Wild birds, farmyard chickens and people are the victims of bird flu not the perpetrators ( Fowl Play in Bird Flu ) . Intensive poultry farming and globalised poultry trade are to blame for creating and spreading the virus ( What Can You Believe About Bird Flu? ) ; but what really causes bird flu outbreaks?
Dr. Sherri Tenpenny points the finger at environmental pollutants that disrupt the immune system, especially dioxins
Most people would agree that people become sick with a cold or with the flu when their immune system fails or is suppressed. People and chickens in Vietnam appear much more susceptible to the deadly effects of H5N1. Has anyone considered why their immune system fails to protect them? Has anyone investigated what is suppressing the immune system of migratory birds? I posed the question to Dr. Alex Thiermann, President of OIE (World Organization for Animal Health) at the Bird Flu Summit held in Washington DC in the United States, February 27-28, 2006. He answered: “No one is looking at this, in fact, no one has even thought about it.” Reporters and scientists raised the same point during the coffee break.
I believe that an in vestigation into the immunosuppressive effects of environmental chemicals, particularly dioxins, may shed light on the seemingly scattered and disconnected outbreaks of bird flu around globe. The association between dioxin and influenza may explain the high death rate in Indonesia.
Influenza viruses are divided into three distinct categories, type A, B, or C, and a large number of subtypes. The outer shell of influenza A viruses is covered with two types of protein antigens: haemagglutinin, (H or HA), and neuraminidase (N or NA). The differences between the H and the N antigens provide the basis for classifying and naming all the many s ubtypes of influenza type A viruses.
Influenza A subtypes are either “mildly pathogenic,” causing minimal or no disease, or “highly pathogenic,” causing serious illnesses and death, particularly among birds. All outbreaks of Highly Pathogenic Avian Influenza (HPAI) viruses since the 1980s have been due to antigen subtypes H5 and H7. The bird flu virus in the news is a highly pathogenic subtype H5N1. See Fowl Play in Bird Flu  for further details.
‘Dioxins' is a general term for a complex family of more than 400 chemicals. Dioxins are by-products of industrial processes that combine chlorine with organic substances such as wood, pulp or paper, in the presence of heat. Production facilities that manufacture pesticides, smelt copper and bleach paper all release dioxins. Dioxins can also enter the environment through the incineration of plastics, particularly those that burn municipal and medical waste.
Dioxins are highly persistent, and can take more than 15 years to degrade to half the original concentration. When released into the local water supplies such as ponds and rivers, they are immediately absorbed by aquatic life and accumulate in fish. If any dioxins remain, they are rapidly deposited into the sediment where they will persist virtually forever. From there, they have the potential to move up the food chain through grasses and frogs, becoming particularly toxic to humans and waterfowl.
Dioxins disrupt the immune system at exposure levels as low as 1.0 ppt (part per trillion). This is the equivalent of a single drop of liquid placed in the centre carriage of a ten- kilometre (6.2 miles) 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 (2,3,7,8-tetrachlorodibenzo-p-dioxin), the most toxic form of dioxin in the world.
Like other dioxins, TCDD suppresses the activity of cytotoxic lymphocytes (CTLs), specialized white blood cells that eliminate viruses and bacteria. There are two main types of “killer” white blood cells, natural killer cells (NK) and CD8+ cells. Both vigilantly circulate through the bloodstream, destroying intruders. NK and CD8+ cells do their work by releasing granules that cause infected cells to break apart, thereby preventing the virus from replicating. Without fully functioning CTLs, the host's defences can become overwhelmed by the replicating viruses or bacteria, which may end up killing the host.
In a healthy individual, only a few NK and CD8+ cells are in circulation, acting as sentinels. However, if the number of viral particles detected is on the rise, this calls for a rapid increase in the number of NK and CD8+ cells in circulation. The CTLs release proteins called cytokines, chemical messengers that recruit dozens of other specialized white blood cells that are necessary to eliminate the 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 recognized symptoms of “the flu.”
Influenza severity has been correlated with cytokine production. In other words, the more cytokines released in the presence of an influenza virus, 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 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.
Studies with laboratory mice have uncovered a link between dioxin exposure and the effect of influenza viruses on the immune system.
It turns out that NK and CD8+ cells are exquisitely sensitive to extremely small concentrations of TCDD. Mice exposed to 100-1 000 ppt of TCDD prior to the common influenza A viruses died significantly more often than control mice that were not pre-exposed to the dioxin . In fact, mice subjected to just 10 ppt of TCDD a week before they were exposed to influenza A viruses had double the mortality rate compared with the controls. The researchers noted that this was the “smallest toxic dose ever demonstrated” to inhibit the ability of the immune system to ward off the flu.
Fluid extracted directly from the lungs of deceased mice demonstrated that the increased mortality seen in TCDD-exposed mice was due to the intense inflammatory action of dioxin, and not due to viral infection alone . In other words, the combination of influenza viruses and dioxin caused so much inflammation in the lungs due to a massive cytokine storm that normal lung tissue was destroyed, thereby killing the mice.
Even though the mechanism of how dioxins disrupt the immune system is not completely understood, there is substantial evidence that exposure to TCDD significantly inhibits the host's ability to resist influenza. First, in the presence of dioxin, the “ramping-up” response to release more of the needed CD8+ and NK cells doesn't occur. Second, TCDD disrupts the immune response in the lung tissue, suppressing 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 inflammation, not only killing infected cells but also causing extreme damage to normal lung cells. The runaway hyper-production of IFN? and other inflammatory cytokines is called a ‘cytokine storm'. It is the complications from the cytokine storm that increases the mortality among TCDD-exposed mice .
Interestingly, researchers report that human deaths from H5N1is also caused by a cytokine st orm [6, 7] ( Where's the Bird Flu Pandemic? ). Recent studies suggest that H5N1 only replicates efficiently in cells that are deep within the tissues of the lungs . Perhaps further study will reveal that it is the combination of H5N1 and dioxin deep in the lung tissue that leads to demise of the small subset of patients who are critically ill in the presence of H5N1.
The volume of herbicides sprayed during the US conflict in Vietnam between 1961 and 1971 has been estimated at more than 19 million litres, with the highest concentrations deposited over the Mekong Delta in what is now southern Vietnam. Produced for the US army by several different chemical companies including T-H Agricultural & Nutrition, Dow Chemical, and Monsanto, the 1:1 mixture of two herbicides 2,4-D and 2,4,5-T was introduced in 1947 for the control of broad-leave weeds. This defoliant was later found contaminated with a third chemical, the deadly TCDD. Although a colourless liquid, the solutions came to be identified by coloured stripes painted on the transport barrels, and came to be known as Agent Orange. More than 30 years later, the persistent chemical has remained in the soil to contaminate the food of local residents and continuing to cause serious health problems.
In the absence of ongoing aerial spraying, the primary route for dioxin to enter the body is through food grown on toxic soils. Canadian researchers found that dioxin levels in soil samples throughout southern Vietnam to be as high as 898 ppt. The most extreme levels of contamination in the area of Bien Hung Lake were measured at greater than 1.1 million ppt .
In 2002, the levels of dioxin were measured in 16 different food samples collected from local markets around the Bien Hung Lake, which included the most commonly consumed meats: free-ranging and cooped chickens, free-ranging ducks, pork, beef, fish, and a toad. Because duck fat is a delicacy in Vietnam, fat that remained attached to the flesh was also tested. The preliminary results were startling. Three of the specimens contained dioxin levels that were so extraordinarily high they were sent to a second, independent laboratory for additional analysis. The second lab confirmed the disturbing results.
Dioxin and other chemical contaminants were detected in all 16 samples. The selection that stood out as “markedly elevated” was duck fat, with levels ranging between 276 and 331 ppt wet weight. When the total toxicity score (TEQ) for the food was tabulated, the score for duck fat ranged from 536 to 550 ppt . The chemicals found in free-ranging chickens ranged from 15 ppt in the meat to 74 ppt in chicken fat, reflecting the contamination in soil. To put these elevated levels in perspective, the usual dioxin level found in food is less than 0.1 ppt .
In May 2006, Indonesia reported a cluster of human bird flu cases that involved eight family members, seven of whom died. All but one person in the family appeared to have contracted the virus from another family member, making this the first reported incidence of H5N1 spreading from one person to another, and then another. Alarmed officials feared that the bird flu virus had acquired characteristics that would soon allow easy passage from human-to-human.
The members of the deceased family lived in a small village in Karo district located in the Indonesian province of North Sumatra. The Karo highland borders on Lake Toba, the world's largest volcanic lake, and the largest lake in Southeast Asia. Lake Toba has been deteriorating since 1998, defen c eless against the onslaught of the province's pulp and paper mills.
The biggest polluter during the past decade was Indorayon, a paper, pulp and rayon manufacturer owned by multinational companies and funded by the World Bank. The mill was forced into temporary closure in 1998 by a grassroots revolt over the company's destruction of the local environment. But in 2003, yielding to pressures of its investors and international bankers, the government allowed the pulp portion of Indorayon to reopen under the name of PT Toba Pulp Lestari. The company's pulp mills are blamed for far-reaching environmental degradation due to the continued release of chlorine and other chlorine compounds such as chlorine oxide, organochlorines, and dioxins, including TCDD.
There has been an explosion in the number of pulp and paper mills built in Southeast Asia and Indonesia over the past 15 years, despite loud protests from local communities. Pulp mills are one of the most polluting processes in the world. Much of that pollution results from the three million tonnes of chlorine used annually to bleach wood paper white. Chlorine bleaching is a major source of dioxin, which is routinely discharged into rivers and streams with wastewater.
In 2005, there were seven pulp mills, 65 paper mills, and 10 pulp and paper mills in Indonesia. According to the WHO  , 42 of the 54 cases of human bird flu in Indonesia have died. Could there be a connection between the arrival of HPIA influenza and the continuing dioxin toxicity in the native population?
Like the Vietnamese, Indonesians too, have an increased exposure to dioxin through food. Backyard and free-range hens makes eggs a useful indicator of overall local environmental contamination through diet.
In 2005, the International POPs Elimination Network (IPEN) sponsored a study to test eggs of free-range chickens from 20 different locations in 17 countries, including eggs from the Philippines .
Dioxin in eggs from the Philippines measured 9.68 ppt, more than 10 times the 2002 European Union (EU) safe limit for dioxins in eggs, which is 0.75 ppt. In fact, 70 percent of the samples from all 17 countries exceeded this limit. Because all humans have some level of dioxin in their bodies, more research is needed to identify the critical dioxin concentration that triggers an explosive cytokine storm when combined with influenza. This “significant minimum level” of dioxin must be established to know who is truly at risk.
Meanwhile, hundreds, perhaps thousands, of individuals with H5N1 influenza have not been sick enough to require medical care, as confirmed by Dick Thompson, spokesperson for the WHO in March, 2005 . However, as of 26 July 2006, there have been 93 reported cases of bird flu in Vietnam with 42 deaths , a high death rate, though not quite as high as Indonesia.
An investigation should be undertaken to determine if those who died had significantly higher concentrations of dioxin in their body than those who have been exposed to H5N1 and remained well.
Recognizing the serious health problems that can occur in the presence of dioxin and other toxic chemicals, the first Stockholm Convention on Persistent Organic Pollutants (POPs), was held in Argentina in May 2001. POPs are chemicals highly toxic to human and wildlife. They persist in the environment for long periods, becoming widely distributed geographically and accumulating in the fatty tissue of living organisms. The international treaty, signed by 98 countries, went into effect in May 2004. Governments have agreed to take measures to eliminate or reduce the release of the 12 most toxic chemicals, including dioxin, dubbed the “Dirty Dozen.” The removal of toxic chemicals from the environment could be the most significant prevention of a global pandemic. Unfortunately, though unsurprisingly, the treaty to protect the environment was not signed by the Bush Administration.
The outbreaks of an aggressive virus among domestic chickens and migratory birds are a wake-up call to the world's countries and international organizations to get serious about improving the environment. The birds are sending an urgent message of impending disaster, similar to the message dead canaries sent to miners deep in the coalmines.
The most serious concern over bird flu is its potential, in combination with dioxin, to cause lethal inflammation of the lungs. Investigations are urgently needed to evaluate the role of dioxin in aggravating influenza.
Part of this article is an excerpt from Dr. Tenpenny's new book, FOWL! Bird Flu: It's Not What You Think , released April 2006. For daily updates on the bird flu and a bi-monthly e-Newsletter go to www.BirdFluHype.com
Dr. Sherri Tenpenny is one of the most knowledgeable and outspoken physicians in the US regarding the impact of vaccines on health. She heads an education company, New Medical Media-Press, which promotes freedom of choice in healthcare, including the freedom to refuse vaccination. Dr. Tenpenny is also a regular columnist for www.NewsWithViews.com and www.RedFlagsDaily.com. She can be contacted through www.Dr.Tenpenny.com or firstname.lastname@example.org
Article first published 19/09/06
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