The Cholesterol Correlation – The Chemical Weapons Correlation

The Cholesterol Correlation – The Chemical Weapons Correlation

The First World War [28 July 1914 – 11 November 1918] was grotesque and deadly.

The total number of deaths includes about 10 million military personnel and about 7 million civilians.

The Entente Powers (also known as the Allies) lost about 6 million military personnel while the Central Powers lost about 4 million.

At least 2 million died from diseases and 6 million went missing, presumed dead.

https://en.wikipedia.org/wiki/World_War_I_casualties

The chemical weapons used during the First World War were especially grotesque.

Chemical weapons in World War I were primarily used to demoralize, injure, and kill entrenched defenders, against whom the indiscriminate and generally slow-moving or static nature of gas clouds would be most effective.

The types of weapons employed ranged from disabling chemicals, such as tear gas and the severe mustard gas, to lethal agents like phosgene and chlorine.

The killing capacity of gas was limited, with four percent of combat deaths caused by gas.

https://en.wikipedia.org/wiki/Chemical_weapons_in_World_War_I

The Hague Declaration of 1899 and the Hague Convention of 1907 forbade the use of “poison or poisoned weapons” in warfare, yet more than 124,000 tons of gas were produced by the end of World War I.

Official figures declare about 1.3 million casualties directly caused by chemical warfare agents during the course of the war.

Of these, an estimated 100,000-260,000 casualties were civilians.

Nearby civilian towns were at risk from winds blowing the poison gases through.

https://en.wikipedia.org/wiki/Chemical_warfare#World_War_I

A poison gas attack using gas cylinders

For example, the British had over 180,000 chemical weapon casualties during the war, and up to one-third of US casualties were caused by gas and mustard.

The Russian Army reportedly suffered roughly 500,000 chemical weapon casualties in World War I.

https://en.wikipedia.org/wiki/Ww1#Chemical_weapons_in_warfare

Lachrymatory [tearing] agents were primarily used to incapacitate.

The earliest military uses of chemicals were tear-inducing irritants rather than fatal or disabling poisons.

https://en.wikipedia.org/wiki/Chemical_weapons_in_World_War_I

In World War I, ethyl bromoacetate was used as a lachrymatory agent and tear gas agent for chemical warfare under the German code Weisskreuz (White Cross), and later as odorant or warning agent in odorless, toxic gases.

https://en.wikipedia.org/wiki/Ethyl_bromoacetate

Tear gas, formally known as a lachrymatory agent or lachrymator (from lacrima meaning “tear” in Latin), is a chemical weapon that stimulates the corneal nerves in the eyes to cause tears, pain, vomiting, and even blindness.

Tear Gas

Pulmonary agents [asphyxiants] were used to incapacitate and kill.

These are the poisonous gases.

This class includes chlorine, phosgene and diphosgene.

Chlorine inflicts damage by forming hydrochloric acid when coming in contact with moisture such as found in the lungs and eyes.

It is lethal at a mix of 1:5000 (gas/air) whereas phosgene is deadly at 1:10,000 (gas/air) – twice as toxic!

Diphosgene, first used by the Germans at Verdun on 22-Jun-1916, was deadlier still and could not be effectively filtered by standard issue gas masks.

http://www.worldwar1.com/arm006.htm

A pulmonary agent, or choking agent, is a chemical weapon agent designed to impede a victim’s ability to breathe.

They operate by causing a build-up of fluids in the lungs, which then leads to suffocation.

Exposure to the eyes and skin tends to be corrosive, causing blurred vision and severe deep burns.

Inhalation of these agents cause burning of the throat, coughing, vomiting, headache, pain in chest, tightness in chest, and respiratory and circulatory failure.

Phosgene is the most dangerous commonly used pulmonary agent (although disulfur decafluoride and perfluoroisobutene are both even more dangerous, with respectively 4 and 10 times the lethality of phosgene, neither is widely used).

It is a colorless gas under ordinary conditions.

It has a vapor density 3.4 times greater than that of air, allowing it to remain low in the air for long periods of times.

Phosgene leads to massive pulmonary edema, which reaches maximum symptoms in 12 hours after exposure, followed by death within 24 to 48 hours.

https://en.wikipedia.org/wiki/Pulmonary_agent

Phosgene

Phosgene vapour was the primary respiratory agent.

It caused severe buring of the alveoli in the lungs, reducing or eliminating the lungs ability to transfer oxygen to the blood stream.

Mucous secreted by the body in response to these burns also caused dry land drowning.

Chemical Agents – Ray Smith
http://www.rjsmith.com/chemical-data.html

Chlorine is a powerful irritant that can inflict damage to the eyes, nose, throat and lungs.

At high concentrations and prolonged exposure it can cause death by asphyxiation.

Chlorine required a concentration of 1,000 parts per million to be fatal, destroying tissue in the lungs, likely through the formation of hydrochloric acid when dissolved in the water in the lungs.

Despite its limitations, however, chlorine was an effective psychological weapon – the sight of an oncoming cloud of the gas was a continual source of dread for the infantry.

Phosgene was a potent killing agent, deadlier than chlorine.

It had a potential drawback in that some of the symptoms of exposure took 24 hours or more to manifest.

In the first combined chlorine–phosgene attack by Germany, against British troops at Wieltje near Ypres, Belgium on 19 December 1915, 88 tons of the gas were released from cylinders causing 1069 casualties and 69 deaths.

https://en.wikipedia.org/wiki/Chemical_weapons_in_World_War_I

Chlorine Gas attack

Vesicant [blistering] agents were used to incapacitate and kill.

A blister agent, or vesicant, is a chemical compound that causes severe skin, eye and mucosal pain and irritation.

They are named for their ability to cause severe chemical burns, resulting in painful water blisters on the bodies of those affected.

Sulfur mustards
A family of sulfur-based agents, including mustard gas.

Nitrogen mustards
A family of agents similar to the sulfur mustards, but based on nitrogen instead of sulfur.

Exposure to a weaponized blister agent can cause a number of life-threatening symptoms, including:
Severe skin, eye and mucosal pain and irritation
Skin erythema with large fluid blisters that heal slowly and may become infected
Tearing, conjunctivitis, corneal damage
Mild respiratory distress to marked airway damage

All blister agents currently known are heavier than air, and are readily absorbed through the eyes, lungs, and skin.

Effects of the two mustard agents are typically delayed: exposure to vapors becomes evident in 4 to 6 hours, and skin exposure in 2 to 48 hours

https://en.wikipedia.org/wiki/Blister_agent

Blister Agents are designed to cause casualties and not necessarily kill, although in high concentrations, or if inhaled, they can cause death.

Blister agents contain powerful irritants which cause large, fluid filled blisters on exposed skin.

These blisters break, making the exposed individual susceptible to infections, causing casualties.

If inhaled, these agents cause blistering of the alveoli in the lungs.

Mucous is secreted which, if exposure is severe enough, can cause the lungs to fill with mucous, causing death by dry land drowning.

The primary blister agent was mustard vapour.

Mustard agent is a highly persistent agent.

There are areas of France that are still contaminated by Mustard Agent that was sprayed by the Germans during World War One.

Chemical Agents – Ray Smith
http://www.rjsmith.com/chemical-data.html

Dichlorethylsulphide:
The most dreaded of all chemical weapons in World War I – mustard gas.

Unlike the other gases which attack the respiratory system, this gas acts on any exposed, moist skin.

This includes, but is not limited to, the eyes, lungs, armpits and groin.

A gas mask could offer very little protection.

The oily agent would produce large burn-like blisters wherever it came in contact with skin.

http://www.worldwar1.com/arm006.htm

Mustard Agents as chemical weapons were first used towards the end of World War I.

It was most commonly used chemical weapon, used to cause severe eye and lung damage.

http://manbir-online.com/diseases/mustard.htm

Mustard Gas

The most widely reported and, perhaps, the most effective gas of the First World War was mustard gas.

Mustard gas is not a particularly effective killing agent (though in high enough doses it is fatal) but can be used to harass and disable the enemy and pollute the battlefield.

Delivered in artillery shells, mustard gas was heavier than air, and it settled to the ground as an oily liquid resembling sherry.

Once in the soil, mustard gas remained active for several days, weeks, or even months, depending on the weather conditions.

The skin of victims of mustard gas blistered, their eyes became very sore and they began to vomit.

Mustard gas caused internal and external bleeding and attacked the bronchial tubes, stripping off the mucous membrane.

This was extremely painful.

Fatally injured victims sometimes took four or five weeks to die of mustard gas exposure.

https://en.wikipedia.org/wiki/Chemical_weapons_in_World_War_I

Blood agents were used to kill.

A blood agent is a toxic chemical agent that affects the body by being absorbed into the blood.

Blood agents are fast-acting, potentially lethal poisons that typically manifest at room temperature as volatile colorless gases with a faint odor.

They are either cyanide- or arsenic-based.

https://en.wikipedia.org/wiki/Blood_agents

A hydrogen cyanide concentration of 300 mg/m3 in air will kill a human within 10–60 minutes.

A hydrogen cyanide concentration of 3500 ppm (about 3200 mg/m3) will kill a human in about 1 minute.

During the First World War, the United States and Italy used hydrogen cyanide against the Central Powers in 1918.

France had used it in combat already in 1916, but this proved to be ineffective due to physical conditions.

https://en.wikipedia.org/wiki/Cyanide_gas#As_a_poison_and_chemical_weapon

Blood agents are designed to interfere with the hemoglobin’s ability to carry oxygen.

They cause asphxiation.

The primary blood agent was Cyanide vapour.

Chemical Agents – Ray Smith
http://www.rjsmith.com/chemical-data.html

Combatants and civilians were exposed to a hideous cocktail of chemicals weapons.

benzyl bromide
German, tearing, first used 1915

bromacetone
Both sides, tearing/fatal in concentration, first used 1916

carbonyl chloride (phosgene)
Both sides, asphyxiant, fatal with delayed action, first used 1915

chlorine
Both sides, asphyxiant, fatal in concentration, first used in 1915, cylinder release only

chloromethyl chloroformate
Both sides, tearing, first used in 1915, artillery shell

chloropircin
Both sides, tearing, first used in 1916, artillery shell (green cross I)

cyanogen (cyanide) compounds
Allies/Austria, asphyxiant, fatal in concentration, first used in 1916, artillery shell

dichlormethylether
German, tearing, first used 1918, artillery shell

dibrommethylethylketone
German, tearing, fatal in concentration, first used in 1916

dichloroethylsulphide (mustard gas)
Both sides, blistering, artillery shell (yellow cross)

diphenylchloroarsine
German, asphyxiant, fatal in concentration, (dust – could not be filtered), first used in 1917, artillery shell (blue cross)

diphenylcyonoarsine
German, more powerful replacement for blue cross, first used in 1918

ethyldichloroarsine
German, less powerful replacement for blue cross, first used in 1918, artillery shell (yellow cross I, green cross III)

ethyl iodoacetate
British, tearing, first used in 1916

monobrommethylethylketone
German, more powerful replacement for bromacetone, first used 1916

trichloromethylchloroformate (diphosgene)
Both sides, asphyxiant, fatal with delayed action, first used 1916

xylyl bromide
German, tearing, first used 1915

Gas Warfare
http://www.worldwar1.com/arm006.htm

Using fire in a World War I battle predated actual flamethrower use, with a petrol spray being ignited by an incendiary bomb in the Argonne-Meuse sector in October 1914.

It was not until 1911 that the German army accepted their first real flamethrowing device, creating a specialist regiment of twelve companies equipped with Flammenwerferapparaten.

Despite this, the weapon went unused in World War I until February 26, 1915, when it was briefly used against the French outside Verdun.

On July 30, 1915, it was first used in a concerted action, against British trenches at Hooge, where the lines were just 4.5 m (4.9 yd) apart – even there, the casualties were caused mainly by soldiers being flushed into the open and being shot by more conventional means rather than from the fire itself.

https://en.wikipedia.org/wiki/World_War_I

A gas and flame attack

By 1918, one in every four artillery shells fired contained gas of one type or another.

Gas Warfare
http://www.worldwar1.com/arm006.htm

The grotesque realities of the First World War didn’t stop with the 1918 armistice for those exposed to mustard gas because it is “strongly mutagenic and carcinogenic”.

Mustard gas has extremely powerful vesicant effects on its victims.

In addition, it is strongly mutagenic and carcinogenic, due to its alkylating properties.

The mutagenic and carcinogenic effects of mustard agent mean that victims who recover from mustard gas burns have an increased risk of developing cancer in later life.

http://en.wikipedia.org/wiki/Mustard_gas#Physiological_effects

In genetics, a mutagen is a physical or chemical agent that changes the genetic material, usually DNA, of an organism and thus increases the frequency of mutations above the natural background level

http://en.wikipedia.org/wiki/Mutagen

A carcinogen is any substance, radionuclide, or radiation that is an agent directly involved in causing cancer. This may be due to the ability to damage the genome or to the disruption of cellular metabolic processes.

http://en.wikipedia.org/wiki/Carcinogen

The “strongly mutagenic” effects of mustard gas became apparent in 1918 when an “unusually deadly influenza” spread around the globe.

The 1918 flu pandemic (January 1918 – December 1920) was an unusually deadly influenza pandemic, the first of the two pandemics involving H1N1 influenza virus.

It infected 500 million people across the world, including remote Pacific islands and the Arctic, and killed 50 to 100 million of them – three to five percent of the world’s population – making it one of the deadliest natural disasters in human history.

The global mortality rate from the 1918/1919 pandemic is not known, but an estimated 10% to 20% of those who were infected died.

With about a third of the world population infected, this case-fatality ratio means 3% to 6% of the entire global population died.

Influenza may have killed as many as 25 million people in its first 25 weeks.

Investigative work by a British team led by virologist John Oxford of St Bartholomew’s Hospital and the Royal London Hospital, identified a major troop staging and hospital camp in Étaples, France as almost certainly being the center of the 1918 flu pandemic.

A significant precursor virus was harbored in birds, and mutated to pigs that were kept near the front.

https://en.wikipedia.org/wiki/1918_flu_pandemic

Étaples or Étaples-sur-Mer (Dutch: Stapel) is a commune in the Pas-de-Calais department in northern France. It is a fishing and leisure port on the Canche river.

The railway, with its network of connections across the north of France, became of strategic importance during World War I, and it was added to temporarily during the period it lasted.

Étaples became the principal depôt and transit camp for the British Expeditionary Force in France and also the point to which the wounded were transported.

The military camp had a reputation for harshness and the treatment received by the men there led to the Étaples Mutiny in 1917.

https://en.wikipedia.org/wiki/%C3%89taples

Etaples was a particularly notorious base camp for those on their way to the front.

The officers and non-commissioned officers (NCOs) in charge of the training, the “canaries”, also had a reputation of not having served at the front, which inevitably created a certain amount of tension and contempt.

Under atrocious conditions, both raw recruits and battle-weary veterans were subjected to intensive training in gas warfare and bayonet drill, and long sessions of marching at the double across the dunes.

After two weeks, many of the wounded would rather return to the front with unhealed wounds than remain at Étaples.

https://en.wikipedia.org/wiki/%C3%89taples_Mutiny

John Oxford, a professor of virology at St. Barts and the Royal London Hospital, has spent a good bit of time researching the Spanish Flu.

His work has led to evidence that traces the Spanish Flu to Northern France to a specific place known as Etaples.

Doctors during that time noted an unusual feature of the flu disease that spelled grave danger.

Those patients who developed a lavendergray hue over their face and ears, or heliotrope cyanosis (deprivation of oxygen to the lungs) as it is called, faced imminent death.

In the winter of 1916/1917, Etaples pathologists described a disease-like flu that ended in heliotrope cyanosis and death.

John Oxford believes the weight of evidence points toward Etaples as a hotbed for viral evolution that produced the 1918 strain of flu.

Etaples was a huge army camp of 100,000 soldiers, almost the size of a city.

The well and wounded moved through the camp daily.

There is evidence that soldiers bought live geese, chickens, and ducks from the local French markets.

Crucially, there existed ample opportunities for a flu virus to move from bird to soldier.

In addition, there were piggeries installed at Etaples.

These animals could also have been intermediaries, although recent genetic analysis of the 1918 virus shows it to be largely of avian origin.

Influenza Pandemic Challenged The Osteopathic Profession
Now and Then – Spring 2006 – National Center for Osteopathic History
https://www.atsu.edu/museum/pdfs/newsletter/museum_spring_06.pdf

The mutation of an “influenza virus” within a host of “young adults” exposed to mustard gas explains why the “unusually deadly” 1918 “influenza virus” disproportionately killed “healthy young adults” by “causing massive hemorrhages and edema in the lung”.

Most influenza outbreaks disproportionately kill juvenile, elderly, or already weakened patients; in contrast the 1918 pandemic predominantly killed previously healthy young adults.

This huge death toll was caused by an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms.

Symptoms in 1918 were so unusual that initially influenza was misdiagnosed as dengue, cholera, or typhoid.

One observer wrote, “One of the most striking of the complications was hemorrhage from mucous membranes, especially from the nose, stomach, and intestine. Bleeding from the ears and petechial hemorrhages in the skin also occurred.”

The majority of deaths were from bacterial pneumonia, a secondary infection caused by influenza, but the virus also killed people directly, causing massive hemorrhages and edema in the lung.

1918 flu pandemic - mortality age-distributions
The difference between the influenza mortality age-distributions of the 1918 epidemic and normal epidemics – deaths per 100,000 persons in each age group, United States, for the interpandemic years 1911–1917 (dashed line) and the pandemic year 1918 (solid line).

https://en.wikipedia.org/wiki/1918_flu_pandemic

The “carcinogenic” effects of mustard gas slowly became apparent after the end of the First World War as the average number of male deaths per year from lung cancer rose from 146 to 3,090 during the period 1919 to 1945 – a total of 35,312 male deaths from lung cancer during this period.

UK Men - Lung Cancer

Smoking and Health – A report of The Royal College of Physicians on smoking in relation to cancer of the lung and other diseases – 1962
http://www.rcplondon.ac.uk/sites/default/files/smoking-and-health-1962.pdf

Gas Casualties

US Death Rates for Heart Disease - 1900-1940

U.S. Department of Health & Human Services – National Institutes of Health
NHLBI Fact Book – Fiscal Year 2012 – Disease Statistics
http://www.nhlbi.nih.gov/about/documents/factbook/2012/chapter4

Unsurprisingly, The Royal College of Physicians discovered male survivors of the First World War [in the 55-59 and 60-64 age groups] were experiencing significantly enhanced levels of mortality in 1959 due to lung cancer and coronary heart disease.

UK 1959 Male Deaths

Smoking and Health – A report of The Royal College of Physicians on smoking in relation to cancer of the lung and other diseases – 1962
http://www.rcplondon.ac.uk/sites/default/files/smoking-and-health-1962.pdf

Therefore, it appears likely that the increased rates of male mortality from lung cancer and coronary heart disease between the First and Second World Wars can be associated with chemical weapons exposure [especially mustard gas] because:

1) “In the early 1900s, lung cancer was a rare disease causing around one death annually in every 100,000 people”.

2) Mortality from coronary heart disease was [also] significantly lower before 1924.

The importance of lung cancer as a cause of death has grown throughout most of the twentieth century.

In the early 1900s, lung cancer was a rare disease causing around one death annually in every 100,000 people.

By 1950, the lung cancer mortality rate had risen six-fold in men and three-fold in women, prompting the first epidemiological study that linked tobacco smoking and lung cancer in Great Britain.

Types of cancer – Lung cancer – Cancer Research UK
http://www.cancerresearchuk.org/cancer-info/print/%20?files=CRUKMIG_100019758,CRUKMIG_100019760,CRUKMIG_100019763,CRUKMIG_100019761,CRUKMIG_100019764,CRUKMIG_100019762,CRUKMIG_1000197598parentfile=CRUKMIG_100019764

WW1 Lung Cancer

UK Trends in Coronary Heart Disease

Secular and geographical trends in sex differences in coronary heart disease mortality
D A Lawlor, S Ebrahim and G Davey Smith – BMJ – 8 September 2001
http://www.bmj.com/content/323/7312/541

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