest respiration rate we can simply increase the times given here by a factor of, say, 2.5. Thus 5 minutes of exposure to 1% CO would suffice to give COHb levels which cause red lividity.

Or use this table:


Ten minutes at half a percent CO would also bring us into the red lividity range zone.

Given that gasoline engines at idle can readily produce 7-12% CO, these concentrations would be rapidly reached. It’s easy to check that oxygen levels would not drop fast enough to pose any danger to life before CO was present in high enough concentrations to rapidly raise COHb levels above 30%.

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