EPA TEACH review of formaldehyde hazards for children does not include
the substantial formaldehyde made by the body from the 11% methanol part
of aspartame: Murray 2007.10.01
http://groups.yahoo.com/group/aspartameNM/message/1477

"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://groups.yahoo.com/group/aspartameNM/messages
group with 82 members, 1,477 posts in a public,
searchable archive http://RMForAll.blogspot.com
////////////////////////////////////////////////////////////


"Cigarette smoke is another important source of formaldehyde.

Formaldehyde may also be present in food, either naturally, as an
additive, or as a result of contamination (1, 3, 57)."

The TEACH review neglects to mention that the body always quickly
converts and retains 40% of ingested methanol as durable cumulative
toxic metabolites of formaldehyde and formic acid. (Bouchard M et al, 2001)

The TEACH review neglects to mention that the 1999 July EPA 468-page
formaldehyde profile admits that four states substantially exceed the
federal EPA limit for lifetime drinking water:

Environmental Protection Agency 2.00 mg in 2 L daily drinking water
California and Maine ---------- 0.06 mg
Maryland ---------------------- 0.02 mg
New Jersey -------------------- 0.20 mg

Maryland's limit is ten times more stringent than the EPA's.

The grave neglect of the TEACH review must be corrected, in view of the
substantial hazard to children from aspartame, a danger that has never
been adequately researched nor publicized.

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
[ Extract, with notes by Rich Murray in square brackets ]

3.1.1 [ 22 mg ingested aspartame releases 2.4 mg methanol, which is 11%
of the aspartame. Stegink, 1987

[ Fully 11% of aspartame is methanol -- 1,120 mg aspartame in 2 L diet
soda, almost six 12-oz cans, gives 123 mg methanol (wood alcohol).

If 30% of the methanol is turned into formaldehyde, the amount of
formaldehyde, 37 mg, is 18 times the USA EPA limit for daily
formaldehyde in drinking water, 2 mg in 2 L water.

For instance, hangover researchers claim that it is the ~150 mg/L
methanol impurity, about one part in 10,000, twice the level from
aspartame in diet sodas, in dark wines and liquors that, turned into
formaldehyde and then formic acid, is the major cause of the dreadful
symptoms of "morning after" hangover. ]


[reference 254:
J. Nutrition 1973 Oct; 103(10): 1454-1459.
Metabolism of aspartame in monkeys.
Oppermann JA, Muldoon E, Ranney RE.
Dept. of Biochemistry, Searle Laboratories,
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680

They found that about 70% of the radioactive methanol in aspartame put
into the stomachs of 3 to 7 kg monkeys was eliminated within 8 hours,
with little additional elimination, as carbon dioxide in exhaled air and
as water in the urine.

They did not mention that this meant that about 30% of the methanol must
transform into formaldehyde and then into formic acid, both of which
must remain as toxic products in all parts of the body.

They did not report any studies on the distribution of radioactivity in
body tissues, except that blood plasma proteins after 4 days held 4% of
the initial methanol.

This study did not monitor long-term use of aspartame. ]
////////////////////////////////////////////////////////////


Oct. 1, 2007 6:38 AM Onc-Env-Med-L
From:
Maryann E. Suero, Ph.D.
US EPA Region 5 (IL, IN, MI, MN, OH, WI)
Children's Health Program Manager
77 W. Jackson Blvd. (LC-8J)
Chicago, IL 60604
Phone (312) 886-9077
Fax (312) 353-4788
suero.maryann@...
////////////////////////////////////////////////////////////


EPA's Toxicity and Exposure Assessment for Children's Health (TEACH)
project has added updated chemical summaries on Formaldehyde and
Trichloroethylene (TCE) .

They can be found at the TEACH website, www.epa.gov/teach

You can also provide feedback to us about TEACH at
http://www.epa.gov/teach/teachsurvey.html

TEACH Background :

The TEACH Web site contains a searchable database of
scientific literature relevant to children's environmental health.

The TEACH database currently includes 18 chemicals of concern.

In addition,
the TEACH website is developing chemical summaries for these chemicals
which provide a survey of the scientific literature and U.S. federal
regulations relevant to children?s environmental health.

The goal of the TEACH project is to complement existing children's
health resources.

TEACH does not provide an evaluation or critique the validity of the
relevant scientific studies; nor does TEACH derive toxicity values.

Instead, the goal of TEACH is to summarize, compile, and organize
information obtained from numerous resources into one online resource.

TEACH is designed to support numerous efforts throughout the country
that target the protection of children's health.

The objective of the TEACH project is to Improve the information base on
children's environmental health risks in order to:

Streamline and facilitate the search for current children's
health information in the scientific literature;

Support existing children's health efforts;

Identify data and information gaps in the literature on
children's environmental health.

The addition of the updated Formaldehyde Chemical Summary and the
Trichloroethylene (TCE) Chemical Summary to the TEACH website brings
the number of completed Chemical Summaries,
http://www.epa.gov/teach/chem_summ/index.html to 16, including:
2,4-Dichlorophenoxyacetic Acid (2,4-D)
Arsenic (As)
Atrazine
Benzene
Benzo(a)pyrene (BaP)
Dichlorvos
Diethyltoluamide (DEET)
Formaldehyde
Manganese
Mercury (Elemental)
Mercury (Inorganic)
Mercury (Methylmercury and Ethylmercury)
Nitrates/Nitrites
Permethrin and Resmethrin (Pyrethroids)
Trichloroethylene (TCE)
Vinyl Chloride

Reminder: you can also provide feedback to us about TEACH at
http://www.epa.gov/teach/teachsurvey.html or
teach@...
*********************************************************


www.epa.gov/teach/chem_summ/Formaldehyde_summary.pdf

Formaldehyde

TEACH Chemical Summary

U.S. EPA, Toxicity and Exposure Assessment for Children’s Health
This TEACH Chemical Summary is a compilation of information derived
primarily from U.S. EPA and ATSDR resources, and the TEACH Database.

The TEACH Database contains summaries of research studies pertaining to
developmental exposure and/or health effects for each chemical or
chemical group.

TEACH does not perform any evaluation of the validity or quality of
these research studies.

Research studies that are specific for adults are not included in the
TEACH Database, and typically are not described in the TEACH Chemical
Summary.

I. INTRODUCTION

Formaldehyde is a colorless flammable gas with a pungent odor, and is
highly reactive with many substances (1-3).

Formalin is a solution of formaldehyde gas in water, and formalin is
used as a disinfectant and as a preservative of biological samples (1-4).

Formaldehyde is also used as a chemical intermediate in industry (1).

Formaldehyde occurs in many biological systems as a metabolic by-product
(1).

Formaldehyde is also commonly found in household products,
e.g., pressed wood products that contain urea-formaldehyde resins,
carpeting,
foam insulation (prior to 1982),
cosmetics,
nail hardeners,
some finger paints
and some cleaning products (1-4).

Formaldehyde is also a component of cigarette smoke (1-4).

Formaldehyde has been found in industrial exhaust, and is used in some
sterilizing and preserving solutions in medical and school settings (1-3).

Although there is some concern about childhood dermal exposure, the
dominant pathway of childhood exposure to formaldehyde is from ambient
and indoor air, particularly in homes with new cabinets made of pressed
wood products or new carpeting (1).

Concentrations of formaldehyde in ambient air may be of concern in
several areas of the U.S. (5-10).

The primary targets affected by formaldehyde exposure are the lungs and
mucous membranes (eyes, nose, and mouth) (1-3).

Occupational studies have demonstrated that adult exposure to
formaldehyde is associated with naso/pharyngeal cancers and possibly
with leukemia (1, 3

Formaldehyde is classified as a probable human carcinogen by the U.S.
EPA (11), and as carcinogenic to humans by the World Health Organization
(3).

In studies of children, exposure to formaldehyde was associated with
irritation of the respiratory tract (12-17), skin (18-21), and eyes (22).

Formaldehyde exposure of children has also been associated with
formaldehyde-specific immunoglobulin (Ig)E antibody production (22, 23).

Supporting references and summaries are provided in the TEACH database
at: http://www.epa.gov/teach/.

Last revised 9/20/2007: includes research articles and other information
through 2006.

II. EXPOSURE MEDIA AND POTENTIAL FOR CHILDREN’S EXPOSURE 1

Exposure; Media; Relative Potential for Children’s Exposure 2,3; Basis 4

Ambient Air
Higher
Concentrations of formaldehyde in ambient air may be of concern in
several areas in the U.S. (see Considerations for Decision Making).

Background levels of formaldehyde exceeded the U.S. EPA Air
Concentration at Specified Risk Level of 1 in one million in over 90% of
census tracts analyzed from 1996 emissions data.

Major sources of formaldehyde in ambient air include emissions from
power plants, manufacturing facilities, and incinerators; and mobile
sources such as cars, trucks, and construction equipment.

Indoor Air
Higher
Formaldehyde contamination of indoor air can result from off-gassing of
certain building materials (e.g., some forms of particle board and other
pressed wood products; new carpeting), and from mainstream and
second-hand cigarette smoke.

For those reasons, indoor levels of formaldehyde can be substantial,
even in non-smoking homes.

Formaldehyde is also used in medical settings, and in preservatives of
biological samples often in school settings.

Diet
Lower
Formaldehyde has been found at low levels in some foods, but diet is not
a major source of exposure.

Sediment
Lower
Formaldehyde is not generally found in sediment.

Soil
Lower
Formaldehyde is not generally found in soil.

Drinking Water
Lower
Formaldehyde is not generally found in drinking water.

Ground and Surface Water
Lower
Formaldehyde is not generally found in surface or groundwater.

1 For more information about child-specific exposure factors, please
refer to the “Child-Specific Exposure Factors Handbook”
(http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=55145).

2 The Relative Potential for Children’s Exposure category reflects a
judgment by the TEACH Workgroup, U.S. EPA, that incorporates potential
exposure pathways, frequency of exposure, level of exposure, and current
state of knowledge.

Site-specific conditions may vary and influence the relative potential
for exposure.

For more information on how these determinations were made, go to
http://www.epa.gov/teach/teachprotocols_chemsumm.html.

3 Childhood represents a lifestage rather than a subpopulation, the
distinction being that a subpopulation refers to a portion of the
population, whereas a lifestage is inclusive of the entire population.

4 Information described in this column was derived from several
resources (e.g., 1-4) including studies listed in the TEACH Database
(http://www.epa.gov/teach).

III. TOXICITY SUMMARY 5, 6

Adult epidemiological studies have found formaldehyde to be
significantly associated with cancer of the respiratory tract, including
nasopharyngeal (nose/throat) cancer (1, 2).

The World Health Organization (WHO) International Agency for Research on
Cancer (IARC) reported “strong but not sufficient evidence for a causal
association between leukemia and occupational exposure to formaldehyde”
(2).

Formaldehyde exposure has also been associated with inflammation and
toxicity of the gastrointestinal tract in adults (1).

In children, inhalation exposure to formaldehyde were associated with
irritation of the respiratory tract (12-17, 22), asthma (12, 13, 15),
and irritation of eyes (22).

Dermal exposure via patch tests have resulted in skin irritation
(positive patch test result), possibly mediated by an allergic response
(18-21).

One study in rats reported that formaldehyde was found to be teratogenic
for fetuses from inhalation-exposed, iron-deficient pregnant mothers (24).

Carcinogenicity Weight-of-Evidence Classification 7:

Formaldehyde is classified by the U.S. EPA as B1, a probable human
carcinogen, based on site-specific neoplasms (tumors) of the respiratory
tract in workers who were occupationally exposed to formaldehyde, and
nasal squamous cell carcinomas in rats and mice
(http://www.epa.gov/iris/subst/0419.htm, II.A.1) (11).

The WHO IARC classified formaldehyde as carcinogenic to humans (Group 1)
(http://monographs.iarc.fr/ENG/Monographs/vol88/volume88.pdf) (2).

5 Please refer to research article summaries listed in the TEACH
Database for details about study design considerations (e.g., dose,
sample size, exposure measurements).

6 This toxicity summary is likely to include information from workplace
or other studies of mature (adult) humans or experimental animals if
child-specific information is lacking for the chemical of interest.

Summaries of articles focusing solely on adults are not listed in the
TEACH Database because the TEACH Database contains summaries of articles
pertaining to developing organisms.

7 For recent information pertaining to carcinogen risk assessment during
development, consult A Guidelines for Carcinogen Risk Assessment and
Supplemental Guidance on Risks from Early Life Exposure@ at
http://www.epa.gov/cancerguidelines.

IV. EXPOSURE AND TOXICITY STUDIES FROM THE TEACH DATABASE

This section provides a brief description of human and animal studies
listed in the TEACH Database.

These descriptions generally include the overall conclusion in each
study without evaluation or assessment of scientific merit by TEACH.

For more details about doses and exposure levels, query the TEACH Database.

Any consideration of adverse events should include an understanding of
the relative exposure on a body weight basis.

In many cases, exposure levels in animal studies are greater than
exposure levels normally encountered by humans.

A. HUMAN EXPOSURE AND EFFECTS

< Childhood exposure to formaldehyde in air may be common.

Sampling of air in schools and homes showed measurable levels of
formaldehyde (5, 8, 14, 15, 25-31).

A survey of formaldehyde sampling in New York City showed levels in air
inside homes of nonsmoking families exceeded levels in outdoor air (15).

Daily formaldehyde intake for individuals in homes with people who smoke
was estimated to be 30-67 μg, based on indoor air formaldehyde
concentrations in those homes (30).

A study of indoor, outdoor, and personal air samples (collected from
individuals’ breathing zone) in Mexico City indicated that 100% of
samples were positive for formaldehyde; concentrations in indoor air and
personal air samples were significantly higher than in outdoor air
samples (31).

< Two studies showed an increased rate of miscarriage in women exposed
to formaldehyde (32, 33), although in both studies the women may have
been exposed to multiple chemicals.

No increased rate of miscarriage was seen in two other occupational
exposure studies of medical personnel (34, 35).

< Formaldehyde is an irritant which can elicit adverse respiratory
responses in children and adults (12-17, 22).

Additional health effects in children associated with formaldehyde
exposure include irritation to eyes and skin (18-22).

In elementary school environments, symptoms of mucous membrane
irritation in adults who worked there were associated with elevated
formaldehyde levels in indoor air (14, 29).

One study of children in China found no significant association between
formaldehyde air concentrations (up to 20 μg/m3) and symptoms of
respiratory irritation (36).

Irritation of mucous membranes of the gums and mouth were reported
following contact formaldehyde exposure at these sites (37).

In the U.S., 6,358 cases of formalin exposure of children ages 13-19
years old, and 1,855 cases of children less than 13 years old, were
reported to poison control centers in 1996-2001 (38).

< Immune system effects of formaldehyde exposure have been studied in
children.

Two children’s studies have detected formaldehyde-specific IgE
antibodies in their blood (22, 23).

One study provided suggestive evidence that children may have an
increased tendency to develop specific antibodies to formaldehyde after
exposure to low levels of formaldehyde in indoor air (22).

Another study found that atopic children (children with multiple
allergies) may be more vulnerable to the irritant effects of
formaldehyde exposure when compared to the general childhood population
(13).

There was no association between formaldehyde exposure and increased
antibody production among children with asthma in one study (39).

Furthermore, the presence of formaldehyde-specific IgE antibodies to
formaldehyde was not associated with incidence of asthma in another
study (23).

< Some studies of formaldehyde exposure found no health effects in children.
In one study, there was no difference in the incidence of respiratory
irritation in children living close to a foundry that used formaldehyde,
as compared to children living further away from the foundry (40).

In another study, no significant differences in respiratory irritation
were measured between children living in homes with urea/formaldehyde
foam insulation, and children living in homes without such insulation (41).

B. EXPERIMENTAL ANIMAL EXPOSURE AND EFFECTS

< Adult male sperm quantity and quality was decreased following
inhalation exposure of rats during adulthood; co-treatment with vitamin
E offered some protective effects (42).

< The nutritional status of exposed pregnant rats may influence the
effects of inhalation exposure to formaldehyde on fetal health.

One study reported that inhalation exposure of pregnant iron-deficient
rats to formaldehyde resulted in a greater incidence of malformations in
fetuses, as compared to pregnant iron-sufficient control rats (24).

< There was no observed increase in resorption (death) of fetuses or
fetal malformations following formaldehyde ingestion exposure in mice
(43), inhalation exposure in rats (44), or dermal exposure in hamsters (45).

< One study reported changes in a region of the brain following neonatal
inhalation exposure of rats to formaldehyde from birth for 30 days, and
some of these changes were significant in adulthood, after formaldehyde
exposure was stopped (46).

This study reported significantly increased volume of the dentate gyrus
region of the brain at 30 days of age, and significantly decreased
numbers of granule cells in this region at 90 days of age (adulthood) (46).

V. CONSIDERATIONS FOR DECISION-MAKERS

This section contains information that may be useful to risk assessors,
parents, caregivers, physicians, and other decision-makers who are
interested in reducing the exposure and adverse health effects in
children for this particular chemical.

Information in this section focuses on ways to reduce exposure, assess
possible exposure, and, for some chemicals, administer treatment.

< A detailed compilation of information pertaining to exposure and
health effects of formaldehyde is available from the U.S. Centers for
Disease Control Agency for Toxic Substances and Disease Registry in the
Toxicological Profile for Formaldehyde (1).

A Hazard Summary for Formaldehyde is also available from the U.S. EPA (4).

< The U.S. Consumer Product Safety Commission provides a summary of
information on formaldehyde, and includes recommendations for avoiding
and reducing exposure to formaldehyde in the home (47).

Recommendations include purchasing wood products labeled to be in
conformance with American National Standards Institute (ANSI) criteria
for formaldehyde emissions (labeled as ANSI grades PBU, D2, or D3 on the
wood panel itself), increasing ventilation in the home by opening doors
and windows, and installing exhaust fans.

< Information about indoor air quality, and recommendations for ways to
reduce exposure to formaldehyde indoors are available from the U.S. EPA
(48).

Recommendations include

1) use "exterior-grade" pressed wood products (lower-emitting because
they contain phenol resins, not urea resins);

2) use air conditioning and dehumidifiers to maintain moderate
temperatures and reduce humidity levels;

and 3) increase ventilation, particularly after bringing new sources of
formaldehyde into the home.

< The U.S. EPA performed statewide estimates of formaldehyde-modeled
ambient air concentrations for all 50 states (5-7, 9, 10).

Using emissions data from 1990 (5), estimated concentrations of
formaldehyde across the U.S. exceeded the U.S. EPA Air Concentration at
Specified Risk Level of 1E-6 (0.08 μg/m3; see Toxicity section) in over
90% of the census tracts analyzed.

More recent information is available based on the 1999 national-scale
assessment, reported on a regional basis (6, 9, 10).

The U.S. EPA concluded from 1999 results that ambient air concentrations
of formaldehyde in some regions may be of concern (i.e., more than
10,000 people living in census tracts where the typical exposure
exceeded the reference concentration for formaldehyde) (9, 10).

Using the current IRIS cancer potency estimate and the 1999 air toxics
assessment, the U.S. EPA concluded that formaldehyde would be considered
a national risk driver for cancer (upper bound lifetime cancer risk
exceeding 10 in a million to more than 25 million people), as it was in
the 1996 national-scale assessment (10).

< Formaldehyde is listed as number 247 out of 275 substances on the 2005
Priority List of Hazardous Substances for the Comprehensive
Environmental Response, Compensation, and Liability Act (CERCLA) section
104 (i), as amended by the Superfund Amendments and Reauthorization Act
(SARA).

This is a prioritized list ranking chemicals in order of concern for
those most commonly found at sites listed on the National Priorities
list (NPL) (49).

< Consult the “Child-Specific Exposure Factors Handbook,”
EPA-600-P-00-002B, for factors to assess children’s inhalation rates (50).

An updated External Draft of the 2006 version of this handbook is
available (51).

VI. TOXICITY REFERENCE VALUES

A. Oral/Ingestion

U.S. EPA Reference Dose (RfD) for Chronic Oral Exposure: 2E-1 (or 0.2)
mg/kg-day, based on reduced weight gain and histopathology of the
gastrointestinal tract in adult rats (www.epa.gov/iris/subst/0419.htm,
I.A.1) (11); last Workgroup Verification Date 6/20/90.

U.S. EPA Drinking Water Advisories (10 kg child): 1 day = 10 mg/L, 10
day = 5 mg/L
(http://www.epa.gov/waterscience/criteria/drinking/standards/dwstandards.pdf)
(52); last revised Winter, 2006.

U.S. ATSDR Minimal Risk Level (MRL) Oral: 0.3 mg/kg/day (intermediate
oral), based on gastrointestinal effects; 0.2 mg/kg/day (chronic oral),
based on gastrointestinal effects
(http://www.atsdr.cdc.gov/mrls/index.html) (53); last revised 7/99.

B. Inhalation

U.S. EPA Cancer Inhalation Exposure Air Unit Risk: 1.3E-5 (or 0.000013)
per (microg/m3), based on nasal squamous cell carcinomas in adult male rats,
using extrapolation methods of linearized multistage procedure, extra
risk (http://www.epa.gov/iris/subst/0419.htm#quainhal, II.C) (11); last
Workgroup Verification Date 2/3/88.

U.S. EPA Air Concentrations at Specified Risk Levels: 1E-4 (or 1 in
10,000), 8E+0 (or 8.0) microg/m3; 1E-5 (or 1 in 100,000), 8E-1 (or 0.8)
microg/m3; 1E-6 (or 1 in 1,000,000), 8E-2 (or 0.08) microg/m3
(http://www.epa.gov/iris/subst/0419.htm#quainhal, II.C) (11); last
Workgroup Verification Date 2/3/88.

U.S. ATSDR Minimal Risk Level (MRL)
Inhalation: 0.04 ppm (acute inhalation), based on respiratory effects;
0.03 ppm (intermediate inhalation), based on respiratory effects;
0.008 ppm (chronic inhalation), based on respiratory effects
(http://www.atsdr.cdc.gov/mrls/index.html) (53); last revised 7/99.

VII. U.S. FEDERAL REGULATORY INFORMATION

< Urea-formaldehyde foam was used as an insulating material until 1982,
when it was banned by the U.S. Consumer Product Safety Commission. The
ban was overturned in the courts, but the action greatly reduced the use
of this foam in residential products (47).

< The U.S. EPA IRIS is currently reviewing toxicity values for
formaldehyde, and review progress is published (54).

< The U.S. EPA Office of Pesticide Programs is currently preparing a
Reregistration Eligibility Decision (RED) for formaldehyde; a RED is a
complete review of the human health and environmental effects of
pesticides first registered before November 1, 1984, to make decisions
about future pesticide uses of formaldehyde (55).

< Formaldehyde is one of 188 hazardous air pollutants (HAPs) listed
under section 112(b) of the 1990 Clean Air Act Amendments, and is
regulated from more than 170 industrial source categories (56).

< The U.S. Food and Drug Administration (FDA) regulates formaldehyde as
a food additive (used as a defoaming agent, and in the feed of animals
used for food sources including some chicken and fish) (57).

< The U.S. EPA requires reporting of quantities of certain chemicals
that exceed a defined reportable quantity, and that quantity varies for
different chemicals.

Under the Emergency Planning and Community Right-to-Know Act (EPCRA)
Section 313 “Toxic Chemicals,” quantities of formaldehyde greater than
25,000 pounds manufactured or processed, or greater than 10,000 pounds
otherwise used, is required; under the Comprehensive Environmental
Response, Compensation, and Liability Act (CERCLA), reporting releases
of formaldehyde of any quantity exceeding 100 pounds is required (58).

VIII. BACKGROUND ON CHEMICAL

A. CAS Number: 50-00-0

B. Physicochemical Properties:

Formaldehyde is a colorless flammable gas, or gas dissolved in water (as
formalin) with a pungent odor, and is highly reactive with many
substances (1, 3).

For more information, go to the National Library of Medicine ChemID Web
site (http://chem.sis.nlm.nih.gov/chemidplus) and search for formaldehyde.

C. Production:

Commercial formaldehyde is produced and sold as an aqueous solution
containing 37 to 50 percent formaldehyde by weight.

The annual production varied from 6.4 to 8.1 billion pounds per year
between 1991-1995 in the U.S. (1).

Formaldehyde occurs in industrial effluents (1, 59).

The major sources of formaldehyde emissions into outdoor air are from
power plants,
manufacturing facilities,
incinerators,
and automobile exhaust.

Cigarette smoke is another important source of formaldehyde.

Formaldehyde may also be present in food, either naturally, as an
additive, or as a result of contamination (1, 3, 57).

D. Uses:

Formaldehyde is used predominantly as a chemical intermediate in
industrial processes (1, 3).

It also has minor uses in agriculture,
concrete and plaster additives,
cosmetics,
disinfectants,
fumigants,
photography,
and wood preservation.

Formaldehyde is used in the manufacture of plastics,
amino and phenolic resins used in construction materials,
paper,
carpets,
textiles,
paint,
particle board,
and plywood.

Total TRI reported disposals and releases of formaldehyde in 2005 were
over 22 million pounds; these releases are likely representative of only
a portion of actual releases because only some facilities (i.e.,
landfills) are required to report to the U.S. EPA (59).

E. Environmental Fate:

Formaldehyde in air is readily broken down by sunlight, with a half-life
of approximately 30-50 minutes (3).

Formaldehyde in liquid form (formalin) is stable over time (1, 3).

F. Synonyms and Trade Names:

BFV, l FA, Fannoform, Floguard 1015, FM 282, Formalin, Formalin 40,
Formalith, Formic aldehyde, Formol, Fyde, Hoch, Ivalon, Karsan,
Lysoform, Methaldehyde, Methyl aldehyde, Methyl oxide, Methylene oxide,
Morbicid, Oxomethane, Oxymethylene, Paraform, Superlysoform

for a more complete list, go to the National Library of Medicine ChemID
Web site (http://chem.sis.nlm.nih.gov/chemidplus) and search for
formaldehyde).

Additional information on formaldehyde is available in the TEACH
Database for Formaldehyde, and at the following Web sites:

http://www.epa.gov/iaq/formalde.html

http://www.surgeongeneral.gov/library/secondhandsmoke/

www.atsdr.cdc.gov/toxprofiles/tp111.pdf

www.epa.gov/ttn/atw/nata/

REFERENCES

1. U.S. Centers for Disease Control Agency for Toxic Substances and
Disease Registry (ATSDR). 1997. "Toxicological Profile for
Formaldehyde." http://www.atsdr.cdc.gov/toxprofiles/tp111.html.

2. World Health Organization. 2006. "IARC Monographs on the Evaluation
of Carcinogenic Risks to Humans: Volume 88 Formaldehyde, 2-Butoxyethanol
and 1-tert-Butoxy-2-propanol."
http://monographs.iarc.fr/ENG/Monographs/vol88/volume88.pdf.

3. World Health Organization. 1999. "International Program on Chemical
Safety, Environmental Health Criteria 89: Formaldehyde."
http://www.inchem.org/documents/ehc/ehc/ehc89.htm.

4. U.S. Environmental Protection Agency. 2003. "Formaldehyde: Hazard
Summary." http://www.epa.gov/ttn/atw/hlthef/formalde.html.

5. Woodruff, T.J., et al. 1998. "Public health implications of 1990 air
toxics concentrations across the United States." Environ.Health
Perspect. 106(5):245-251.

6. U.S. Environmental Protection Agency. 1999. "Technology Transfer
Network 1999 National-Scale Air Toxics Assessment: 1999 Emission Density
Maps." http://www.epa.gov/ttn/atw/nata1999/mapemis99.html.

7. U.S.Environmental Protection Agency. 2006. "Technology Transfer
Network 1996 National-Scale Air Toxics Assessment."
http://www.epa.gov/ttn/atw/nata/ .

8. Rosenbaum, A.S., et al. 1999. "National estimates of outdoor air
toxics concentrations." J.Air Waste Manag.Assoc. 49(10):1138-1152.
9. U.S. Environmental Protection Agency. 2006. "Technology Transfer
Network 1999 National-Scale Air Toxics Assessment: Summary of Results
for the 1999 National-Scale Assessment."
http://www.epa.gov/ttn/atw/nata1999/risksum.html.

10. U.S. Environmental Protection Agency. 2006. "Technology Transfer
Network 1999 National-Scale Air Toxics Assessment: Formaldehyde."
http://www.epa.gov/ttn/atw/nata1999/formald.html.

11. U.S. Environmental Protection Agency. 2006. "Integrated Risk
Information System (IRIS): Formaldehyde."
http://www.epa.gov/iris/subst/0419.htm.

12. Rumchev, K.B., et al. 2002. "Domestic exposure to formaldehyde
significantly increases the risk of asthma in young children."
Eur.Respir.J. 20(2):403-408.

13. Smedje, G., and D. Norback. 2001. "Incidence of asthma diagnosis and
self-reported allergy in relation to the school environment--a four-year
follow-up study in schoolchildren." Int.J.Tuberc.Lung Dis. 5(11):1059-1066.

14. Olsen, J.H., and M. Dossing. 1982. "Formaldehyde induced symptoms in
day care centers." Am.Ind.Hyg.Assoc.J. 43(5):366-370.

15. Krzyzanowski, M., et al. 1990. "Chronic respiratory effects of
indoor formaldehyde exposure." Environ.Res. 52(2):117-125.

16. Tuthill, R.W. 1984. "Woodstoves, formaldehyde, and respiratory
disease." Am.J.Epidemiol. 120(6):952-955.

17. Franklin, P., et al. 2000. "Raised exhaled nitric oxide in healthy
children is associated with domestic formaldehyde levels."
Am.J.Respir.Crit Care Med. 161(5):1757-1759.

18. de Groot, A.C., et al. 1988. "The allergens in cosmetics."
Arch.Dermatol. 124(10):1525-1529.

19. Sharma, V.K., and A. Chakrabarti. 1998. "Common contact sensitizers
in Chandigarh, India. A study of 200 patients with the European standard
series." Contact Dermatitis 38(3):127-131.

20. Sugai, T., et al. 1979. "Age distribution of the incidence of
contact sensitivity to standard allergens." Contact Dermatitis 5(6):383-388.

21. Boyvat, A., et al. 2005. "Contact sensitivity to preservatives in
Turkey." Contact Dermatitis 52(6):329-332.

22. Wantke, F., et al. 1996. "Exposure to gaseous formaldehyde induces
IgE-mediated sensitization to formaldehyde in school-children."
Clin.Exp.Allergy 26(3):276-280.

23. Doi, S., et al. 2003. "The prevalence of IgE sensitization to
formaldehyde in asthmatic children." Allergy 58(7):668-671.

24. Senichenkova, I.N., and N.A. Chebotar. 1996. "[The effect of benzine
and formaldehyde on the prenatal development of rats with induced iron
trace-element disorder]." Ontogenez 27(2):108-113.

25. Kinney, P.L., et al. 2002. "Exposures to multiple air toxics in New
York City." Environ.Health Perspect. 110(Suppl 4):539-546.

26. Stock, T.H., and S.R. Mendez. 1985. "A survey of typical exposures
to formaldehyde in Houston area residences." Am.Ind.Hyg.Assoc.J.
46(6):313-317.

27. Lemus, R., et al. 1998. "Potential health risks from exposure to
indoor formaldehyde." Rev.Environ.Health 13(1-2):91-98.

28. Smedje, G., and D. Norback. 2001. "Irritants and allergens at school
in relation to furnishings and cleaning." Indoor.Air 11(2):127-133.

29. Norback, D., et al. 2000. "Indoor air pollutants in schools: nasal
patency and biomarkers in nasal lavage." Allergy 55(2):163-170.

30. Nazaroff, W.W., and B.C. Singer. 2004. "Inhalation of hazardous air
pollutants from environmental tobacco smoke in US residences."
J.Expo.Anal.Environ.Epidemiol. 14 Suppl 1:S71-7.:S71-S77.

31. Serrano-Trespalacios, P.I., et al. 2004. "Ambient, indoor and
personal exposure relationships of volatile organic compounds in Mexico
City Metropolitan Area." J.Expo.Anal.Environ.Epidemiol. 14 Suppl
1:S118-32.:S118-S132.

32. John, E.M., et al. 1994. "Spontaneous abortions among
cosmetologists." Epidemiology 5(2):147-155.

33. Taskinen, H., et al. 1994. "Laboratory work and pregnancy outcome."
J.Occup.Med. 36(3):311-319.

34. Hemminki, K., et al. 1982. "Spontaneous abortions in hospital staff
engaged in sterilising instruments with chemical agents."
Br.Med.J.(Clin.Res.Ed) 285(6353):1461-1463.

35. Hemminki, K., et al. 1985. "Spontaneous abortions and malformations
in the offspring of nurses exposed to anaesthetic gases, cytostatic
drugs, and other potential hazards in hospitals, based on registered
information of outcome." J.Epidemiol.Community Health 39(2):141-147.

36. Mi, Y.H., et al. 2006. "Current asthma and respiratory symptoms
among pupils in Shanghai, China: influence of building ventilation,
nitrogen dioxide, ozone, and formaldehyde in classrooms." Indoor.Air
16(6):454-464.

37. Ozcelik, O., et al. 2005. "Iatrogenic trauma to oral tissues." J
Periodontol. 76(10):1793-1797.

38. Spiller, H.A. 2004. "Epidemiology of volatile substance abuse (VSA)
cases reported to US poison centers." Am.J.Drug Alcohol Abuse 30(1):155-165.

39. Erdei, E., et al. 2003. "Indoor air pollutants and immune biomarkers
among Hungarian asthmatic children." Arch.Environ.Health 58(6):337-347.

40. Symington, P., et al. 1991. "Respiratory symptoms in children at
schools near a foundry." Br.J.Ind.Med. 48(9):588-591.

41. Norman, G.R., et al. 1986. "Respiratory function of children in
homes insulated with urea formaldehyde foam insulation." CMAJ.
134(10):1135-1138.

42. Zhou, D.X., et al. 2006. "The protective effect of vitamin E against
oxidative damage caused by formaldehyde in the testes of adult rats."
Asian J Androl 8(5):584-588.

43. Marks, T.A., et al. 1980. "Influence of formaldehyde and Sonacide
(potentiated acid glutaraldehyde) on embryo and fetal development in
mice." Teratology 22(1):51-58.

44. Martin, W.J. 1990. "A teratology study of inhaled formaldehyde in
the rat." Reprod.Toxicol. 4(3):237-239.

45. Overman, D.O. 1985. "Absence of embryotoxic effects of formaldehyde
after percutaneous exposure in hamsters." Toxicol.Lett. 24(1):107-110.

46. Aslan, H., et al. 2006. "Effects of formaldehyde exposure on granule
cell number and volume of dentate gyrus: a histopathological and
stereological study." Brain Res 1122(1):191-200.

47. U.S. Consumer Products Safety Commission. 2004. "An Update on
Formaldehyde: 1997 Revision." http://www.cpsc.gov/CPSCPUB/PUBS/725.html
CPSC Document #725.

48. U.S. Environmental Protection Agency. 2006. "Indoor Air Quality: An
Introduction to Indoor Air Quality: Formaldehyde."
http://www.epa.gov/iaq/formalde.html.

49. U.S. Environmental Protection Agency. 2005. "Priority List of
Hazardous Substances for the Comprehensive Environmental Response,
Compensation, and Liability Act (CERCLA) Section 104(i)."
http://www.atsdr.cdc.gov/cercla/.

50. U.S. Environmental Protection Agency. 2002. "Child-Specific Exposure
Factors Handbook (Interim Report) 2002."
http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=55145.

51. U.S. Environmental Protection Agency. 2006. "Child-Specific Exposure
Factors Handbook 2006 (External Review Draft)."
http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=56747.

52. U.S. Environmental Protection Agency. 2006. "2006 Edition of the
Drinking Water Standards and Health Advisories."
http://www.epa.gov/waterscience/criteria/drinking/dwstandards.pdf.

53. U.S. Centers for Disease Control (ATSDR). 2006. "Minimal Risk Levels
(MRLs) for Hazardous Substances." http://www.atsdr.cdc.gov/mrls/index.html.

54. U.S. Environmental Protection Agency. 2005. "IRIS Chemical
Assessment Tracking System." http://cfpub.epa.gov/iristrac/index.cfm.

55. U.S. Environmental Protection Agency. 2006. "Pesticides:
Reregistration - Pesticide Reregistration Status."
http://cfpub.epa.gov/oppref/rereg/status.cfm?show=rereg.

56. U.S. Environmental Protection Agency. 2006. "Technology Transfer
Network Air Toxics Assessment: Original List of Hazardous Air
Pollutants." http://www.epa.gov/ttn/atw/188polls.html.

57. U.S. Food and Drug Administration. 2006. "Food Additive Status
List." http://www.cfsan.fda.gov/~dms/opa-appa.html#ftnT.

58. U.S. Environmental Protection Agency. 2001. "Lists of Lists:
Consolidated List of Chemicals Subject to the Emergency Planning and
Right-to-Know Act (EPCRA) and Section 112(r) of the Clean Air Act."
http://www.epa.gov/ceppo/pubs/title3.pdf.

59. U.S. Environmental Protection Agency. 2006. "TRI Explorer: Providing
Access to EPA's Toxic Release Inventory Data."
http://www.epa.gov/triexplorer/.


http://www.epa.gov/teach/

The TEACH Database currently contains over 2,300 summaries of articles
published from January 1972 through mid-2006.

These article summaries provide information on 18 chemicals of concern
that potentially impact children’s health.

The TEACH Database is updated annually and will soon contain the
remainder of 2006 article summaries.

The TEACH project was created and developed by the U.S. EPA Region 5
TEACH Workgroup and is funded through the U.S. EPA Office of Children’s
Health Protection.

Technical support was provided by Environmental Health Consulting, Inc.

1: Childhood represents a lifestage rather than a subpopulation -- the
distinction being that a subpopulation refers to a portion of the
population, whereas a lifestage is inclusive of the entire population.

2: Exposure to lead can pose significant health hazards to children, and
extensive information is provided elsewhere by the U.S. EPA at the
National Lead Information Center.
////////////////////////////////////////////////////////////


http://cfpub.epa.gov/teach/queryresults.cfm

Query Results
Query Summary:

* Chemical: Formaldehyde

The Query returned 60 results. Click on a citation to view details for
that report.

1. Aslan, H., et al. 2006. "Effects of Formaldehyde Exposure on
Granule Cell Number and Volume of Dentate Gyrus: A Histopathological and
Stereological Study." Brain Research 1122:191-200.

2. Axelsson, G., et al. 1984. "Exposure to Solvents and Outcome of
Pregnancy in University Laboratory Employees." British Journal of
Industrial Medicine 41:305-312.

3. Berne, B., et al. 1996. "Adverse Effects of Cosmetics and
Toiletries Reported to the Swedish Medical Products Agency." Contact
Dermatitis 34:359-362.

4. Boyvat, A., et al. 2005. "Contact Sensitivity to Preservatives in
Turkey." Contact Dermatitis 52:329-332.

5. Caldwell, J.C., et al. 1998. "Application of Health Information
to Hazardous Air Pollutants Modeled in EPA's Cumulative Exposure
Project." Toxicology and Industrial Health 14(3):429-454.

6. Casas, M.J., et al. 2005. "Do We Still Need Formocresol in
Pediatric Dentistry?" Journal Canadian Dental Association 71(10):749-751.

7. Collins, J.J., et al. 2001. "A Review of Adverse Pregnancy
Outcomes and Formaldehyde Exposure in Human and Animal Studies."
Regulatory Toxicology and Pharmacology 34:17-34.

8. deGroot, A.C., et al. 1988. "The Allergens in Cosmetics."
Archives of Dermatology 124:1525-1529.


9. Doi, S., et al. 2003. "The Prevalence of IgE Sensitization to
Formaldehyde in Asthmatic Children." Allergy 58:668-671.

10. Erdei, E., et al. 2003. "Indoor Air Pollutants and Immune
Biomarkers Among Hungarian Asthmatic Children." Archives of
Environmental Health 58(6):337-347.

11. Feinman, S.E. 1988. "Formaldehyde Genotoxicity and
Teratogenicity." In Formaldehyde Sensitivity and Toxicity. S. E.
Feinman, Ed. CRC Press, FL; pp. 168-178.

12. Franklin, F., et al. 2000. "Raised Exhaled Nitric Oxide in
Healthy Children Is Associated with Domestic Formaldehyde Levels."
American Journal of Respiratory and Critical Care Medicine 161:1757-1759.

13. Garrigos, M.C., et al. 2001. "Potentially Toxic Colorant
Precursors and Preservatives Used in Finger-Paints." Bulletin of
Environmental Contamination and Toxicology 66:557-562.


14. Hemminki, K., et al. 1982. "Spontaneous Abortions in Hospital
Staff Engaged in Sterilising Instruments with Chemical Agents." British
Medical Journal 285:1461-1463.


15. Hemminki, K., et al. 1985. "Spontaneous Abortions and
Malformations in the Offspring of Nurses Exposed to Anaesthetic Gases,
Cytostatic Drugs, and Other Potential Hazards in Hospitals, Based on
Registered Information of Outcome." Journal of Epidemiology and
Community Health 39:141-147.


16. John, E.M., et al. 1994. "Spontaneous Abortions Among
Cosmetologists." Epidemiology 5(2):147-155.


17. Kaniwa, M.A., et al. 1994. "Identification of Causative Chemicals
of Allergic Contact Dermatitis Using a Combination of Patch Testing in
Patients and Chemical Analysis." Contact Dermatitis 30:26-34.

18. Kinney, P.L. et al. 2002. "Exposures to Multiple Air Toxics in
New York City." Environmental Health Perspectives 110(Supplement 4):539-546.

19. Koltai, P.J. 1994. "Effects of Air Pollution on the Upper
Respiratory Tract of Children." Otolaryngology-Head and Neck Surgery
111:9-11.


20. Krzyzanowski, M., J.J. Quackenboss, and M.D. Lebowitz. 1990.
"Chronic Respiratory Effects of Indoor Formaldehyde Exposure."
Environmental Research 52:117-125.

21. Kusy, R.P., and J.Q. Whitley. 2005. "Degradation of Plastic
Polyoxymethylene Brackets and the Subsequent Release of Toxic
Formaldehyde." American Journal of Orthodontics and Dentofacial
Orthopedics 127(4):420-427.

22. Lemus, R., et al. 1998. "Potential Health Risks from Exposure to
Indoor Formaldehyde." Reviews on Environmental Health 11(1-2):91-98.

23. Marks, T.A., et al. 1980. "Influence of Formaldehyde and
Sonacide® (Potentiated Acid Glutaraldehyde) on Embryo and Fetal
Development in Mice." Teratology 22:51-58.


24. Martin, W.J. 1990. "A Teratology Study of Inhaled Formaldehyde in
the Rat." Reproductive Toxicology 4:237-239.

25. Mendell, M.J., and G.A. Heath. 2005. "Do Indoor Pollutants and
Thermal Conditions in Schools Influence Student Performance? A Critical
Review of the Literature." Indoor Air 15:27-52.


26. Mi, Y.-H., et al. 2006. "Current Asthma and Respiratory Symptoms
Among Pupils in Shanghai, China: Influence of Building Ventilation,
Nitrogen Dioxide, Ozone, and Formaldehyde in Classrooms." Indoor Air
16:454-464.


27. Milnes, A.R. 2006. "Persuasive Evidence that Formocresol Use in
Pediatric Denistry is Safe." Journal Canadian Dental Association
72(3):247-248.

28. Naya, M., and J. Nakanishi. 2005. "Risk Assessment of
Formaldehyde for the General Population in Japan." Regulatory Toxicology
and Pharmacology 43:232-248.

29. Nazaroff, W.W., and B.C. Singer. 2004. "Inhalation of Hazardous
Air Pollutants from Environmental Tobacco Smoke in U.S. Residences."
Journal of Exposure Analysis and Environmental Epidemiology 14:S71-S77.

30. Nelson, B.K. 1986. "Developmental Neurotoxicology of In Utero
Exposure to Industrial Solvents in Experimental Animals."
NeuroToxicology 7(2):441-448.

31. Norback, D., et al. 2000. "Indoor Air Pollutants in Schools:
Nasal Patency and Biomarkers in Nasal Lavage." Allergy 55:163-170.

32. Norman, G., et al. 1986. "Respiratory Function of Children in
Homes Insulated with Urea Formaldehyde Foam Insulation." Canadian
Medical Association Journal 134:1135-1138.

33. Olsen J.H., and M. Dossing. 1982. "Formaldehyde Induced Symptoms
in Day Care Centers." American Industrial Hygiene Association Journal
43:366-370.

34. Overman, D.O. 1985. "Absence of Embryotoxic Effects of
Formaldehyde After Percutaneous Exposure in Hamsters." Toxicology
Letters 24(1):107-110.

35. Ozcelik, O., et al. 2005. "Iatrogenic Trauma to Oral Tissues."
Journal of Periodontology 76(10):1793-1797.

36. Pike-Paris, A. 2004. "Indoor Air Quality: Part I - What It Is."
Pediatric Nursing 30(5):430-433.

37. Ritchie, I.M., and R.G. Lehnen. 1987. "Formaldehyde-Related
Health Complaints of Residents Living in Mobile and Conventional Homes."
American Journal of Public Health 77(3):323-328.

38. Rosenbaum, A.S., et al. 1999. "National Estimates of Outdoor Air
Toxics Concentrations." Journal of the Air and Waste Management
Association 49:1138-1152.

39. Rumchev, K.B., et al. 2002. "Domestic Exposure to Formaldehyde
Significantly Increases the Risk of Asthma in Young Children." European
Respiratory Journal 20(2):403-408.

40. Senichenkova, I.N., and N.A. Chebotar. 1996. "Effects of Gasoline
and Formaldehyde on Prenatal Development of Rats with Induced Iron
Microelementosis." Russian Journal of Developmental Biology 27(2):90-94.

41. Serrano-Trespalacios, P.I., et al. 2004. "Ambient, Indoor and
Personal Exposure Relationships of Volatile Organic Compounds in Mexico
City Metropolitan Area." Journal of Exposure Analysis and Environmental
Epidemiology 14:S118-S132.

42. Sharma, V.L., and A. Chakrabarti. 1998. "Common Contact
Sensitizers in Chandigarh, India." Contact Dermatitis 38:127-131.

43. Smedje, G. and D. Norback, 2001. "Incidence of Asthma Diagnosis
and Self-Reported Allergy in Relation to the School Environment- A
Four-Year Follow-up Study in Schoolchildren." International Journal of
Tuberculosis and Lung Disease 5(11):1059-1066.

44. Smedje, G. and D. Norback, 2001. "Irritants and Allergens at
School in Relation to Furnishings and Cleaning." Indoor Air 11:127-133.


45. Sommer, S., et al. 1999. "Contact Dermatitis Due to
Urea-Formaldehyde Resin in Shin-Pads." Contact Dermatitis 40:159-60.

46. Spengler, J.D., and K. Sexton. 1983. "Indoor Air Pollution: A
Public Health Perspective." Science 221:9-17.

47. Spiller, H.A. 2004. "Epidemiology of Volatile Substance Abuse
(VSA) Cases Reported to U.S. Poison Centers." The American Journal of
Drug and Alcohol Abuse 30(1):155-165.

48. Steensberg, J. 1984. "Indoor Climate Problems in Day Institutions
for Children." Institution of Medical Officers of Health, Frederiksborg
County, DK-3400 Hillerod, Denmark.

49. Stock, T.H., and S.R. Mendez. 1985. "A Survey of Typical
Exposures to Formaldehyde in Houston Area Residences." American
Industrial Hygienist Assocation Journal 46(6):313-317.

50. Sugai, T., et al. 1979. "Age Distribution of the Incidence of
Contact Sensitivity to Standard Allergens." Contact Dermatitis 5:383-388.

51. Suk, W.A., et al. 2003. "Environmental Threats to Children's
Health in Southeast Asia and the Western Pacific."Environmental Health
Perspectives 111(10):1340-1347.

52. Symington, P., et al. 1991. "Respiratory Symptoms in Children at
Schools near a Foundry." British Journal of Industrial Medicine 48:588-591.


53. Taskinen, H., et al. 1994. "Laboratory Work and Pregnancy
Outcome." Journal of Occupational Medicine 36(3):311-319.

54. Thrasher, J.D., and K.H. Kilburn. 2001. "Embryo Toxicity and
Teratogenicity of Formaldehyde." Archives of Environmental Health
56(4):300-311.

55. Tuthill, R.W. 1984. "Woodstoves, Formaldehyde, and Respiratory
Disease." American Journal of Epidemiology 120(6):952-955.


56. U.S. Environmental Protection Agency (EPA). 2001.
"Formaldehyde-Statewide estimates." 1996 Modeled Ambient Concentrations.
/www.epa.gov/ttn/atw/nata/pdf/forma_conc.pdf.

57. Wantke, F., et al. 1996. "Exposure to Gaseous Formaldehyde
Induces IgE-Mediated Sensitization to Formaldehyde in School-Children."
Clinical and Experimental Allergy 26:276-280.

58. Wjst, M., et al. 1994. "Indoor Factors and IgE Levels in
Children." Allergy 49:766-771.

59. Woodruff, T.J., et al. 1998. "Public Health Implications of 1990
Air Toxics Concentrations Across the United States." Environmental
Health Perspectives 106(5):245-251.

60. Zhou, D.-X., et al. 2006. "The Protective Effect of Vitamin E
Against Oxidative Damage Caused by Formaldehyde in the Testes of Adult
Rats." Asian Journal of Andrology 8(5):584-588.
////////////////////////////////////////////////////////////



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/1286
methanol products (formaldehyde and formic acid) are main cause of
alcohol hangover symptoms [same as from similar amounts of methanol, the
11% part of aspartame]: YS Woo et al, 2005 Dec: Murray 2006.01.20

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@...

http://groups.yahoo.com/group/aspartameNM/message/1143
methanol (formaldehyde, formic acid) disposition: Bouchard M et al, full
plain text, 2001: substantial sources are degradation of fruit pectins,
liquors, aspartame, smoke: Murray 2005.04.02
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169


Fully 11 % of aspartame is methanol -- 1,120 mg aspartame
in 2 L diet soda, almost six 12-oz cans, gives 123 mg methanol
(wood alcohol).

The methanol is immediately released into the body after drinking .

Within hours, the liver turns much of the methanol into formaldehyde,
and then much of that into formic acid, both of which in time
are partially eliminated as carbon dioxide and water.

However, about 30 % of the methanol remains in the body
as cumulative durable toxic metabolites of formaldehyde
and formic acid -- 37 mg daily, a gram every month,
accumulating in and affecting every tissue.

If only 10 % of the methanol is retained daily as formaldehyde,
that would give 12 mg daily formaldehyde accumulation -- about
60 times more than the 0.2 mg from 10 % retention
of the 2 mg EPA daily limit for formaldehyde in drinking water.

Bear in mind that the EPA limit for formaldehyde in drinking water is
1 ppm, or 2 mg daily for a typical daily consumption of 2 L of water.

http://groups.yahoo.com/group/aspartameNM/message/835
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999:
Murray 2002.05.30

This long-term low-level chronic toxic exposure leads to typical
patterns of increasingly severe complex symptoms,
starting with headache, fatigue, joint pain, irritability, memory loss,
rashes, and leading to vision and eye problems, and even seizures.
In many cases there is addiction. Probably there are immune system
disorders, with a hypersensitivity to these toxins and other chemicals.
////////////////////////////////////////////////////////////


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
[ Extracts re formaldehyde, made in body from methanol ]

[ http://groups.yahoo.com/group/aspartameNM/message/835
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999:
Murray 2002.05.30

"The EPA recommends that an adult should not drink water containing more
than 1 milligram of formaldehyde per liter of water (1 mg/L) for a
lifetime exposure, and a child should not drink water
containing more than 10 mg/L for 1 day or 5 mg/L for 10 days."

http://groups.yahoo.com/group/aspartameNM/message/1140
EPA Preliminary Remedial Goals, PRGs, 2003 Oct, air and tap water --
methanol, formaldehyde, formic acid -- not mentioned is methanol from
aspartame, dark wines and liquors: Murray 2004.11.20

http://groups.yahoo.com/group/aspartameNM/message/1108
faults in 1999 July EPA 468-page formaldehyde profile:
Elzbieta Skrzydlewska PhD, Assc. Prof., Medical U. of Bialystok, Poland,
abstracts -- ethanol, methanol, formaldehyde, formic acid, acetaldehyde,
lipid peroxidation, green tea, aging: Murray 2004.08.08 2005.07.11 ]

"The 1999 July EPA 468-page formaldehyde profile admits that four states
substantially exceed the federal EPA limit:

Environmental Protection Agency 2.00 mg in 2 L daily drinking water
California and Maine ---------- 0.06 mg
Maryland ---------------------- 0.02 mg
New Jersey -------------------- 0.20 mg

Maryland's limit is ten times more stringent than the EPA's." ]



[ This study by Jones AW (1987) found next-morning hangover
from red wine with 100 to 150 mg methanol
(9.5 % w/v ethanol, 100 mg/l methanol, 0.01 %).
Fully 11% of aspartame is methanol --
1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol).

Pharmacol Toxicol. 1987 Mar; 60(3): 217-20.
Elimination half-life of methanol during hangover.
Jones AW. wayne.jones@...
Department of Forensic Toxicology,
University Hospital, SE-581 85 Linkoping, Sweden.

This paper reports the elimination half-life of methanol in human
volunteers.

Experiments were made during the morning after the subjects had
consumed 1000-1500 ml red wine
(9.5 % w/v ethanol, 100 mg/l methanol)
the previous evening. [ 100 to 150 mg methanol ]

The washout of methanol from the body
coincided with the onset of hangover.

The concentrations of ethanol and methanol in blood were
determined indirectly by analysis of end-expired alveolar air.

In the morning when blood-ethanol dropped
below the Km of liver alcohol dehydrogenase (ADH)
of about 100 mg/l (2.2 mM),
the disappearance half-life of ethanol was 21, 22, 18 and 15 min.
in 4 test subjects respectively.

The corresponding elimination half-lives of methanol
were 213, 110, 133 and 142 min. in these same individuals.

The experimental design outlined in this paper can be used
to obtain useful data on elimination kinetics of methanol
in human volunteers without undue ethical limitations.

Circumstantial evidence is presented to link methanol
or its toxic metabolic products, formaldehyde and formic acid,
with the pathogenesis of hangover. PMID: 3588516


http://groups.yahoo.com/group/aspartameNM/message/1052
DMDC: Dimethyl dicarbonate 200mg/L in drinks adds methanol 98 mg/L
( becomes formaldehyde in body ): EU Scientific Committee on Foods
2001.07.12: Murray 2004.01.22

[ DMDC would be a very useful alternative source of methanol for human
studies, as controls to compare with aspartame and wines. ] ]


http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause of
alcohol hangover symptoms [same as from similar amounts of methanol, the
11% part of aspartame]: YS Woo et al, 2005 Dec: Murray 2006.01.20

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

[ Han-Kyu Lee ]

A hangover is characterized by the unpleasant physical and mental
symptoms that occur between 8 and 16 hours after drinking alcohol.

After inducing experimental hangover in normal individuals,
we measured the methanol concentration prior to
and after alcohol consumption
and we assessed the association between the hangover condition
and the blood methanol level.

A total of 18 normal adult males participated in this study.

They did not have any previous histories of psychiatric
or medical disorders.

The blood ethanol concentration prior to the alcohol intake
(2.26+/-2.08) was not significantly different from that
13 hours after the alcohol consumption (3.12+/-2.38).

However, the difference of methanol concentration
between the day of experiment (prior to the alcohol intake)
and the next day (13 hours after the alcohol intake)
was significant (2.62+/-1.33/l vs. 3.88+/-2.10/l, respectively).

A significant positive correlation was observed
between the changes of blood methanol concentration
and hangover subjective scale score increment when covarying
for the changes of blood ethanol level (r=0.498, p<0.05).

This result suggests the possible correlation of methanol
as well as its toxic metabolite to hangover. PMID: 16318957

[ The toxic metabolite of methanol is formaldehyde, which in turn
partially becomes formic acid -- both potent cumulative toxins
that are the actual cause of the toxicity of methanol.] ]


[ It is remarkable how little is known about the disposition of
formaldehyde and formic acid in human tissues, according to a sober
review by Bouchard M, 2001:

"Exposure to methanol also results from the consumption of certain
foodstuffs (fruits, fruit juices, certain vegetables, aspartame
sweetener, roasted coffee, honey) and alcoholic beverages (Health
Effects Institute, 1987; Jacobsen et al., 1988)."

"A biologically based dynamic model was developed to simulate the uptake
and disposition of methanol and its metabolites (formaldehyde, formate,
CO2) in animals and humans."

"Systemic methanol is extensively metabolized by liver alcohol
dehydrogenase and catalase-peroxidase enzymes to formaldehyde, which is
in turn rapidly oxidized to formic acid by formaldehyde dehydrogenase
enzymes (Goodman and Tephly, 1968; Heck et al., 1983; Røe, 1982; Tephly
and McMartin, 1984)."

"Formaldehyde, as it is highly reactive, forms relatively stable adducts
with cellular constituents (Heck et al., 1983; Røe, 1982)."

"Thus, in monkeys and plausibly humans, a much larger fraction of body
formaldehyde is rapidly converted to unobserved forms rather than passed
on to formate and eventually CO2."

"Inversely, in monkeys and in humans, a larger fraction of body burden
of formaldehyde is rapidly transferred to a long-term component.
The latter represents the formaldehyde that (directly or after oxidation
to formate) binds to various endogenous molecules..."

"However, fits to the available data in rats and monkeys of Horton et
al. 1992) and Dorman et al. (1994) show that, once formed, a substantial
fraction of formaldehyde is converted to unobserved forms.

This pathway contributes to a long-term unobserved compartment.

The latter, most plausibly, represents either the formaldehyde that
(directly or after oxidation to formate) binds to various endogenous
molecules (Heck et al., 1983; Røe, 1982)...

That substantial amounts of methanol metabolites or by-products are
retained for a long time is verified by Horton et al. (1992) who
estimated that 18 h following an iv injection of 100 mg/kg of
14C-methanol in male Fischer-344 rats, only 57% of the dose was
eliminated from the body.

From the data of Dorman et al. (1994) and Medinsky et al. (1997), it can
further be calculated that 48 h following the start of a 2-h inhalation
exposure to 900 ppm of 14C-methanol vapors in female cynomolgus monkeys,
only 23% of the absorbed 14C-methanol was eliminated from the body.

These findings are corroborated by the data of Heck et al. (1983)
showing that 40% of a 14C-formaldehyde inhalation dose remained in the
body 70 h postexposure."

http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169
free full text
Toxicological Sciences 64, 169-184 (2001)
A Biologically Based Dynamic Model for Predicting the Disposition of
Methanol and Its Metabolites in Animals and Humans
Michèle Bouchard *, #,1, bouchmic@...
Robert C. Brunet, # brunet@...
Pierre-Olivier Droz, #
Gaétan Carrier* gaetan.carrier@...

http://groups.yahoo.com/group/aspartameNM/message/1143
methanol (formaldehyde, formic acid) disposition, Bouchard M et al, full
plain text, 2001 -- substantial sources are degradation of fruit
pectins, liquors, aspartame, smoke: Murray 2005.01.05 ]
////////////////////////////////////////////////////////////


13 mainstream research studies in 24 months showing aspartame toxicity,
also 3 relevant studies on methanol and formaldehyde: Murray 2007.10.01
http://groups.yahoo.com/group/aspartameNM/message/1464

resia.pretorius@...,j.o.warner@...,tara.dean@...,jsteven@\
soton.ac.uk,crcfr@...,inchildh@...,stsakir@...,
biochem@...,katalin_gombos@...,niecl1022@...,step@su\
n5.ibp.ac.cn,liuy@...,sperrett@...,herq@...,
aritaven@...,w.g.mclean@...,c.v.howard@...,dom@...\
.uk,karenlau@...,

cogliano@...,grosse@...,baan@...,straif@...,secretan@...,elg\
hissassi@...,cie@...,chhabrar@...,john.cocker@...,
dnc@...,Rconolly@...,pdemers@...,david.eastmond@...\
u,faustman@...,gerinm@...,
marcel.goldberg@...,bdgold@...,roland.grafstrom@...,\
johnni@...,tjunghans@...,dkrewski@...,solin@...,
martine.reynier@...,yshaham@...,lstayner@...,wolf.doug@...,


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.
////////////////////////////////////////////////////////////


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 ~7 to 11
cans of soft drinks daily) compared with the lowest categories,
and the associations were similarly null in both men and women."

[ 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
http://groups.yahoo.com/group/aspartameNM/message/1475


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 2,000 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 cohert ---------- 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. ]

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. ]
////////////////////////////////////////////////////////////


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', 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&#8722;17177 Stockholm, Sweden Telefax: +46–8&#8722;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. Lézère, 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


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
////////////////////////////////////////////////////////////


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

"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://groups.yahoo.com/group/aspartameNM/messages
group with 82 members, 1,475 posts in a public,
searchable archive http://RMForAll.blogspot.com


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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