Shofar FTP Archive File: camps/auschwitz/cyanide/cyanide.001
Newsgroups: alt.revisionism
Subject: Cyanide, Zyklon-B & Mass Murder
Archive/File: camps/auschwitz/cyanide cyanide.001
Last-Modified: 1994/10/03
From: Raskolnikov
TECHNICAL ASPECTS OF THE HOLOCAUST:
Cyanide, Zyklon-B, and Mass Murder
Brian Harmon
I. Introduction
Because many holocaust deniers find themselves unable to
dismiss the many volumes of historical information documenting
the Holocaust, they often turn to other methods. A very
common tactic is to claim that the Holocaust was "technically
impossible", improperly citing chemical and physical data as
"proof". The most well known example is the "Leuchter Report"
where Fred Leuchter, a self-proclaimed engineer, claimed that
"no one was gassed at Auschwitz", using a combination of poor
chemical analysis and technical difficulties as "proof".
Another example, "The Luftl Report", written by the Austrian
Walter Luftl, erroneously claims that not enough people could
be crammed into the chambers, and that Zyklon was too
dangerous to use for extermination. Many of these documents
are shrouded in pseudo-scholarly terminology and methodology,
and use confusing statements to make their lies seem more
tenable. The deniers hope to play on the common individual's
lack of knowledge in chemistry and physiology to confuse and
obfuscate the issue.
I will not deal directly with the claims of Leuchter and
Luftl here, rather I hope to provide the knowledge necessary
to take on Holocaust denier's claims directly, so they can
easily be discredited by anyone. As I hope to show, a little
knowledge of physiology and chemistry is all that is required
to see through their fabrications.
In this paper, I will discuss how cells make and use
energy via aerobic metabolism. Then, I will show exactly how
cyanide kills by shutting down aerobic (oxygen-using)
metabolism in organisms, including how much cyanide can kill,
and why warm blooded mammals are the most susceptible to
cyanide poisoning. The supporting biochemical and
toxicological data will set the context for the next section,
which discusses how the gassing of people could be carried
out. I will extrapolate from the Degesch manual on Zyklon B
to show that Zyklon cloud be used quite easily in a number of
situations, even at very low temperatures. I will then present
a "hypothetical gassing", where I will run some basic
calculations showing how easily a large number of people
(about 1.8 million) could be killed in one and one half years
with only one gassing a day. Comparing this with documents on
how the camps actually were run, It should be self-evident
that gassings with cyanide were quite easy for the Nazis to
carry out.
This document may be of a somewhat technical and
detailed nature. It is also exceptionally long, much longer
than I had anticipated. To remedy this, I also will write a
shorter "reference sheet" that takes the major conclusions
and points of this paper without all of the laborious
calculations and explanations. I intended this document
primarily as a reference resource rather than a document to be
completely absorbed at one sitting.
II. Structure of the Paper
Part one: Physiological Basis of Cyanide Poisoning
A. Cells and energy
-- How cells use energy
-- How the electron transport system works
-- How oxidative phosphorylation provides energy
B. Cytochromes in the Electron Transport System
-- Different cytochromes, and hemoglobin
B. How Cyanide Kills
-- Poisoning the ETS
-- Hemoglobin
D. Data on Cyanide
Part Two: Use of Zyklon B
A. Extrapolate from Nuremburg doc N1-9912
B. A Hypothetical Gassing
C. Compare to Existing Documents
Conclusion
A Brief Aside: What is Cyanide?
Cyanide refers to a large number of compounds that
contain the negatively charged cyanide ion: CN-. This ion
consists of one carbon atom triple-bonded to one nitrogen
atom. The negative charge primarily rests on the carbon atom.
Cyanide can be found both as a gas and as a salt. When bound
to hydrogen, it's referred to as hydrogen cyanide (HCN), and
is a gas at room temperature. When bound to ions like sodium
(Na+) or Potassium (K+), it's a salt and is a water soluble
solid. Its name varies depending on the ion it binds. KCN is
potassium cyanide, for example.
More information is presented in the "Data on Cyanide"
section (see below).
Part One: The Physiological Basis of Cyanide Poisoning
A. Cells and Energy {1}.
Cells need energy to grow and maintain their function.
In cells, energy is carried in the form of a transport
molecule, namely Adenosine Triphosphate (ATP). The metabolism
of molecules such as glucose (sugar), lipids (fats), etc.
release energy that is used to make more ATP. ATP is
essentially an "energy carrier" that allows cells to utilize
energy derived from food. Without ATP, a cell will die, as
will the organism itself. If a chemical interrupts a cell's
ATP producing machinery, that cell will die once it runs out
of ATP. Cyanide eliminates a cell's ability to produce ATP.
Before we can discuss how this happens, we must first deal
with how cells produce ATP under normal conditions.
Almost all ATP is produced in the mitochondria, a small
cellular organelle (literally "small organ"). The
mitochondria are, in essence, the "power plants" of a cell. A
mitochondrion has two membranes, an inner one and and outer
one. The outer membrane is highly permeable, and it will
allow just about anything through. The inner membrane, on the
other hand, is very impermeable. Only carbon dioxide (CO2),
water (H2O) and oxygen (O2) can pass through this membrane
without transport proteins to carry them across{2}. The
impermeable nature of the inner mitochondrial membrane (IMM)
will be important later.
Cells produce ATP through a combination of the electron
transport system (ETS) and oxidative phosphorylation (OP),
both in the mitochondrial inner membrane. The electron
transport system can be compared to an electric motor, where
current supplied to the motor allows work to be done. The
current passing through an electric motor is just a stream of
electrons, and the "current" passing through the ETS is no
different. High energy molecules generated by metabolism like
NADH and FADH2 supply the ETS with electrons, just as a
battery would supply a motor with current. This current
allows the ETS to do work. The "work" done is the pumping of
positively charged hydrogen atoms (protons, H+) across the
inner mitochondrial membrane. As I stated earlier, this
membrane will not allow anything back across without help from
a transport protein. At the end of the ETS, electrons have to
"go somewhere" to keep the current flowing -- they must leave
the ETS. In a battery, electrons go to the positive pole. In
the ETS, electrons are dumped onto oxygen, in effect acting
like an electron "sink". This is where oxygen is used in
metabolism, and will be dealt with later.
After a certain time, a significant number of protons
will be pumped out of the inner mitochondria, with many more
protons outside the mitochondria than inside. As the protons
are positively charged, the area outside the mitochondria will
have a relative positive charge, and the inside will have a
relative negative charge. There now exists a net potential
across the membrane, much like a fully charged battery. This
potential can be relieved to do work, namely the synthesis of
ATP.
The positive charges outside the mitochondria will
"want" to flow back in for two reasons: (1) the electrical
potential between the inner mitochondrial membrane and the
outer mitochondria. The positively charged H+ ions (protons)
will flow, if allowed, into the more negatively charged inner
mitochondria. This is much like how a battery works, but in
reverse. (2) The chemical gradient across the membrane.
Simply by random motions, molecules will flow from areas of
high concentration (outside the mitochondria) to those of low
concentration (inside the mitochondria). This is the same
reason a drop of dye in water will spread out over time even
if undisturbed. If molecules are prevented from diffusing by
a barrier (the inner membrane), a net pressure will result
from their impacts on the membrane, called the osmotic
pressure. The combination of electrical potential and osmotic
pressure is what provides the energy to make ATP in a cell
{3}.
Oxidative phosphorylation (making ATP) requires a
membrane-bound protein enzyme called ATP synthetase {4}. ATP
synthetase allows H+ ions back across the membrane, relieving
the pressure like letting air out a balloon. This flow of
protons allows the enzyme to combine Adenosine Diphosphate
(low E) and inorganic phosphate to make ATP (high energy).
This type of ATP synthesis is called oxidative
phosphorylation. It takes about two or three protons moving
through the enzyme to make one ATP molecule. The enzyme
requires a proton gradient across the membrane, with a higher
concentration on the outside than the inside. If anything
prevents the electron transport system from setting up this
proton gradient, ATP synthesis will not occur and the cell
will die.
-- Cyanide Poisoning
At the very end of the ETS, four electrons are added to
an oxygen molecule (see above). These electrons are added to
an oxygen molecule (O2), which combines with protons to make 2
water molecules. The ETS must dump electrons onto oxygen just
to keep the steady flow of electrons going, otherwise
electrons will "back up" and the current will stop.
Metabolism has an absolute requirement for oxygen, and it will
stop without it. If the ETS stops, the proton gradient will
fade away, ATP synthesis will stop, and the cell with die.
This last step, where electrons are given to oxygen to make
water, is where our cells utilize oxygen in metabolism.
Cyanide prevents the transfer of electrons to oxygen from the
last protein in the electron transport system, called a
cytochrome.
Cyanide reaches cells primarily through the blood, and
readily diffuses across the lungs during normal breathing.
Ingestion with food or drink is also lethal, as cyanide will
diffuse across the stomach wall and small intestine. Cyanide
will also very slowly diffuse across the skin, but this can
take over an hour {5}. Therefore cyanide intake through the
lungs and digestive tract is a very significant source of
poisoning, but very little occurs from absorption through the
skin.
B. Cytochromes in the ETS
Electrons passing through ETS are carried by three types
of molecules: iron-sulfur proteins, ubiquinone, and
cytochromes {6}. When talking about cyanide poisoning, the
cytochromes are the most important. Cytochromes contain a
very important structure called a porphyrin ring, which is an
aromatic, planar carbon-based ring with an iron atom
conjugated in the middle. A similar porphyrin ring structure
is also the oxygen binding structure in hemoglobin, a
vertebrate oxygen carrier protein in the blood. The iron has
two oxidation, or "charge" states, +2 (when it holds and
electron) and +3 (when it doesn't). The iron atom holds one
electron at a time, and passes it on the next molecule in the
ETS.
The iron atom, in addition to being bound by the
porphyrin ring, is often conjugated by the amino acids
histidine or cysteine. As the ring structure is planar, there
are two faces that can be conjugated by amino acids:
His
|
---- Fe(+3)-- Porphyrin molecule (side view)
|
His
Some cytochromes, however, are open on one of their two
faces:
--- Fe(+3)---
|
His
This open face is where hemoglobin in the blood cells
and a specific cytochrome in the ETS (Cytochrome a3, to be
exact) bind oxygen. Cytochrome a3 is the terminal cytochrome
that passes on electrons to oxygen to make water:
O2 + (2)H2 + 4 electrons ----> (2)H20
Cyt a3 binds oxygen at its open face {7}:
02
|
---- Fe(+2)--
|
His
When all works well, cytochrome a3 passes electrons to
oxygen, producing water. Dumping electrons onto oxygen acts as
a "sink" which allows electrons to flow continuously through
the ETS. The only problem is, certain poisons bind to this
cytochrome more strongly than oxygen, specifically cyanide and
carbon monoxide {8}.
C. How Cyanide Kills
-- Poisoning the ETS
Cyanide binds cytochromes much in the same way that
oxygen does, by conjugating at its open site. Unlike oxygen,
cyanide cannot receive electrons from cytochrome a3.
-:C=N: (note - actually a triple bond between C and N)
|
---Fe(+2)--
|
His
With the ETS deprived of its electron "sink", the whole
system backs up. Without the ETS, oxidative phosphorylation
will dissipate the H+ gradient, ATP synthesis will stop, and
the cell will die. Cyanide binds cytochromes more tightly
than oxygen, and as a result is lethal at very low
concentrations, at about 300 ppm. The effect also occurs at
hemoglobin, as cyanide will bind to that too, preventing
oxygen from reaching cells. In essence, this is how cyanide
kills cells and whole organisms.
-- Hemoglobin
Cyanide is most effective on warmblooded animals such as
mammals, but is less effective on insects. While insect
mitochondria and vertebrate mitochondria are not radically
different, one thing is: Hemoglobin. Vertebrates carry oxygen
in their blood via hemoglobin, while insects do not carry
oxygen in their blood at all. Instead, insects have air
tubules that carry oxygen directly to all cells in their body.
Because cyanide poisons hemoglobin too, animals that use it
are all the more susceptible. Also (while I am not sure of
this) insects may be more tolerant of anaerobic metabolism
than vertebrates.
Since cyanide binds to hemoglobin much in the same fashion
as it binds cytochrome a3, cyanide takes hemoglobin out of
commission as well {9}. With their oxygen carrying molecules
bound by cyanide, vertebrates die all the faster from
asphyxiation. Mammals are also very dependent on oxygen-
utilizing metabolism, and will die in minutes if it is shut
off. Insects, lacking hemoglobin, die more slowly as their
cells must be starved of ATP. Insects may also be able to
survive longer on anaerobic (non-O2 utilizing) metabolism.
Cyanide kills by binding to cytochrome a3 in the electron
transport system. As this site is usually bound by oxygen,
the passage of electrons from the ETS to oxygen is prevented,
backing up the system. Unable to maintain a proton gradient
without a properly functioning ETS, ATP synthesis stops and
the cell dies. In vertebrate organisms, cyanide also binds to
the porphyrin ring in hemoglobin, exacerbating cyanide's toxic
effects.
D. Data on Hydrogen Cyanide:
Here's what the 10th edition (1983) of the Merck Index had
to say on Hydrogen Cyanide:
HYDROGEN CYANIDE: Hydrocyanic acid, Blauseare, prussic acid.
[preparation info deleted] Colorless gas or liquid;
characteristic odor; very weakly acidic; burns in air with a
blue flame. INTENSELY POISONOUS EVEN MIXED WITH AIR.
Gas density: 0.941 (air = 1)
Liquid density: 0.687 [g/cm^3, I assume]
melting point: -13.4 deg Celsius
Boiling Point: 25.6 deg Celsius
The LC50 (lethal dose for 50% of animals) in rats -- 544
ppm (5min), mice 169 ppm (30 min), dogs 300 ppm (3 min).
HUMAN TOXICITY: [..] exposure to 150 ppm for 1/2 to 1 hour
may endanger life. Death may result from a few min. exposure
to 300 ppm. Average fatal dose: 50 to 60 milligrams.
USE: The compressed gas is used for exterminating rodents
and insects in ships and for killing insects on trees, etc.
MUST BE HANDLED BY SPECIALLY TRAINED EXPERTS.
Here's what _Chemistry of Industrial Toxicology_ had to say
about it (p94) [added emphasis is mine]:
"Hydrogen cyanide, or hydrocyanic or prussic acid, owes
its toxicity not to its acidity but to the cyanide ion (CN-).
Thus the soluble cyanides-- sodium, potassium,etc. -- are
equally toxic in the same molar concentrations. Unlike carbon
monoxide, hydrogen cyanide is a protoplasmic poison, killing
insects and other lower [sic] forms of animal life. _It does
not kill bacteria, however_. ^^^^^^^
^^^^^^^^^^^^ ^^^^^^^^^^^^^^
Hydrogen cyanide acts by inhibiting tissue oxidation, that is,
by preventing useful employment of oxygen carried by the
blood.
Cyanides are very rapid in their effects, killing
instantly if present in sufficient amounts. It is this speed
of action, rather than the minuteness of the fatal dose, which
accounts for the reputation of cyanide as the most powerful
common poison [..]
Hydrogen cyanide is used as a fumigant in dwellings,
warehouses, and ships. _Although such fumigations are
potentially very dangerous, accidents can be avoided by proper
precautions._
In high concentrations, hydrogen cyanide is absorbed through
the skin; therefore complete reliance cannot be placed on a
gas mask. After 1 hour exposure, 100 to 250 ppm of HCN are
dangerous."
[assumed the 100-250 ppm value is for absorption through skin]
Some things I'd like to point out:
Cyanide will not kill bacteria, and is completely useless
for disinfecting a morgue or hospital. Its only medical use
is to kill vermin (rats, mice, lice) that may harbor
pathogens. Some Holocaust deniers claim that cyanide was used
to disinfect "morgues" in Auschwitz. This is clearly a
ludicrous notion.
The sources I listed make specific references to HCN's
widespread use as a fumigant, and that it can be done easily
with the right precautions.
Major Modes of Poisoning
HCN will pass through the skin, and poisoning can result.
Absorption through the skin is a much slower process than
through lungs, so a short exposure to skin is not very
dangerous. It also takes a higher concentration of the gas
{10}. Absorption of cyanide through the skin is not
significant unless the concentration is high over a long
exposure.
According to July 1993 issue of _American Family
Physician_, cyanide poisoning through the skin is very rare: