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Table of Contents...

The Faroes Statement
  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."
Scientists Warn of Dangers Chemicals Pose to Fetuses, Kids
  This is how Marla Cone of the Los Angeles Times -- one of the best
  science writers working today -- covered the Faroes Statement.
BBC: 'No Hard Evidence' for Wi-Fi Scare
  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."
Mendocino County, California, One-year Update
  Here is an update on precautionary policies in Mendocino County,
  California.

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From: PPTOX 2007, May 24, 2007
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THE FAROES STATEMENT

Human health effects of developmental exposure to environmental
toxicants

Consensus statement issued by the International Conference on Fetal
Programming and Developmental Toxicity

[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)
Sjúrður Olsen (Denmark)
Beate Ritz (IARC)
Greet Schoeters (Belgium)
Niels E Skakkebæk (Denmark)
Staffan Skerfving (Sweden)

Copyright 2006 by Thomas Steen Christensen

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From: Los Angeles Times, May 24, 2007
[Printer-friendly version]

SCIENTISTS WARN OF DANGERS CHEMICALS POSE TO FETUSES, KIDS

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

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From: PC Pro, May 24, 2007
[Printer-friendly version]

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

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

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From: Mendocino Partnership for the Precautionary Principle, May 27, 2007
[Printer-friendly version]

MENDOCINO COUNTY, CALIFORNIA, ONE-YEAR UPDATE

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

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  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
  
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