Saturday, January 12, 2008

The polio vaccine, AIDS, and their US-made viruses

By Jerry Mazza

Jan 11, 2008,

When I was a teenager growing up in Brooklyn, my parents warned me every summer to stay away from public pools or taking any chances running under opened fire hydrants to cools us from the brick-and-tar baking heat. Their fear was the epidemic of polio that haunted the US -- 52,000 cases in 1952 alone. My parents worried that polio “germs” could be carried in the highly used and abused public waters.

Yet in April 1955, in my 17th year, lo and behold Dr. Jonas Salk, a funny looking guy from Pittsburgh, announced from the University of Michigan that he had developed a polio vaccine for distribution. Eureka. Thousands of families like mine flooded to the local doctors, clinics, and hospitals. It seemed all those rosaries my friends’ mothers and mine gave up to the Holy Mother paid off. But did they?

As William Carlsen reports in his SFGATE article “Rogue virus in the vaccine:” Salk’s vaccine was produced by actually growing live polio virus on kidney tissue from the Asian rhesus monkey. The virus was then killed with formaldehyde. Thus, when the vaccine was injected in humans, the dead virus generated antibodies that could fend off live polio. What a simple, beautiful idea. Or so it seemed.

What the millions of people who were injected didn’t know, nor would they until 1959, when Bernice Eddy, looking in her microscope at the National Institutes of Health (NIH), found that monkey kidney cells, the very same kind used to make the vaccine, were dying with no known cause. So she experimented.

She prepared extracts from kidneys from eight to 10 rhesus monkeys. She then injected tiny amounts beneath the skin of 23 newborn hamsters. In nine months, “large, malignant, subcutaneous tumors” showed up on 20 of the animals -- and the world shook. Or did it?

Eddy tried to spread the word

Horrified that a monkey virus could be contaminating the famous polio vaccine, on July 6, 1960, Eddy shared her findings with Dr. Joseph Smadel, chief of NIH’s biologics division, who summarily dismissed the tumors as harmless “lumps.” Meanwhile at a Pennsylvania Merck lab, Dr. Maurice Hilleman and Dr. Ben Sweet isolated the virus. They named it Simian Virus 40 or SV40 for being the 40th virus found in rhesus kidney tissue. So much for miracle drugs.

Nevertheless, by then we seemed to be winning the polio war. Sixty percent of the population, some 98 million Americans, had gotten at least one shot of the Salk vaccine and the number of cases was diving downwards.

Concurrently, an oral polio vaccine developed by virologist Albert Sabin was in its final trials in Russia and Eastern Europe. Tens of millions of people had been given it, and it was ready to be licensed in the US. Its big difference was that unlike the Salk vaccine, Sabin’s version contained a live but weakened form of polio virus that “promised” lifelong immunity.

Fortunately, US Public Health Service (PHS) officials had conducted tests and found SV40 in both the Sabin and Salk vaccines. The US PHS estimated that a third of the Salk vaccine was tainted, and that SV40 was causing cancer in lab animals. Picture the corporate and government panic at this news, which was less than mildly shared with the public.

Early in 1961, PHS officials met quietly with the agency’s top vaccine advisers. Strangely, the agency found no evidence the virus had been harmful to humans. Yet in March, officials ordered manufacturers to eliminate SV40 from all future vaccine. New plans to neutralize the tainted polio virus seed stock were adopted and SV40-free African green monkeys were used to make the bulk vaccine instead of rhesus monkeys. More monkey business.

Amazingly, officials didn’t recall the contaminated Salk vaccine, that is, more than a year’s supply. It stayed in the hands of the country’s doctors. And they didn’t notify the public of the contamination and SV40’s effect on new born hamsters. Their strange reasoning was that any negative information could start a panic and put the vaccination campaign in danger. What about the millions of people who took the vaccines? Weren’t they being put in danger?

The first disclosure

The Salk vaccine contamination story crept on cat’s feet on July 26, 1961, onto page 33 of the New York Times. It reported Merck and other manufacturers had halted production until they could get “monkey virus” out of the vaccine. Asked for comments, the US PHS said there was no evidence the virus was dangerous. Except, of course, to the 20 baby hamsters it blew away.

In 1962, a Harvard epidemiologist, Dr. Joseph Fraumeni, joined the National Cancer Institute and was assigned to find out if there was any cancer increase among those injected with the Salk vaccine. With two Colleagues, Fraumeni tested vaccine samples from May and June of 1955, the first months of the national immunization campaign. Then they ranked the samples according to “no,” “low” or “high” amounts of SV40 they contained.

It was the only time US health officials would measure such level in the 55-62 vaccine. Stored samples were later dumped. Fraumeni pinpointed states where contaminated vaccines were distributed during the key months. California received a vaccine with a low level of the virus. The study also looked at cancer death rates for 6-to-8-year olds vaccinated during that narrow time frame and tracked the group for four years.

Findings, published in the Journal of the American Medical Association, showed no significant difference in cancer deaths in states with high or low levels of SV40 in the vaccine when compared with cancer deaths in states with no SV40 in the vaccine.

Yet some 14 years later, after “isolated reports” linking the virus to human cancers, Fraumeni deemed another group should be looked at that had received contaminated vaccine. This group was the subject of trials conducted in the early '60s at Cleveland Metropolitan general Hospital. To see the effect of different amounts of SV40 in vaccines, hospital researchers inoculated newborns from mostly lower-income black families. Noticeably, doses ranged up to more than 100 times the dose recommended for adults, not a nice thing to do to those black kids.

The experiments spanned three years, involving 1,073 infants. The majority were given Sabin oral, which later was shown to contain SV40. A 1982 report in the New England Journal of Medicine hedged the study’s limitations: that a majority of the kids had not responded; but SV40-realted cancers could take longer than 17 to 19 years to appear; and SV40 appeared less likely to infect humans through the oral vaccine.

Despite these critical caveats, the whitewash called the findings “reassuring and consistent with the prevailing view that SV40 is not carcinogenic in human beings.” Then they called a halt to the studies, claiming “mountains of complexities and obstacles in tracing this particular group and the negative results to date.” This is not to mention their destructive racism, which would remain part of the government’s position for years.

BOOM, 1988

In Boston, Dr. Robert Garcea and assistant, Dr. John Bergsagel, used a new tool, a polymerase chain reaction, PCR, to look for a pair of common human viruses in kids’ brain tumors. A different DNA footprint popped up in more than half the tumors. It finally hit them that they were seeing SV40.

The PCR was capable of amplifying the smallest fragments of DNA, making detections far more credible than earlier more primitive tests for SV40-like proteins in human tumors. The findings were disturbing, indicating that the children were too young to have received the contaminated vaccine, yet somehow the virus infected them and embedded itself in their tumors.

In that same year, Dr. Michele Carbone found a milky, rind-like tumor in a laboratory at the National Insitutes of Health in Bethesda, Md. Carbone performed a variety of experiments showing that sixty percent of hamsters, after having SV40 injected into their hearts, contracted the fatal cancer, mesothelioma. Something awful was happening.

Carbone finally used PCR to test 48 human mesotheliomas stored at the NIH. He was stunned when 28 of them contained SV40. PCR went on to unleash a wave of SV40 discoveries. By the end of 1996, dozens of scientists reported SV40 in a variety of bone cancers and a wide range of brain cancers, a rise of 30 percent over the previous 20 years.

At the National Cancer Institute in Bethesda, officials were growing increasingly concerned about the SV40 discoveries. And these findings were of particular interest to Fraumeni, who had been promoted to director of the NCI (National Cancer Institute)’s Division on Cancer Epidemiology and Genetics. His early studies concluding that SV40 posed little or no health risk were now under challenge . . .

More about the NCI, National Cancer Institute

The deadly truth is that the National Cancer Institute (NCI-Frederick) and 37 mission partners are located at Fort Detrick, about 20 minutes from Bethesda, Maryland. The Fort is home to the United States Army Medical Research and Materiel Command (ISAMRMC). The primary missions include biomedical research and development. This is where the AIDS virus was developed, but not from monkeys.

In my 2005 Online Journal article, The AIDS virus: Made in the USA?, I reported that “Dr. Robert Strecker indicated that the AIDS virus was in fact developed by the National Cancer Institute, in cooperation with the World Health Organization (WHO), in a laboratory at Ft. Detrick in Maryland. From 1970–74, this laboratory facility was part of the U.S. Army’s germ warfare unit, known as the Army Infectious Disease Unit, or Special Operations Division, also referred to as the Army’s Chemical and Biological Warfare Laboratory. Post 1974, the facility was renamed the National Cancer Institute (NCI). According to researcher William Cooper (former Navy Intelligence officer), noted in Larry Jamison’s article Is The AIDS Virus Man Made?, this work was supervised by the CIA under a project called MK-NAOMI. [To get to this site click link, then “All News,” then “Next page”].

“Dr. Strecker has also traced some of the research and researchers at Ft. Detrick/NCI to a group of Japanese scientists captured at WW II’s end and given amnesty in exchange for information on racial and ethnic bio-weaponry, their research dating back to 1930. What’s more, expatriated Russian scientists were brought in to help as well.

“Dr. Strecker, one of the original and foremost authorities on the AIDS virus, found that the virus creation was conducted under the leadership of Dr. Robert Gallo, who later claimed to discover the virus. Dr. Gallo and his team created the AIDS virus by combining the bovine (cattle) leukemia virus and visna (sheep) virus, and injecting them into human tissue cultures.

“They discovered, as Strecker did, that bovine leukemia virus is lethal to cattle, but not to humans. And the visna virus is deadly to sheep, but not to man. However, when combined, they produce a retro-virus that can change the genetic composition of the cells they enter. In fact, as Larry Jamison points out, early field tests on prison convicts led to sickness then death, which inspired Gallo and friends to bigger and more terrible things, including injecting brothers and sisters with the tainted vaccine to see who died first. This was done to study HLA (human leukocyte antigen processing), to see how related people reacted. Frighteningly, whole families got sick at once! And there was worse to come.

“The AIDS retro-virus works, as Dr. Strecker states, by causing the destruction of the immune system, fundamentally the body's white blood or T-cells essential to the effectiveness of the immune system particularly against opportunistic infections diseases. The B-cells deal with more benign, bacterial infections. AZT, the drug which is a kind of junk food that starves the AIDS virus, often kills the patient as well. It provides dubious consolation. . . ."

As an updating underscore, I quote from Dr. Alan Cantwell’s 11/4/04 article at, The Man-Made Origin Of AIDS -- Important Notes . . . in which he unqualifiedly states: “VISNA VIRUS WAS MOVED INTO PORCINE, BOVINE, AND HUMAN CELLS CAUSING PRODUCTIVE INFECTION PRIOR TO ANY ADVENT OF HIV ANYWHERE.

“ . . . The capital-lettered statement above is uncontestable. It is a fact.”

The polio virus was monkey-derived, but AIDS was not . . .

I repeat the above so that the idea of a monkey biting an African’s butt or of Simian Virus 40 being the culprit for HIV-AIDS is not the case. There is a desire to surrender to this idea because it seems convenient. African populations live in jungle areas and are largely black and may be in contact with monkeys. Unfortunately, to a lesser degree AIDS has struck white communities in America as well, either white and/or gay in addition to black and/or Latino, i.e. minorities, ergo expendable to the elites. The question is, was the CIA/NCI behind the polio virus as well? It’s timeline flows into and parallels the AIDS virus.

Again, the AIDS virus was weaponized at Fort Detrick. As Cantwell reports, “I believe, based on now some 16 years of investigation of this whole thing that HIV is a strategic biological weapon designed to kill billions of people in a slow-unfolding relentless holocaust which was released in two different vaccination programs: a) the smallpox vaccination program in Africa commencing in the late 1960s, b) the hepatitis-B vaccination program in the United States in the mid-to-late 1970s.

“Moreover, so it is perfectly clear, this contamination was no accident. It was done on purpose with the goal of ‘thinning the herd’ in a Nazi-like mindset that has covertly governed population control politics since the 1870s. These same politics had pervaded the WHO [World Health Organization] and most of western medical experimental science throughout the 20th century. And, to be very pointed: the same political ideology is still there. Non-whites [and gay whites] are detrimental to the gene pool's evolution so says the political philosophy. To see a bit of this in history, go here:


“This belief system is pervasive in the molecular sciences as it is at the heart of eugenics, cloning, evolution, and heritability.”

Yet, little did my Brooklyn family, friends, myself and America know what darker forces were lurking about us in the 50s and 60s, especially in the post WW-ll surge in our economy, military strength, intelligence community and the confidence that America was the best, safest, the most noble place to grow up in and ultimately defend.

In fact, was the polio vaccine weaponized from the get-go with SV40 the way the World Health Organization laced a smallpox vaccine for millions of Africans with the AIDS virus? Or was the polio virus a Pandora’s box opened by a well-meaning Salk? If so, why did it take so long to unearth and never really correct it? And how many millions of Americans have paid with their lives via the SV40 cancer-link? Here is one doctor’s answer, again from my article . . .

“Also, concerning green monkeys, Dr. William Campbell Douglass, MD, writes in 1987 in W.H.O. Murdered Africa: “This is the origin of the green monkey theory. The polio vaccine was grown on green monkey kidney cells and the geniuses who brought us polio vaccine said: ‘We got away with it once so let's use it again.’ But they didn't get away with it and in spite of the fact that polio was rapidly disappearing without any medical intervention, 64 million Americans were vaccinated with SV-40 contaminated vaccine in the 60s. An increase in cancer of the brain, possibly multiple sclerosis and God only knows what else is the tragic result. The delay between vaccination and the onset of cancer with this virus is as long as 20–30 years. Nineteen sixty-five plus 20 equals 1985. Get the picture?”

Unfortunately, it’s a rather grim picture, but as close as the truth as I can get on this awful subject. I suggest you read the entirety of my first AIDS article, including all links. Knowledge is power as they say. And even back in 2005, I reported Bilderberger involvement in all this, the power beyond the powers that rule, going about its deadly business.

Jerry Mazza is a freelance writer living in New York. Reach him at

Rogue virus in the vaccine: Early polio vaccine harbored virus now feared to cause cancer in humans

Rogue virus in the vaccine / Early polio vaccine harbored virus now feared to cause cancer in humans
Students at St. Vibiana's school in Los Angeles were among the first to receive the Salk vaccine. Associated Press File Photo

A growing number of medical researchers fear that a monkey virus that contaminated polio vaccine given to tens of millions of Americans in the 1950s and '60s may be causing rare human cancers.

For four decades, government officials have insisted that there is no evidence the simian virus called SV40 is harmful to humans. But in recent years, dozens of scientific studies have found the virus in a steadily increasing number of rare brain, bone and lung-related tumors - the same malignant cancer SV40 causes in lab animals.

Dr. Howard Strickler, chief investigator for the National Cancer Institute, said that none of his studies of SV40 have shown "an inkling of an effect on the population." Photo by Craig Allen, special to the Chronicle

Even more troubling, the virus has been detected in tumors removed from people never inoculated with the contaminated vaccine, leading some to worry that those infected by the vaccine might be spreading SV40.

The discovery of SV40 in human tumors has generated intense debate within the scientific community, pitting a handful of government health officials, who believe that the virus is harmless, against researchers from Boston to China who now suspect SV40 may be a human carcinogen. At stake are millions of research dollars and potential medical treatments for those afflicted with the cancers SV40 may be causing.

In April, more than 60 scientists met in Chicago to discuss the controversial virus and how it works to defeat certain cells' natural defenses against cancer.

"I believe that SV40 is carcinogenic (in humans)," said Dr. Michele Carbone of Loyola University Medical Center in Maywood, Ill. "We need to be creating therapies for people who have these cancers, and now we may be able to because we have a target - SV40."

"I belives that SV40 is carcinogenic (in humans). We need to be creating therapies for people who have these cancers, and now we may be able to because we have a target -- SV40." -- Dr. Michele Carbone of Loyola University Medical Center in Maywood, ILL.

But scientists at the National Cancer Institute say their studies show almost no SV40 in human tumors and no cancer increase in people who received the contaminated vaccine.

"No one would dispute there's been a widespread, very scary exposure to the population of potentially cancer-causing virus," said Dr. Howard Strickler, NCI's chief investigator. "But none of our studies and other major analyses have shown an inkling of an effect on the population."

Critics charge, however, that the few studies done by the government are scientifically flawed and that health officials have downplayed the potential risks posed by SV40 ever since they learned in 1961 that the virus contaminated the polio vaccine and caused tumors in rodents.

"How long can the government ignore this?" asked Dr. Adi Gazdar, a University of Texas Southwestern Medical Center cancer researcher. "The government has not sponsored any real research. Here's something possibly affecting millions of Americans, and they're indifferent.

"Maybe they don't want to find out."

The recent SV40 discoveries come at a time of growing concern over the dangers posed by a range of animal viruses that have crossed the species barrier to humans, including HIV, which scientists now believe came from chimpanzees and ultimately caused the AIDS epidemic.

Based on dozens of interviews and a review of the medical research, this is the story of how the campaign to eradicate polio may have inadvertently permitted another potentially deadly monkey virus to infect millions of people - and why the government for years discounted the accumulating evidence suggesting that SV40 may be a health risk for humans.

Polio epidemic, 1955

During the first half of the 20th century, polio struck down hundreds of thousands of people, leaving many paralyzed - some in iron lung machines - and killing others. The worst year was 1952, when more than 57,000 polio cases were reported in the United States. Three thousand died.

Then on April 12, 1955, Dr. Jonas Salk, a slightly built, soft-spoken researcher from Pittsburgh, mounted the podium at the University of Michigan and announced that he had developed a vaccine. That afternoon, the government licensed the vaccine for distribution.

Salk's vaccine was made by growing live polio virus on kidney tissue from Asian rhesus monkeys. The virus was then killed with formaldehyde. When the vaccine was injected in humans, the dead virus generated antibodies capable of fending off live polio.

Dr. Dwight Murray, then chairman of the American Medical Association, called Salk's announcement "one of the greatest events in the history of medicine."

Within weeks, the stockpiled vaccine was being injected into the arms of millions of people worldwide.

Virus and the tumors, 1959

Four years later, Bernice Eddy, a researcher at the National Institutes of Health, noticed something strange while looking through her microscope. Monkey kidney cells - the same kind used to make the vaccine - were dying without apparent cause.

So she tried an experiment. She prepared kidney extracts from eight to 10 rhesus monkeys and injected tiny amounts under the skin of 23 newborn hamsters. Within nine months, "large, malignant, subcutaneous tumors" appeared on 20 of the animals.

On July 6, 1960, concerned that a monkey virus might be contaminating the polio vaccine, Eddy took her findings to Dr. Joseph Smadel, chief of the NIH's biologics division. Smadel dismissed the tumors as harmless "lumps."

The same year, however, at a Merck laboratory in Pennsylvania, Dr. Maurice Hilleman and Dr. Ben Sweet isolated the virus. They called it simian virus 40, or SV40, because it was the 40th virus found in rhesus kidney tissue.

Immunization campaign, 1961

By then, the nation was winning the war against polio. Nearly 98 million Americans - more than 60 percent of the population - had received at least one injection of the Salk vaccine, and the number of cases was plummeting.

At the same time, an oral polio vaccine developed by virologist Albert Sabin was in final trials in Russia and Eastern Europe, where tens of millions had been inoculated, and it was about to be licensed in the United States. Unlike the Salk vaccine, the oral version contained a live but weakened form of polio virus and promised lifelong immunity.

But U.S. Public Health Service officials were worried. Tests had found SV40 in both the Sabin and Salk vaccines - it was later estimated that as much as a third of the Salk vaccine was tainted - and that SV40 was causing cancer in lab animals.

In early 1961, they quietly met with the agency's top vaccine advisers. The agency found no evidence that the virus had been harmful to humans, but in March, the officials ordered manufacturers to eliminate SV40 from all future vaccine.

New procedures were adopted to neutralize the tainted polio virus seed stock and SV40-free African green monkeys were used to produce the bulk vaccine instead of rhesus monkeys.

But officials did not recall contaminated Salk vaccine - more than a year's supply - still in the hands of the nation's doctors.

And they did not notify the public of the contamination and SV40's carcinogenic effect on newborn hamsters.

Hilleman would later explain that government officials were worried that any potentially negative information could ignite a panic and jeopardize the vaccination campaign.

The first public disclosure that the Salk vaccine was contaminated came in the New York Times on July 26, 1961. A story on Page 33 reported that Merck and other manufacturers had halted production until they could get a "monkey virus" out of the vaccine.

When asked to comment, the U.S. Public Health Service stressed there was no evidence the virus was dangerous.

No cause for alarm, 1962

The next year, a young Harvard-trained epidemiologist named Dr. Joseph Fraumeni joined the National Cancer Institute and was assigned one of the agency's most important projects: to determine if there was any cancer increase among those injected with the Salk vaccine.

His research would form the basis of the government's position for decades.

Working with two colleagues, Fraumeni tested stored vaccine samples from May and June of 1955, the first months of the national immunization campaign, then ranked the samples according to how much SV40 they contained - no, low or high amounts.

It would be the only time U.S. health officials measured the level of SV40 in the 1955-1962 vaccine. Stored samples from that period were later discarded.

Fraumeni identified the states where the SV40-contaminated vaccines had been distributed during those two months. California, for example, received vaccine with a low level of the virus.

The study looked at cancer mortality rates for 6- to 8-year-old children vaccinated during that narrow time frame, tracking the group for four years.

The findings, which were published in the Journal of the American Medical Association, showed no significant difference in cancer deaths in states with high or low levels of SV40 in the vaccine when compared with cancer deaths in states with no SV40 in the vaccine.

Cleveland children, 1976

Fourteen years later, after isolated reports linking the virus and human cancers, Fraumeni decided to look at another group that had received contaminated vaccine.

The group had been the subject of experiments conducted in the early 1960s at Cleveland Metropolitan General Hospital. To determine the effect of different amounts of the vaccines, researchers at the hospital inoculated newborns from mostly lower-income black families with doses ranging up to more than 100 times the dose recommended for adults.

The experiments took place over three years and involved 1,073 infants. Most were given Sabin oral vaccine later determined to contain SV40.

From 1976 to 1979, Fraumeni and his associates sent letters to the children - now age 17 to 19 - but fewer than half responded. The researchers found no SV40-related health problems from exposure to contaminated vaccine.

However, their 1982 report published in the New England Journal of Medicine acknowledged the study's limitations: A majority of the children had not responded; SV40-related cancers might take longer than 17 to 19 years to develop, and SV40 appears less likely to infect humans through the oral vaccine.

Nevertheless, they called their findings "reassuring and consistent with the prevailing view that SV40 is not carcinogenic in human beings."

Then they decided to end the study, citing "the mounting complexities and obstacles in tracing this particular group and the negative results to date."

The study's closure appeared to end the government's research into the virus. But a few years later there would be a tectonic shift in SV40 research.

First discovery, 1988

In Boston, two researchers stumbled onto something disturbing.

Dr. Robert Garcea and his assistant, Dr. John Bergsagel, were using a powerful new tool called polymerase chain reaction, or PCR, to look for a pair of common human viruses in children's brain tumors.

But a different DNA footprint kept popping up in more than half the tumors. They finally realized they were seeing SV40.

For more than a decade, scientists had reported sporadic findings of SV40- like proteins in human tumors. But the earlier tests were primitive and the results suspect. PCR, however, is capable of amplifying infinitesimal fragments of DNA, which makes detections far more credible.

The findings were troubling. The researchers noted in their published report that the children were too young to have received the contaminated vaccine. But somehow the virus had infected them and embedded itself in their tumors.

Mesothelioma, 1988

That same year, Dr. Michele Carbone was surprised to find a milky, rindlike tumor in a laboratory hamster at the National Institutes of Health in Bethesda, Md.

The animal was one of a group given an SV40 injection directly into their hearts. Sixty percent of those hamsters developed the fatal cancer called mesothelioma.

Carbone, a postdoctoral fellow at the institute, knew that SV40 caused tumors in hamsters but only in specific locations where large doses of virus were injected. Here the mesothelial membrane lining the lungs apparently became cancerous from minuscule amounts of SV40 shed by the tip of the needle on the way to the hamsters' hearts.

So he tried another experiment, this time injecting SV40 directly into the thin mesothelial walls of another group of hamsters. Within six months, every animal developed mesothelioma.

Carbone was puzzled. Mesothelioma is a rare cancer. Few human cases were reported before the 1950s, but its incidence had been increasing steadily, reaching several thousand cases a year in the United States by 1988.

Studies had linked mesothelioma to asbestos exposure - with tumors usually appearing many decades later. Yet 20 percent of victims had no asbestos exposure.

Carbone decided to use PCR to test 48 human mesotheliomas stored at the NIH.

He was stunned: 28 of them contained SV40.

More cancers, 1996

PCR unleashed a wave of SV40 discoveries.

By the end of 1996, dozens of scientists reported finding SV40 in a variety of bone cancers and a wide range of brain cancers, which had risen 30 percent over the previous 20 years.

Then, Italian researchers reported finding SV40 in 45 percent of the seminal fluid samples and 23 percent of the blood samples they had taken from healthy donors.

That meant SV40 could have been spreading through sexual activity, from mother to child, or by other means, which could explain how those never inoculated with the contaminated vaccine, such as the Boston children, were being infected.

Government assurances, 1996

At the National Cancer Institute in Bethesda, officials were growing increasingly concerned about the SV40 discoveries.

The findings were of particular interest to Fraumeni, who had been promoted to director of NCI's Division on Cancer Epidemiology and Genetics. His earlier studies concluding that SV40 posed little or no health risk were now under challenge.

But the scientific community was skeptical of the recent SV40 discoveries. As a potent carcinogen in lab animals, SV40 had been used for years as a tool to study cancer. Therefore, the powerful PCR test was suspected of finding stray SV40 fragments that might have contaminated laboratories.

So Dr. Howard Strickler, one of Fraumeni's epidemiologists, led a study using PCR on 50 mesotheliomas from Armed Forces hospitals across the country. And he found no SV40.

Although the findings bolstered the government's long-standing position that SV40 did not appear to be a health risk, federal officials decided to convene a conference on the virus.

In January 1997, 30 scientists gathered at the National Institutes of Health in Maryland. Garcea, Carbone and others presented their evidence showing SV40 in tumors and pleaded for research funding.

Strickler presented his mesothelioma study, as well as new research he had just completed, this time working with Fraumeni.

Their new study compared 20 years of cancer rates of people born between 1947 and 1963, and therefore likely to have been exposed to the contaminated polio vaccine, with people born after 1963, who they believed weren't exposed.

Their study found no significant difference between the two groups.

Letter of protest, 1998

But when Susan Fisher read Strickler and Fraumeni's study in the Journal of the American Medical Association, she fired off a letter of protest to the publication.

An epidemiologist at Loyola University Medical Center in Maywood, Ill., Fisher challenged the study's methodology, calling it "an error in judgment" and misleading.

Using the same 20-year national cancer database for the two groups, Fisher compared people of the same age - "because these cancers are highly correlated with age" - and she came up with very different results.

Studying 18- to 26-year-olds who probably had been exposed to the contaminated vaccine, Fisher found a 19.6 percent greater incidence of the two major brain cancers linked to SV40 when compared with the incidence in people the same age who were not exposed. She also found 16.6 percent more bone cancers and 178 percent more mesotheliomas among those exposed to the vaccine.

But Fisher cautioned against comparing the two groups. She argued that if SV40 is being transmitted and circulating in the population, then many people in the "unexposed" group would also be carrying the virus and that would undermine the comparison.

Two types of SV40, 1999

For years, researchers had believed that all SV40-contaminated Salk vaccine made between 1955 and 1963 had been used or discarded.

Then in 1999, Carbone was contacted by a former public health director in Oak Park, Ill., who said he had seven sealed vials of vaccine dated October 1955 in a refrigerator in his basement.

Carbone, who had left the NIH and joined the faculty at Loyola University Medical Center, ran tests on the vaccine and made a startling discovery: Not only was the vaccine contaminated, it contained a second form of the virus - an "archetypal" SV40 strain.

Although manufacturers switched from rhesus monkeys to SV40-free green African monkeys to grow the bulk vaccine in 1961, they have continued to use potentially contaminated polio seed strains originally grown on the rhesus monkey tissue to start the bulk vaccine process.

Manufacturers check the purity of their vaccine with a series of 14-day tests to detect whether any SV40 slipped through.

But when Carbone replicated the tests, he found that the second, slower- growing "archetypal" strain took 19 days to emerge.

It was possible, Carbone noted in a published report, that this second strain of SV40 had been evading manufacturers' screening procedures for years - and infecting vaccine recipients after 1962.

Controversial study, 2000

Meanwhile, a new study led by Strickler had bogged down in bitter internal conflict.

After the NIH's 1997 conference, nine laboratories were recruited to participate in a government-sponsored study to determine if tests were really finding SV40 in tumors or whether earlier detections were the result of laboratory contamination.

Carbone and other researchers considered the study unnecessary. A similar multilab study led by Dr. Joseph Testa of Philadelphia had just been completed, and it virtually eliminated the contamination theory. The prestigious journal Cancer Research published Testa's findings in 1998.

But Strickler pressed on.

An independent laboratory in Maryland prepared mesothelioma samples for the nine labs.

When tests revealed almost no SV40 in the tumor samples, some participants questioned the preparation methods used by the Maryland lab. They also challenged Strickler's written conclusion implying that contamination had caused the earlier findings of SV40 in tumors.

If Strickler was right, the earlier SV40 detections were probably the result of stray SV40 in the labs. But critics argued that the study was scientifically flawed and should be scrapped.

The dispute became so contentious that FDA officials were forced to intervene and a neutral arbitrator assigned to mediate.

Finally, in early 2000, more than two years after the study was initiated, a carefully rewritten report emerged for publication.

It concluded that contamination was an unlikely explanation for earlier SV40 findings. Then it struggled to explain the discrepancy between earlier detections of SV40 in about half of all mesotheliomas tested and the fact that the nine labs found the virus in only slightly more than 1 percent of the study's tumor specimens.

The report noted that discrepancy might be because of the inefficiency of the method used by the Maryland lab to recover DNA - like the genetic sequences of SV40 - from the mesothelial tissue to create the test samples.

The Maryland lab also had inadvertently contaminated some of the laboratory controls and "theoretically" could have contaminated others.

The report concluded by calling for further research.

Despite the study's ambivalent conclusions and technical problems, the NCI submitted it to Cancer Research, the journal that had published Testa's study.

It was rejected.

Further discoveries, 2000

In laboratories around the world, researchers continued to find SV40 in a widening range of tumors that now included pituitary and thyroid cancers and some lymphomas.

Meanwhile, an NCI investigator named Dr. David Schrump was able to gut a common respiratory virus and use it to deliver genetic material called "antisense" into SV40-infected mesothelial cells and stop the cells' malignant growth.

His discovery, which was patented by the government, strongly suggested that SV40 contributed to mesothelioma and that a treatment might be possible.

Then in August, Carbone and several colleagues published a major study providing a "mechanistic" explanation of how SV40 contributes to the uncontrolled growth of mesothelial cells. The key, they found, was the large number of "tumor suppressor" proteins found in the mesothelial cells that makes them unusually susceptible to SV40.

In most human cells, they said, the virus reproduces itself and kills the infected cell in the process. But in mesothelial cells, SV40 is especially attracted to the "tumor suppressor" proteins and binds to them, knocking them out of action. The virus then lives on in the cell.

The result, they said, is a rate of malignant cell transformation in tissue cultures 1,000 times higher than has ever been observed.

In a paper published in the Proceedings of the National Academy of Science, Carbone further explained that asbestos fibers appear to act as a co- carcinogen in mesothelioma by somehow suppressing the immune system's response, which is designed to kill the infected cells.

Chicago conference, 2001

Carbone and others believed that the time had come for another conference on the virus he calls "a perfect little war machine."

In April, more than 60 scientists gathered on a warm weekend at the University of Chicago's downtown conference center. Despite numerous faxes and certified letters inviting him, Strickler declined to attend.

Carbone opened the conference by confronting the question of whether SV40 is present in humans.

"Sixty-two papers from 30 laboratories from around the world have reported SV40 in human tissues and tumors," he said. "It is very difficult to believe that all of these papers, all of the techniques used and all of the people around the world are wrong."

For two days, scientists from as far away as China and New Zealand presented the results of their studies, with almost every speaker concluding that SV40 was present in the tissues they examined.

One of the newest discoveries came from Dr. Jeffrey Kopp, an NIH scientist who reported finding SV40 in a high percentage of patients with kidney disease. The virus was also present, he said, in 60 percent of a new "collapsing" type of renal disease that was unknown before 1980 but has since increased rapidly in incidence.

There were also reports on efforts to develop a vaccine, recently funded by the NCI, that would allow the immune system to target and eliminate SV40.

At times, the meeting took on almost revivalist overtones as scientist after scientist said he or she was initially very skeptical of SV40's presence in human tumors but was now a believer.

"I was a hard sell," said Testa, the Philadelphia geneticist who conducted the first multilaboratory tests, noting that the study had convinced him.

Gazdar, the cancer researcher from Texas, showed a slide describing his transformation: "Nonbeliever -- Believer - Zealot."

The conference concluded with a consensus among the leading scientists that SV40's presence in human tumors was no longer in question. They were more circumspect about the virus' possible role in causing cancer.

If SV40 is a human carcinogen, they said, the virus probably requires interaction with other cancer-causing substances like asbestos.

Dr. Janet Butel from Baylor Medical College in Houston said that it simply might be too soon to make a determination, citing the many years it has taken to establish that other viruses cause cancer.

But even renowned tumor biologist George Klein from Sweden said he was impressed by Carbone and Schrump's work.

"This strongly suggests that the virus plays a role (in causing tumors)," said Klein, a former chairman of the Nobel Assembly.

Low priority, 2001

In May, shortly after the conference, Strickler's multilab study was published in a small journal called Cancer Epidemiology, Biomarkers & Prevention.

Carbone and other SV40 experts dismissed the study.

"A garbage paper in a garbage journal," said Garcea, now on the faculty at the University of Colorado School of Medicine.

But Strickler strongly defends the study. He said it was the first to use strict controls not used in other studies. He acknowledged, however, that the study "doesn't prove that SV40 is not out there."

Strickler, who now teaches at Albert Einstein School of Medicine in New York, said he remains skeptical about whether SV40 has infected humans, a suspicion he says is shared by the broader scientific community.

But the NCI recently acknowledged that there is evidence to suggest that SV40 "may be associated with human cancer." The NCI statement, released last month, also said that SV40's interaction with "tumor suppressor proteins" indicates "possible mechanisms that could contribute to the development of cancer."

Top NCI officials declined to be interviewed on the record for this report. Fraumeni also declined several requests for an interview.

Dr. James Goedert, the chief of the NCI's Viral Epidemiology Branch who supervised Strickler's work, said that if SV40 is in human tumors, it must be at extremely low levels. To critics who claim the government has downplayed SV40's potential health risks, Goedert responded: "Absolutely not."

He acknowledged that research is needed to resolve the question of whether SV40 is prevalent in the human population and, if so, how it might be spreading. But Goedert said he has no plans for such studies.

"It's not our highest priority," he said.

Key figures in developing vaccines and tracing SV40

Dr. Jonas Salk Developed the first polio vaccine using killed virus in 1955.

Virologist Albert Sabin Developed an oral vaccine using weakened live virus.

Dr. Robert Garcea Used new technology to trace SV40 in children's brain tumors.

Q&A on polio vaccine contaminated with SV40 Q: How widespread is the SV40 infection?

A: Scientists and government health officials don't know because no comprehensive studies have addressed the question.

What is known: During the 1950s and '60s, more than 100 million people worldwide were given SV40-contaminated polio vaccine. The virus also has been found in people who did not receive contaminated vaccine, as well as laboratory workers and monkey handlers. No studies, however, have examined how SV40 might be transmitted between people, or if somehow humans might have become infected with SV40 before the introduction of the tainted vaccines.

Q: Can I be tested for SV40?

A: An accurate blood test does not exist. Current antibody blood tests can be inaccurate, scientists say, because they may also detect the presence of other closely related viruses, and SV40 may be present at such a low level that no antibodies are produced. Researchers are working to create an effective test.

Q: Is the current

polio vaccine safe?

A: Vaccine producers, health officials and most scientists believe that it is safe. Manufacturers say they take elaborate steps to test their vaccine for SV40, and the government says it recently tested vaccine samples back to 1972 and found no trace of SV40.

Some scientists, including Dr. Michele Carbone, have raised questions about whether manufacturers' testing techniques have been adequate. Carbone, however, tested vaccine from 1996 and found no SV40. He has had his children inoculated.

Q: In which kinds of cancers has SV40 been found?

A: The virus has been detected in rare cancers:

-- Mesothelioma, a fatal tumor of the membrane surrounding the lungs. Few cases were reported prior to 1950, but the incidence has grown in the United States to 2,000 to 4,000 cases a year, with greater incidence in Europe.

-- Brain cancers: Primarily ependymoma and choroid plexus tumors, but also astrocytoma, glioblastoma, medulloblastoma and meningioma. These make up a total of less than 1,000 U.S. cases each year.

-- Bone cancers: Primarily osteosarcoma but also chondrosarcoma and giant cell tumors. These also make up less than 1,000 cases annually.

-- Other cancers: A few detections in pituitary and thyroid tumors and lymphomas.

Report sources

The sources for this report include the books "The Saga of Jonas Salk" by Richard Carter and "The Health Century" by Edward Shorter; articles in Atlantic Monthly and New York magazine; newspaper archives at The Chronicle and the New York Times; transcript of the 1997 National Institutes of Health Conference in Bethesda; a review of dozens of scientific journal articles and scores of interviews.

Related series: Quest for the Origin of AIDS.

How SV40 contaminated polio vaccine

When Dr. Jonas Salk introduced the first polio vaccine in 1955, it was hailed as "one of the greatest events in medicine." Within 10 years, U.S. polio cases plummeted from 30,000 to less than 1,000. But in 1960, a monkey virus called SV40 was found in the Salk vaccine. As much as one-third of the vaccine was contaminated. SV40 was also found in earlier versions of an oral vaccine developed by Dr. Albert Sabin that replaced the Salk vaccine in the 1960s. When it was discovered that SV40 caused cancer in lab animals, U.S. health officials ordered vaccine manufacturers in 1961 to eliminate the virus from all future vaccine, although questions remain about whether they succeeded with the Sabin vaccine. .

Making the Sabin vaccine: 1955-1961 Starting in the mid-1950s, both Sabin and Salk vaccines are made by growing polio virus on kidney tissue from Asian rhesus monkeys, which are natural hosts for the simian virus known as SV40. Special weakened seed strain of polio virus developed by Sabin is grown on rhesus kidney tissue to make large bulk amounts of vaccine. SV40 from the kidney tissue contaminates the vaccine. .

Making the vaccine safe: 1961 In 1961, after SV40 is discovered in the vaccines, U.S. health officials order manufacturers to eliminate SV40. Antiserum is used to neutralize SV40 in seed stock, and SV40-free African green monkeys are used to grow bulk vaccine. But some researchers believe small amounts of SV40 may have survived. .

Testing Manufacturers check the safety of the vaccine pools by using a series of 14- day growth tests to see if SV40 is present.

Making the Salk vaccine: 1955-1961 Full strength polio virus is grown on rhesus kidney to make bulk Salk vaccine. SV40 from the kidney tissue contaminates the vaccine. The polio virus is then killed with formaldehyde, but some SV40 survives. .

Making the vaccine safe: 1961 In the original vaccine, the SV40 survives, contaminating up to 30 million Americans. But after 1961, African green monkeys are used to grow bulk vaccine and SV40 is eliminated.

Sources: Children's Hospital of Philadelphia; SEER; virus images by Jean Yves Sgro, University of Wisconsin; Chronicle research


For more information about the simian virus SV40, the following studies or scientific reviews were published during that past year:

A multicenter evaluation of assays of detection of SV40 DNA and results in masked mesothelioma specimens. Strickler H, Goedert J., Cancer Epidemiology, Biomarkers & Prevention. Vol. 10, 523-532, May 2001.

Simian virus 40 and human cancers, Strickler H., Einstein Quarterly J. Biol. and Med. (2001) 18:14-21. This includes a detailed bibliography that will lead readers to earlier scientific articles.

Oral polio vaccine and human cancer: a reassessment of SV40 as a contaminant based upon legal documents. Kops S., Anticancer Research (2000) 20: 4745-4750.

Human mesothelial cells are unusually susceptible to SV40-mediated transformation and asbestos cocarcinogenicity. Bocchetta M, Di Resta I, Powers A, Fresco R, Tosolini A, Testa J, Pass H, Rizzo P, Carbone M., Proc. Natl. Acad. Sci. USA, Vol. 97, Issue 18, 10214-10219, Aug. 29, 2000.

In addition, a bibliography of journal articles by leading SV40 researcher Dr. Michele Carbone can be viewed by clicking on the following link:

Monday, January 7, 2008

Nerve Cell Damage in Mammalian Brain after Exposure to Microwaves from GSM Mobile Phones

The possible risks of radio-frequency electromagnetic fields for the human body is a growing concern for our society. We have previously shown that weak pulsed microwaves give rise to a significant leakage of albumin through the blood-brain barrier. In this study we investigated whether a pathologic leakage across the blood-brain barrier might be combined with damage to the neurons. Three groups each of eight rats were exposed for 2 hr to Global System for Mobile Communications (GSM) mobile phone electromagnetic fields of different strengths. We found highly significant (p < alt="" src="">

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Figure 1. Cross-section of central parts of the brain of (A) an unexposed control rat and (B) an RF EMF-exposed rat, both stained for albumin, which appears brown. In (A), albumin is visible in the central inferior parts of the brain (the hypothalamus), which is a normal feature. In (B), albumin is visible in multiple small foci representing leakage from many vessels. Magnification, about times symbol3.

The voluntary exposure of the brain to microwaves from hand-held mobile phones by one-fourth of the world's population has been called the largest human biologic experiment ever (Salford et al. 2001). In the near future, microwaves will also be emitted by an abundance of other appliances in the cordless office and also in the home. The possible risks of radio-frequency electromagnetic fields (RF EMFs) for the human body is a growing concern for our society (for a review, see Hyland 2000). Most researchers in the field have dwelled on the question of whether RF EMFs may induce or promote cancer growth. Although some have indicated increased risk (Hardell et al. 2002; Repacholi et al. 1997), most studies, including our own, have shown no effects (Salford et al. 1997a) or even a decreased risk (Adey et al. 1999).

The possible risks of microwaves for the human body has attracted interest since the 1960s (i.e., before the advent of mobile phones), when radar and microwave ovens posed a possible health problem. Oscar and Hawkins (1977) performed early studies on effects of RF EMFs on the blood-brain barrier. They demonstrated that at very low energy levels (<>2), the fields in a restricted exposure window caused a significant leakage of 14C-mannitol, inulin, and also dextran (same molecular weight as albumin) from the capillaries into the surrounding cerebellar brain tissue. These findings, however, were not repeated in a study using 14C-sucrose (Gruenau et al. 1982). A recent in vitro study has shown that EMF at 1.8 GHz increase the permeability of the blood-brain barrier to sucrose (Schirmacher et al. 2000). Shivers and colleagues (Shivers et al. 1987; Prato et al. 1990) examined the effect of magnetic resonance imaging upon the rat brain. They showed that the combined exposure to RF EMFs and pulsed and static magnetic fields gave rise to a significant pinocytotic transport of albumin from the capillaries into the brain.

Inspired by this work, since 1988 our group has studied the effects of different intensities and modulations of 915 MHz RF EMFs in a rat model where the exposure takes place in a transverse electromagnetic transmission line chamber (TEM-cell) during various time periods. In series of more than 1,600 animals, we have proven that subthermal power densities from both pulse-modulated and continuous RF EMFs--including those from GSM (Global System for Mobile Communications) mobile phones--have the potency to significantly open the blood-brain barrier such that the animals' own albumin (but not fibrinogen) passes out of the bloodstream into the brain tissue and accumulates in the neurons and glial cells surrounding the capillaries (Malmgren 1998; Persson et al. 1997; Persson and Salford 1996; Salford et al. 1992, 1993, 1994, 1997b, 2001) (Figure 1). These results have been duplicated recently in another laboratory (Töre et al. 2001). Similar results have been reported by others (Fritze et al. 1997).

We and others (Oscar and Hawkins 1977; Persson et al. 1997) have pointed out that when such a relatively large molecule as albumin can pass the blood-brain barrier, so too can many other smaller molecules, including toxic ones, which may escape into the brain because of exposure to RF EMFs. We have hitherto not concluded that such leakage is harmful for the brain. However, Hassel et al. (1994) have shown that autologous albumin injected into the brain tissue of rats leads to damage to neurons at the injection site when the concentration of albumin in the injected solution is at least 25% of that in blood. In the present study, we investigated whether leakage across the blood-brain barrier might cause damage to the neurons.

Materials and Methods

TEM-cells used for the RF EMF exposure of rats were designed by dimensional scaling from previously constructed cells at the National Bureau of Standards (Crawford 1974). TEM-cells are known to generate uniform electromagnetic fields for standard measurements. A genuine GSM mobile phone with a programmable power output was connected via a coaxial cable to the TEM-cell; no voice modulation was applied.

The TEM-cell is enclosed in a wooden box (15 times symbol 15 times symbol 15 cm) that supports the outer conductor and central plate. The outer conductor is made of brass net and is attached to the inner walls of the box. The center plate, or septum, is constructed of aluminum.

The TEM-cells were placed in a temperature-controlled room, and the temperature in the TEM-cells was kept constant by circulating room air through holes in the wooden box.

The specific absorption rate (SAR) distribution in the rat brain has been simulated with the finite-difference time-domain method (Martens et al. 1993) and found to vary <>

The rats were placed in plastic trays (12 times symbol 12 times symbol 7 cm) to avoid contact with the central plate and outer conductor. The bottom of the tray was covered with absorbing paper to collect urine and feces.

Thirty-two male and female Fischer 344 rats 12-26 weeks of age and weighing 282 ± 91 g were divided into four groups of eight rats each. The peak output power of 10 mW, 100 mW, and 1,000 mW per cell from the GSM mobile telephone was fed into two TEM-cells simultaneously for 2 hr. This exposed the rats to peak power densities of 0.24. 2.4, and 24 W/m2, respectively. This exposure resulted in average whole-body SARs of 2 mW/kg, 20 mW/kg, and 200 mW/kg, respectively. For further details about exposure conditions and SAR calculations, see Martens et al. (1993) and Malmgren (1998). The fourth group of rats was simultaneously kept for 2 hr in nonactivated TEM-cells. The animals were awake during the exposure and could move and turn within the exposure chamber.

The animals in each exposure group were allowed to survive for about 50 days after exposure. They were carefully observed daily for neurologic and behavioral abnormalities during this period, at the end of which they were anesthetized and sacrificed by perfusion fixation with 4% formaldehyde.

The brains were removed from the skull by nontraumatic technique (resection of bone structures at the skull base, followed by a midline incision from the foramen magnum to the nose) after an extended in situ postmortem fixation time of 30 min. Each brain was sectioned coronally in 1-2-mm-thick slices, which all were embedded in paraffin, cut in 5-µm sections, and stained for RNA/DNA with cresyl violet to show dark neurons. Applying albumin antibodies (Dakocytomation Norden AB, Älvsjö, Sweden) reveals albumin as brownish spotty or more diffuse discolorations (Salford et al. 1994).

The occurrence of "dark neurons" was judged semiquantitatively by the neuropathologist as 0 (no or occasional dark neurons), 1 (moderate occurrence of dark neurons), or 2 (abundant occurrence). The microscopic analysis was performed blind to the test situation. The Kruskal-Wallis one-way analysis of variance by ranks was used for a simultaneous statistical test of the score distributions for the four exposure conditions. When the null hypothesis could be rejected, comparisons between controls and each of the exposure conditions was made with the Mann-Whitney nonparametric test for independent samples.

Results and Discussion

Controls and test animals alike showed the normal diffuse positive immunostaining for albumin in hypothalamus, a kind of built-in method control.

Control animals showed either no positivity or an occasional and often questionable positivity for albumin outside the hypothalamus (Figure 1A). In one control animal we observed a moderate number of dark neurons, but no such change was observed in all the other controls.

Exposed animals usually showed several albumin-positive foci around the finer blood vessels in white and gray matter (Figure 1B). Here the albumin had spread in the tissue between the cell bodies and surrounded neurons, which either contained no albumin or contained albumin in some foci. Scattered neurons, not associated with albumin leakage between the neurons, were also positive.

The cresyl violet staining revealed scattered and grouped dark neurons, which were often shrunken and darkly stained, homogenized with loss of discernible internal cell structures. Some of these dark neurons were also albumin positive or showed cytoplasmic microvacuoles indicating an active pathologic process. There were no hemorrhages and no discernible glial reaction, astrocytic or microglial, adjacent to changed neurons. Changed neurons were seen in all locations, but especially the cortex, hippocampus, and basal ganglia, mixed in among normal neurons (Figure 2). The percentage abnormal neurons is roughly appreciated to be maximally around 2%, but in some restricted areas they dominated the picture.

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Figure 2. Photomicrograph of sections of brain from an RF EMF-exposed rat stained with cresyl violet. (A) Row of nerve cells in a section of the pyramidal cell band of the hippocampus; among the normal nerve cells (large cells) are interspersed black and shrunken nerve cells, so-called dark neurons. (B) The cortex, top left, of an RF EMF-exposed rat showing normal nerve cells (pale blue) intermingled with abnormal, black and shrunken "dark neurons" at all depths of the cortex, but least in the superficial upper layers. Magnification, times symbol160.

The occurrence of dark neurons under the different exposure conditions is presented in Figure 3, which shows a significant positive relation between EMF dosage (SAR) and number of dark neurons.

A combined nonparametric test for the four exposure situations simultaneously revealed that the distributions of scores differed significantly between the groups (p <>

We present here for the first time evidence for neuronal damage caused by nonthermal microwave exposure. The cortex as well as the hippocampus and the basal ganglia in the brains of exposed rats contained damaged neurons. We realize that our study comprises few animals, but the combined results are highly significant and exhibit a clear dose-response relation.

We considered the observed dark neurons not to be artifacts for the following reasons: first, the brains were removed atraumatically and perfusion fixed in situ; second, the dark neurons were intermingled with normal-appearing neurons (see Figure 2). Also, the presence of vacuoles in several of the dark neurons is a clear sign that damage occurred in the living animal. We cannot exclude that the neuronal change described may represent apoptotic cell death.

The neuronal albumin uptake and other changes described would seem to indicate serious neuronal damage, which may be mediated through organelle damage with release of not only hydrolytic lysosomal enzymes but also, for example, sequestered harmful material, such as heavy metals, stored away in cytoplasmic organelles (lysosomes).

The time between last exposure and sacrifice is of great importance for the detection of foci of leakage because extravasated albumin rapidly diffuses down to, and beyond, concentrations possible to demonstrate accurately immunohistologically. However, the initial albumin leakage into the brain tissue (seen within hours in ~40% of exposed animals in our previous studies) may start a secondary blood-brain barrier opening, leading to a vicious circle--because we demonstrate albumin leakage even 8 weeks after the exposure.

We chose 12-26-week-old rats because they are comparable with human teenagers--notably frequent users of mobile phones--with respect to age. The situation of the growing brain might deserve special concern from society because biologic and maturational processes are particularly vulnerable during the growth process. The intense use of mobile phones by youngsters is a serious consideration. A neuronal damage of the kind described here may not have immediately demonstrable consequences, even if repeated. In the long run, however, it may result in reduced brain reserve capacity that might be unveiled by other later neuronal disease or even the wear and tear of aging. We cannot exclude that after some decades of (often) daily use, a whole generation of users may suffer negative effects, perhaps as early as in middle age.


Figure 1 in the original manuscript was cited in "Materials and Methods" and illustrated albumin leakage that we had reported earlier. The figure showed examples of cross-sections of the brains of rats sacrificed immediately after exposure to microwaves. Because this could be misunderstood, in the interest of clarity and with the permission of the editor, we have replaced that figure.

The new Figure 1 is now cited in "Results" and shows animals from the present study. Figure 1A illustrates the brain of a sham-exposed control animal, and Figure 1B illustrates an animal exposed to 2 mW/kg for 2 hr.


Adey W, Byus C, Cain C, Higgins R, Jones R, Kean C, et al. 1999. Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fisher 344 rats exposed to 836 MHz modulated microwaves. Radiat Res 152:293-302.

Crawford M. 1974. Generation of standard EM field using TEM transmission cells. IEEE Trans Electromagn Compat EMC 16:189-195.

Fritze K, Sommer C, Schmitz B, Mies G, Hossman K, Kiessling M, et al. 1997. Effect of global system for mobile communication (GSM) microwave exposure on blood-brain barrier permeability in rat. Acta Neuropathol (Berl) 94:465-470.

Gruenau SP, Oscar KJ, Folker MT, Rapoport SI. 1982. Absence of microwave effect on blood-brain-barrier permeability to [C-14]-labeled sucrose in the conscious rat. Exp Neurol 75:299-307.

Hardell L, Hallquist A, Hansson Mild K, Carlberg M, Påhlson A, et al. 2002. Cellular and cordless telephones and the risk for brain tumours. Eur J Cancer Prev 11:377-386.

Hassel B, Iversen E, Fonnum F. 1994. Neurotoxicity of albumin in-vivo. Neurosci Lett 167:29-32.

Hyland G. 2000. Physics and biology of mobile telephony. Lancet 356:1833-1836.

Malmgren L. 1998. Radio Frequency Systems for NMR Imaging: Coil Development and Studies of Non-Thermal Biological Effects [PhD thesis]. Lund, Sweden:Department of Applied Electronics, Lund University.

Martens L, Van Hese J, De Sutter D, De Wagter C, Malmgren L, Persson BRR, et al. 1993. Electromagnetic field calculations used for exposure experiments on small animals in TEM-cells. Bioelectrochem Bioenerg 30:73-81

Oscar K, Hawkins T. 1977. Microwave alteration of the blood-brain barrier system of rats. Brain Res 126:281-293.

Persson B, Salford L. 1996. Permeability of the blood-brain barrier in rats induced by continuous wave and pulse-modulated 915 MHz electromagnetic radiation exposure in TEM-cells. In: Proceedings of the COST 244 Workshop, Kuopio Finland, 3-4 September 1995 (Chiabrera A, Juutilainen J, eds). EU DG XIII. Brussels:COST 244, 66-72.

Persson B, Salford L, Brun A. 1997. Blood-brain barrier permeability in rats exposed to electromagnetic fields used in wireless communication. Wireless Networks 3:455-461.

Prato F, Frappier J, Shivers R, Kavaliers M, Zabel P, Drost D, et al. 1990. Magnetic resonance imaging increases the blood-brain barrier permeability to 153-gadolinium diethylenetriaminepentaacetic acid in rats. Brain Res 523:301-304.

Repacholi M, Basten A, Gebski V, Noonan D, Finnie J, Harris A. 1997. Lymphomas in Eµ-Pim1 transgenic mice exposed to pulsed 900 MHz electromagnetic fields. Radiat Res 147:631-640.

Salford LG, Brun A, Eberhardt J, Malmgren L, Persson B. 1992. Electromagnetic field-induced permeability of the blood-brain barrier shown by immunohistochemical methods. In: Interaction Mechanism of Low-Level Electromagnetic Fields in Living Systems (Nordén B, Ramel C, eds). Oxford, UK:Oxford University Press, 251-258.

Salford LG, Brun A, Eberhardt J, Persson B. 1993. Permeability of the blood-brain barrier induced by 915 MHz electromagnetic radiation, continuous wave and modulated at 8, 16, 50, 200 Hz. Bioelectrochem Bioenerg 30:293-301.

Salford LG, Brun A, Persson B. 1997a. Brain tumour development in rats exposed to electromagnetic fields used in wireless communication. Wireless Networks 3:463-469.

Salford LG, Brun A, Sturesson K, Eberhardt J, Persson B. 1994. Permeability of the blood-brain barrier induced by 915 MHz electromagnetic radiation, continuous wave and modulated at 8, 16, 50, and 200 Hz. Microsc Res Techn 27:535-542.

Salford LG, Persson B, Brun A. 1997b. Neurological aspects on wireless communication. In: Non-Thermal Effects of RF Electromagnetic Fields (Bernhardt JH, Matthes R, Repacholi MH, eds). Munich, Germany:International Commission on Non-Ionizing Radiation Protection, 131-143.

Salford LG, Persson B, Malmgren L, Brun A. 2001. Téléphonie mobile et barrière sang-cerveau. In: Téléphonie Mobile--Effets Potentiels sur la Santé des Ondes Électromagnétiques de Haute Fréquence (Pietteur Marco, ed). Embourg, Belgium:Collection Resurgence, 141-152.

Schirmacher A, Winters S, Fischer S, Goeke J, Galla HJ, Kullnick U, et al. 2000. Electromagnetic fields (1.8 GHz) increase the permeability to sucrose of the blood-brain barrier in vitro. Bioelectromagnetics 21:338-345.

Shivers R, Kavaliers M, Teskey G, Prato F, Pelletier R. 1987. Magnetic resonance imaging temporarily alters blood-brain barrier in the rat. Neurosci Lett 76:25-31.

Töre F, Dulou P-E, Haro E, Veyret B, Aubineau P. 2001. Two-hour exposure to 2 W/kg, 900 MHz GSM microwaves induces plasma protein extravasation in rat brain. In: Proceedings from the 5th International Congress of the European Bioelectromagnetics Association, 6 September 2001, Helsinki, Finland (Hietanen M, Jokela K, Juutilainen, J, eds). Helsinki:Finnish Institute of Occupational Health, 43-45.

Depleted Uranium - Iraq

The effects of fallout from depleted uranium shells used in the First Gulf War is a matter of controversy. What is the reality of DU pollution in Iraq?

In the hospitals of Basra doctors are speaking of a crime against humanity. Flicking though his casebook from the last four years, Doctor Abdul Karin shows pictures of babies born without skin, with over-sized heads and with noses where a mouth should be. Doctors here firmly point the finger of blame at the Allies' use of Depleted Uranium shells during the Gulf War. Over a million rounds of the weapon were fired during the short and decisive round of bombing. Favoured for its armour piercing qualities, a DU bomb penetrates its target with intense radioactive heat, incinerating its victims. "It's ...a flash, bang sort of toaster," describes Nuclear Consultant John Range. Once detonated DU particles remain radioactive for 4000 million years. Irradiated particles travel on the wind polluting water and soil and entering the food chain.

Depleted Uranium - US weapons causing Iraqi birth defects

This won't make you proud to be an American.

You CAN Handle The Truth - Poison DUst

Depleted Uranium Kills -- US soldiers are
returning from Iraq to die of "mysterious"
ailments - and the depleted uranium
(DU) poisoning scandal just won't go away,
despite efforts to cover it up.

Protesters in New Haven spoke out
against the U.S. military's use of DU,
its effects on US troops, and cutbacks
in veterans' medical benefits.

The DU test costs $1,000, so the U.S.
government won't test for DU poisoning.
"More than 240,000 Gulf War veterans are
on permanent medical disability and more
than 11,000 are dead. They have been
denied testing, medical care,
and compensation for depleted uranium
exposure and related illnesses since 1991,"
say reports. A U.S. government study found
that 67% of post-Gulf War babies have serious
birth defects or serious illnesses.

In Italy, eight soldiers home from Iraq
died of cancer, probably caused by DU
exposure. Today, Italy proposed new
legislation to censor media covering
the military. The new law would bar
any reporting on the health effects of
depleted uranium. Anyone who breaks the
law could face up to 20 years
in a military prison, including
civilians. You thought they came home safely from
the war. They didn't.

Poison DUst tells the story of three
young men from New York who could not
answers for their mysterious ailments
after their National Guard unit's 2003
tour of duty in Iraq. A mother reveals
her fears about the extent of her
child's birth defects and the growing
disablity of her young husband - a vet.

This Generation has the ability since
the beginning of mankind to be the most
informed about the world around you.

Terminator Technology

The Threat to World Food Security

Monsanto's latest flagship technology makes a nonsense of its claim that it seeks to feed the worlds hungry. On the contrary, it threatens to undermine the very basis of traditional agriculture - that of saving seeds from year to year. What's more, this “gene cocktail" will increase the risk that new toxins and allergens will make their way into the food chain.

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In 1860, fully five years before Abbé Gregor Mendel published his obscure tome on the genetics of peas, launching so-called "modern" plant breeding, a certain Major Hallett, F.L.S., of Brighton was warning farmers and fellow seedsmen that any abuse of his "pedi-gree" trademark for cereals would be "severely dealt with".(1) But his seeds were not patentable and there was little he could do to keep farmers from buying his wheat varieties, sowing them, selecting the best seed for the next season, and breeding their own varieties uniquely adapted to local soils, slopes, and weather.

It was only in 1908 that George Shull came up with what Major Hallett really wanted - a biological weapon to keep farmers from saving and developing their own seeds. Called "hybridization", a wonderfully euphemistic term that led farmers to think that crossing two distant plant relatives could create a "hybrid vigour" that so improved yield as to make the resulting seed sterility - meaning it could not be replanted - financially worthwhile.(2) Today, almost every ear of corn grown from California to Kazakhstan is a hybrid controlled by any one of a handful of very large seed companies.

Exactly 90 years after Shull's revelation, one of the biggest and most powerful of those companies, Monsanto, is fighting for control of the most important seed monopoly technology since the hybrid. But unlike 1860, this piece of life control can be patented. On March 3rd, the US Department of Agriculture (USDA) and a little-known cotton-seed enterprise called Delta and Pine Land Company, acquired US patent 5,723,765 - or the Technology Protection System (TPS). Within days, the rest of the world knew TPS as Terminator Technology. Its declared goal is to promulgate plants that will produce self-terminating off-spring - suicide seeds. Terminator Technology epitomizes what the genetic engineering of crops is all about and gives an insight into the driving forces behind the corporate campaign to control and own life.

The Terminator rides to the rescue of long-suffering multi-nationals who have been unable to hold farmers back from their 12,000 year tradition of saving and breeding seeds. Farmers buy the seed once do their own work thereafter. Patents and Pinkerton detectives have been employed to stop farmers from doing so. The Terminator though provides a built-in biological "patent", enforced by egineered genes. Small farming communities of the Third World especially, rely upon their
own plant breeding since neither corporate nor public breeders show much interest or aptitude in breeding for their often ficult environments. Old-fashioned hybrids and the Terminator Technology with its terminated seeds force farmers back to the market every season. Terminator also scuttles community conservation of agricultural biodiversity. There's nothing to conserve. It is the "neutron bomb" of agriculture.

Hybrid seeds

Following the rediscovery of Mendel's Laws in 1900, money-minded plant breeders pursued strategies that would force farmers back to the marketplace every season to spend their hard-earned money on seeds. Although the concept of hybrids evolved with George Shull in 1908, the first hybrid maize was not commercialized until 1924 by Henry A. Wallace. Two years later, Wallace formed Pioneer Hi-Bred the world's largest seed company and still largely controlled by the founding family. Wallace went on to become US Secretary of Agriculture and, finally (in 1941), Vice-President of the United States. Wallace's championship of hybrids made it an immutable, if unscientific, Act of Faith to argue that "hybrid
vigour" made maize the "bin-busting" bonanza it is today. More recently, however, respected scientific and economic critics like Jean-Pierre Berlan of France's INRA and Richard C. Lewontin of Harvard, as well as Jack R Kloppenburg Jr. of
the University of Wisconsin, have challenged this assumption insisting that conventional maize-breeding programmes would always out-perform hybrids given the same research invest-ment. According to these critics, the only advantage to hybrids lies in their profitability for companies.

How hybrids work

Hybrid seeds are the first generation (Fl) progeny of two distinct and distant parental lines of the same species. The seed will incorporate and express the desired genetic traits of each parent for just one generation. Seeds taken from an Fl hybrid may either be sterile or, more commonly, fail to "breed true", not express the desirable genetic qualities found in Fl. Farmers in industrialized agricultural systems rarely attempt to replant a hybrid because of the exacting requirements of machine-harvesting and food-processing for crop uniformity. Resource-poor farmers in countries such as Brazil, on the other hand, will often take F2 (second generation) hybrid seeds as a source of breeding material to be blended with their traditional varieties. In this way, skilled local breeders, mostly women, be they in Brazil, Burundi or Bangladesh, isolate useful genetic characteristics and adapt them to their immediate market. The most commonly hybridized crops are maize, cotton, sunflowers and sorghum.

Until recently, small grain cereals such as rice, wheat, barley, oats, and rye and leguminous crops such as soybeans, have defied such commercial hybridization. Now this is changing. Public breeding initiatives led by governments such as China and institutions such as the Rockefeller Foundation and Cornell University have developed commercial rice hybrids. The seed multinationals are hot on their heels. Most recently, giants like Monsanto and Novartis have been waxing poetic over the prospect of Fl hybrid wheat. With more land sown to wheat than any other crop on the planet, a new hybrid monopoly for this crop would be a windfall for seed companies. (3)

Terminator Technology: The Terminator as Biological Warfare on Farmers and Food Security

The Terminator does more than ensure that farmers can't successfully replant their harvested seed. It is the "platform" upon which companies can load their proprietary genetic traits - patented genes for herbicide-tolerance or insect-resistance - and get the farmers hooked on their seeds and caught in the chemical treadmill. The Terminator is a guarantee that even Brazil's innovative farmers will have to buy access to these traits every year.

The target market for the Terminator is explicitly the South's farmers. Beginning with company news releases announcing the patent, Delta and Pine has trumpeted that its Technology Protection System will make it economically safe for seed companies to sell their high-tech varieties in Africa, Asia and Latin America. The company has even estimated that 405 million hectares will be sown with Terminator seeds within a few years. This is a land mass almost equal to South Asia. Although Terminator Technology has only been tested in cotton and tobacco, its designers are convinced that it can be applied to any species. Delta and Pine has specifically suggested that rice and wheat farmers in countries like India, China and Pakistan are a priority market. According to the company, Terminator Technology's value could run as high as $4.00 per hectare for upmarket garden crops. The patent could be worth a billion dollars.(4)

"The centuries old practice of farmer-saved seed is really a gross disadvantage to Third World farmers who inadvertently become locked into obsolete varieties because of their taking the "easy road" and not planting newer, more productive varieties." - Dr Harry B. Collins, Delta and Pine Land Co, VicePresident for Technology Transfer (June 12, 1998) (5)

How the Terminator Technology works

The Terminator Technology is the main application of a broadly framed patent for the "control of plant gene expression". The Terminator is basically a genetically engineered suicide mechanism that can be triggered off by a specific outside stimulus. As a result the seeds of the next generation will self-destruct by self-poisoning. The preferred trigger is the antibiotic tetracycline applied to seeds. The main version of the Terminator consists of a set of three novel genes inserted into one plant [see Box I ]; another version divides two or three genes on to two plants, which are later to be cross-pollinated. The end-result is always a dead seed in the following generation.

Terminator Technology is the Trojan Horse for the spread of genetically-engineered crops in the South. In the absence of "effective" patent regimes, companies can still market their wares and enforce constant returns for their investments. In the absence of adequate biosafety legislation, countries might be persuaded to accept the Terminator on the assumption that the technology is safe and that transgenic traits cannot survive to a second generation. even by cross-pollination. This assumption is ill-founded. As with all genetic engineering, its direct effect and its side-effects are unpredictable and carry all the risks inherent in this technology. The gene-cocktail of the Terminator increases the risks that new toxins and allergens will show up in our food and animal fodder.

Most alarming though is the possibility that the Terminator genes themselves could infect the agricultural gene pool of the neighbour's crops and of wild and weedy relatives, placing a time-bomb. Temporary "gene silencing" of the poison gene or failed activation of the Terminator countdown enables such infection [see Box 2].

Between 15 and 20 per cent of the world's food supply is grown by poor farmers who save their seed. These farmers feed at least 1.4 billion people. The Terminator "protects" companies by risking the lives of these people. Since Terminator Technology has absolutely zero agronomic benefit, there is no reason to jeopardize the food security of the poor by gambling with genetic engineering in the field. Whether the Terminator works immediately or later, in either instance it is biological warfare on farmers and food security.

The Terminator also portends a hidden dark side. As a Trojan Horse for other transgenic traits, the technology might also be used to switch any trait off or on. At least in theory, the technology points to the possibility that crop diseases could be triggered by seed exports that would not have to "kick in" immediately - or not until activated by specific chemicals or conditions. This form of biological warfare on people's food and economies is becoming a hot topic in military and security circles.(6)

Terminator meets the "Monster"

Scarcely two months after USDA and Delta & Pine Land announced the receipt of the Terminator patent, Monsanto bought the company. The announcement of the $1.76 billion purchase came on May 11th even as parties to the Convention on Biological Diversity were meeting in Bratislava. The Terminator had already elbowed its way into conference debates when press stories reached delegations. Overnight the US delegation, who had not uttered a word when even the USDA was under attack for its Terminator involvement, came out fighting for Monsanto. With former Clinton White House staffers on Monsanto's lobby payroll and Mickey Cantor, the US Trade Representative for much of the Uruguay Round, on Monsanto's board, the American government's zeal was less than surprising.[See Ferrara in this issue]

Seed technology has moved a long way since 1860 and the proprietary passions of Major Hallett. Short months before the Major trade-marked his pedigreed seed, the keynote speaker to the Wisconsin agricultural fair warned the farmers and scientists to beware of new technologies that distance farmers from their crops. Although his immediate concern was the steam engine's use in agriculture - he wasn't against it, just worried about whose interests it was serving - the speaker opined that the task of agricultural technology is to provide a decent living for farmers and to feed people. Clinton's administration might do well to heed Abraham Lincoln's advice before allowing the Terminator to enslave the world's farmers today.' (7)

Terminating the Terminator

People's organizations and governments can halt the Terminator. Legal means are available through International Law and existing intergovernmental convention to outlaw the technology. Here are a few possibilities.

1. The USDA/Delta patent is pending around the world. The patent can and should be rejected on the grounds that it is in conflict with public morality. The Terminator is a threat to food security and destructive of agricultural biodiversity. On these grounds, governments are fully entitled under the terms of even the quarrelsome TRIPS chapter of the WTO (World Trade Organization) agreement to refuse the patent. In doing so, governments are also (according to the WTO) agreeing not to allow the technology to be exploited by others within their territory.

2. Pressure (within and without the United States) should be put on the USDA to refuse to surrender the patent to the company. In fact, the USDA (which surprised itself with the March 3rd patent announcement) should also petition the US Patent and Trademark Office to revisit the claims and determine whether or not it is indeed in conflict with public morality.

3. The 100+ member states to the Convention on the Prohibition of the Development, Production, and Stockpiling of Bacteriological and Toxic Weapons, and on Their Destruction (1972) should call for the abolition of Terminator Technology as a form of economic biological warfare that not only makes war on farming communities but could be manipulated to threaten national food security and destroy the national agricultural economy.

4. At its October 1998 meeting the Consultative Group on International Agricultural Research (CGIAR), the world's largest international public plant breeding network) should announce its opposition to the Terminator and its refusal to use it itself.

5. At its May 1999 meeting, the Convention on Biological Diversity's Subsidiary Body on Science and Technology should pass a resolution declaring the Terminator a threat to agricultural biodiversity and calling for its removal. Such an initiative would strengthen national efforts to ban the patent and the technology under the terms of the World Trade Agreement.

Dr. Ricarda A. Steinbrecher is a geneticist and biologist. She is coordinating the Test Tube Harvest Campaign of the Women's Environmental Network, is Science Director of the Genetics Forum, UK and is biolechnology advisor to many non-governmental organisations.

Pat Roy Mooney has worked for more than 30 years with civil society organisations on international trade and development issues related to agnculture and biodiversity and is the author of several books on the subject. He lives in Winnipeg, Canada, where he is Executive Director of RAFI.

References and Notes

1. Berlan, Jean-Pierre and Richard C.Lewontin, "Agricultural Genetics and Sterifix Breeding" (1998) unpublished manuscript from an advertisment inserted at pages 5 -6.

2. Lewontin, Richard C., and Berlan, Jean-Pierre,"The Political Economy of Agricultural Research. The Case of Hybrid Corn" Chapter 23, p. 625 in Carroll, Ronaid, C., Vandermeer, John H., and Rossett, Peter, Agroecology, McGraw-Hill Publishing Co.

3. For further information about the new push for cereal hybrids, please see RAFI Communiqué "Seed Industry Consolidation - 1988: Who Owns Whom?" (July/August, 1988) at the RAH website

4. Freiburg, Bill, "Is Delta and Pine Land's Terminator Gene a Billion Dollar
Discover?" in Seeds and Crop Digest, May-June, 1998.

5. Collins, Harry B. "New Technologies and Modemizing World Agriculture", an unpublished paper distributed by Dr. Collins during a debate on Terminator held June 12th, 1998 during the FAO Commission on Genetic Resources for Food and Agriculture (Rome).

6. Via a Freedom of Information application to the US Army, RAFI recently received documentation from a military seminar titled, "Biotechnology Workshop 20/20" (May 29-30, 1996, held at the Army War College. The papers outline a wide range of military uses for biotechnology which the authors believe to be feasible by the year 2020.

7. Abraham Lincoln, "Annual Address by Hon. Abram Lincoln of Illinois delivered at Milwaukee, Sept. 30, 1859" pages 287-299 in Transactions of the Wisconsin State Agricultural Society, Carpenter and Hyer, (Madison) 1860.