Category: Diseases

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Why the United States Leaves Deadly Chemicals on the Market

November 21, 2015  

By Valerie Brown and Elizabeth Grossman



Scientists are trained to express themselves rationally. They avoid personal attacks when they disagree. But some scientific arguments become so polarized that tempers fray. There may even be shouting.

Such is the current state of affairs between two camps of scientists: health effects researchers and regulatory toxicologists. Both groups study the effects of chemical exposures in humans. Both groups have publicly used terms like “irrelevant,” “arbitrary,” “unfounded” and “contrary to all accumulated physiological understanding” to describe the other’s work. Privately, the language becomes even harsher, with phrases such as “a pseudoscience,” “a religion” and “rigged.”

The rift centers around the best way to measure the health effects of chemical exposures. The regulatory toxicologists typically rely on computer simulations called “physiologically based pharmacokinetic” (PBPK) modeling. The health effects researchers—endocrinologists, developmental biologists and epidemiologists, among others—draw their conclusions from direct observations of how chemicals actually affect living things.

The debate may sound arcane, but the outcome could directly affect your health. It will shape how government agencies regulate chemicals for decades to come: how toxic waste sites are cleaned up, how pesticides are regulated, how workers are protected from toxic exposure and what chemicals are permitted in household items. Those decisions will profoundly affect public health: the rates at which we suffer cancer, diabetes, obesity, infertility, and neurological problems like attention disorders and lowered IQ.

The link from certain chemicals to these health effects is real. In a paper published earlier this year, a group of leading endocrinologists concluded with 99 percent certainty that environmental exposure to hormone-disrupting chemicals causes health problems. They estimate that this costs the European Union healthcare system about $175 billion a year.

Closer to home, Americans are routinely sickened by toxic chemicals whose health effects have been long known. To cite one infamous example, people exposed to the known carcinogen formaldehyde in FEMA trailers after Hurricane Katrina suffered headaches, nosebleeds and difficulty breathing. Dozens of cancer cases were later reported. Then there are workplace exposures, which federal government estimates link to as many as 20,000 cancer deaths a year and hundreds of thousands of illnesses.

“We are drowning our world in untested and unsafe chemicals, and the price we are paying in terms of our reproductive health is of serious concern,” wrote the International Federation of Gynecology and Obstetrics in a statement released on October 1.

Yet chemical regulation in the United States has proceeded at a glacial pace. And corporate profit is at the heart of the story.

That the chemical industry exerts political influence is well documented. What our investigation reveals is that, 30 years ago, corporate interests began to control not just the political process but the science itself. Industry not only funds research to cast doubt on known environmental health hazards; it has also shaped an entire field of science—regulatory toxicology—to downplay the risk of toxic chemicals.

Our investigation traces this web of influence to a group of scientists working for the Department of Defense (DOD) in the 1970s and 1980s—the pioneers of PBPK modeling. It quickly became clear that this type of modeling could be manipulated to minimize the appearance of chemical risk. PBPK methodology has subsequently been advanced by at least two generations of researchers—including many from the original DOD group—who move between industry, government agencies and industry-backed research groups, often with little or no transparency.

The result is that chemicals known to be harmful to human health remain largely unregulated in the United States—often with deadly results. For chemicals whose hazards are just now being recognized, such as the common plastics ingredient bisphenol A (BPA) and other , this lack of regulation is likely to continue unless the federal chemical review process becomes more transparent and relies less heavily on PBPK modeling.

Here we lay out the players, the dueling paradigms and the high-stakes health consequences of getting it wrong.

The dawn of PBPK simulation

The 1970s and 1980s saw a blizzard of environmental regulation. The Clean Air Act, Clean Water Act and Toxic Substances Control Act, along with the laws that established Superfund and Community Right-to-Know Programs, for the first time required companies— and military bases—using and producing chemicals to account for their environmental and health impacts. This meant greater demand for chemical risk assessments as the Occupational Safety and Health Administration (OSHA) and the Environmental Protection Agency (EPA) began to establish safety standards for workplace exposures and environmental cleanups.

In the 1980s, the now-defunct Toxic Hazards Research Unit at the Wright-Patterson Air Force Base in Dayton, Ohio, was investigating the toxicity and health effects of chemicals used by the military. Of particular concern to the DOD were the many compounds used by the military to build, service and maintain aircraft, vehicles and other machinery: fuels and fuel additives, solvents, coatings and adhesives. The military is responsible for about 900 of the approximately 1,300 currently listed Superfund sites, many of which have been contaminated by these chemicals for decades.

In the mid-1980s, scientists at the Wright-Patterson Toxic Hazards Research Unit began using PBPK simulations to track how chemicals move through the body. Known as in silico (in computers) models, these are an alternative to testing chemicals in vivo (in live animals) or in vitro (in a test tube). They allow scientists to estimate what concentrations of a chemical (or its breakdown products) end up in a particular organ or type of tissue, and how long they take to exit the body. The information can then be correlated with experimental data to set exposure limits—or not.

PBPK simulations made testing faster and cheaper, something attractive to both industry and regulators. But the PBPK model has drawbacks. “It tells you nothing about effects,” says Linda Birnbaum, director of both the National Institute of Environmental Health Sciences (NIEHS) and National Toxicology Program (NTP). Observational studies and laboratory experiments, on the other hand, are designed to discover how a chemical affects biological processes.

Even regulatory toxicologists who support PBPK acknowledge its limitations: “[PBPK models] are always going to be limited by the quality of the data that go into them,” says toxicologist James Lamb, who worked for the NTP and EPA in the 1980s and is now principal scientist at the consulting firm Exponent.

The late health effects researcher Louis Guillette, a professor at the Medical University of South Carolina famous for studies on DDT’s hormonedisrupting effects in Florida alligators, put it more bluntly: “PBPK? My immediate response: Junk in, junk out. The take-home is that most of the models [are] only as good as your understanding of the complexity of the system.”

Many biologists say PBPK-based risk assessments begin with assumptions that are too narrow, and thus often fail to fully capture how a chemical exposure can affect health. For example, a series of PBPK studies and reviews by toxicologist Justin Teeguarden of the Pacific Northwest National Laboratory in Richland, Wash., and his colleagues suggested that BPA breaks down into less harmful compounds and exits the body so rapidly that it is essentially harmless. Their research began with certain assumptions: that BPA only mimics estrogen weakly, that it affects only the body’s estrogen system, and that 90 percent of BPA exposure is through digestion of food and beverages. However, health effects research has shown that BPA mimics estrogen closely, can affect the body’s androgen and thyroid hormone systems, and can enter the body via pathways like the skin and the tissues of the mouth. When PBPK models fail to include this evidence, they tend to underestimate risk.

Because of its reliance on whatever data are included, PBPK modeling can be deliberately manipulated to produce desired outcomes. Or, as University of Notre Dame biologist Kristin Shrader-Frechette, who specializes in human health risk assessment, says: “Models can offer a means of avoiding the conclusions derived from actual experiments.” In other words, PBPK models can be customized to provide results that work to industry’s advantage.

That’s not to say PBPK itself is to blame. “Let’s not throw the baby out completely with the bathwater,” says New York University associate professor of environmental medicine and health policy Leo Trasande. “However, when you have biology telling you there are basic flaws in the model, that’s a compelling reason that it’s time for a paradigm shift.”

A handy tool for industry

That PBPK studies could be used to make chemicals appear safer was as clear in the 1980s as it is now. In a 1988 paper touting the new technique, Wright-Patterson scientists explained how their modeling had prompted the EPA to stop its regulation process for a chemical of great concern to the military: methylene chloride.

Methylene chloride is widely used as a solvent and as an ingredient in making plastics, pharmaceuticals, pesticides and other industrial products. By the 1990s, the U.S. military would be the country’s second greatest user. Methylene chloride was—and remains—regulated under the Clean Air Act as a hazardous air pollutant because of its carcinogenic and neurotoxic effects.

Between 1985 and 1986, the National Institute for Occupational Safety and Health estimated that about 1 million workers a year were exposed to methylene chloride, and the EPA classified the compound as a “probable human carcinogen.” A number of unions, including United Auto Workers and United Steelworkers, also petitioned OSHA to limit on-the-job exposure to methylene chloride.

In 1986, OSHA began the process of setting occupational exposure limits. Stakeholders were invited to submit public comments.

Among the materials submitted was a PBPK study by Melvin Andersen, Harvey Clewell—both then working at Wright-Patterson—and several other scientists, including two employed by methylene chloride product manufacturer Dow Chemical. Published in 1987, this study concluded, “Conventional risk analyses greatly overestimate the risk in humans exposed to low concentrations [of methylene chloride].”

Later that year, the EPA revised its previous health assessment of methylene chloride, citing the Wright-Patterson study to conclude that the chemical was nine times less risky than previously estimated. The EPA “has halted its rulemaking on methylene chloride [based on our studies],” wrote Wright-Patterson scientists in 1988.

OSHA, too, considered the Wright-Patterson study in its methylene chloride assessment—and its rulemaking dragged on another 10 years before the agency finally limited exposure to the chemical.

The usefulness of PBPK modeling to industry did not escape the Wright-Patterson researchers. “The potential impact,” wrote Andersen, Clewell and their colleagues in 1988, “is far reaching and not limited to methylene chloride.” Using PBPK models to set exposure limits could help avoid setting “excessively conservative”—i.e., protective— limits that could lead to “unnecessary expensive controls” and place “constraints on important industrial processes.” In other words, PBPK models could be used to set less-stringent environmental and health standards, and save industry money.

So far, they’ve been proven right. The work done at Wright-Patterson set the stage for the next 30-plus years. Results obtained using PBPK modeling—especially in industry-funded research, often conducted by former Wright-Patterson scientists—have downplayed the risk and delayed the regulation of numerous widely used and commercially lucrative chemicals. These include formaldehyde, styrene, tricholorethylene, BPA and the pesticide chlorpyrifos. For many such chemicals, PBPK studies contradict what actual biological experiments conclude. Regulators often defer to the PBPK studies anyway.

A web of influence

At the time that PBPK modelling was being developed, the chemical industry was struggling with its public image. The Bhopal, India, disaster—the methyl isocyanate release that killed and injured thousands—happened in 1984. The following year, a toxic gas release at a West Virginia Union Carbide plant sent about 135 people to hospitals.

In response to these incidents, new federal regulations required companies to account for the storage, use and release of hazardous chemicals. The minutes from a May 1988 Chemical Manufacturers Association (CMA) meeting show industry was feeling the pressure. Noting the federal scrutiny and the growing testing requirements, the CMA recommended that industry help “develop exposure data” and “explore innovative ways to limit required testing to that which is needed.”

Industry had already begun to do this by founding a number of research institutes such as the Chemical Industry Institute of Toxicology (CIIT), a nonprofit toxicology research institute (renamed the Hamner Institutes in an act of linguistic detoxification in 2007). This period also saw the rise of for-profit consulting firms like Environ (1982), Gradient (1985), ChemRisk (1985) and K.S. Crump and Company (1986), with which industry would collaborate advantageously in the following decades.

“Our goal was to do the science that would help the EPA and other regulatory bodies make the policies,” explained William Greenlee, Hamner president and CEO, in an interview for a business website. Indeed, over the past 30 years, Hamner and these consultancies have produced hundreds of PBPK studies, often with the support of chemical companies or trade groups. Overwhelmingly, these studies downplay or cast doubt on chemicals’ health effects—and delay regulation.

“I have seen how scientists from the Hamner Institutes can present information in a way that carefully shapes or controls a narrative,” says Laura Vandenberg, an assistant professor of environmental health sciences at University of Massachusetts Amherst. She explains that Hamner scientists often use narrow time windows or present data in a limited context, rejecting information that does not conform to their models. “These are the kinds of tactics used to manufacture doubt,” she says.

A close look at the authors of studies produced by these industry-linked research groups reveals a web of influence traceable to Wright-Patterson (see chart on following page). At least 10 researchers employed at or contracted by Wright-Patterson in the 1980s went on to careers in toxicology at CIIT/Hamner, for-profit consulting firms or the EPA. About half have held senior positions at Hamner, including the co-authors of many of the early Wright-Patterson PBPK studies: Melvin Anderson, now a chief scientific officer at Hamner, and Harvey Clewell, now a senior investigator at Hamner and principal scientist at the consulting firm ENVIRON. “I’m probably given credit as the person who brought PBPK into toxicology and risk assessment,” Andersen told In These Times.

A revolving door between these industry-affiliated groups and federal regulators was also set in motion. More than a dozen researchers have moved from the EPA to these for-profit consultancies; a similar number have gone in the other direction, ending up at the EPA or other federal agencies.

Further blurring the public-private line, CIIT/Hamner has received millions of dollars in both industry and taxpayer money. The group stated on its website in 2007 that $18 million of its $21.5 million annual operating budget came from the “chemical and pharmaceutical industry.” Information about its corporate funders is no longer detailed there, but Hamner has previously listed as clients and supporters the American Chemistry Council (formerly the CMA, and one of the most powerful lobbyists against chemical regulation), American Petroleum Institute, BASF, Bayer CropScience, Dow, ExxonMobil, Chevron and the Formaldehyde Council. At the same time, over the past 30 years, CIIT/Hamner has received nearly $160 million in grants and contracts from the EPA, DOD and Department of Health and Human Services. In sum, since the 1980s, these federal agencies have awarded hundreds of millions of dollars to industry-affiliated research institutes like Hamner.

But the federal reliance on industry-linked researchers extends further. Since 2000, the EPA has signed a number of cooperative research agreements with the ACC and CIIT/ Hamner. All involve chemical toxicity research that includes PBPK modeling. And in 2014, Hamner outlined additional research it will be conducting for the EPA’s next generation of chemical testing—the ToxCast and Tox21 programs. Over the past five years, Hamner has received funding for this same research from the ACC and Dow.

Meanwhile, the EPA regularly contracts with for-profit consultancies to perform risk assessments, assemble peer review panels and select the scientific literature used in chemical evaluations. This gives these private organizations considerable sway in the decision-making process, often with little transparency about ties to chemical manufacturers. The upshot: Experts selected to oversee chemical regulation often overrepresent the industry perspective.

These cozy relationships have not gone unnoticed; the EPA has been called to task by both its own Office of Inspector General and by the U.S. Government Accountability Office. “These arrangements have raised concerns that ACC or its members could potentially influence, or appear to influence, the scientific results that may be used to make future regulatory decisions,” wrote the GAO in a 2005 report.

Asked for comment by In These Times, the EPA said these arrangements do not present conflicts of interest.

Decades of deadly delay

PBPK studies have stalled the regulation of numerous chemicals. In each case, narrowly focused models developed by industry-supported research concluded that risks were lower than previously estimated or were not of concern at likely exposure levels.

Take, for example, methylene chloride, the subject of the 1987 paper Wright-Patterson scientists bragged had halted the EPA’s regulatory process. Despite the chemical being identified as “probably carcinogenic to humans” by the U.N. International Agency for Research on Cancer, a “reasonably anticipated” human carcinogen by the U.S. National Toxicology Program, and an “occupational carcinogen” by OSHA, the EPA has yet to limit its use. EPA researchers noted this year that the 1987 PBPK model by the Wright-Patterson scientists remains the basis for the agency’s risk assessment.

Today, methylene chloride remains in use—to produce electronics, pesticides, plastics and synthetic fabrics, and in paint and varnish strippers. The Consumer Product Safety Commission, OSHA and NIOSH have issued health warnings, and the FDA bars methylene chloride from cosmetics— but no U.S. agency has totally banned the chemical. The EPA estimates that some 230,000 workers are exposed directly each year. According to OSHA, between 2000 and 2012, at least 14 people died in the United States of asphyxiation or heart failure after using methylene chloride-containing products to refinish bathtubs. The Center for Public Integrity reports that methylene chloride exposure prompted more than 2,700 calls to U.S. poison control centers between 2008 and 2013.

Another telling example of industry-funded PBPK studies’ influence is formaldehyde. This chemical remains largely unrestricted in the United States, despite being a well-recognized respiratory and neurological toxicant linked to nasal cancer and leukemia, as well as to allergic reactions and skin irritation. The EPA’s toxicological review of formaldehyde, begun in 1990, remains incomplete, in no small part because of delays prompted by the introduction of studies—including PBPK models conducted by CIIT/Hamner—questioning its link to leukemia.

If that link is considered weak or uncertain, that means formaldehyde—or the companies that employ the sickened workers—won’t be held responsible for the disease. The chemical industry is well aware that “more people have leukemia … than have nasal tumors,” says recently retired NIEHS toxicologist James Huff.

Some of this CIIT/Hamner research was conducted between 2000 and 2005 with funding from an $18,750,000 EPA grant. In 2010, Hamner received $5 million from Dow, a formaldehydeproduct manufacturer, for toxicity testing, including PBPK modeling. The ACC, which opposes formaldehyde restriction, also supported this research.

Consequently, apart from a few state regulations and a pending EPA proposal to limit formaldehyde emissions from composite wood products like plywood, companies can still use the chemical—as in the FEMA trailers.

Cosmetics and personal-care products can also be sources of formaldehyde exposure. This made headlines in 2011 after hair salon workers using a smoothing product called Brazilian Blowout reported nausea, sore throats, rashes, chronic sinus infections, asthma-like symptoms, bloody noses, dizziness and other neurological effects. “You can’t see it … but you feel it in your eyes and it gives you a high,” salon owner and hair stylist Cortney Tanner tells In These Times. “They don’t teach this stuff in beauty school,” she says, and no one warns stylists about these products or even suggests using a ventilator.

OSHA has issued a hazard alert for these products and the FDA has issued multiple warnings, most recently in September, but regulations prevent federal agencies from pulling the products from store shelves. So, for formaldehyde, as in the case of the paint strippers containing methylene chloride, exposures continue.

BPA rings alarm bells

The chemical currently at the center of the most heated debates about consumer exposure is BPA. The building block of polycarbonate plastics, BPA is used in countless products, including the resins that line food cans and coat the thermal receipt paper at cash registers and ATMs. While scientific evidence of adverse health effects from environmentally typical levels of BPA mounts, and many manufacturers and retailers have responded to public concern by changing their products, federal regulatory authorities still resist restricting the chemical’s use.

BPA does not produce immediate, acute effects, like those experienced by salon workers exposed to formaldehyde or machinists working with methylene chloride. But in laboratory tests on animals, BPA is a known endocrine disruptor. Structurally similar to natural hormones, endocrine disruptors can interfere with normal cellular processes and trigger abnormal biochemical responses. These can prompt numerous health problems, including cancer, infertility, and metabolic and neurological disorders. BPA has also been linked to increased risk of cardiovascular disease, diabetes and obesity.

To promote the idea that BPA is safe, the chemical industry routinely lobbies policymakers and “educates” consumers. What has not been widely discussed, however, is how industry has backed PBPK studies that marginalized research showing risks from environmentally typical levels of BPA. Many of these doubt-inducing studies have been conducted by researchers whose careers can be linked to the PBPK work done at Wright-Patterson. In published critiques, health effects researchers—among them Gail Prins and Wade Welshons—have detailed the many ways in which these PBPK models fail to accurately reflect BPA exposure.

PBPK and endocrine disruption

Over the past several decades, our evolving understanding of our bodies’ responses to chemicals has challenged previous toxicological assumptions— including those that are fed into PBPK models. This is particularly true of endocrine disruptors.

Cause-and-effect relationships between endocrine disruptors and health problems can be hard to pinpoint. We now know that early—even prenatal— exposure to endocrine disruptors can set the stage for adult disease. In addition, a pregnant woman’s exposures may affect not only her children but also her grandchildren. These transgenerational effects have been documented in animal experiments. The classic human evidence came from victims of DES, a drug prescribed in the 1940s, 1950s and 1960s to prevent miscarriages. Daughters of women who took the endocrine disruptor developed reproductive cancers, and preliminary research suggests their daughters may be at greater risk for cancer and other reproductive problems.

“The transgenerational work raises an incredible specter,” says Andrea Gore, who holds the Vacek Chair in Pharmacology at the University of Texas at Austin and edits the influential journal Endocrinology. “It’s not just what you’re exposed to now, it’s what your ancestors were exposed to.”

Complicating PBPK modeling further, hormone-mimicking chemicals, just like hormones, can have biological effects at concentrations as low as parts per trillion. In addition, environmental exposures most often occur as mixtures, rather than in isolation. And each individual may respond differently.

“PBPK doesn’t come close” to capturing the reality of endocrine disruption, the late developmental biologist Louis Guillette told In These Times, in part because modelers are “still asking questions about one chemical exposure with one route of exposure.” Even for health effects researchers, understanding of mixtures’ effects is in its infancy.

The debate over how endocrine disruption can be represented in PBPK models has intensified the unease between regulatory toxicologists and health effects researchers. That tension is particularly well-illustrated by a recent series of events that also reveal how some journal editors privilege the industry’s point of view.

A life-and-death debate

In February 2012 the World Health Organization (WHO) and the U.N. Environment Programme (UNEP) published a report intended to inform regulation worldwide. The authors were an international group of health effects researchers with long experience studying endocrine disruption.

“There is an increasing burden of disease across the globe in which [endocrine disruptors] are likely playing an important role, and future generations may also be affected,” said the report. These diseases, it continued, are being seen in humans and wildlife, and include male and female reproductive disorders, changes in the numbers of male and female babies born, thyroid and adrenal gland disorders, hormone-related cancers and neurodevelopmental diseases.

The backlash from toxicologists was immediate. Over the next few months—as the EU prepared to begin its regulatory decision-making on endocrine disruptors—the editors of 14 toxicology journals each published an identical commentary harshly criticizing the WHO/UNEP conclusions.

The commentary included a letter from more than 70 toxicologists urging the EU not to adopt the endocrine disruption framework. The letter said that the WHO/UNEP report could not be allowed to inform policy because its science is “contrary to all accumulated physiological understanding.”

This commentary was followed by further attacks. One critique, published in the journal Critical Reviews in Toxicology, was funded and vetted by the ACC.

These commentaries infuriated health effects researchers. Twenty endocrine journal editors, 28 associate editors and 56 other scientists—including several WHO/UNEP report authors—signed a statement in Endocrinology, saying in part:

The dismissive approach to endocrine disruption science put forth … is unfounded, as it is [not] based on the fundamental principles of how the endocrine system works and how chemicals can interfere with its normal function.

Endocrinology editor Andrea Gore tells In These Times that she and other health effects researchers don’t think the scientifically demonstrated dangers of endocrine disruptors are subject to debate. “There are fundamental differences between regulatory toxicologists and what I refer to as ‘people who understand the endocrine science.’ ”

The outcome of this debate and the structure of future regulatory toxicity testing in the United States and Europe is not yet clear. The EPA appears to be attempting to incorporate endocrine disruption into PBPK models, but many scientists are skeptical the process will produce reliable results, given the models’ limitations and the complexity of endocrine effects.

From science to activism

Although couched in complex language, these arguments are not academic, but have profound implications for public health. Disorders and diseases, increasingly linked to exposure to endocrine disruptors— including metabolic, reproductive, developmental and neurological problems—are widespread and increasing. About 20 percent of U.S. adults show at least three of the five indicators of metabolic syndrome: obesity, diabetes, high blood pressure, high cholesterol and heart disease. Neurological problems, including behavioral and learning disabilities in children as well as Parkinson’s disease, are increasing rapidly. Fertility rates in both men and women are declining. Globally, the average sperm count has dropped 50 percent in the last 50 years.

Scientists typically shy away from activism, but many now believe it’s what’s needed to punch through the machinations and inertia regarding chemical regulation. Shanna Swan, Mount Sinai professor of preventive medicine, obstetrics, gynecology and reproductive medicine, notes that some of the biggest reductions in chemical exposures have happened in response to consumer pressure on both industry and policymakers. Or, as the University of California’s Bruce Blumberg says, “I think we need to take the fight to the people.”

The Endocrine Society stressed the urgency of addressing these public health impacts in a statement released September 28. Not surprisingly, industry disagreed, calling this science “unsupported” and “still-unproven.”

Meanwhile, PBPK studies continue to succeed in sowing doubt about adverse health effects of endocrine disorders. Their extremely narrow focus leads to narrow conclusions that often result in calls for more research before regulation. In regulatory decisions, “the assumption is that if we don’t know something, it won’t hurt us,” says University of Massachusetts, Amherst professor of biology R. Thomas Zoeller. In other words, the burden of proof remains on health effects researchers to prove harm, not on industry to prove safety—and proving harm is difficult, especially when other scientists are seeding doubt.

But the clock is ticking. As Washington State University geneticist Pat Hunt told In These Times, “If we wait [to make regulatory decisions] for ‘proof’ in the form of compelling human data, it may be too late for us as a species.”

This investigation was supported by the Leonard C. Goodman Institute for Investigative Reporting and published originally in In These Times.

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Zika virus: Health alerts in South America and Caribbean following fears illness may cause birth deformities

Doctors believe the illness may be linked to a rise in cases of microcephaly in infants
  • Alexandra Sims
  • Thursday 19 November 2015 Zika virus is a mosquito-borne disease similar to dengue fever VALERY HACHE/AFP/Getty Images


A virus believed to cause under-developed brains and skulls in newborn babies has sparked a public health emergency in Brazil and the Caribbean.

The Zika virus, a mosquito-borne disease similar to dengue fever, was first identified on Easter Island, Chile in February last year and has since spread to Brazil, Columbia and the Caribbean.

On Monday, the Caribbean Public Health Agency confirmed five cases of the Zika virus in a territory of the Caribbean Community, according to Liverostrum News Agency.

The territory where the cases were confirmed has not been revealed.

Reports say the disease surveillance system operated by one of the community’s members, Grenada, has since been heightened and health officials are on alert.


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Research: Plants Cure Cancer, Not Chemicals

Plants Are The Cure For Cancer, Not Chemicals

Unbeknownst to most, a Copernican revolution has already taken place in cancer theory. Today, the weight of evidence indicates that plants and not chemicals are the solution for reversing the global cancer epidemic.

Our understanding of what causes cancer has undergone something akin to a Copernican revolution in the past decade. Biological fatalism has been the predominant force in medicine over the past half century, where most conditions including cancer were believed predestined ‘in the genes,’ and therefore impossible to reverse. Instead of looking for root cause resolution of disease (RCRD), we resigned ourselves to ‘finding it early’ and in the case of cancer, when doing so (even when it was benign), we waged war against it, quite literally using weapons grade materials (mustard gas- and nuclear materials-derived agents). Now, however, in this post-Genomic era, factors above (epi-) the control of the genes – epigenetic factors – are taking center stage; these include environmental exposures, stress, nutritional factors, and various lifestyle-based variables that are within the ambit of our control and volition, and which are often reversible.

In other words, cancer is now being understood as epigenetic dysfunction, a direct and even adaptive response to the post-industrial, carcinogen-saturated environment, in addition to a diet of faux, mostly chemically-produced ‘food,’ combining to produce an environment – ‘inner terrain–  within the body ideal for cancer promotion.

Indeed, in a new study published in the journal Food and Chemical Toxicology titled, “The use of plant-derived bioactive compounds to target cancer stem cells and modulate tumor microenvironment,” the authors note the powerful implications of this new epigenetic view of cancer:

“A fundamental aspect to be taken into account is that epigenetic changes can possibly be reversed by modifying epigenetic factors, such as diet and lifestyle. Nowadays, identification of these factors is crucial to develop epigenetically-based preventions and more effective anti-cancer intervention strategies.”

Moreover, they note that natural interventions are once again (after countless millennia of worldwide use), at the cutting edge of medical intervention:

“Virtually, all dietary compounds have the ability to act at the epigenetic level in cancer cells thus influencing the epigenome in a positive or negative way. Particularly, plant derived compounds, such as polyphenols, have the capacity to reverse adverse epigenetic mutations in cancer cells, to inhibit tumorigenesis progression, to prevent the metastatic process or to sensitize cancer cells to chemo and radiotherapy (Vanden Berghe, 2012).”

The new study highlighted the following points, the implications for the future of cancer treatment are truly revolutionary:

  • Cancer stem cells (CSCs) are chemo-radiotherapy resistant, causing tumor relapse.
  • CSCs are known to reside within specific hypoxic and acidic tumor niches.
  • Phytocompounds affect CSC self-renewal, metabolism and microenvironment.
  • Phytocompounds might be exploited for cancer prevention and treatment.


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 Health Nut News

1,000 McDonald’s Customers Exposed To Hepatitis A, Sparking Class Action Lawsuit

People buying fast-food from McDonald's Restaurant

In November, more than 1,000 customers were potentially exposed to Hepatitis A after having their meal at McDonald’s prepared by an employee who was recently diagnosed (Nov. 13th) with the virus. The employee who works at a location in Waterloo, New York, could have contaminated food, utensils or dishes if they didn’t wash their hands after using the bathroom. The Seneca County Health Department has advised the community that if they ate at the Waterloo McDonald’s on Nov. 2nd, 3rd, 5th, 6th and or 8th, that they need to be tested and vaccinated.

However, one customer is suing.

The branch’s owner, Jascor Inc., is being sued by Christopher Welch in a class-action lawsuit, filed on Nov. 18th, for potentially exposing people to the virus, which causes liver infections. Mr. Welch ate at the restaurant on at least one occasion when the worker was present so he received the vaccination. Some of the customers who ate there during that time have said they will get tested but not get the vaccine.

According to the Centers for Disease Control and Prevention (CDC):

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Activist Post

Interrupt Your Regularly Scheduled Program

Electromagnetic Hypersensitivity from Microwave Technology Finally Medically Proven

wifi emfsBy Catherine J. Frompovich

Finally, there’s documented medical proof that electromagnetic hypersensitivity is a real-time health issue that actually can be verified using standard medical procedures and testing capabilities.

An international group of researchers aced it when they published their findings from the clinical study “Metabolic and Genetic Screening of Electromagnetic Hypersensitive Subjects as a Feasible Tool for Diagnostics and Intervention” in the November 2014 issue of Mediators of Inflammation.

So, the million-dollar-question has to be, “When will utility companies get up to speed on the latest in microwave technology damage to the human body?” Also, “When will public utility commissions nationwide institute proper procedures to protect consumers from such damage?”

Pennsylvanians currently are being bombarded by non-thermal health problems from public utility companies’ electric, natural gas and water Smart Meters, which operate using microwave technology.

Furthermore, the PA House Consumer Affairs Committee Chair Robert Godshall sits on Opt-Out Bills that will permit electrosensitive consumers and others to keep safe analog meters, which have been in use for decades.


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The Return of Whooping Cough in High Vaccination Areas

Pertussis (whooping cough) has re-emerged in countries with high vaccination coverage and low mortality. Although it is listed as one of the top causes of vaccine preventable deaths, reports of a global resurgence originated in countries with low mortality and high vaccination coverage. Priorities are to decrease infant mortality by improving coverage and timeliness of vaccination and implementing pertussis surveillance, but vaccinations don’t seem to be working and this is of great concern.

More recently some countries with sustained high vaccine coverage have experienced increases in pertussis, especially in older children and adults, the reasons for which are complex. The issue may stem from under diagnosis or missed diagnosis and under-reporting, which hinder surveillance, as well as gaps in our knowledge of levels of herd immunity generated by the vaccination programs.Whooping cough is a relatively new infectious disease afflicting human beings, compared with other infectious diseases, and is undergoing a resurgence despite decades of vaccination.

One study found that the body’s response to a pertussis infection was correlated with vaccination status. There was a primary response in unvaccinated children.

Another study in the Center For Infectious Disease Dynamics showed that pertussis vaccination actually enhances the colonization Bordetella parapertussis, the bacteria that causes pertussis, and that the vaccination itself may have contributed to the observed increase in whooping cough over the last decade.

How common is whooping cough in a non-vaccinating country?

In Sweden, general vaccination with a whole cell pertussis vaccine was recommended from 1953. In 1979 the recommendation was withdrawn because the Swedish-made vaccine had become ineffective. In order to determine the incidence of the disease in a non-vaccinating country, 400 children born in 1980 were randomly selected from the population register of Goteborg, Sweden. The parents of the children were interviewed in 1990, when the children were 10 years old. The parents of 377 children could be reached, and of those 372 were not vaccinated against pertussis. Of the nonvaccinated children 61% had experienced clinically typical whooping cough; 195 (119 with and 76 without a history of whooping cough) agreed to donate a serum sample for determination of antibodies against pertussis toxin, filamentous hemagglutinin and pertactin. Of the children with a history of whooping cough, 91% had antibodies against pertussis toxin, as had 64% of the children without a history of disease. All but 3 children had antibodies against filamentous hemagglutinin and all 195 children had antibodies against pertactin. The antibody titers against the 2 last mentioned proteins did not differ between children with and without a history of whooping cough or between children with and without antibodies against pertussis toxin.

In light of the solid Swedish study why is the rest of the world still heavily vaccinating its citizens for whooping cough / pertussis when it has proven unsuccessful and appears to be increasing in the vaccinated groups? Could this enzyme deficiency in vaccinated subjects be linked to a lack of naturally occurring anti-bodies? From the time we are born our body’s immune system begins to create anti-bodies and depending on the region of birth they create anti-bodies specifically to the threats of their own community. In the western world we heavily vaccine children beginning at childbirth, is this resurgence of pertussis the result of not having their own antibodies due to a life time of vaccinations, this avenue of thought must be considered regardless of the outcome or the profits lost in the world wide vaccination programs?

It used to be that infants were not vaccinated as early as today they allowed 6 months for the child’s own immune defense to develop now they are vaccinated before leaving the hospitals. How can the individuals immune system develop if they are being shut down or altered with vaccinations, how can they hope to adapt to new virus protection when bacteria begin mutating? Do you think what is done in a laboratory is more efficient than what is done within the body pertaining to the individual needs and region to where they live? Will we look back at this generation and see the errors of our ways when antibiotics fail or will we line up for vaccinations each time a new strain of bacteria is discovered since we no longer have our own immune defense? This is an age of discovery but the question that remains unanswered is what the discovery will be?

Products to help build our immunity are: Laktokhan, Colloidal Silver, Full Spectrum Digestive Enzyme, Zinc Picolinate, Thymus Gland and L-Lysine.

Eldon Dahl, Doctorate in natural medicine.

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Is This The Common Denominator Of All Disease?

Pigeonholing Diseases

Diseases display a variety of symptoms, but curiously enough, there is a common denominator!

The Truth About “All Disease”

A recent series presented via GreenMedInfo, “The Truth About Cancer” could have been more accurately titled, “The Truth about All Disease.” The elements of cancer protocols: nutrient/mineral correction, detoxification, helpful supplements, various energy therapies and lifestyle choices, really apply to healing all chronic disease. The idea of personal empowerment applies to all disease as well. Survivors emerged from the shock of a cancer diagnosis, stepped away from conventional treatments and “willed” their healing, which proves once again the critical importance of mental states and the reality of placebo-nocebo effects. Yes, it can be done!

We get misdirected by complex medical studies and lose sight of the common denominator in chronic disease; all are symptoms of oxidative stress and inflammation. Every symptom that ever occurs starts with a shortage of cellular bio-energy: electrons. Colds, bronchitis, indigestion, high blood pressure, bleeding gums or depression are first signs of inflammation and a progression toward heart disease, arthritis and cancers that arrive decades later. The fooler is that symptoms may appear in different locations in the body, yet reflect a predictable correlation with a range of specific insults. So cut to the cure, identify the root causes that come from toxins, wrong nutrition, poor lifestyle choices and negative personality traits/emotional stress/fear of death. Take appropriate steps at this seed level.

The public is not only convinced pharma-medicine is “real” medicine, but is deprived of accurate information and even the very idea of alternative treatments…and doctors have little time to coach patients on self-care. The best interests of the patient would be better served by a Nurse Advocate (schooled in CAM) offering personal instructions rather than a quick prescription. Leave the allopathic paradigm of a drug for every symptom…behind. Natural health proponents borrow the same pigeonhole framework by substituting an herb or supplement for a drug, repeating the idea that there is a specific silver bullet for each malady. Not so! Basic oxidation-reduction (redox) chemistry, though it seems foreign to medical thinking, is the most certain scientific and holistic point of view that goes to the root of health and healing.


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Natural Blaze

gardasil death boy

By Norma Erickson

Gardasil®-related fatal myocardial infarction in a teenage boy – case filed in United States Court of Federal Claims Office of Special Masters.

Gomez versus USDOH: Petition No. 15-0160V1 filed by the Roberts Law Firm of Newport Beach, California for petitioners Adan Gomez and Raquel Ayon, on behalf of their deceased son Joel Gomez, states:

Joel Gomez received a Merck Gardasil vaccine on June 19, 2013 and again on August 19, 2013, and died in his sleep the following day on August 20, 2013. The death was caused in fact by receiving the Gardasil Vaccine.

This statement is reinforced by a supportive Expert Report written by Sin Hang Lee, MD, stating:

Gardasil® did cause or contributed to a myocardial infarction in the decedent, and that the second dose of Gardasil®finally caused a fatal hypotension in this case on the day of vaccination. There was no other plausible cause for the death of Joel Gomez at the night of August 19, 2013.

The record shows that Joel Gomez, the decedent, a 14-year old healthy boy who had regular visits to the pediatrician’s office for periodic check-ups since birth showed no evidence of any pre-existing health issues, specifically no evidence of cardiac abnormalities, psychological disorders or substance abuse. The teenager had been training for the high school football team from four to five hours a day for the two months prior to his death without incident.


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The seven hundred years-old expression, “curses are like chickens; they always come home to roost,” rarely has been more appropriate than to describe what is happening to the world’s largest purveyor of gene-manipulated or GMO seeds and paired chemical toxins. It couldn’t happen to a nicer bunch of genocidal eugenicists. Monsanto Corporation of St Louis is apparently in a deep decline.


Ever since 1992 when that nasty US President George H. W. Bush conspired–yes, Virginia, conspiracies exist– with the leadership of Monsanto to unleash GMOs on an unwitting American population, Monsanto seemed unstoppable.

With the help of Bush, who made a decree that no US Government agency be allowed to independently test GMO seeds or their chemicals for health and safety–the fraudulent and totally unscientific Doctrine of Substantial Equivalence–Monsanto could make its own fraudulent doctored tests and give them to US or EU agencies as valid. As a result, GMO seeds took over American agriculture, based on a pack of lies to farmers that they would raise yields and decrease chemical use. Monsanto spread its GMO far around the world, through bribery as in Indonesia, and through the unusual machinations of the Government of the United States. Monsanto paid scientists to lie about its products safety.

It used the corrupt Brussels European Food Safety Authority (EFSA) to back its position, even when alarming studies such as the famous September 2012 Food and Chemical Toxicology peer-reviewed study by Prof. Gilles-Eric Seralini created shock waves around the world. The Seralini study, the first ever long term, two year study of GMO diet with a group of 200 rats found shocking effects. Among them that,”female rats fed Monsanto GMO maize died 2–3 times more than controls, and more rapidly… Females developed large mammary tumors almost always more often than, and before, controls; the pituitary was the second most disabled organ; the sex hormonal balance was modified by GMO and Roundup treatments.”

Monsanto then set about to kill the messenger by pressuring the Food & Chemical Toxicology journal to hire a former Monsanto employee, Richard E. Goodman, who promptly declared Seralini’s study “unscientific” and deleted it, an act almost without precedent in science journals. A year later both Goodman and the journal’s editor-in-chief were forced to step down and Seralini’s article was republished in another scientific journal. But the scientific character assassination against Seralini had a chilling effect as Monsanto wanted.

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The Telegraph

First genetically modified humans could exist within two years

Biotech company Editas Medicine is planning to start human trials to genetically edit genes and reverse blindness

Humans who have had their DNA genetically modified could exist within two years after a private biotech company announced plans to start the first trials into a ground-breaking new technique.

Editas Medicine, which is based in the US, said it plans to become the first lab in the world to ‘genetically edit’ the DNA of patients suffering from a genetic condition – in this case the blinding disorder ‘leber congenital amaurosis’.

The disorder prevents normal function of the retina; the light-sensitive layer of cells at the back of the eye. It appears at birth or in the first months of life and eventually sufferers can go completely blind.

“Hereditary eye disease in an obvious place to start given that there is already precedent in classical gene therapy”
Professor Darren Griffin, University of Kent

The rare inherited disease is caused by defects in a gene which instructs the creation of a protein that is essential to vision.

But scientists at Editas Medicine in the US believe they can fix the mutated DNA using the ground-breaking gene-editing technology Crispr.

Katrine Bosley, the chief executive of Editas Medicine, told a conference in the US that the company hopes to start trialling the technology on blind patients in 2017.

It would be the first time the technology has been used on humans. Gene editing is currently banned in the US, so the company would need special permission from health regulators.

“It feels fast, but we are going at the pace science allows,” Bosley told the EmTech conference in Cambridge, Massachusetts.


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