the tobacco industry violated the Racketeer Influenced Corrupt
Organizations Act RICO law to "defraud the public." with huge amounts of
false research to mislead people about its addictive toxin, Elisa K
Tong, Stanton A Glantz, Circulation 2007 Oct. 16: Murray 2007.10.17
http://RMForAll.blogspot.com October 17, 2007
http://groups.yahoo.com/group/aspartameNM/message/1480

[ Rich Murray comments: Sadly, this probably throws a lot of light on
similar manipulations by the aspartame industry. ]


EXCERPT: [ SHS = second hand smoke ]

"People should understand how hard the tobacco industry has worked to
undermine scientific evidence," said Elisa Tong, an assistant professor
of internal medicine at UC Davis School of Medicine and lead author of
the study”

"The tobacco industry's efforts at manipulating scientific literature as
a way to serve their economic and political needs continues to this
day," said Glantz. "Despite the overwhelming and unbiased
epidemiological and biological evidence, our analysis of industry
documents shows how tobacco companies are continuing to market a
dangerous product in any way they can."

"The tobacco industry’s efforts to subvert scientific conclusions on SHS
have been previously described for lung cancer 15, 22–24 and sudden
infant death syndrome. 25"

"The tobacco industry’s efforts to manipulate the scientific process,
including the use of "special [scientific] projects" managed by lawyers,
was a central element of the 2006 federal court ruling that the tobacco
industry violated the Racketeer Influenced Corrupt Organizations Act
(RICO) law to "defraud the public." 147"

"Because the OSHA proposal 27 addressed all indoor air pollution, not
just SHS, the tobacco industry’s actions have repercussions on
regulating other pollutants and environmental chemicals that have
significance in the emergent field of environmental cardiology. 137"

The full paper is available at
http://circ.ahajournals.org/cgi/reprint/116/16/1845?ijkey=v6vvZyY12zJrium&keytyp\
e=ref
pdf free full text

https://exchange.ucsf.edu/exchweb/bin/redir.asp?URL=http://circ.ahajournals.org/\
cgi/reprint/116/16/1845?ijkey=v6vvZyY12zJrium%26keytype=ref

http://circ.ahajournals.org/cgi/content/full/116/16/1845?ijkey=v6vvZyY12zJrium&k\
eytype=ref
html free full text


FOR IMMEDIATE RELEASE: OCT. 15, 2007

UC STUDY UNCOVERS TOBACCO INDUSTRY EFFORTS TO UNDERMINE SECONDHAND SMOKE
LINK TO CARDIOVASCULAR DISEASE

(SACRAMENTO, Calif.) -- After combing through nearly 50 million pages of
previously secret internal, tobacco industry documents, UC Davis and UC
San Francisco researchers say they have documented for the first time
how the industry funded and used scientific studies to undermine
evidence linking secondhand smoke to cardiovascular disease.

In a special report published in the Oct. 16 issue of the journal
Circulation, authors Elisa K. Tong and Stanton A. Glantz say that the
tobacco-related documents they reviewed show how the industry initially
worked to question scientific evidence about the harmful effects of
secondhand smoke as a way to fight smoke-free regulations.

More recently, they suggest, tobacco company-funded studies have been
conducted to support the development of so-called "reduced-harm" cigarettes.

"People should understand how hard the tobacco industry has worked to
undermine scientific evidence," said Elisa Tong, an assistant professor
of internal medicine at UC Davis School of Medicine and lead author of
the study. "It's not just about fighting smoke-free regulations. Our
analysis of the documents indicates an industry that also wants to
influence the debate about how 'reduced-harm' tobacco products should be
evaluated."

Tong conducted a computerized search involving millions of pages of
tobacco industry materials, including memos, letters and scientific
reports. The documents are publicly available as part of several major
legal settlements in recent years. Of the 5,000 documents ultimately
reviewed, she identified 47 closely tied to secondhand smoke and
cardiovascular disease issues.

Co-author Glantz, a professor of medicine in the cardiology division at
UCSF and director of the university's Center for Tobacco Control
Research and Education, helped analyze the information and develop a
detailed picture of tobacco industry practices.

The documents show how tobacco companies funded epidemiological and
biological research that was designed to support claims that secondhand
smoke posed little or no harm.

The Circulation article identifies a pattern within the studies that
misclassified study subjects as nonsmokers when they were actually
"passive smokers," who were being exposed to background air filled with
secondhand smoke.

This type of misclassification helped bias study results against finding
an effect from secondhand smoke.

The results were used to call into question other evidence linking
secondhand smoke to the increased risks of cardiovascular disease.

Such studies, the authors also say, were often published in scientific
journals that had industry representatives on their editorial boards.

In one case cited by Tong and Glantz, the manuscript by RJ Reynolds'
scientists was reviewed for Inhalation Toxicology by an employee of RJ
Reynolds before its publication in 1998.

"The process was presented to the outside world as having peer review,"
noted Glantz. "The true level of the tobacco industry's involvement in
such studies was rarely disclosed in an adequate manner."

Unfavorable research results also were suppressed by the tobacco
industry, according to Tong and Glantz.

Their report cites a 1995 industry study that found nonsmokers exposed
to more than seven hours of secondhand smoke suffered statistically
significant changes in blood lipids, inflammatory markers, pulmonary
function tests and urinary mutagenicity. Those findings, say Tong and
Glantz, appear to have been briefly revealed at a conference and only
partially published elsewhere.

The pair note in their report that when tobacco-funded studies in the
early 1990s demonstrated that secondhand smoke increased
atherosclerosis, the industry criticized the findings and withdrew funding.

Tong and Glantz also point to several industry studies that attempted to
provide alternative explanations for the direct cardiovascular effects
of secondhand smoke by attributing findings to an unproven "stress"
response in individuals from the odor of smoke rather than its inherent
toxicity.

Tong and Glantz suggest one of the key reasons why tobacco companies
have hindered efforts to ban smoking in public places is to maintain
corporate viability in the marketplace.

They note that smoke-free workplace rules can reduce cigarette
consumption among smokers by approximately three cigarettes per day, or
about 30 percent.

"What the documents we reviewed show is an industry strategy that, in
their own words, will continue to question the evidence about secondhand
smoke as a way 'to keep controversy alive,'" said Tong. "Tobacco
companies want to debate this forever because it helps challenge
no-smoking policies. And since such policies diminish cigarette
consumption, it obviously strikes at the heart of corporate revenue."

The Circulation report suggests the tobacco industry is preparing for
another scientific battle, this one involving the allegedly
"reduced-harm" tobacco products.

Policy makers, tobacco companies and their critics are currently
debating claims about the possibility of a less harmful cigarette and
whether the U.S. Food and Drug Administration should regulate such products.

Tong and Glantz describe an industry executive as stating that the
research priorities in developing biomarker assays for the so-called
"reduced-harm" products is not to establish any real effects or
long-term clinical impacts from secondhand smoke.

They suggest such efforts by the industry are being done to demonstrate
the elimination of potential elements, such as odor or a chemical
compound, in cigarette products without admitting existing health impacts.

The two authors emphasize that their overall analysis of the industry's
memos, letters and reports indicates the need for caution in the current
debates about tobacco industry regulation and the potential development
of what the industry claims are "reduced-harm" products.

"The tobacco industry's efforts at manipulating scientific literature as
a way to serve their economic and political needs continues to this
day," said Glantz. "Despite the overwhelming and unbiased
epidemiological and biological evidence, our analysis of industry
documents shows how tobacco companies are continuing to market a
dangerous product in any way they can."

The Circulation study was funded by an American Heart Association
Western States Postdoctoral Fellowship and a grant from the National
Cancer Institute.
The primary source for tobacco industry documents was UC San
Francisco's Legacy Tobacco Document Library,
http://legacy.library.ucsf.edu/

Media Contacts:
Charles Casey, UC Davis Health System: (916) 734-9064
Corinna Kaalela, UC San Francisco: (415) 476-8254

About the University of California, Davis
Along with being a leader in health-care research, UC Davis School of
Medicine is known for its commitment to people from underserved
communities and a passion for clinical care.
The university's research strengths include clinical and translational
science, regenerative medicine, infectious disease, vascular biology,
neuroscience, functional genomics and mouse biology, comparative
medicine and nutrition, among many others.

About the University of California, San Francisco
UCSF is a leading university dedicated to defining health worldwide
through advanced biomedical research, graduate level education in the
life sciences and health professions, and excellence in patient care.

Public Affairs
UC Davis Health System
4900 Broadway, Suite 1200
Sacramento, CA 95820
Phone: (916) 734-9040
FAX: (916) 734-9066
E-mail: publicaffairs@...,
Web address: http://www.ucdmc.ucdavis.edu/newsroom/


In addition, the AHA released the following statement on our paper:

EMBARGOED UNTIL 4:00 PM EDT CONTACT: Aaron Tallent
Monday, October 15, 2007 202-785-7946

Statement of M. Cass Wheeler
CEO, American Heart Association,
on "Tobacco Industry Efforts Undermine Evidence Linking Secondhand Smoke
with Cardiovascular Disease"
by Elisa Tong, MA, MD and Stanton Glantz, PhD
October 15, 2007

Since the late 1990s, researchers have searched millions of pages of
documents and uncovered evidence of suggesting that tobacco companies
attempting to sully scientific findings, duping consumers and
aggressively preying on our children.

Their despicable tactics have confused generations of Americans and
policymakers about the dangers of smoking and of secondhand smoke exposure.

Fortunately, lawmakers need not be misled by these practices when
debating smoke-free workplace ordinances.

This special report by researchers Drs. Elisa Tong and Stanton Glantz
published in Circulation exposes the deceitful practices of the tobacco
industry in its attempts to fight smoke-free regulations and serves as
an eye-opener for the public health community and the federal government
as the "reduced harm product" debate picks up steam.

According to the U.S. Surgeon General, secondhand smoke exposure is
estimated to cause 46,000 coronary heart disease deaths each year and
increase a nonsmoker's risk for heart disease by as much as 30 percent.

These statistics should alarm workers, employers and policymakers in
cities and towns that have yet to implement smoke-free workplace laws.

It is inhumane to expect workers and patrons, including those in
restaurants and bars, to inhale someone else's deadly cigarette smoke.

More than 20 states and a large number of cities have passed
comprehensive smoke-free workplace laws.

It is time for the rest of the nation to do so as well.

It is also time for Congress to pass the Family Smoking Prevention and
Tobacco Control Act, legislation giving the Food and Drug Administration
meaningful regulatory authority over tobacco products.

Big Tobacco is currently able to make misleading health claims about its
products without showing evidence of reduced harm.

That gaping loophole would be closed with the passage of this legislation.

Regardless, in creating "reduced harm" products, the tobacco industry's
focus should be reducing the effects of cardiovascular disease and other
diseases, rather than removing a few carcinogens to meet their so-called
standards of a safer cigarette.



[ [occ-env-med-l] FYI -- Tobacco industry undermining of secondhand
smoke literature
From: David Wallinga dWallinga@...,
Date: 2007.10.16 2:25 pm

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Circulation. 2007; 116: 1845-1854.
© 2007 American Heart Association, Inc.
Special Report
Tobacco Industry Efforts Undermining Evidence Linking Secondhand Smoke
With Cardiovascular Disease [ 152 references ]
Elisa K. Tong, MD, MA; Stanton A. Glantz, PhD
From the Division of General Internal Medicine, Department of Medicine,
University of California, Davis (E.K.T.),
and Division of Cardiology, Department of Medicine, Cardiovascular
Research Institute, and Center of Tobacco Control Research and
Education, University of California, San Francisco (S.A.G.).

Correspondence to Stanton Glantz, 530 Parnassus, Ste 366, University of
California, San Francisco, San Francisco, CA 94143–1390.
E-mail glantz@...,

Background -- The scientific consensus that secondhand smoke (SHS)
increases cardiovascular disease (CVD) risk by 30 % is based on
epidemiological and biological evidence.

The tobacco industry has contested this evidence that SHS causes CVD,
but how and why they have done it has not been described.

Methods and Results -- About 50 million pages of tobacco industry
documents were searched using general keywords and names of industry
consultants and scientists.

Tobacco industry–funded epidemiological analyses of large data sets were
used to argue against an epidemiological association between SHS and CVD
and smoke-free regulations, but these analyses all suffered from
exposure misclassification problems that biased the results toward the null.

More recent industry-funded publications report an increased risk of CVD
associated with SHS but claim a low magnitude of risk.

When early tobacco industry–funded work demonstrated that SHS increased
atherosclerosis, the industry criticized the findings and withdrew funding.

RJ Reynolds focused on attacking the biological plausibility of the
association between SHS and CVD by conducting indirect platelet
aggregation studies, exposure chamber experiments, and literature reviews.

Although these studies also suffered from exposure misclassification
problems, several produced results that were consistent with a direct
effect of SHS on blood and vascular function.

Instead, RJ Reynolds attributed these results to an unproven
epinephrine-related stress response from odor or large smoke exposure,
which supported their regulatory and "reduced-harm" product development
efforts.

Philip Morris’ recent "reduced-harm" efforts seem supportive of a
similar corporate agenda.

Conclusions -- The tobacco industry attempted to undermine the evidence
that SHS causes CVD to fight smoke-free regulations while developing
approaches to support new products that claim to reduce harm.

The industry interest in preserving corporate viability has affected the
design and interpretation of their cardiovascular studies, indicating
the need for great caution in current debates about future tobacco
industry regulation and development of reduced-harm tobacco products.

Key Words: epidemiology • lipids • platelets • public policy • tobacco
smoke pollution

Introduction

The first epidemiological studies linking secondhand smoke (SHS) with
heart disease were published in the mid-1980s, 1,2 with reviews
concluding that SHS caused cardiovascular disease (CVD) published in
19883 and 1991. 4

In 1992, the American Heart Association’s Council on Cardiopulmonary and
Critical Care concluded that SHS was a "major preventable cause of
cardiovascular disease and death." 5

With the accumulation of published literature, scientific and public
health organizations have consistently concluded 5-8 that SHS increases
CVD risk by 30 % and accounts for about 46 000 nonsmoker deaths a year
7; newer research strongly suggests a larger effect. 9

Initially, many were concerned that the observed effect was too large,
given the much lower dose of smoke a passive smoker receives than an
active smoker.

It is now clear that small exposures to tobacco smoke such as with SHS
or smoking 1 or 2 cigarettes a day substantially affect heart disease
risk because of the nonlinear dose-response effects on platelet
activation, endothelial dysfunction, and other factors. 4, 10–14

The tobacco industry has contested the conclusion that SHS is dangerous
because widespread acceptance of this fact builds support for smoking
restrictions, 15,16 which reduce cigarette consumption 17 and thus
industry profits.

Beginning in 1988, the tobacco industry developed an "International ETS
[environmental tobacco smoke, the industry’s name for SHS] Consultants
Program" to "keep the controversy alive" on SHS by recruiting physicians
and scientists to develop and promote viewpoints favorable to the
industry. 16,18

The industry’s now-disbanded Center for Indoor Air Research (CIAR) has
been a mechanism for funding "special-reviewed" projects selected by
lawyers and industry executives that support the industry position
against smoking regulations. 19

(CIAR has, however, been essentially reconstituted as the Philip Morris
External Research Program. 20,21)

The tobacco industry’s efforts to subvert scientific conclusions on SHS
have been previously described for lung cancer 15, 22–24 and sudden
infant death syndrome. 25

The tobacco industry used similar strategies to undermine the evidence
that SHS causes CVD to fight smoke-free regulations while later
developing approaches to support new products that claim to "reduce harm."

Discussion

This is the first article to describe how the tobacco industry initiated
and funded scientific work to counter epidemiological and biological
conclusions that SHS causes CVD.

The industry pursued this work initially to fight smoke-free
regulations; later, the work also was done to promote allegedly
"reduced-harm" products.

Tobacco industry–funded epidemiological analyses 57,58,73 of large data
sets were used to argue against an epidemiological association between
SHS and CVD, but these analyses all suffered from exposure
misclassification problems that eventually even some in the tobacco
industry 71 recognized.

More recent industry-funded publications 68,75 report an increased risk
of CVD associated with SHS but claim that the magnitude of the risk is
far below the generally accepted 30 % increase. 7,8

When early tobacco industry–funded work demonstrated that SHS increased
atherosclerosis, 39,45,46 the industry criticized the findings for using
smoke concentrations larger than that in the real world and withdrew
funding.

RJR focused on attacking the biological plausibility of the association
between SHS and CVD by conducting indirect platelet aggregation studies,
exposure chamber experiments, and literature reviews.

Although many of the RJR studies also suffered from exposure
misclassification problems, several 85,86,91 produced results that were
consistent with a direct effect of SHS on blood and vascular function.

RJR, however, chose to interpret the cardiovascular effects associated
with SHS as actually reflecting an unproven epinephrine-related stress
response from odor or large smoke exposure (which the industry had tried
unsuccessfully 83 to remove).

RJR’s stress hypothesis supported their regulatory and "reduced-harm"
product development efforts, and PM’s recent interest in these products
seems similar in developing scientific work to support the viability of
the industry rather than products with long-term clinical significance.

These industry efforts have not, however, prevented the scientific
community from concluding that SHS causes CVD. 7,8,67

It is now accepted that some of the key cardiovascular effects of SHS
are nearly as large as those of smoking. 12–14

However, the industry’s efforts to slow national regulation of SHS by
OSHA -- one of its original motivations for its efforts to challenge the
conclusion that SHS caused CVD -- were successful.

Although OSHA conducted its own review and concluded that SHS increased
the risk for lung cancer and CVD in 1994, 27 it withdrew its proposal
for smoke-free workplaces in 2001 after the tobacco industry
successfully delayed and weakened the proposal. 136

Because the OSHA proposal 27 addressed all indoor air pollution, not
just SHS, the tobacco industry’s actions have repercussions on
regulating other pollutants and environmental chemicals that have
significance in the emergent field of environmental cardiology. 137

Simply eliminating SHS exposure through regulatory policies immediately
reduces morbidity and mortality from CVD.

Smoke-free workplaces reduce absolute smoking prevalence by 3.8 % and
reduce cigarette consumption among continuing smokers by about 3
cigarettes a day. 17

Implementation of smoke-free laws in public places and workplaces
results in subsequent significant reductions in acute myocardial
infarction hospitalizations 138–141 by about 27 %. 142

The California Tobacco Control program, which has a strong smoke-free
component, significantly accelerated both the decline in cigarette
consumption and cardiovascular mortality, with 59 000 fewer
cardiovascular deaths estimated between 1989 and 1997. 143,144

A model of the first-year benefits of making all unregulated workplaces
smoke free in 1999, when {approx}30 % workers were not covered by
smoke-free policies, 145 estimated that such a policy would have
prevented about 1500 myocardial infarctions and 350 strokes and resulted
in nearly $49 million in savings in direct medical costs. 146

The tobacco industry’s efforts to manipulate the scientific process,
including the use of "special [scientific] projects" managed by lawyers,
was a central element of the 2006 federal court ruling that the tobacco
industry violated the Racketeer Influenced Corrupt Organizations Act
(RICO) law to "defraud the public." 147

The court did not, however, specifically address industry efforts to
undermine the science on the CVD effects of SHS, perhaps because nothing
had been published evaluating these efforts.

As of 2007, PM and RJR still did not publicly acknowledge that their
companies believe SHS causes disease.

(These public positions contradict analyses of unpublished data from
tobacco industry’s internal studies, which demonstrate that sidestream
smoke from a burning cigarette [85 % of SHS] is 4 times more toxic per 1
g TPM than mainstream smoke. 148

Their unpublished research also shows that as sidestream smoke ages, it
becomes another 4 times more toxic than fresh smoke, 149 suggesting that
aged sidestream smoke is an order of magnitude more toxic than fresh
mainstream smoke.)

For several years, PM has admitted that public health officials (but not
PM itself) conclude SHS causes disease and that this concern is
sufficient to warrant regulating smoking in public places 150;

RJR’s Web site previously stated that although public health officials
have reached this conclusion, the company believes SHS is unlikely to
present any significant harm to otherwise healthy nonsmoking adults. 151

After the federal RICO ruling, 147 RJR’s Web site was revised to state
that adults should avoid exposing minors to SHS and that public
policymakers should encourage the development of tobacco products that
reduce harm or risk of serious disease. 152

In addition, the court identified the Philip Morris External Research
Program, which continues to fund cardiovascular research in
universities, as an element of the continuing fraud.

This fact has contributed to the decision by many universities to adopt
policies to decline tobacco industry research funding.

Understanding the context in which the tobacco industry operates to
preserve its corporate interests is important in evaluating the research
funded by the tobacco industry on SHS, including that on CVD.

The industry interest in preventing smoke-free regulations and
supporting claims of "reduced-harm" products to preserve corporate
viability has affected the design and interpretation of its scientific
cardiovascular studies.

The question of whether CVD effects, not just carcinogens, can be
eliminated with the large number of chemicals in tobacco smoke must be
on the forefront in the ongoing "reduced-harm" product debate, 126,127 a
debate that will intensify if the federal Food and Drug Association is
granted authority to regulate tobacco products.

The industry’s past and recent cardiovascular scientific activities
indicate the need for great caution in current debates about future
tobacco industry regulation and development of "reduced-harm" tobacco
products.

Acknowledgments

Sources of Funding

This research was supported by an American Heart Association Western
States Postdoctoral Fellowship and National Cancer Institute grant
CA-87472. The funding agencies had no role in the conduct of the
research or preparation of the manuscript.

Disclosures

None.


http://pediatrics.aappublications.org/cgi/content/full/115/3/e356
free full html text

Published online March 1, 2005
PEDIATRICS Vol. 115 No. 3 March 2005, pp. e356-e366
(doi:10.1542/peds.2004-1922)

ELECTRONIC ARTICLE
Changing Conclusions on Secondhand Smoke in a Sudden Infant Death
Syndrome Review Funded by the Tobacco Industry
Elisa K. Tong, MD *,{d dagger},
Lucinda England, MD §
and Stanton A. Glantz, PhD {d dagger},||

* Division of General Internal Medicine Fellowship Program
{d dagger} Center for Tobacco Control Research and Education
|| Institute for Health Policy Studies, Cardiovascular Research
Institute, University of California, San Francisco, California
§ Division of Reproductive Health, Centers for Disease Control and
Prevention, Department of Health and Human Services, Atlanta, Georgia

ABSTRACT

Background.
Prenatal and postnatal exposure to tobacco smoke adversely affects
maternal and child health.
Secondhand smoke (SHS) has been linked causally with sudden infant death
syndrome (SIDS) in major health reports.
In 1992, the US Environmental Protection Agency (EPA) first noted an
association between SHS and SIDS, and both prenatal exposure and
postnatal SHS exposure were listed as independent risk factors for SIDS
in a 1997 California EPA report (republished in 1999 by the National
Cancer Institute) and a 2004 US Surgeon General report.

The tobacco industry has used scientific consultants to attack the
evidence that SHS causes disease, most often lung cancer.
Little is known about the industry’s strategies to contest the evidence
on maternal and child health.
In 2001, a review was published on SIDS that acknowledged funding from
the Philip Morris (PM) tobacco company.
Tobacco industry documents related to this review were examined to
identify the company’s influence on the content and conclusions of this
review.

Methods.
Tobacco industry documents include 40 million pages of internal memos
and reports made available to the public as a result of litigation
settlements against the tobacco industry in the United States.
Between November 2003 and January 2004, we searched tobacco industry
document Internet sites from the University of California Legacy Tobacco
Documents Library and the Tobacco Documents Online website.
Key terms included "SIDS" and names of key persons.
Two authors conducted independent searches with similar key terms,
reviewed the documents, and agreed on relevancy through consensus.
Thirty documents were identified as relevant.
Two drafts (an early version and a final version) of an industry-funded
review article on SIDS were identified, and 2 authors independently
compared these drafts with the final publication.
Formal comments by PM executives made in response to the first draft
were also reviewed.
We used Science Citation Index in July 2004 to determine citation
patterns for the referenced SIDS reviews.

Results.
PM executives feared that SHS and maternal and child health issues would
create a powerful and emotional impetus for smoke-free areas in the
home, public areas, and the workplace.
In response to the 1992 US EPA report on SHS, the Science and Technology
Department of PM’s Switzerland subsidiary, Fabriques de Tabac Reunies,
searched for "independent" consultants to publish articles addressing SHS.
The first industry-funded article was a literature review focusing on
smoking and SIDS, conducted by consultant Peter Lee and co-author
Allison Thornton, which stated that the association between parental
smoking and SIDS could have been attributable to the failure to control
fully for confounders.
That first review has only been cited once, in the subsequent
industry-funded review.

In 1997, PM commissioned a consultant, Frank Sullivan, to write a
review, with coauthor Susan Barlow, of all possible risk factors for SIDS.
The first draft concluded that prenatal and postnatal smoking exposures
are both independent risk factors for SIDS.
After receiving comments and meeting with PM scientific executives,
Sullivan changed his original conclusions on smoking and SIDS.
The final draft was changed to emphasize the effects of prenatal
maternal smoking and to conclude that postnatal SHS effects were "less
well established."
Changes in the draft to support this new conclusion included
descriptions of Peter Lee’s industry-funded review, a 1999 negative but
underpowered study of SIDS risk and urinary cotinine levels, and
criticisms of the conclusions of the National Cancer Institute report
that SHS was causally associated with SIDS.
In April 2001, the Sullivan review was published in the United Kingdom
journal Paediatric and Perinatal Epidemiology, with a disclosure
statement that acknowledged financial support from PM but did not
acknowledge contributions from PM executives in the preparation of the
review.
By 2004, the Sullivan SIDS review had been cited at least 19 times in
the medical literature.

Conclusions.
PM executives responded to corporate concerns about the possible adverse
effects of SHS on maternal and child health by commissioning consultants
to write review articles for publication in the medical literature.
PM executives successfully encouraged one author to change his original
conclusion that SHS is an independent risk factor for SIDS to state that
the role of SHS is "less well established."
These statements are consistent with PM’s corporate position that active
smoking causes disease but only public health officials conclude the
same for SHS.
The author’s disclosure of industry funding did not reveal the full
extent of PM’s involvement in shaping the content of the article.
This analysis suggests that accepting tobacco industry funds can disrupt
the integrity of the scientific process.

The background of this SIDS review is relevant for institutions engaged
in the debate about accepting or eschewing funding from the tobacco
industry.
Those who support acceptance of tobacco industry funds argue that
academic authors retain the right to publish their work and maintain
final approval of the written product, but this argument fails to
recognize that the tobacco industry funds work to ensure that messages
favorable to the industry are published and disseminated.

Clinicians, parents, and public health officials are most vulnerable to
the changed conclusions of the SIDS review.
The national SIDS "Back to Sleep" campaign has been very successful in
reducing SIDS rates.
However, estimates of SIDS risk from SHS (odds ratios range from 1.4 to
5.1) have considerable overlap with estimates of risk from prone sleep
positioning (odds ratios range from 1.7 to 12.9).
With the Back to Sleep campaign well underway, efforts to address
parental smoking behavior in both the prenatal and postnatal periods
should be intensified.
The tobacco industry’s disinformation campaign on SHS and maternal and
child health can be counteracted within clinicians’ offices.

Key Words: secondhand smoke • tobacco industry • sudden infant death
syndrome

Abbreviations: SIDS, sudden infant death syndrome
EPA, Environmental Protection Agency
SHS, secondhand smoke
PM, Philip Morris
FTR, Fabriques de Tabac Reunies
NCI, National Cancer Institute
ETS, environmental tobacco smoke

Prenatal and postnatal exposure to tobacco smoke adversely affects
maternal and infant health.
Adverse outcomes that have been causally associated with prenatal
tobacco exposure include premature rupture of membranes, preterm
delivery, fetal growth restriction, and impaired pulmonary function
among infants. 1
Exposure of infants and children to secondhand smoke (SHS) has also been
associated with a number of adverse health outcomes, including induction
and exacerbation of asthma, otitis media, and sudden infant death
syndrome (SIDS).
National estimates of annual pediatric morbidity and mortality rates
associated with SHS exposure include 1900 to 2700 SIDS deaths,
0.7 to 1.6 million office visits for treatment of otitis media,
8,000 to 26,000 new cases of asthma,
400,000 to 1,000,000 asthma exacerbations,
and 150,000 to 300,000 cases of bronchitis or pneumonia among infants
and toddlers. 2

SHS has been causally linked with SIDS in a number of major health reports.
The landmark 1992 report from the US Environmental Protection Agency
(EPA) 3 not only confirmed that SHS causes lung cancer among nonsmokers
4,5 but also noted an association between SHS exposure and an increased
risk of SIDS.
Subsequent research on SIDS and smoking explored the roles of in utero
exposure (prenatal), exposure to SHS after birth (postnatal), or both.
In 1997, the California EPA concluded that both prenatal exposure and
postnatal SHS exposure are independent risk factors for SIDS. 2
The California EPA report was republished by the National Cancer
Institute (NCI) as part of its Smoking and Health Monograph Series in
1999, 6 with a preface by the US Surgeon General endorsing the report’s
conclusions.
In 1999, a World Health Organization report called for the elimination
of exposure to tobacco smoke in utero
and exposure to SHS in childhood. 7
Most recently, the 2004 Surgeon General’s report on smoking concluded
that there is "a causal relationship between SIDS and maternal smoking
during and after pregnancy." 1(pp 4–5)
////////////////////////////////////////////////////////////


"Of course, everyone chooses, as a natural priority,
to actively find, quickly share, and positively act
upon the facts about healthy and safe food, drink,
and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 117 members, 1,480 posts in a public,
searchable archive

http://groups.yahoo.com/group/aspartameNM/message/1472
bias, omissions, incuriosity = opportunity, aspartame safety evaluation,
Magnuson BA, Burdock GA, Williams GM, 7 more, 2007 Sept, Ajinomoto
funded 98 pages html [$ 32 781888262_content.pdf]: Murray 2007.09.15
////////////////////////////////////////////////////////////


13 mainstream research studies in 24 months showing aspartame toxicity,
also 3 relevant studies on methanol and formaldehyde: Murray 2007.10.17
http://groups.yahoo.com/group/aspartameNM/message/1464

Aspartame toxicity was shown in thirteen detailed mainstream research
studies in 24 months in work by expert teams in South Africa, England,
Italy, Greece, Hungary, and Mexico.

Very little has been publicized in mass print and broadcast media.

Also highly relevant are a study in South Korea that finds levels of
methanol similar to those from aspartame drinks cause the hangovers from
alcohol drinks, a study in China on Alzheimer's type damage in nerve
cells from low dose formaldehyde, and an IARC review by 25 experts that
determines formaldehyde to be a human carcinogen.
////////////////////////////////////////////////////////////


http://RMForAll.blogspot.com October 12, 2007
http://groups.yahoo.com/group/aspartameNM/message/1479
13,620 seniors using more than 1 can/week artificially sweetened
[aspartame] soft drinks had 8 % higher death risk, 1981-2004,
Paganini-Hill A, Kawas CH, Corrada MM, U. Southern Cal., Prev. Med. 2007
April 44(4) 305-10: Murray 2007.10.12


http://groups.yahoo.com/group/aspartameNM/message/1475
19,000 people, the 4 % of users of aspartame who drink average 5 cans
daily, have more problems in NIH AARP study of 474,000 people: Murray
2007.09.21
http://RMForAll.blogspot.com September 21, 2007


This is the first good data about the percentage of aspartame users who
use over 3 cans daily, averaging 5 cans daily at 200 mg per 12 oz can
diet soda.

About 4 % of 473,984 is 19,000 people, with a peak intake of 17 cans
daily, and average 5 cans daily.

It would be worthwhile to investigate a wide variety of symptoms for the
0.1 % of highest level users, about 500 people.

For about 200 million USA aspartame users, this would be 200,000 people.

Table 1 reveals consistent increase in problems from

--------------------- zero to (400-600) to (over 600) mg/d
aspartame intake:

% of cohort ---------- 46 -------- 5 -------- 4 %

mean aspartame mg/d --- 0 -------441 ------ 986

16+ education -------- 37 ------- 40 ------- 34 %

diabetes history ------ 3 ------- 22 ------- 26 %

alcohol g/d ---------- 14 ------- 11 ------- 13

never smoke ---------- 36 ------- 31 ------- 29 %

Body Mass Index ------ 26 ------- 29 ------- 29

18.5 - 25 ------------ 42 ------- 21 ------- 19 %

30 - 35 -------------- 13 ------- 23 ------- 26 %

over 35 -------------- 4 ------- 10 ------- 13 %

Physical activity %:

under 3-4/mo --------- 32 ------- 32 ------- 37 %

under 1-2/wk --------- 22 ------- 21 ------- 19 %

over 3-4/wk ---------- 45 ------- 45 ------- 43 %

Calories kcal ----- 1,919 ---- 1,855 ---- 2,044 %

Caffeine mg/d ------ 393 ------ 364 ------ 424

There do seem to be many increases of problems
from the second to third row, as mean aspartame use doubles.

Granted, this is cherry picking the data, selecting interesting patterns.

Correlations alone do not prove any direction of causation.

Nevertheless, it may be of value to study the correlations for
increasing aspartame intake among the 4 % using over 600 mg, the
equivalent of 3 cans 12-oz cans diet soda daily. The average use for
this group is 5 cans daily.

For instance, are a minority of these heavy users displaying the great
majority of the problems that are reflected in the mean for each level
of use, with most users only having little or no increase in problems?

This is a group of about 20,000 people.


http://groups.yahoo.com/group/aspartameNM/message/1141
Nurses Health Study can quickly reveal the extent of aspartame
(methanol, formaldehyde, formic acid) toxicity: Murray 2004.11.21

The Nurses Health Study is a bonanza of information about the health of
probably hundreds of nurses who use 6 or more cans daily of diet soft
drinks -- they have also stored blood and tissue samples from their
immense pool of subjects, over 100,000 for decades.


Cancer Epidemiol Biomarkers Prev. 2006 Sep; 15(9): 1654-9.
Comment in:
Cancer Epidemiol Biomarkers Prev. 2007 Jul; 16(7): 1527-8;
author reply 1528-9.
Consumption of aspartame-containing beverages and incidence of
hematopoietic and brain malignancies.
Lim U, Subar AF, Mouw T, Hartge P, Morton LM, Stolzenberg-Solomon R,
Campbell D, Hollenbeck AR, Schatzkin A.
Division of Cancer Control and Population Sciences,
National Cancer Institute, 6130 Executive Boulevard, EPN 4005,
Rockville, MD 20852-7344, USA. PMID: 16985027

Unhee Lim 1,
Amy F. Subar 2, subara@...,
Traci Mouw 1,
Patricia Hartge 1,
Lindsay M. Morton 1,
Rachael Stolzenberg-Solomon 1,
David Campbell 3,
Albert R. Hollenbeck 4
and Arthur Schatzkin 1

1 Division of Cancer Epidemiology and Genetics,

2 Division of Cancer Control and Population Sciences, National Cancer
Institute, NIH, Department of Health and Human Services;

3 Information Management Services, Inc., Rockville, Maryland; and

4 AARP, Washington, District of Columbia

Requests for reprints: Amy Subar,
Division of Cancer Control and Population Sciences,
National Cancer Institute,
6130 Executive Boulevard, EPN 4005, Rockville, MD 20852-7344.
Phone: 301-594-0831; Fax: 301-435-3710. E-mail: subara@...

http://cebp.aacrjournals.org/cgi/content/full/15/9/1654 free full text

BACKGROUND:
In a few animal experiments, aspartame has been linked to hematopoietic
and brain cancers.

Most animal studies have found no increase in the risk of these or other
cancers.

Data on humans are sparse for either cancer.

Concern lingers regarding this widely used artificial sweetener.

OBJECTIVE:
We investigated prospectively whether aspartame consumption is
associated with the risk of hematopoietic cancers or gliomas (malignant
brain cancer).

METHODS:
We examined 285,079 men and 188,905 women ages 50 to 71 years in the
NIH-AARP Diet and Health Study cohort

Daily aspartame intake was derived from responses to a baseline
self-administered food frequency questionnaire that queried consumption
of four aspartame-containing beverages (soda, fruit drinks, sweetened
iced tea, and aspartame added to hot coffee and tea) during the past year.

Histologically confirmed incident cancers were identified from eight
state cancer registries.

Multivariable-adjusted relative risks (RR) and 95% confidence intervals
(CI) were estimated using Cox proportional hazards regression that
adjusted for age, sex, ethnicity, body mass index, and history of diabetes.

RESULTS:
During over 5 years of follow-up (1995-2000), 1,888 hematopoietic
cancers and 315 malignant gliomas were ascertained.

Higher levels of aspartame intake were not associated with the risk of
overall hematopoietic cancer
(RR for over 600 mg/d, 0.98; 95 % CI, 0.76-1.27),
glioma (RR for over 400 mg/d, 0.73; 95 % CI, 0.46-1.15;
P for inverse linear trend = 0.05),
or their subtypes in men and women.

CONCLUSIONS:
Our findings do not support the hypothesis that aspartame increases
hematopoietic or brain cancer risk. PMID: 16985027

"We cannot exclude the possibility that higher aspartame consumption
than that observed in this study may be associated with an elevated risk
of hematopoietic or brain cancers.

In the laboratory study with positive findings, animals were fed doses
starting from 4 mg up to 5,000 mg per kg body weight.

Significantly elevated lymphomas and leukemias were observed in female
rats fed 20 mg of aspartame and higher (e.g., 1,200 mg for humans
weighing 60 kg or 132 lb; refs. 13, 14).

The reported aspartame intake in our data ranged from 0 to 3,400 mg/d
with sparse numbers in the upper intake categories (under 1 % consuming
over 1,200 mg/d).

However, we did not detect any increase in risk estimates in the highest
categories (over 1,200 or 2,000 mg/d, which is equivalent to about 7 to
11 cans of soft drinks daily) compared with the lowest categories,
and the associations were similarly null in both men and women."

Table 1. NIH-AARP Diet and Health Study aspartame intake levels from
beverages, 1995-2000 (N = 473,984) [ adapted from article ]

0 - under 100 - 100-200 - 200-400 - 400-600 - 600-1200 - over 1200 mg/d

cohort %
46 ------- 25 ------ 13 ------ 7 -------- 5 -- about 3 --- under 1
////////////////////////////////////////////////////////////


http://groups.yahoo.com/group/aspartameNM/message/1472
bias, omissions, incuriosity, opportunity, aspartame safety evaluation,
Magnuson BA, Burdock GA, Williams GM, 7 more, 2007 Sept, Ajinomoto
funded 98 pages html [$ 32 781888262_content.pdf]: Murray 2007.09.14


Eur J Clin Nutr. 2007 Aug 8; [Epub ahead of print]
Direct and indirect cellular effects of aspartame on the brain.
Humphries P,
Pretorius E, resia.pretorius@...,
Naudé H.
[1] Department of Anatomy, University of Pretoria, Pretoria, Gauteng,
South Africa
[2] Department of Anatomy, University of the Limpopo, South Africa.
http://groups.yahoo.com/group/aspartameNM/message/1463


Ultrastruct Pathol. 2007 Mar-Apr; 31(2): 77-83.
Ultrastructural changes to rabbit fibrin and platelets due to aspartame.
Pretorius E,
Humphries P.
Department of Anatomy, Faculty of Medicine,
University of Pretoria, South Africa.
[ Humphries P also at
Department of Anatomy, University of Limpopo.
Medunsa Campus, Garankuwa. South Africa ]
*Correspondence to E. Pretorius,
BMW Building, PO Box 2034,
Faculty of Health Sciences,
University of Pretoria, Pretoria 0001, South Africa
http://groups.yahoo.com/group/aspartameNM/message/1452


[ not about aspartame, but highly suggestive... ]
http://groups.yahoo.com/group/aspartameNM/message/1471
Food additives and hyperactive behaviour in kids, McCann D, Grimshaw K,
Sonuga-Barke, Warner JO, Stevenson J, et al, The Lancet 2007.09.06 pdf
454 KB: Murray 2007.09.06

www.dailymail.co.uk/pages/live/articles/health/womenfamily.html?in_article_id=45\
\3431&in_page_id=1799
By UK Daily Mail Newspaper
The proof food additives ARE as bad as we feared
By SEAN POULTER Last updated at 09:53am on 18th May 2007

[ This team will publish their confirming study later in 2007. ]
http://adc.bmj.com/cgi/content/full/89/6/506
Archives of Disease in Childhood 2004; 89(6): 506-511
Erratum in: Arch Dis Child. 2005 Aug; 90(8): 875.
© 2004 BMJ Publishing Group & Royal College of Paediatrics and Child Health
The effects of a double blind, placebo controlled, artificial food
colourings and benzoate preservative challenge on hyperactivity in a
general population sample of preschool children
B Bateman 1,
J O Warner 1, j.o.warner@...,
E Hutchinson 3,
T Dean 5, tara.dean@...,
P Rowlandson 4, Dr. Piers Rolandson, Paediatric Tutor
C Gant 5,
J Grundy 5,
C Fitzgerald 3
and J Stevenson 2 jsteven@...,
1 Infection, Inflammation and Repair Division, University of
Southampton, Southampton, UK
2 Department of Psychology, University of Southampton, Southampton, UK
3 Department of Clinical Psychology, St Mary’s Hospital, Isle of Wight, UK
4 Department of Paediatrics, St Mary’s Hospital, Isle of Wight, UK
5 David Hide Asthma and Allergy Research Centre, St Mary’s Hospital,
Isle of Wight, UK
http://groups.yahoo.com/group/aspartameNM/message/1461


www.ehponline.org/members/2007/10271/10271.pdf free full text 24 pages
National Institutes of Health
U.S. Department of Health and Human Services
ENVIRONMENTAL HEALTH PERSPECTIVES
Lifespan Exposure to Low Doses of Aspartame Beginning During Prenatal
Life Increases Cancer Effects in Rats
doi:10.1289/ehp.10271 (available at http://dx.doi.org/)
Online 13 June 2007
Morando Soffritti 1,
Fiorella Belpoggi 1,
Eva Tibaldi 1,
Davide Degli Esposti 1,
Michela Lauriola 1
1 Cesare Maltoni Cancer Research Center, European Ramazzini Foundation
of Oncology and Environmental Sciences, Bologna Italy
Address of the institution: Cesare Maltoni Cancer Research Center,
European Ramazzini Foundation of Oncology and Environmental Sciences
Castello di Bentivoglio, Via Saliceto, 3, 40010 Bentivoglio, Bologna,
Italy +39 051 6640460 fax +39 051 6640223
crcfr@..., www.ramazzini.it
Address correspondence to: M. Soffritti
Acknowledgements:
This research was supported entirely by the European Ramazzini
Foundation Environmental Sciences.
The authors declare that they have no competing financial interests.
http://groups.yahoo.com/group/aspartameNM/message/1441


http://www.ramazzini.it/fondazione/docs/NYAS_Aspartame_Ramazzini.pdf
Results of Long-Term Carcinogenicity Bioassay on Sprague-Dawley Rats
Exposed to Aspartame Administered in Feed
Ann. N.Y. Acad. Sci. 2006 Sep; 1076: 559-577.
Fiorella Belpoggi,
Morando Soffritti,
Michela Padovani,
Davide Degli Esposti,
Michelina Lauriola, and
Franco Minardi.
The end judges everything -- HERODOTUS (480-425 B.C.) The History
Cesare Maltoni Cancer Research Center,
European Foundation of Oncology and Environmental Sciences
'B. Ramazzini',ť 40010 Bentivoglio, Bologna, Italy
http://groups.yahoo.com/group/aspartameNM/message/1382
[ and, previously ]
First experimental demonstration of the multipotential
carcinogenic effects of aspartame administered in the feed to
Sprague-Dawley rats.
Environ. Health Perspect. 2006 Mar; 114: 379-385. PMID: 16507461
Soffritti M, Belpoggi F, Degli Esposti D, Lambertini L, Tibaldi E, Rigano A.
Environmental Health Perspectives Volume 113, Number 11
November 2005 Current print issue
The full version of this article is available for free in PDF format.
http://ehp.niehs.nih.gov/members/2005/8711/8711.pdf 35 pages
First Experimental Demonstration of the
Multipotential Carcinogenic Effects of Aspartame
Administered in the Feed to Sprague-Dawley Rats.
Morando Soffritti, Fiorella Belpoggi, Davide Degli Esposti,
Luca Lambertini, Eva Tibaldi, and Anna Rigano.
doi:10.1289/ehp.8711 (available at http://dx.doi.org/)
Online 17 November 2005
The National Institute of Environmental Health Sciences
National Institutes of Health
U.S. Department of Health and Human Services
http://www.ehponline.org/
Cesare Maltoni Cancer Research Center,
European Ramazzini Foundation of Oncology and
Environmental Sciences
Sofritti, M. et al. 2005.
Aspartame induces lymphomas and leukaemias in rats.
Eur. J. Oncol. 2005; 10: 107-116.
http://groups.yahoo.com/group/aspartameNM/message/1250


Food Chem Toxicol. 2007 Jun 16;[Epub ahead of print]
The effect of aspartame metabolites on the suckling rat
frontal cortex acetylcholinesterase. An in vitro study.
Simintzi I,
Schulpis KH, inchildh@...,
Angelogianni P,
Liapi C,
Tsakiris S. stsakir@...,
Department of Experimental Physiology, Medical School,
University of Athens,
P.O. Box 65257, GR 15401 Athens, Greece.
http://groups.yahoo.com/group/aspartameNM/message/1459


Toxicology. 2007 May 18; [Epub ahead of print]
l-Cysteine and glutathione restore the reduction of rat hippocampal
Na(+),K(+)-ATPase activity induced by aspartame metabolites.
Simintzi I,
Schulpis KH,
Angelogianni P,
Liapi C,
Tsakiris S.
Department of Experimental Physiology,
Medical School, Athens University,
P.O. Box 65257, GR-15401 Athens, Greece.
http://groups.yahoo.com/group/aspartameNM/message/1447


Pharmacol Res. 2007 May 13; [Epub ahead of print]
The effect of aspartame on acetylcholinesterase activity in
hippocampal homogenates of suckling rats.
Simintzi I,
Schulpis KH,
Angelogianni P,
Liapi C,
Tsakiris S.
Department of Experimental Physiology,
Medical School, University of Athens,
P.O. Box 65257, GR-15401 Athens, Greece.
http://groups.yahoo.com/group/aspartameNM/message/1444


Eur J Clin Nutr. 2005 Dec 14; [Epub ahead of print]
The effect of L-cysteine and glutathione on inhibition of
Na(+), K(+)-ATPase activity by aspartame metabolites
in human erythrocyte [red blood cell] membrane.
Schulpis KH, Kleopatra H. Schulpis, MD, PhD.
Institute of Child Health, Aghia Sophia Children's Hospital,
GR-11527 Athens (Greece) +30 1 7708291, Fax +30 1 7700111
inchildh@...
Papassotiriou I, biochem@...,
Tsakiris T,
Tsakiris S. Stylianos Tsakiris. stsakir@...,
1 Institute of Child Health, Research Center,
'Aghia Sophia' Children's Hospital, Athens, Greece.
ggbriass@... ersi_voskaridou@...
mmoschov@... siahanidou@...
http://groups.yahoo.com/group/aspartameNM/message/1279


Pharmacol Res. 2005 Aug 26; [Epub ahead of print]
The effect of aspartame metabolites on human [red blood cell]
erythrocyte membrane acetylcholinesterase activity.
Tsakiris S,
Giannoulia-Karantana A,
Simintzi I,
Schulpis KH.
Department of Experimental Physiology, Medical School,
University of Athens, P.O. Box 65257, GR-154 01 Athens, Greece.
Stylianos Tsakiris. stsakir@...,
Giannoulia-Karantana A. First Department of Pediatrics,
Aghia Sophia Children's Hospital, University of Athens, Greece.
Kleopatra H. Schulpis, MD, PhD. Institute of Child Health,
Aghia Sophia Children's Hospital, GR-11527 Athens (Greece)
Tel. +30 1 7708291, Fax +30 1 7700111 inchildh@...
[ Papoutsakis T. tina.papoutsakis@...,
Papadopoulos G. Department of Biochemistry and Biotechnology,
University of Thessaly, Ploutonos 26, 41221 Larisa, Greece
papg@..., ]
http://groups.yahoo.com/group/aspartameNM/message/1213


In Vivo. 2007 Jan-Feb; 21(1): 89-92.
The effect of aspartame administration on oncogene and suppressor gene
expressions.
Gombos K, katalin_gombos@...,
Varjas T,
Orsos Z,
Polyak E,
Peredi J,
Varga Z,
Nowrasteh G,
Tettinger A,
Mucsi G,
Ember I.
Faculty of Medicine, Institute of Public Health University of Pecs,
Pecs, Hungary.
http://groups.yahoo.com/group/aspartameNM/message/1414


Hum Exp Toxicol. 2006 Aug; 25(8): 453-9.
The effect of aspartame on rat brain xenobiotic-metabolizing enzymes.
Vences-Mejia A 1,
Labra-Ruiz N 1,
Hernandez-Martinez N 1,
Dorado-Gonzalez V 1,
Gomez-Garduno J 1,
Perez-Lopez I 1,
Nosti-Palacios R 1,
Camacho Carranza R 2,
Espinosa-Aguirre JJ 2.
Laboratorio de Toxicologia Genetica,
1: Instituto Nacional de Pediatria, Insurgentes Sur, 3700-C,
04530 Mexico, DF Mexico.
2: Instituto de Investigaciones Biomédicas, UNAM, Apartado postal 70228,
Ciudad Universitaria 04510 México, D.F., México
http://www.biomedicas.unam.mx/index.asp
*Correspondence: JJ Espinosa-Aguirre, Instituto de Investigaciones
Biome´dicas, UNAM, Apartado postal 70228, Ciudad
Universitaria 04510 Me´xico, D.F., Me´xico
Human & Experimental Toxicology (2006) 25(8): 453 - 459.
www.sagepublications.com
c 2006 SAGE Publications 10.1191/0960327106het646oa
[ Dra. Araceli Vences M
Jefa de Laboratorio de Toxicologia Genetica
6° P de Hospital Laboratorios
10 84 09 00 Ext.1410 -1448 aritaven@..., ]
http://groups.yahoo.com/group/aspartameNM/message/1373


Toxicol Sci. 2006 Mar;90(1):178-87.
Synergistic interactions between commonly used food additives in a
developmental neurotoxicity test.
Lau K, McLean WG, Williams DP, Howard CV.
Developmental Toxicopathology Unit,
Department of Human Anatomy & Cell Biology,
University of Liverpool, Sherrington Buildings, Liverpool L69 3GE, UK;
Department of Pharmacology & Therapeutics,
University of Liverpool, Sherrington Buildings, Liverpool L69 3GE, UK.
W. Graham McLean w.g.mclean@...,
C. V. Howard c.v.howard@...,
D. P. Williams dom@..., 0151 794 5791 http://www.liv.ac.uk/
Miss. Karen Lau karenlau@..., 0151 795 4223
http://groups.yahoo.com/group/aspartameNM/message/1271


http://www.biomedcentral.com/content/pdf/1471-2202-8-9.pdf
free full text 28 pages
This Provisional PDF corresponds to the article as it appeared upon
acceptance.
Copyedited and fully formatted PDF and full text (HTML) versions will be
made available soon.
Amyloid-like aggregates of neuronal tau induced by formaldehyde promote
apoptosis of neuronal cells
BMC Neuroscience 2007 Jan 23, 8(1): 9 doi: 10.1186/1471-2202-8-9
Chunlai Nie niecl1022@...,
Xing sheng Wang step@...,
Ying Liu liuy@...,
Sarah Perrett sperrett@...,
Rongqiao He herq@...,
ISSN 1471-2202
Article type Research article
Submission date 15 August 2006
Acceptance date 23 January 2007
Publication date 23 January 2007
Article URL http://www.biomedcentral.com/1471-2202/8/9
Chun Lai Nie 1,3,
Xing Sheng Wang 1,3,
Ying Liu 1,
Sarah Perrett 2 and
Rong Qiao He 1,3*
1 State Key Laboratory of Brain and Cognitive Science,
Institute of Biophysics, 15 Datun Rd, Chaoyang District, Beijing 100101,
China
2 National Laboratory of Biomacromolecules,
Institute of Biophysics, 15 Datun Rd, Chaoyang District, Beijing 100101,
China
3 Graduate School, Chinese Academy of Sciences, 19 Yuquan Rd, Shijingshan
District, Beijing 100049, China
*Corresponding author
http://groups.yahoo.com/group/aspartameNM/message/1406


Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
http://www.cuk.ac.kr/eng/ sysop@...
Songsin Campus: 02-740-9714 Songsim Campus: 02-2164-4116
Songeui Campus: 02-2164-4114
http://www.cuk.ac.kr/eng/sub055.htm eight hospitals
http://groups.yahoo.com/group/aspartameNM/message/1394


" Absorbed formaldehyde can be oxidized to formate and carbon dioxide or
can be incorporated into biologic macromolecules. "

[ References include: Soffritti M, Belpoggi F, Lambertini L, Lauriola M,
Padovani M, Maltoni C. 2002. Results of long-term experimental studies
on the carcinogenicity of formaldehyde and acetaldehyde in rats. Ann NY
Acad Sci 982: 87-105.

Soffritti M, Maltoni C, Maffei F, Biagi R. 1989. Formaldehyde: an
experimental multipotential carcinogen. Toxicol Ind Health 5:699-730. "
Morando Soffritti is a member of the Working Group. ]

http://www.ehponline.org/members/2005/7542/7542.html free full text

After a thorough discussion of the epidemiologic, experimental, and
other relevant data, the working group concluded that formaldehyde is
carcinogenic to humans, based on sufficient evidence in humans and in
experimental animals.

In the epidemiologic studies, there was sufficient evidence that
formaldehyde causes nasopharyngeal cancer, "strong but not sufficient"
evidence of leukemia, and limited evidence of sinonasal cancer.

The working group also concluded that 2-butoxyethanol and
1-tert-butoxy-2-propanol are not classifiable as to their
carcinogenicity to humans, each having limited evidence in experimental
animals and inadequate evidence in humans.

These three evaluations and the supporting data will be published as
Volume 88 of the IARC Monographs. PMID: 16140628

Environ Health Perspect. 2005 Sep; 113(9): 1205-8.
Meeting report: summary of IARC monographs on formaldehyde,
2-butoxyethanol, and 1-tert-butoxy-2-propanol.
Cogliano VJ, Vincent James Cogliano cogliano@...,
Grosse Y, Yann Grosse grosse@...,
Baan RA, Robert A. Baan baan@...,
Straif K, Kurt straif@...,
Secretan MB, Marie Béatrice Secretan secretan@...,
El Ghissassi F, Fatiha El Ghissassi elghissassi@...,
Working Group for Volume 88.

IARC, 150 Cours Albert Thomas, 69372 Lyon CEDEX 08, France
Tel: +33 (0)4 72 73 84 85 - Fax: +33 (0)4 72 73 85 75
© IARC 2004 - All Rights Reserved
http://monographs.iarc.fr cie@...,

Monographs Recently Published

IARC Monographs Vol 88
Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol
December 2006
478 pages
ISBN 92 832 1288 6
US$ 40

This volume re-evaluates the available evidence on the carcinogenic
potential of formaldehyde, a substance that is found in the workplace
and in the environment.
Formaldehyde is widely used in resins that bind wood products, pulp and
paper; in glasswool and rockwool insulation; in plastics and coatings,
textile finishing, chemical manufacture; and as a disinfectant and
preservative.
Also evaluated are two glycol ethers, 2-butoxyethanol and
1-tert-butoxypropan-2-ol,
which are widely used as solvents in paints and paint thinners,
coatings, glass and surface cleaners, inks, adhesives, personal-care
products, and as chemical intermediates.
As for formaldehyde, there is sufficient evidence in epidemiological
studies for nasopharyngeal cancer, strong but not sufficient evidence
for leukaemia, and limited evidence for sinonasal cancer.
The extensive scientific database on the mechanisms by which
formaldehyde can induce nasal-tract cancer in humans is considered.
These data provide strong support for the empirical observation of
nasopharyngeal cancer in humans.
In contrast, the lack of information on possible mechanisms by which
formaldehyde might increase the risk for leukaemia in humans tempered
the interpretation of the epidemiological data on that cancer.
Although this volume focuses on a qualitative assessment of the
carcinogenic potential of formaldehyde, subsequent predictions of the
risks for nasopharyngeal cancer should consider pertinent information on
mechanisms of carcinogenesis, including genotoxicity and dose-dependent
cytoxicity.
A theme common to the three evaluations is the consideration of
mechanistic information to develop and evaluate hypotheses on the
sequence of steps that lead to the induction of tumours in experimental
animals.
The hypothesized mechanisms described provide an interesting set of
cases that range from a vast literature on respiratory tract tumours in
rats induced by the inhalation of formaldehyde to some more tentative
hypotheses on the various tumours observed in animals following exposure
to both glycol ethers.
Recurring issues were the criteria that characterize a rare tumour or
how to introduce additional information to resolve difficult questions;
for example, how to consider the results of historical controls.

International Agency for Research on Cancer, Lyon, France.

An international, interdisciplinary working group of expert scientists
met in June 2004 to develop IARC Monographs on the Evaluation of the
Carcinogenic Risk of Chemicals to Humans (IARC Monographs) on
formaldehyde, 2-butoxyethanol, and 1-tert-butoxy-2-propanol.

Each IARC Monograph includes a critical review of the pertinent
scientific literature and an evaluation of an agent's potential to cause
cancer in humans.

Key words: 1-tert-butoxy-2-propanol, 2-butoxyethanol, carcinogen,
formaldehyde, glycol ethers, hazard identification, IARC Monographs,
leukemia, nasopharyngeal cancer, sinonasal cancer. Environ Health
Perspect 113: 1205-1208 (2005) .
doi:10.1289/ehp.7542 available via http://dx.doi.org/ [Online 12 May 2005]

Address correspondence to V.J. Cogliano, Carcinogen Identification and
Evaluation, International Agency for Research on Cancer, 150 cours
Albert Thomas, 69372 Lyon cedex 08, France.
33-4-72-73-84-76. fax 33-4-72-73-83-19 cogliano@...,

The Working Group for Volume 88 of the IARC Monographs includes:

Ulrich Andrae (Germany) , andrae@..., Dr. Ulrich Andrae, GSF-Institut
für Toxikologie,. Postfach 1129, D-85758 Neuherberg, Germany Fax:
149-089-3187-3449 Sherwood Burge (UK),

Rajendra S Chhabra (USA) , http://dir.niehs.nih.gov/dirtob/chhabra.htm
chhabrar@..., General Toxicology Group, TOB, ETP, DIR

John Cocker (UK) , Health and Safety Laboratory, Buxton, UK
john.cocker@...,

David N Coggon (UK) , MRC Environmental Epidemiology Unit at the
University of Southampton, UK dnc@...,

Rory Conolly (USA) , Rconolly@..., Senior Research Biologist,
National Center for Computational Toxicology, Office of Research and
Development, U.S. Environmental Protection Agency

Paul Demers (Canada) , pdemers@..., Occupational Hygiene
Institute, University of British Columbia

David A Eastmond (USA) , david.eastmond@..., Enviromental Toxicology
Graduate Program, University of California Riverside, CA 92521 (951)
827-4497 (Voice) (951) 827-3087 (Fax)

Elaine Faustman (USA) , faustman@..., Professor, Env. and
Occ. Health Sciences, Adjunct Professor, Evans School 206–685–2269

Victor J Feron (the Netherlands) , TNO Nutrition and Food Research
(retired), The Netherlands TNO-CIVO TOXICOLOGY AND NUTRITION INSTITUTE
Utrechtseweg 48 3704 HE Zeist The Netherlands (31)-3404 44 144

Michel Gérin (Canada, Chair) , gerinm@..., Departement de
medecine du travail et d'hygiene du milieu, Universite de Montreal,
Quebec, Canada.

Marcel Goldberg (France) , marcel.goldberg@..., France
-- National Institute of Health and Medical Research INSERM Unite 88,
HNSM 14 Rue de Val d'Osne F-94410 St. Maurice France [33] 1-451-83859
[33] 1-451-83889 Departement Sante Travail, Institut de Veille
Sanitaire, 12, rue du Val d'Osne, 94410 Saint Maurice, France

Bernard D Goldstein (USA) , bdgold@..., Director of the
Environmental and Occupational Health Sciences Institute and Professor
and Chair of the Department of Environmental and Community Medicine at
UMDNJ - Robert Wood Johnson Medical School. Dean's Office, University of
Pittsburgh Graduate School of Public Health, A624 Crabtree Hall, 130
DeSoto St., Pittsburgh, PA 15261, USA.

Roland C Grafström (Sweden) , roland.grafstrom@..., Roland C
Grafström, Institute of Environmental Medicine, Karolinska Institutet,
Box 210, S−17177 Stockholm, Sweden Telefax: +46–8−329402

Johnni Hansen (Denmark) , johnni@..., PhD, Senior researcher,
Danish Cancer Registry , Institute of Cancer Epidemiology, Danish Cancer
Society, Strandboulevarden 49, DK-2100, Copenhagen, Denmark.

Michael Hauptmann (USA) , The National Cancer Institute

Kathy Hughes (Canada) , Head, Existing Substances Section 1, Health Canada,

Ted Junghans (USA) , tjunghans@..., Technical Resources
International, Inc., 6500 Rock Spring Drive, Suite 650, Bethesda, MD
20817, USA.

Dan Krewski (Canada) , MHA, MSc, PhD dkrewski@..., Professor
Director, R. Samuel McLaughlin Centre for Population Health Risk
Assessment, Institute of Population Healt, 1 Stewart Street, Room 320,
Phone: (613) 562-5381 Fax: (613)562-5380

Steve Olin (USA) , solin@..., ILSI International Life Sciences
Institute

Martine Reynier (France) , martine.reynier@..., Mme Martine REYNIER,
Institut National de Recherche et de Sécurité (INRS), 30, rue Olivier
Noyer, 75680 Paris Cedex 14 (France) Tel : +33 (0)1 40 44 30 81 Fax :
+33 (0)1 40 44 30 54

Judith Shaham (Israel) , yshaham@..., Occupational Cancer
Department, National Institute of Occupational and Environmental Health,
Raanana, Israel. MD, Occupational Cancer Unit, Occupational Health &
Rehabilitation Institute, P.O. Box 3, Raanana 43100, ISRAEL

Morando Soffritti (Italy) , crcfr@..., European Foundation of
Oncology and Environmental Sciences “B. Ramazzini”, Cesare Maltoni
Cancer Research Center, Bologna, Italy

Leslie Stayner (USA) , lstayner@..., Division of Epidemiology and
Biostatistics, University of Illinois at Chicago School of Public Health
(M/C 923), 1603 West Taylor Street, Room 971, Chicago, IL 60612. E-mail:

Patricia Stewart (USA) , National Food Safety and Toxicology Center, 165
Food Safety and Toxicology Building, Michigan State University, East
Lansing, MI 48824; fax (517) 432-2310

Douglas Wolf (USA) , wolf.doug@..., DVM, PhD, USEPA, (Toxicology)

We gratefully acknowledge the important contributions of the
administrative staff of the IARC Monographs: S. Egraz, M. Lézčre, J.
Mitchell, and E. Perez.
The IARC Monographs are supported, in part, by grants from the U.S.
National Cancer Institute, the European Commission, the U.S. National
Institute of Environmental Health Sciences, and the U.S. Environmental
Protection Agency.
The authors declare they have no competing financial interests.
Received 31 August 2004 ; accepted 12 May 2005.
http://groups.yahoo.com/group/aspartameNM/message/1417
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http://groups.yahoo.com/group/aspartameNM/message/1467
4 cases of aspartame-induced thrombocytopenia [ very low platelets in
blood ], HJ Roberts MD, Letter in Southern Medical Journal 2007 May:
100(5); 543: Murray 2007.08.25

http://groups.yahoo.com/group/aspartameNM/message/1468
Formaldehyde induced urticarial vasculitis in male medical student,
age 40, Michael Pellizzari, Gillian Marshman, Flinders U.,
Australasian J. Dermatol. 2007 Aug: Murray 2007.08.29

http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is made by
the body from 100 mg doses of methanol from dark wines and liquors,
dimethyl dicarbonate, and aspartame: Murray 2007.08.31

http://groups.yahoo.com/group/aspartameNM/message/1470
new details on how formaldehyde and formic acid from methanol are
neurotoxic: Chun Lai Nie, Rong Giao He, et al, PLoS ONE 2(7): e629
2007.07.18 Chinese Academy of Sciences, Beijing: Murray 20097.09.01
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http://groups.yahoo.com/group/aspartameNM/message/1457
aspartame bans, tis more an avalanche than a trend...: Rich Murray
2007.08.17

[ see also:
http://groups.yahoo.com/group/aspartameNM/message/1458
ASDA, Wal-Mart's UK supermarket chain, bans artificial colors, trans
fats, MSG and aspartame, Marguerite Kelly, The Washington Post: Murray
2007.08.03 ]

So far, USA print and broadcast media are deaf, blind, and dumb,
regarding recent major bans of aspartame and MSG in the UK and EU.

The EU Parliament voted July 12 to ban artificial sweeteners
in newly born and infant foods.

On May 15 four huge UK supermarket chains announced bans
of aspartame and MSG, food dyes, and many additives
to protect kids from ADHD --
Sainsbury, Tesco, Marks & Spencer, and ASDA, a unit of WalMart.

May 31: Coca-Cola and the much larger Cargill Inc.,
after years of secret development, with 24 patents,
will soon sell rebiana (stevia) in drinks and food
in the many nations where it is approved as a sweetener --
for decades a major sweetener in Japan, China, Korea, Taiwan,
Thailand, Malasia, Saint Kitts, Nevis,
Brazil, Peru, Paraguay, Uruguay, and Israel,
and an approved supplement in USA, Australia, and Canada,
according to Wikipedia.


http://groups.yahoo.com/group/aspartameNM/message/1454
recent research and news re aspartame and stevia: Murray 2007.08.16

http://groups.yahoo.com/group/aspartameNM/message/1395
Aspartame Controversy, in Wikipedia democratic
encyclopedia, 72 references (including AspartameNM # 864
and 1173 by Murray, brief fair summary of much more research:
Murray 2007.01.01

http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation
cancer studies 2007.06.25: Murray 2007.07.18

http://groups.yahoo.com/group/aspartameNMmessage/1451
Artificial sweeteners (aspartame, sucralose) and coloring
agents will be banned from use in newly-born and baby foods,
the European Parliament decided: Latvia ban in schools 2006:
Murray 2007.07.12

http://groups.yahoo.com/group/aspartameNMmessage/1437
stevia to be approved and cyclamates limited by
Food Standards Australia New Zealand:
JMC Geuns critiques of two recent stevia studies by Nunes:
Murray 2007.05.29

http://groups.yahoo.com/group/aspartameNM/message/1427
more from The Independent, UK, Martin Hickman, re ASDA
(unit of Wal-Mart Stores) and Marks & Spencer ban of
aspartame, MSG, artificial chemical additives and dyes
to prevent ADHD in kids: urray 2007.05.16
http://news.independent.co.uk/uk/health_medical/article2548747.ece

http://groups.yahoo.com/group/aspartameNM/message/1426
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
will join Tesco and also Sainsbury to ban and limit
aspartame, MSG, artificial flavors dyes preservatives additives,
trans fats, salt "nasties" to protect kids from ADHD:
leading UK media: Murray 2007.05.15

http://groups.yahoo.com/group/aspartameNM/message/1438
Coca-Cola and Cargill Inc., after years of development,
with 24 patents, will soon sell rebiana (stevia)
in drinks and foods: Murray 2007.05.31

www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed search PubMed
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