A virus is not a living organism, but its ability to make copies of itself that can be spread to other hosts is what gives the impression that it is alive. Influenza viruses are divided into three distinct categories — types A, B, or C — and a large number of subtypes based on protein antigens on their outer coatings. One protein is called hemagglutinin, (H) or (HA), the other is called neuraminidase, identified as (N) or (NA). The differences between the H and the N antigens provide the basis for classifying and naming all the many subtypes of influenza type A viruses.
Influenza A subtypes are further delineated as either ‘mildly pathogenic’, meaning they cause minimal or no disease, or ‘highly pathogenic’, meaning their presence has been associated with widespread death among birds [emphasis added] and occasionally among people.
Viral identification: A big concern for birds
But just because a virus is present doesn’t mean that it is causing a problem. In fact, influenza A viruses can be completely benign. Most are silent passengers in the intestinal tracts of waterfowl. However, when thousands of ducks and geese congregate in available lakes and ponds during their migration, tens of billions of influenza A particles and as many as 130 viral subtypes have been identified in the waters.
It is presumed that once a highly pathogenic influenza virus is found in a flock, the virus will be transmitted indefinitely through the stool of the birds. Complete destruction of all the birds is considered to be the only option for eradicating the outbreak, even if the birds show no sign of the infection. That practice, called culling, continues today with the large-scale elimination of flocks in the presence of a killer virus.
Records show that since 1959 there have been 21 reported outbreaks of highly pathogenic avian influenza worldwide. The majority have occurred in Europe, with a few emerging in Mexico, Canada and even the US. Of the 21 incidents, five resulted in significant losses to regional economies.
Recently, 36 countries have reported outbreaks in birds and 10 countries have reported human deaths from the virus. The news continually buzzes with reports of outbreaks of the flu. With each incident, scientists and global organisations wring their hands and wonder if this is ‘the one’ that will start wreaking havoc on every continent.
Other pandemics: Why the hysteria?
The most highly discussed outbreak is the global influenza pandemic of 1918. It has been reported that more than 20 million people died due to the virus. Called the Spanish flu, it gained its name from the press in politically neutral Spain, where some of the earliest printed reports of the flu’s impact were not censored during World War I.
A unique feature of the 1918 influenza pandemic was the demographics of the people who died. Normally, flu is only a threat to the very old, the very young and people with compromised immune systems. But in 1918, men between the ages of 20 and 40 were the most common victims; in fact, men were 35% more likely than women to die from flu. This statistic, left unexplained in the history books, exposes a clue to be discussed later in this article.
Two other global pandemics have occurred during the 20th century. In 1957, a new influenza virus named H2N2 caused many to become sick worldwide. Ultimately the virus was blamed for nearly one million deaths worldwide. Like a typical flu, the highest mortality rates occurred among the elderly.
A third global pandemic, in 1968, was distinctly different from the previous two. The clinical symptoms were mild, the mortality was low and the disease seemed to spread slowly rather than explosively. In some countries, absentee rates and increased death rates were slight or non-existent. Canada, for example, experienced practically no deaths from the flu. In the UK, deaths from influenza-like illness and pneumonia were actually lower than in the year preceding the new outbreak. A similar picture was seen in most of Europe, where flu symptoms were mild and excessive deaths were negligible.
Scientists have proclaimed that the world is ‘overdue’ for another pandemic. Strident experts have made foreboding predictions, stating that if an influenza pandemic struck today, ‘borders would close, the global economy would shut down, international vaccine supplies and health-care systems would be overwhelmed, and panic would reign’.
But could the ‘next pandemic’, if and when it occurred, be less than catastrophic? Could it be similar to the one in 1957 or 1968? No one dropped dead in the streets during those influenza seasons. There were no detention centres set up at airports and no plans for mass vaccination. Why all this hysteria?
Exaggerated death rates
The WHO (World Health Organisation) reports that urgency is necessary because the H5N1 virus seems to be highly aggressive, with the media reporting a nearly 50% death rate. At one point, the media had pushed the death statistic to 76%.
The truth is, the real death rate is completely unknown. Only the deaths of very ill persons who died in hospitals and tested positive for the H5N1 virus have been included in death statistics. Hundreds, perhaps thousands, of individuals exposed to the H5N1 influenza have not been sick enough to require medical care, as has been confirmed by Dick Thompson, spokesperson for the WHO. In March, 2005, Thompson stated, ‘The obvious assumption is that others are infected and have either not got sick, or have not gotten sick enough to seek treatment at a hospital. Factoring those patients into the death rate [makes it] impossible to determine, because the denominator is unknown.’
Dr. John Allen Paulos, Professor of Mathematics at Temple University, concurred with Thompson’s observation. Paulos asserted that because the death rate is based only on cases of severely ill persons, it is an ‘almost textbook case’ of sample bias. He explained that asymptomatic people and those who have recovered uneventfully aren’t part of the mortality rate calculations. As a consequence, the numbers are skewed substantially upward. In our fear-based, drug-driven society, emphasis is placed on the death rate, not on the survival rate. That small change alters the entire structure of the discussion.
Overlooked connection: Dioxin and the flu?
Dioxin is a general term that describes a complex family of more than 400 chemicals. An unintentional waste product, dioxin is formed during industrial processes which combine chlorine with an organic substance, such as wood, pulp or paper, in the presence of heat. Production facilities that manufacture pesticides, smelt copper and bleach paper all release dioxins as by-products. Additionally, dioxin can enter the environment through the incineration of plastics, particularly in burning municipal and medical waste.
A highly persistent chemical, dioxin can take more than 15 years to degrade to half its original concentration. If released into the local water supplies, it can accumulate in fish and other aquatic life, or be deposited in muddy sediment. Once in the soil, it will remain there virtually forever unless it moves up the food chain through grasses and frogs, becoming particularly toxic to humans and waterfowl.
The effects of dioxin on the immune system
Dioxin has been shown to disrupt the immune system at exposures as low as 1.0 ppt. This is the equivalent of a single drop of liquid placed in the centre car of a 10-kilometre long cargo train. Because chemicals are usually a mixture of toxic and non-toxic compounds, a score for each chemical is developed called its Toxic Equivalency (TEQ). The TEQ of any chemical is established by comparing it to TCDD, the most toxic form of dioxin in the world.
TCDD and other dioxins suppress the activity of white blood cells called cytotoxic lymphocytes (CTLs). These are specialised white blood cells that eliminate viruses and bacteria. They do their work by releasing granules that cause infected cells to break apart; hence the virus ‘dies’ because it cannot replicate. It is believed that without fully functioning CTLs, a host’s defences can become overwhelmed by the replicating germs, sometimes leading to death.
Once activated, the CTLs release proteins called cytokines, chemical proteins that recruit dozens of other specialised white blood cells necessary to eliminate a virus. Cytokines are responsible for causing acute reactions in the body including pain, fever, and inflammation. It is this ‘ramping-up’ of the immune system that produces the readily recognised symptoms of the flu. ‘Influenza severity’ has been correlated with cytokine production. In other words, the more cytokines that are released the more serious the infection and the more potentially deadly the outcome.
There are many different cytokines involved in this complex process, but the two that are particularly important are IL-12 (interleukin 12) and IFN (interferon-gamma). Cytokine IL-12 plays the key role in coordinating the efforts of the entire immune system’s campaign against a virus, while IFN facilitates the destruction of cells that contain replicating viruses.
Even though the mechanism for how dioxins disrupt the immune system is not completely understood, there is substantial evidence in experimental mice that exposure to TCDD significantly inhibits the host’s ability to resist influenza. In the presence of dioxin, the ‘ramping-up’ response to release more of the needed CTLS doesn’t occur. Additionally, TCDD suppresses the production of cytokine IL-12. Without IL-12, other white blood cells are not recruited to aid in the elimination of the virus. At the same time, TCDD increases the levels of IFN by more than 10-fold, leading to massive damage to normal lung cells. The runaway hyper-production of IFN and other inflammatory cytokines is called a cytokine storm. It is the complexities of the cytokine storm that increases the mortality among TCDD-exposed mice. Whether this mechanism applies directly to humans deserves careful consideration. Of note, researchers have demonstrated that human deaths from H5N1 are associated with a cytokine storm.
Recent studies suggest that H5N1 only replicates efficiently in cells that are deep within the tissues of the lungs. Further studies are needed to determine if it was the combination of H5N1 and dioxin deep in the lung tissue that led to the demise of a small subset of patients living in Vietnam.
Dioxin in Vietnam
The volume of herbicides sprayed during the US conflict in Vietnam between 1961 and 1971 has been estimated to be more than 19 million litres, with the highest concentrations deposited over the Mekong Delta in what is now southern Vietnam. The defoliant was later found to be contaminated with TCDD, commonly known as Agent Orange. More than 30 years later, the persistent chemical remains in the soil and food of local residents, continuing to cause serious health problems.
Absent ongoing aerial spraying, dioxin’s primary route for entering the body is through food grown on toxic soils. Canadian researchers found that dioxin levels in soil samples throughout different regions of southern Vietnam to be as high as 898 ppt. The most extreme levels of contamination — in the area of Bien Hung Lake — were measured to be greater than 1.1 million ppt.
In 2002, levels of dioxin were measured in 16 different food samples collected from local markets around the Bien Hung Lake. The preliminary, startling results were confirmed by a second, independent laboratory. The selections that stood out as ‘markedly elevated’ were the fat of ducks, with levels ranging between 276 ppt and 331 ppt wet weight. When the total toxicity score (TEQ) for the food was tabulated, the score for duck fat ranged from 536 ppt to 550 ppt. To put these elevated levels in perspective, the usual dioxin level found in food is less than 0.1 ppt.
Similar to the people in Vietnam, Indonesians have an increased exposure to dioxin through environmental exposures. An explosive number of pulp and paper mills have been built in Southeast Asia and Indonesia over the last 15 years over the loud protest of local communities. Pulp mills are among the most polluting processes in the world. Chlorine, used to bleach paper white, is a major source of dioxin.
Coming full circle: 1918 pandemic and chemical warfare
The cornerstone argument for planning for the next pandemic is the possibility of the supposed similarity between the H5N1 virus and the virus that caused the 1918 pandemic. However, little attention has been given to the similar correlation between the global contamination with dioxin and the massive use of chemical warfare from 1915 to 1917, just prior to the outbreak of the Great Influenza Pandemic.
The Leavenworth Papers, published by the US Army in 1984, is a collection of monographs about military history. Leavenworth Paper No. 10 chronicles ‘the introduction of chemical agents in World War I, the US Army’s tentative preparations for gas warfare’.
During World War I, chemists investigated more than 3,000 chemical substances for use as weapons. The most widely used chemical, mustard gas, was known to be toxic in concentrations undetected by smell. The symptoms of severe burning and blistering didn’t show up until many hours later. Mustard gas was used from 1915 until the end of the war.
On April 6, 1917, when the US declared war on Germany, its military had no practical knowledge concerning chemical warfare equipment. By the summer of 1917, US troops began to arrive at French ports with only minimal protective preparations. It wasn’t until January 1918 that the US military established gas training camps.
The training was brutal. For example, a minimum of three surprise gas attacks were included as part of the drills. To test alertness and correct such ‘carelessness as leaving their masks out of reach’, chemical attacks were often scheduled while the troops were asleep. During night marches, men were subjected to gas attacks to ‘teach them how to overcome confusion’.
Widespread susceptibility
The troops experienced tight travel quarters which increased their exposure. During the day, three men were crammed into every double seat on the trains. In the sleeping cars, one man slept in the upper bunk and two in the lower. Many were ill en route. The chemical-laden military troops carried an influenza virus that may have gotten started by an interaction with toxicities in their lungs.
The Spanish flu epidemic was not severe worldwide. In fact, it seemed to crest in England in June 1918; China and Japan had versions of the Spanish flu that was referred to as the ‘three-day fever’ or sometimes, ‘wrestler’s fever’. This suggests that — similar to H5N1 outbreaks — mild cases of the Spanish flu occurred and fatal cases had a contributing factor.
For the three years prior to the first outbreak in the US at Fort Riley, Kansas, millions of kilos of toxic liquids and poisonous gases had been in the air over the military theatre in Europe. The suspended chemicals could have traversed the globe, contaminating civilians in diverse places, increasing their risk to a fatal outcome from influenza.
Outrageous hypothesis?
The idea that chemical contamination was the backdrop for increased susceptibility to the flu is not as unbelievable as it may first sound. Pollen has been discovered deep in the ice of Antarctica. Dust from China has been delivered to the US through the air after massive wind storms. The smoke and particulates from the massive timber fires in Indonesia were measured in the air on the other side of the globe. Satellite instruments showed that sulfur dioxide released during the eruption of Mt. Pinatubo, Philippines, in 1991 circumvented the globe in only three weeks, and then slowly dispersed to cover much of the Earth in the following two years.
The idea of mustard gas and the 30-odd other chemicals released into the environment during three years of daily explosions finding their way around the globe and causing health problems thousands of miles from their course is not an absurdity. By December 1918, approximately 18 months after the epidemic began, the outbreaks stopped and history reported that the Spanish flu ‘mysteriously disappeared’. The massive use of chemicals during WWI could have been responsible for the major spike in susceptibility to influenza worldwide.
A key symptom in many sufferers was a blue discoloration of the face caused by rapid accumulation of fluid in the lungs. For patients who developed the grotesque, lavender-gray hue over their face and ears, death was imminent. Historical records reported that people without symptoms could be ‘struck suddenly’ and rendered ‘too feeble to walk’ within hours, dying as soon as the next day. Does that sound like a case of the flu?
What can you do?
On a personal level, eliminate as much toxicity as you possibly can. Clean up your diet by minimising — or better, eliminating — refined white sugar, white flour, food additives, and other toxic components that you eat. The highest concentrations of dioxin come from dairy products and animal meat. Consider a vegan lifestyle, or at the very least, be sure to eat organic meat, eggs and cheese. Get a good home water filtration system. There are many well-written books available on these topics. Pick one and get started; which one you choose is much less important than that you simply begin.
Select a form of healing for yourself and your family that is outside the Western paradigm of using chemicals called ‘drugs’ for something called ‘medicine’. Although occasionally necessary for critical health problems, prescription drugs given for chronic conditions are nothing more than suppressive medicine. They eliminate a symptom, but do nothing to correct the underlying cause of the problem. Health is defined as being well in the absence of pharmaceuticals; health is not defined as the absence of symptoms in the presence of drugs.
Putting these suggestions into play will keep you and your family healthy, regardless of what type of influenza virus may be in circulation.
Some Sources of Dioxin in Australia
- Bushfires
- Burning of crops, sugarcane
- Motor vehicle emissions
- Pesticides, including popular ones like Round-Up
- Fish, oysters, mussels, especially those collected from urban / industrial areas
- All food products are likely to contain dioxins. Higher levels are found in those containing animal fats (dairy products, meat and meat products, eggs) and peanut butter. When compared with New Zealand, concentrations are higher in a range of foods.
With thanks to a National Toxic Network Review of the summary of the findings of studies conducted for rgw Department of the Environment and Heritage (DEH) for the National Dioxins Program. “Dioxins in Australia: a summary conducted from 2001 to 2004”
- OIE. http://www.oie.int/downld/AVIAN%20INFLUENZA/A_AI-Asia.htm
- Cumulative Number of Confirmed Human Cases of Avian Influenza A/(H5N1) Reported to WHO as of July 26, 2006. http://www.who.int
- Noymer, Andrew and Garenne, Michel. ‘The 1918 Influenza Epidemic’s Effects on Sex Differentials in Mortality in the United States’, Population and Development Review. 26(3):565–581. September 2000.
- Osterholm, Michael. ‘Preparing for the Next Pandemic’, Foreign Affairs, July/August 2005.
- ‘Airports would be a battleground for bird flu fight’, Kathleen Doheny. LATimes.com May 7, 2006.
- ‘Bird-flu vaccine may be available in mass quantities’, APPress. USA Today. July 26, 2006. http://www.usatoday.com/news/health/2006-07-26-birdflu-vaccine_x.htm
- ‘Bird flu “has pandemic potential”’, by Michelle Roberts. BBC News. February 20, 2005.
- Roos, Robert. ‘Relatives of avian flu patients have asymptomatic cases’, CIDRAP News, 9 March 2005.
- Paulos, John Allen. ‘Who’s Counting: Flu Deaths, Iraqi Dead Numbers Skewed’, ABC News.
- Quynh, Hoang Trong, MD, et al. ‘Long-term consequences of Vietnam War’, Nordic News Network, Report to the Environmental Conference on Cambodia, Laos and Vietnam. (http://www.nnn.se/vietnam/health.pdf.)
- Warren, T. K., Mitchell, K. A., Lawrence, B. P. ‘Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Suppresses the Humoral and Cell-Mediated Immune Responses to Influenza A Virus without Affecting Cytolytic Activity in the Lung’, Toxicological Sciences 56 (2000): 114–123.
- Chan, M. C., et al. ‘Proinflammatory cytokine responses induced by influenza A(H5N1) viruses in primary human alveolar and bronchial epithelial cells’, Respiratory Research 6 (2005): 135. PMID 16283933.
- ‘Bird flu too deep in human lungs to spread easily’, by Joyce Howard Price. The Washington Times. March 23, 2006.
- Schecter, A., Quynh, H. T., Pavuk, M., Papke, O., Malisch, R., Constable, J. D. “Food as a source of dioxin exposure in the residents of Bien Hoa City, Vietnam,” Journal of Occupational and Environmental Medicine 45 (2003): 781–788. PMID: 12915779.
- “Chemicals,” D Ekonomik Kurulu Foreign Economic Relations Board, June 2002.
- Sparks, S. & Self. S., et al. “Super-eruptions: global effects and future threats,” The Geological Society of London, June 2005.
Published in byronchild/Kindred, issue 19, September 06