Rachel's Precaution Reporter #92
Wednesday, May 30, 2007

From: PPTOX 2007 ..........................................[This story printer-friendly]
May 24, 2007

THE FAROES STATEMENT

[Rachel's introduction: In this powerful consensus statement, more than 200 scientists from five continents call for a precautionary approach to toxic chemicals, to protect fetuses and children from chemical exposures that may doom them to disease (cancer, diabetes, attention deficits, others) later in life, which may also be inherited by their children and grandchildren. The Faroes Statement defines a "new paradigm of understanding in toxicology."]

[Introduction: This consensus statement was issued March 24, 2007, by the International Conference on Fetal Programming and Developmental Toxicity held May 20-24, 2007, at Torshavn, Faroe Islands, which was attended by more than 200 biologists, toxicologists, epidemiologists, nutrion researchers, and pediatricians. The conference was organized jointly with, and sponsored by, BCPT (the journal, Basic & Clinical Pharmacology and Toxicology); the World Health Organization; the European Environment Agency; the Centers for Disease Control and Prevention; National Institute of Environmental Health Sciences and National Institute of Child Health and Human Development, National Institutes of Health. The conference was co-chaired by Philippe Grandjean (University of Southern Denmark and Harvard School of Public Health) and Pal Weihe (The Faroese Hospital System).]

Background

Fetal life and early infancy are periods of remarkable susceptibility to environmental hazards. Toxic exposures to chemical pollutants during these windows of increased susceptibility can cause disease and disability in infants, children, and across the entire span of human life. Among the effects of toxic exposures recognised in the past have been congenital malformations and other adverse pregnancy outcomes. These outcomes may be readily apparent and have been linked to toxicant exposures during or prior to pregnancy. Even subtle effects caused by chemical exposures during early development may lead to important functional deficits and increased risks of disease later in life. The notion of developmental plasticity of organ functions and disease risks has gained much support from both experimental and epidemiological studies. The timing of exposure -- with an emphasis on critical windows of susceptibility -- has therefore become a crucial factor to be considered in toxicological assessments.

During May 20-24, 2007, researchers in the fields of environmental health, environmental chemistry, developmental biology, toxicology, epidemiology, nutrition, and paediatrics gathered at the International Conference on Fetal Programming and Developmental Toxicity, in Torshavn, Faroe Islands. The conference goal was to highlight new insights into the effects of prenatal and early postnatal exposure to toxicants, and their sustained effects on the individual throughout their lifespan. The Conference brought together, for the first time, key researchers to focus on human data and translation of laboratory results to elucidate the environmental risks to human health.

Research state of the art

The developing fetus is extraordinarily susceptible to perturbation of the intrauterine environment. Fetal development is adjusted to the intrauterine environment of nutrients and energy supply to fit the anticipated postnatal environmental conditions. If a disparity arises between prenatal and postnatal environments, it can cause abnormalities in energy metabolism, endocrine functions, and organ development. Evolution seems to have favoured a "thrifty" phenotype that optimizes the energy use, but which, in an environment with ample food and limited energy expenditure, can increase the likelihood of developing obesity, metabolic syndrome, and associated diseases.

The physiological mechanisms involved in the development of energy and nutrient metabolism are also highly vulnerable to toxic effects of environmental chemicals. Chemical exposures during prenatal and early postnatal life can bring about important effects on gene expression, which determines normal development and also predisposes to disease risks during adolescence and adult life. Many environmental chemicals can alter gene expression by DNA methylation and chromatin remodelling. These epigenetic changes can cause lasting functional changes in specific organs and tissues and increased susceptibility to disease that may even affect successive generations.

New research on rodent models shows that developmental exposures to toxic chemicals, such as the hormonally active substances, diethylstilbestrol, tributyl tin, bisphenol A, genistein, can increase the incidence of reproductive abnormalities, metabolic disorders, including obesity and diabetes, and cancer, presumably through epigenetic mechanisms that do not involve changes to DNA sequences but may be heritable.

Prenatal exposure to diethylstilbestrol, an estrogenic drug no longer used on pregnant women, causes an increased risk of vaginal, uterine, and breast cancer. Low-level developmental exposure to a plastics ingredient, bisphenol A, can result in increased susceptibility to breast cancer or prostate cancer, and prenatal exposure to vinclozoline, a common fungicide, also promotes later development of cancer. These substances are only weak carcinogens, if at all, in the adult organism but are nonetheless hazardous to the growing fetus. In addition, when exposure to a carcinogenic substance occurs during early development, the expected life-span will exceed the normal latency period for development of the disease.

Functioning of the human reproductive system is highly vulnerable to changes in the intrauterine hormonal environment. In men, increasing occurrence of testicular cancer, poor semen quality, and cryptorchidism have all been linked to developmental exposures to maternal smoking and endocrine disrupting chemicals, such as diethylstilbestrol. Additional risk factors include fertility treatment of the mother, phthalate exposure, and occupational exposure to pesticides with suspected estrogenic and antiandrogenic activity. Perinatal exposure to endocrine disrupting chemicals, such as polychlorinated or polybrominated biphenyls, endosulfan, or DDT compounds, may affect puberty development and sexual maturation at adolescence. Expression of some of these effects may be promoted by predisposing genetic traits.

The brain is particularly sensitive to toxic exposures during development, which involves a complex series of steps that must be completed in the right sequence and at the right time. Slight decrements in brain function may have serious implications for social functioning and economic activities, even in the absence of mental retardation or obvious disease. Each neurotoxic contaminant may perhaps cause only a negligible effect, but the combination of several toxic chemicals, along with other adverse factors, such as maternal stress or decreased thyroid function, may trigger substantial decrements in brain function and may predispose to the development of serious degenerative disease.

The immune system also undergoes important development both before and after birth. New evidence suggests that exposure to some immunotoxic chemicals, such as polychlorinated biphenyls and atrazine, and maternal stress may cause aberrant reactions of the immune system to foreign proteins, including vaccines. Such effects may be related to a shift in immune system balance, with an increased susceptibility to infections and an increased risk of development of allergy in the child.

While the research on developmental toxic effects has to date emphasised maternal exposures and the neonatal environment, the possibility exists that paternal exposures may also affect the child's development. Experimental studies suggest that ionizing radiation, smoking, and certain chemicals may be of importance, and some exposures may also affect the sex ratio of the children.

Conclusions

Three aspects of children's health are important in conjunction with developmental toxicity risks. First, the mother's chemical body burden will be shared with her fetus or neonate, and the child is then likely to be exposed to larger doses relative to the body weight. Second, susceptibility to adverse effects is increased during development, from preconception through adolescence. Third, developmental exposures to toxicants can lead to life-long functional deficits and manifestations of increased disease risks.

Research into the environmental influence on developmental programming of health and disease has therefore led to a new paradigm of toxicologic understanding. The old paradigm, developed over four centuries ago by Paracelsus, was that "the dose makes the poison". However, for exposures sustained during early development, the most important issue is that "the timing makes the poison". This extended paradigm deserves wide attention to protect the fetus and child against preventable hazards.

Part of the new insight derives from numerous animal studies on fetal programming being responsible for reproductive, immunological, neurobehavioural, cardiovascular, and endocrine dysfunctions and diseases, as well as certain cancers and obesity. These adverse effects have been linked to chemical pollutants at realistic human exposure levels similar to those occurring from environmental sources. Among the mechanisms involved, particular concern is raised about changes in gene expression due to altered epigenetic marking, which may not only lead to increased susceptibility to diseases later in life, but the effects may also be passed on to subsequent generations. Most chronic disease processes are characterised by multi-causality and complexity. Understanding such processes requires a more holistic approach that focuses on systems and tissue biology.

Recommendations

** Studies on the etiology of human disease therefore need to incorporate early development and characterise appropriately the factors that determine organ functions and subsequent disease risks. Such associations can best be examined in long-term prospective studies, and existing and planned birth cohorts should be utilized for this purpose.

** Cross-disciplinary approaches and translation of animal data on exposure biomarkers and disease susceptibility need to be promoted for application in studies of the etiology of human disease. Communication and clarification of key concepts and terms needs to be stimulated between the scientific disciplines involved and between these scientists and policymakers.

Environmental chemical exposure assessment should emphasise the time period of early development. Exposure data already routinely collected need to be optimised for application in epidemiological studies. Cord blood, cord tissue, human milk and other biological samples can be applied for assessment of exposure biomarkers and for determination of gene expression changes.

Since humans are exposed to numerous chemicals during development and throughout life, mixed exposures need to be considered in a life- course approach to disease. Further, the interaction due to other life-style factors, such as intake of essential nutrients and societal environment, needs to be explored. This research should also involve the impact of genetic variation and genetic predisposition to disease.

** Toxicological tests and risk assessment of environmental chemicals need to take into account the susceptibility of early development and the long-term implications of adverse programming effects. Although test protocols exist to assess reproductive toxicity or developmental neurotoxicity, such tests are not routinely used, and the potential for such effects is therefore not necessarily considered in decisions on safety levels of environmental exposures.

The accumulated research evidence suggests that prevention efforts against toxic exposures to environmental chemicals should focus on protecting the fetus and small child as highly vulnerable populations. Given the ubiquitous exposure to many environmental toxicants, there needs to be renewed efforts to prevent harm. Such prevention should not await detailed evidence on individual hazards to be produced, because the delays in decision-making would then lead to propagation of toxic exposures and their long-term consequences. Current procedures therefore need to be revised to address the need to protect the most vulnerable life stages through greater use of precautionary approaches to exposure reduction.

Note: This statement has been developed by the International Scientific Committee of the conference, taking into account comments and suggestions from the conference participants. The statement (pending minor editorial revision) will be included in the conference proceedings.

Members of the International Scientific Committee

David Barker (UK) David Bellinger (USA) Ake Bergman (Sweden) Roberto Bertollini (WHO) Sylvaine Cordier (France) Terri Damstra (WHO) George Davey-Smith (UK) Erik Dybing (BCPT) Brenda Eskenazi (USA) David Gee (EEA) Kimberly Gray (NIEHS) Mark Hanson (UK) Peter van den Hazel (The Netherlands) Jerry Heindel (NIEHS) Birger Heinzow (Germany) Irva Hertz-Picciotto (USA) Howard Hu (USA) Terry Huang (NICHD) Tina Kold Jensen (Denmark) Philip J Landrigan (USA) Caroline McMillen (Australia) Katsuyuki Murata (Japan) Larry L Needham (USA) Sjśršur Olsen (Denmark) Beate Ritz (IARC) Greet Schoeters (Belgium) Niels E Skakkebęk (Denmark) Staffan Skerfving (Sweden)

Copyright 2006 by Thomas Steen Christensen

::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::

From: Los Angeles Times ..................................[This story printer-friendly]
May 24, 2007

SCIENTISTS WARN OF DANGERS CHEMICALS POSE TO FETUSES, KIDS

[Rachel's introduction: This is how Marla Cone of the Los Angeles Times -- one of the best science writers working today -- covered the Faroes Statement.]

By Marla Cone

In a strongly worded declaration, many of the world's leading environmental scientists warned Thursday that exposure to common chemicals makes babies more likely to develop an array of health problems later in life, including diabetes, attention deficit disorders, prostate cancer, fertility problems, thyroid disorders and even obesity.

The declaration by about 200 scientists from five continents amounts to a vote of confidence in a growing body of evidence that humans are vulnerable to long-term harm from toxic exposures in the womb and during the first years after birth.

Convening in the Faroe Islands in the North Atlantic, toxicologists, pediatricians, epidemiologists and other experts warned that when fetuses and newborns encounter various toxic substances, growth of critical organs and functions can be skewed. In a process called "fetal programming," the children then are susceptible to diseases later in life -- and perhaps could even pass on those altered traits to their children and grandchildren.

The scientists' statement also contained a rare international call to action. The effort was led by Dr. Philippe Grandjean of Harvard University and University of Southern Denmark, and Dr. Pal Weihe of the Faroese Hospital System, who both have studied children exposed to mercury for more than 20 years.

Many governmental agencies and industry groups, particularly in the United States, have said there is no or little human evidence to support concerns about most toxic residue in air, water, food and consumer products. About 80,000 chemicals are registered in the United States.

Yet, the scientists urged government leaders not to wait for more scientific certainty and recommended that governments revise regulations and procedures to take into account subtle effects on fetal and infant development.

"Given the ubiquitous exposure to many environmental toxicants, there needs to be renewed efforts to prevent harm. Such prevention should not await detailed evidence on individual hazards," the scientists wrote in the four-page statement.

The scientists are particularly concerned that the newest animal research suggests that chemicals can alter gene expression -- turning on or off genes that predispose people to disease. Although the DNA itself would not be altered, such genetic misfires in the womb may be permanent, and all of the subsequent generations could be at greater risk of diseases, too.

"Toxic exposures to chemical pollutants during these windows of increased susceptibility can cause disease and disability in childhood and across the entire span of human life," the scientists concluded. "Recent research now shows that even subtle effects caused by chemical exposures during early development may lead to important functional deficits and increased risks of disease."

The Barker Hypothesis, conceived by a British scientist in 1992, says human fetuses are "programmed" for diseases by their early environment. The scientists concluded that this is now well-documented for toxic exposures by a large collection of animal experiments and some human data.

"A sad aspect with many of these prenatal exposures is that they leave the mother unscathed while causing injury to her fetus," said Dr. Philip Landrigan, a pediatrician who chairs the Mount Sinai School of Medicine's Department of Community and Preventive Medicine. He was one of the statement's authors.

In a more optimistic vein, the researchers said that if contaminants do play a big role in human health problems, some diseases could be prevented.

"Reducing exposure would lead to tremendous benefits," said Dr. Bruce Lanphear, director of the Environmental Health Center at Cincinnati Children's Hospital Medical Center. "We shouldn't wait for an epidemic to fully mature before we develop policies to protect children."

For centuries, the basic rule of toxicology has been "the dose makes the poison." Now, the scientists say "the timing makes the poison" -- in other words, when a toxic exposure occurs is as important as how much people are exposed to.

The fetus "is extraordinarily susceptible to perturbation of the intrauterine environment," they wrote.

The growing brain is the most sensitive. Mothers' exposure to mercury and polychlorinated biphenyls (PCBs) in fish and other seafood can cause slight declines in IQ and motor skills. In addition, early exposure to pesticides might trigger Parkinson's and Alzheimer's diseases.

Also, children exposed to lead, organophosphate pesticides or cigarette smoke have greater risk of attention deficit hyperactivity disorder. One of every three cases of the neurological disorder, affecting an estimated 560,000 children in the United States, can be attributed to either lead exposure or prenatal tobacco smoke exposure, Lanphear reported in a study published last December.

The immune, reproductive and cardiovascular systems also are vulnerable to early damage. Children exposed prenatally to PCBs have a high rate of infections and weak response to vaccinations. Many chemicals also can mimic hormones, and in animal tests, they feminize newborns, lowering sperm counts and promoting prostate, testicular, uterine and breast cancers.

In the newest area of research, metabolic systems -- which control how nutrients are converted into energy -- have been altered by chemicals administered in animal experiments, changes that may contribute to obesity and diabetes.

"These adverse effects have been linked to chemical pollutants at realistic human exposure levels similar to those occurring from environmental sources," the scientists wrote.

Among the risky chemicals they named are bisphenol A, found in polycarbonate plastic food and water containers, the pesticides atrazine, vinclozolin and DDT, lead, mercury, phthalates used in some cosmetics and soft plastics, brominated flame retardants, arsenic, which contaminates some water supplies, and PCBs, banned but ubiquitous, particularly in fish.

Some of the chemicals already have been regulated in the United States, but many have not. Moreover, the scientists said, tests for developmental effects are not routinely required, so "the potential for such effects is therefore not necessarily considered in decisions on safety levels of environmental exposures."

"We have absolutely solid evidence for certain chemicals -- lead, methyl mercury, PCBs, arsenic and the organophosphate pesticides," Landrigan said. "We know with great certainty that prenatal exposure to any of these materials can damage the developing brain with resulting lifelong loss of intelligence and disruption of behavior."

Yet there is "an incredible gap," he said, because 80 percent of major chemicals in commerce have never been tested to see if they damage early development.

Although the statement did not include any reference to it, some of the U.S. scientists said Congress should adopt a new law, similar to one enacted by the European Union last year, that requires more chemical testing and could ban many hazardous substances.

The conference was funded by the World Health Organization, National Institutes of Health, European Environment Agency and the Centers for Disease Control and Prevention.

Denmark's Faroe Islands, just south of the Arctic Circle, was the venue because it is home to the longest-running human experiment analyzing prenatal toxic exposure. Since 1986, Grandjean and Weihe have tracked Faroese children from the womb to adolescence to monitor neurological effects of mercury in seafood. Their findings prompted U.S. advisories that women of childbearing age and children avoid swordfish and other highly contaminated fish.

Ten U.S. scientists served on the 28-member committee that wrote the consensus: Landrigan; Brenda Eskenazi of the University of California, Berkeley; Irva Hertz-Picciotto of UC Davis; Beate Ritz of UCLA; Jerry Heindel and Kimberly Gray of the National Institute of Environmental Health Sciences; Larry Needham of the CDC; Terry Huang of the National Institute of Child Health and Human Development; David Bellinger of Harvard University; and Howard Hu of University of Michigan.

Copyright 2007, Los Angeles Times

::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::

From: PC Pro ..............................................[This story printer-friendly]
May 24, 2007

BBC: 'NO HARD EVIDENCE' FOR WI-FI SCARE

[Rachel's introduction: BBC: "Wi-Fi is being rolled out into classrooms around the country by the Government contrary to the precautionary approach recommended by the head of its own advisory body Sir William Stewart -- chair of the Health Protection Agency."]

By Simon Aughton

The BBC has admitted 'there is no hard evidence' on the long-term effects of Wi-Fi equipment, following its controversial Panorama investigation.

The admission comes in a letter sent from the BBC in reaction to viewers' complaints, and it has subsequently been published on the Bad Science website.

The letter begins with an apology for the lack of 'hard evidence' within the programme: 'Unfortunately, the truth is that as things stand, there is no hard evidence regarding the effects of long term exposure to Wi-Fi which is why we made the programme,' it says.

'The programme attempted to raise concern without causing alarm - always a difficult balance to strike but one which we believe we achieved,' the BBC says

'Wi-Fi is being rolled out into classrooms around the country by the Government contrary to the precautionary approach recommended by the head of its own advisory body Sir William Stewart -- chair of the Health Protection Agency,' the letter explains. 'As you will have seen in the programme, he believes that where radiation is concerned we should base policy on the precautionary principle particularly when it comes to children. This therefore raises questions as to whether Wi-Fi should be rolled out into the classroom without any long term health research being carried out.'

The letter then touches on the veracity of the programmes sources. Panorama contrasted the views of Swedish scientist Dr Olle Johansson, who said that the Swedish government recognises radiation sensitivity as a disability that affects three per cent of the population, with the UK Government's position that this condition does not exist.

But Swedish blogger DennisJ notes on badscience.net that Johnasson was the 2004 recipient of the Misleader of the Year award.

'I have found no indications that there are such things as official disabilities in Sweden or that "the Swedish government recognises radiation sensitivity as a disability",' he says. 'That it affects three per cent of the population is perhaps a half truth at best.'

The BBC has confirmed the validity of the letter, and told us that 19 complaints have been raised against the programme.

Copyright Copyright Dennis Publishing Limited licensed by Felden

f

::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::

From: Mendocino Partnership for the Precautionary Principle [This story printer-friendly]
May 27, 2007

MENDOCINO COUNTY, CALIFORNIA, ONE-YEAR UPDATE

[Rachel's introduction: Here is an update on precautionary policies in Mendocino County, California.]

By Britt Bailey

Dear Precautionary Principle Endorsers,

It has been nearly a year since Mendocino County passed the Precautionary Principle Policy. I want to take this opportunity to update you on our progress.

As you may know, the Precautionary Principle Policy states that the "implementation of the policy will begin with a pilot project utilizing two (2) County Departments to be recommended by the CEO and selected by the BOS. Implementation guidelines for the precautionary principle will be developed during this initial phase that will then be disseminated to other county departments for use and implementation. "

In October 2006, the interim CEO, Mr. Al Beltrami, proposed that the Water Agency and Environmental Health participate with the Precautionary Principle Partnership (hereinafter the Partnership) in developing a framework or procedure for implementing the objectives of the Principle. The Partnership has been meeting monthly with involved officials and we are on the brink of having a final draft framework or procedure to guide staff through the new decision-making process.

The procedure for implementing the Precautionary Principle will be applied to two different projects. Environmental Health has chosen to apply the Principle to its mosquito control program to manage for West Nile Virus. Currently the County recommends the use of mosquito fish and larvicides.

The Water Agency will be using the Precautionary Principle for an element of its Stormwater Management Program. The Stormwater Management Program, mandated by the Clean Water Act, holds considerable potential for controlling sediment run-off, illicit toxic discharges, and educating residents about the effects of such run-off into surface waters of Mendocino.

A major aspect of the Precautionary Principle includes transparency and public participation. To that end, our website (www.mendoprecaution.org) has been an active portal for any and all information related to our progress in Mendocino. Our meetings are posted and always open to the public. By the end of June the draft framework will be available for review. In addition, we strongly encourage public involvement in the upcoming pilot projects. Thank you for your continued interest in the Mendocino County Precautionary Principle.

Sincerely,

Britt Bailey Mendocino Partnership for the Precautionary Principle

http://www.mendoprecaution.org

::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::

Rachel's Precaution Reporter offers news, views and practical examples of the Precautionary Principle, or Foresight Principle, in action. The Precautionary Principle is a modern way of making decisions, to minimize harm. Rachel's Precaution Reporter tries to answer such questions as, Why do we need the precautionary principle? Who is using precaution? Who is opposing precaution?

We often include attacks on the precautionary principle because we believe it is essential for advocates of precaution to know what their adversaries are saying, just as abolitionists in 1830 needed to know the arguments used by slaveholders.

Rachel's Precaution Reporter is published as often as necessary to provide readers with up-to-date coverage of the subject.

As you come across stories that illustrate the precautionary principle -- or the need for the precautionary principle -- please Email them to us at rpr@rachel.org.

Editors:
Peter Montague - peter@rachel.org
Tim Montague - tim@rachel.org

::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::

To start your own free Email subscription to Rachel's Precaution Reporter send a blank Email to one of these addresses:

Full HTML edition: join-rpr-html@gselist.org
Table of Contents edition: join-rpr-toc@gselist.org

::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::

Environmental Research Foundation
P.O. Box 160
New Brunswick, N.J. 08901
rpr@rachel.org

::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::