As School Doors Open, Food and Beverage Industries Rush In

unexamined diet research cofactors: formaldehyde from tobacco and wood smoke, it also forms from methanol in dark wines and liquors and 11% methanol part of aspartame: Murray 2006.09.16

http://groups.yahoo.com/group/aspartameNM/message/1340
aspartame groups and books: updated research review of 2004.07.16:
Murray 2006.05.11

http://groups.yahoo.com/group/aspartameNM/message/1366
toxicity in rat brains from aspartame, Vences-Mejia A,
Espinosa-Aguirre JJ et al 2006 Aug: Murray 2006.09.06

http://groups.yahoo.com/group/aspartameNM/message/1341
Connecticut bans artificial sweeteners in schools, Nancy Barnes,
New Milford Times: Murray 2006.05.25

http://groups.yahoo.com/group/aspartameNM/message/1353
carcinogenic effect of inhaled formaldehyde, Federal Institute of Risk
Assessment, Germany -- same safe level as for Canada:
Murray 2006.06.02

http://groups.yahoo.com/group/aspartameNM/message/1352
Home sickness -- indoor air often worse, as our homes seal in pollutants
[one is formaldehyde, also from the 11% methanol part of aspartame],
Megan Gillis, WinnipegSun.com: Murray 2006.06.01

"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@comcast.net
505-501-2298 1943 Otowi Road Santa Fe, New Mexico 87505

http://groups.yahoo.com/group/aspartameNM/messages
group with 77 members, 1,368 posts in a public, searchable archive
http://RMForAll.blogspot.com

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://groups.yahoo.com/group/aspartameNM/message/1349
NIH NLM ToxNet HSDB Hazardous Substances Data Bank
inadequate re aspartame (methanol, formaldehyde, formic acid):
Murray 2006.08.19

http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~HwoSfJ:1
HSDB Hazardous Substances Data Bank: Aspartame

ASPARTAME CASRN: 22839-47-0
METHANOL CASRN: 67-56-1
FORMALDEHYDE CASRN: 50-00-0
FORMIC ACID CASRN: 64-18-6

http://groups.yahoo.com/group/aspartameNM/message/1307
formaldehyde from 11% methanol part of aspartame or from red wine
causes same toxicity (hangover) harm: Murray 2006.05.24

Dark wines and liquors, as well as aspartame, provide
similar levels of methanol, above 120 mg daily, for
long-term heavy users, 2 L daily, about 6 cans.

Within hours, methanol is inevitably largely turned into formaldehyde,
and thence largely into formic acid -- the major causes of the dreaded
symptoms of "next morning" hangover.

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 18.5 times the USA EPA limit for daily formaldehyde in
drinking water, 2.0 mg in 2 L average daily drinking water.

Any unsuspected source of methanol, which the body always quickly
and largely turns into formaldehyde and then formic acid, must be
monitored, especially for high responsibility occupations, often with
night shifts, such as pilots and nuclear reactor operators.

http://www.HolisticMed.com/aspartame mgold@holisticmed.com
Aspartame Toxicity Information Center Mark D. Gold
12 East Side Drive #2-18 Concord, NH 03301 603-225-2100

http://www.holisticmed.com/aspartame/abuse/methanol.html
"Scientific Abuse in Aspartame Research"
*******************************************************

ASPARTAME CASRN: 22839-47-0

Human Health Effects:

Human Toxicity Excerpts:

. . . Adverse effects: urticaria, angiodema, granulomatous
panniculitis, cross-reactivity with sulfonamides,
renal tubular acidosis (with large amounts) /From table/
[Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger.
Ellenhorn's Medical Toxicology: Diagnosis and Treatment of
Human Poisoning. 2nd ed.
Baltimore, MD: Williams and Wilkins, 1997., p. 996]
**PEER REVIEWED**

METHANOL CASRN: 67-56-1

Human Health Effects:

Toxicity Summary:

Methanol occurs naturally in humans, animals and plants.
It is a natural constituent in blood, urine, saliva and expired air.
... The two most important sources of background body burdens
for methanol and formate are diet and metabolic processes.
Methanol is available in the diet principally from fresh fruits and
vegetables, fruit juices ... fermented beverages
... and diet foods (principally soft drinks).

The artificial sweetner aspartame is widely used and, on hydrolysis,
10% (by weight) of the molecule is converted to free methanol,
which is available for absorption. ... Exposures to methanol can occur
in occupational settings through inhalation or dermal contact.
... Methanol is readily absorbed by inhalation, ingestion and dermal
exposure, and it is rapidly distributed to tissues according to the
distribution of body water. A small amount of methanol is excreted
unchanged by the lungs and kidneys.

[ Alcohol Clin Exp Res. 1997 Aug; 21(5): 939-43.
Endogenous production of methanol after the consumption of fruit.
Lindinger W, Taucher J, Jordan A, Hansel A, Vogel W.
Institut fur Ionenphysik, Leopold Franzens Universitat Innsbruck,
Austria.

After the consumption of fruit, the concentration of methanol in the
human body increases by as much as an order of magnitude.
This is due to the degradation of natural pectin
(which is esterified with methyl alcohol) in the human colon.
[ by bacteria ]
In vivo tests performed by means of proton-transfer-reaction mass
spectrometry show that consumed pectin in either a pure form
(10 to 15 g)
or a natural form (in 1 kg of apples) induces a significant increase of
methanol in the breath (and by inference in the blood) of humans.
The amount generated from pectin (0.4 to 1.4 g) [ 400 to 1400 mg ]
is approximately equivalent to the total daily endogenous production
(measured to be 0.3 to 0.6 g/day) [ 300 to 600 mg ]
or that obtained from 0.3 liters of 80-proof brandy
(calculated to be 0.5 g). [ 500 mg ]
This dietary pectin may contribute to the development
of nonalcoholic cirrhosis of the liver. PMID: 9267548

Alcohol Clin Exp Res. 1995 Oct; 19(5): 1147-50.
Methanol in human breath.
Taucher J, Lagg A, Hansel A, Vogel W, Lindinger W.
Institut fur Ionenphysik, Universitat Innsbruck, Austria.

Using proton transfer reaction-mass spectrometry for trace gas analysis
of the human breath, the concentrations of methanol and ethanol have
been measured for various test persons consuming alcoholic beverages
and various amounts of fruits, respectively.
The methanol concentrations increased from a natural (physiological)
level of approximately 0.4 ppm up to approximately 2 ppm a few hours
after eating about 1/2 kg of fruits,
and about the same concentration was reached
after drinking of 100 ml brandy
containing 24% volume of ethanol and 0.19% volume of methanol.
PMID: 8561283 [ My earlier errors were corrected 2005.07.11:
24 ml means 19 g ethanol,
and 0.19 ml means 0.15 g = 150 mg methanol.
One L diet soda has 61.5 mg methanol in the aspartame molecule,
so 100 ml diet soda has 6.15 mg methanol,
so the brandy has 24.4 times more methanol than diet soda.
A pound of fruit gives about as much methanol as 2 L
(nearly 6 cans) diet soda. ] ]

... Methanol is metabolized primarily in the liver
by sequential oxidative steps
to formaldehyde, formic acid and carbon dioxide.
The initial step
involves oxidation to formaldehyde by hepatic alcohol dehydrogenase
... In step 2, formaldehyde is oxidized by formaldehyde dehydrogenase
to formic acid/or formate depending on the pH.
In step 3, formic acid is detoxified to carbon dioxide
by folate-dependent reactions.

Elimination of methanol from the blood via the urine and exhaled air
and by metabolism appears to be slow in all species,
especially when compared to ethanol.
... It is the rate of metabolic detoxification, or removal of formate
that is vastly different between rodents and primates and is the
basis for the dramatic differences in methanol toxicity observed
between rodents and primates.
The acute and short term toxicity of methanol varies greatly
between different species, toxicity being highest in species with a
relatively poor ability to metabolize formate.
In such cases of poor metabolism of formate,
fatal methanol poisoning occurs as a result of metabolic acidosis
and neuronal toxicity, whereas, in animals that readily metabolize
formate, consequences of CNS depression (coma, respiratory
failure, etc.) are usually the cause of death.

Sensitive primate species (humans and monkeys)
develop increased blood formate concentrations following methanol
exposure, while resistant rodents, rabbits and dogs do not.

Humans and non-human primates are uniquely sensitive
to the toxic effects of methanol.

Overall methanol has a low acute toxicity to non-primate animals.
... In the rabbit, methanol is a moderate irritant to the eye.
It was not skin sensitizing ... There is no evidence from animal
studies to suggest that methanol is a carcinogen

... The inhalation of methanol by pregnant rodents throughout the
period of embryogenesis induces a wide range of
concentration-dependent teratogenic and embryolethal effects.
Treatment-related malformations, primarily extra or rudimentary
cervical ribs and urinary or cardiovascular defects, were found
in fetuses of rats ... Increased incidences of exencephaly and cleft
palate were found in the offspring of ... mice ... There was increased
embryo/fetal death ... and an increasing incidence of full litter
resorptions. Reduced fetal weight was observed
... Fetal malformations ... included neural and ocular defects,
cleft palate, hydronephrosis and limb anomalies.

Humans (and non-human primates) are uniquely sensitive to
methanol poisoning and the toxic effects in these species are
characterized by formic acidemia, metabolic acidosis,
ocular toxicity, nervous system depression, blindness, coma and death.
Nearly all of the available information on methanol toxicity
in humans relates to the consequences of acute
rather than chronic exposures.

A vast majority of poisonings involving methanol have occurred
from drinking adulterated beverages and from methanol-containing
products. Although ingestion dominates as the most frequent route
of poisoning, inhalation of high concentrations of methanol vapor
and percutaneous absorption of methanolic liquids are as effective
as the oral route in producing acute toxic effects.

The most noted health consequences of longer term exposure
to lower levels of methanol is a broad range of ocular effects.
... The toxicity is manifest if formate generation continues at a rate
that exceeds its rate of metabolism.
... The minimum lethal dose of methanol in the absence of
medical treatment is between 0.3 and 1 g/kg.
The minimum dose causing permanent visual defects is unknown.
... Wide interindividual variability of the toxic dose is a prominent
feature in acute methanol poisoning.
Two important determinants of human susceptibility
to methanol toxicity appear to be
(1) concurrent ingestion of ethanol, which slows the entrance of
methanol into the metabolic pathway, and
(2) hepatic folate status, which governs the rate
of formate detoxification.

The symptoms and signs of methanol poisoning, which may not appear
until after an asymptomatic period ... include visual disturbances,
nausea, abdominal and muscle pain, dizziness, weakness and
disturbances of consciousness ranging from coma to clonic seizures.
Visual disturbances ... range from mild photophobia and misty or
blurred vision to markedly reduced visual acuity
and complete blindness.
In extreme cases death results.
The principal clinical feature is severe metabolic acidosis of the
anion-gap type. The acidosis is largely attributed to the
formic acid produced when methanol is metabolized.
... Visual disturbances of several types (blurring, constriction of
the visible field, changes in color perception, and temporary or
permanent blindness) have been reported in workers
... No other adverse effects of methanol have been reported
in humans except minor skin and eye irritation. ... Methanol is of
low toxicity to aquatic organisms, and effects due to environmental
exposure to methanol are unlikely to be observed,
except in the case of a spill.
[Environmental Health Criteria 196: Methanol pp. 1-9 (1997)
by the International Programme on Chemical Safety (IPCS)
under the joint sponsorship of the
United Nations Environment Programme,
the International Labour Organisation and
the World Health Organization.]**PEER REVIEWED**

Human Toxicity Excerpts:

/HUMAN EXPOSURE STUDIES/ ...Teacher aides who
worked at or near spirit duplicators that used a 99% methanol
duplicator fluid /were studied/. The exposures ranged
from 1 hr/day for 1 day/wk to 8 hr/day for 5 days/wk
and had occurred for 3 years.

Since the introduction of the equipment, the aides
began to experience headaches, dizziness and eye irritation,
blurred vision and nausea/upset stomach while working
near the machines.

Fifteen-minute breathing zone samples near 21 operating machines
contained between 475 and 4000 mg/cu m of methanol vapor.
Fifteen of these samples exceeded the NIOSH recommended
15-min standard of 1050 mg/cu m (800 ppm).
The aides were also exposed while collating and stapling papers
impregnated with the fluid up to 3 hr earlier and these exposures
ranged from 235-1140 mg/cu m .

The results suggested that chronic effects may occur when
methanol concentrations exceed the threshold limit value (TLV)
of 260 mg/cu m (200 ppm). The effects reported in the study
... were similar in nature but appeared less severe than those
reported from acute poisoning by methanol
[WHO; Environ Health Criteria 196: Methanol p.111 (1997).
Available from:
http://www.inchem.org/documents/ehc/ehc/ehc196.htm
as of July 19, 2005. ]**PEER REVIEWED**

FORMALDEHYDE CASRN: 50-00-0

Human Health Effects:

Evidence for Carcinogenicity:

CLASSIFICATION: B1; probable human carcinogen.
BASIS FOR CLASSIFICATION: Based on limited evidence
in humans, and sufficient evidence in animals.
Human data include nine studies that show statistically significant
associations between site-specific respiratory neoplasms and exposure
to formaldehyde or formaldehyde-containing products.
An increased incidence of nasal squamous cell carcinomas
as observed in long-term inhalation studies in rats and in mice.
The classification is supported by in vitro genotoxicity data
and formaldehyde's structural relationships to other
carcinogenic aldehydes such as acetaldehyde.

HUMAN CARCINOGENICITY DATA:
Limited. ANIMAL CARCINOGENICITY DATA: Sufficient.
[U.S. Environmental Protection Agency's
Integrated Risk Information System
(IRIS) on Formaldehyde (50-00-0)
Available from:
http://www.epa.gov/ngispgm3/iris
on the Substance File List as of March 15, 2000]**PEER REVIEWED**

... SYMPTOMATOLOGY:

A. Inhalation:
1. Irritation of mucous membranes, especially of eyes,
nose & upper respiratory tract.
2. With higher concn, cough, dysphagia, bronchitis, pneumonia,
edema or spasm of the larynx. Pulmonary edema is uncommon.

B. Ingestion.
1. Immediate intense pain in mouth, pharynx & stomach.
2. Nausea, vomiting, hematemesis, abdominal pain & occasionally
diarrhea (which may be bloody).
3. Pale, clammy skin & other signs of shock.
4. Difficult micturition, hematuria, anuria.
5. Vertigo, convulsions, stupor, & coma.
6. Death due to respiratory failure.

C. Skin contact:
1. Irritation & hardening of skin. Strong solutions produce
coagulation necrosis.
2. Dermatitis & hypersensitivity from prolonged or repeated exposure.
[Gosselin, R.E., R.P. Smith, H.C. Hodge.
Clinical Toxicology of Commercial Products. 5th ed.
Baltimore: Williams and Wilkins, 1984., p. III-197]
**PEER REVIEWED**

. . . The effect of formaldehyde exposure on medical students
conducting dissections in the gross anatomy laboratory course
/was evaluated using/ self-administered questionnaires designed
to assess the frequency of occurrence of various symptoms
indicating the acute effects of formaldehyde exposure.

The questionnaires were given to a cohort of 1st-yr medical students
on completion of the gross anatomy lab course.
Air sampling of formaldehyde levels in the anatomy labs
was carried out on one day during the time in which these students
were conducting dissections.
... Although the results of the air sampling showed formaldehyde levels
to be well below current occupational standards,
significant numbers of students reported experiencing symptoms
associated with formaldehyde exposure.
Estimates of the relative risk of experiencing formaldehyde-related
symptoms in the anatomy laboratories compared to the control
laboratories ranged from 2.0-19.0,
depending on the particular symptom.
In addn, it was found that female students were 3 times more likely
to report formaldehyde-related symptoms than male students.
[Fleischer JM; NY J Med 87 (7): 385-8 (1987)]
**PEER REVIEWED**

. . . Symptoms:

Local: Conjunctivitis, corneal burns; brownish discoloration of skin;
dermatitis, urticaria (hives), pustulovesicular eruption.

Inhalation: rhinitis & anosmia (loss of sense of smell);
pharyngitis, laryngospasm; tracheitis & bronchitis;
pulmonary edema, cough, constriction in chest;
dypsnea (difficult breathing), headache, weakness,
palpitation (rapid heart beat), gastro enteritis (inflammation of the
stomach & intestines).

Ingestion: Burning in mouth & esophagus; nausea & vomiting;
abdominal pain, diarrhea, vertigo (dizziness), unconsciousness,
jaundice, albuminuria, hematuria, anuria, acidosis, convulsions.
[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual.
Tokyo, Japan:
The International Technical Information Institute, 1988., p. 249]
**PEER REVIEWED**

. . . Four groups of patients with long-term inhalation exposure to
formaldehyde were compared with controls who had short-term
periodic exposure to formaldehyde.
The following were determined for all groups:
total white cell, lymphocyte, and T cell counts;
helper/suppressor ratios;
total Ta1+, IL2+, and B cell counts;
antibodies to formaldehyde-human serum albumin conjugate
and autoantibodies.
When compared with the controls, the patients
had significantly higer antibody titers to formaldehyde-human
serum albumin.
In addition, significant increases in Ta1+, IL2+, and B cells and
autoantibodies were observed.
Immune activation, autoantibodies, and anti formaldehyde-human
erum albumin antibodies are associated with long-term
formaldehyde inhalation.
[Thrasher JD et al; Arch Environ Health 45 (4): 217-23 (1990)]
**PEER REVIEWED**

[ http://groups.yahoo.com/group/aspartameNM/message/915
formaldehyde toxicity: Thrasher & Kilburn: Shaham: EPA: Gold:
Wilson: CIIN: Murray 2002.12.12 rmforall

Thrasher (2001): "The major difference is that the Japanese
demonstrated the incorporation of FA and its metabolites
into the placenta and fetus.
The quantity of radioactivity remaining in maternal and fetal tissues
at 48 hours was 26.9% of the administered dose." [ Ref. 14-16 ]

Arch Environ Health 2001 Jul-Aug; 56(4): 300-11.
Embryo toxicity and teratogenicity of formaldehyde. [100 references]
Thrasher JD, Kilburn KH. toxicology@drthrasher.org
Sam-1 Trust, Alto, New Mexico, USA.
http://www.drthrasher.org/formaldehyde_embryo_toxicity.html full text

http://www.drthrasher.org/formaldehyde_1990.html full text
Jack Dwayne Thrasher, Alan Broughton, Roberta Madison.
Immune activation and autoantibodies in humans with long-term
inhalation exposure to formaldehyde.
Archives of Environmental Health. 1990; 45: 217-223.
PMID: 2400243 ]

... measured the formation of DNA-protein cross links in peripheral
white blood cells of occupationally exposed workers (n=12)
& unexposed controls (n=8).
The avg length of ... exposure was 13 yr.
... Venous blood samples were collected ... .
Personal & room concn of formaldehyde were collected at
various periods during the working day among the exposed subjects,
with formaldehyde room concn ranging from 1.38-1.6 ppm.
Personal monitoring devices indicated formaldehyde concn
of 2.8-3.1 ppm during peak work & an
avg concn of 1.46 ppm at times when work was usually completed.
Exposure to formaldehyde resulted in a significant incr in the
incidence of DNA-protein cross links.
Mean ... incidences in exposed & nonexposed workers were
28 + or - 6 & 22 + or - 6%, respectively.
Within the exposed workers group,
technicians had significantly greater levels of DNA-protein cross links
than physicians (32.3 + or - 4.3 & 26.3 + or - 4.4%, respectively).
A linear relationship between yr of exposure & DNA-protein cross
links formation was also detected.
When the data were analyzed considering worker smoking habits,
DNA-protein cross links was consistently elevated among
formaldehyde-exposed versus corresponding controls (p=0.03).
[DHHS/ATSDR; Toxicological Profile for Formaldehyde p. 86 (1999)]
**PEER REVIEWED**

. . . No biologic monitoring techniques exist at present, either for
the reliable determineation of formaldehyde levels in tissue or for the
determination of formaldehyde adducts formed with macromolecules.
Techniques are under development for nonspecific monitoring of
exposure through periodic assessment of chromosome damage
(micronucleus formation or sister chromatid exchange frequency)
in workers exposed to formaldehyde.
[Rom, W.N. (ed.). Environmental and Occupational Medicine. 2nd ed.
Boston, MA: Little, Brown and Company, 1992., p. 868]
**PEER REVIEWED**

. . . The assessment of formaldehyde exposure can be accomplished
through measurement of the metabolite formic acid. Formic acid is also
an endogenously produced substance
formed by the degradation of glycine.
There was no information in the literature that showed a correlation
between urinary formic acid levels & formaldehyde exposure levels.
This measurement is also a poor indicator of the extent of formaldehyde
absorption, due to the high endogenous levels of formic acid.
Urine Reference Ranges:
Normal-normal population level: 21 mg/l
(endogenously produced formic acid);
Exposed- not established; Toxic- not established.
[Ryan, R.P., C.E. Terry, S.S. Leffingwell (eds.)
Toxicology Desk Reference 5th ed. Volumes 1-2.
Taylor & Francis Philadelphia, PA. 2000, p. 714]
**PEER REVIEWED**

. . . Release of /formaldehyde/ vapors in mobile homes
has been associated with headache & pulmonary & dermal irritation.
/Occupants of mobile homes are possibly exposed/.
[Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger.
Ellenhorn's Medical Toxicology:
Diagnosis and Treatment of Human Poisoning. 2nd ed.
Baltimore, MD: Williams and Wilkins, 1997., p. 1214]
**PEER REVIEWED**

. . . Smokers and persons who live in a home with a cigarette smoker
also may be exposed to higher levels of formaldehyde.
Environmental tobacco smoke, which is a combination of diluted
sidestream smoke released form a cigarette's burning end and
mainstream smoke exhaled by an active smoker,
can contribute 10-25% (0.1-1 mg/day) of the total average indoor
exposure to formadehyde ... .
[DHHS/ATSDR; Toxicological Profile for Formaldehye p. 311 (1999)]

[ 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, Lyme disease:
Murray 2004.08.08 ]

**PEER REVIEWED**

. . . Cigarette smoke and products of combustion
contain formaldehyde(1).
Cigarette smoke contains 15 to 20 mg formaldehyde per cigarette(1).
Avg formaldehyde exposure from passive smoking
is between 0.23 to 0.27 ppm(1).
A 'pack-a-day' smoker may inhale
as much as 0.4-2.0 mg formaldehyde(1).
[ See below for
Federal Drinking Water Guidelines:
EPA 1000 ug/l [ 1.0 mg/l gives 2 mg for daily 2 l drinking water ]]

[(1) Bingham E et al, eds; Patty's Toxicology. 5th ed.
NY, NY: John Wiley & Sons Inc. 5: 980-3 (2001)]
**PEER REVIEWED**

Food Survey Values:

Formaldehyde occurs naturally in foods,
and foods may be contaminated as a result of fumigation
(of e.g. grain),
cooking (as a combustion product) and
release from formaldehyde resin-based tableware(1).
It has been used as a bacteriostatic agent in some foods,
such as cheese(1).
Fruits and vegetables typically contain 3-60 mg/kg,
and meat and fish, 6-20 mg/kg(1).
[(1) IARC; Monographs on the Evaluation of the Carcinogenic Risk
of Chemicals to Man. Geneva, Switzerland:
WHO 62: 243 (1995)]**PEER REVIEWED**

Federal Drinking Water Guidelines:

EPA 1000 ug/l [ 1.0 mg/l gives 2 mg for daily 2 l drinking water ]
[USEPA/Office of Water; Federal-State
Toxicology and Risk Analysis Committee
(FSTRAC).
Summary of State and Federal Drinking Water Standards and
Guidelines (11/93), p. ]**QC REVIEWED**

FORMIC ACID CASRN: 64-18-6

Human Health Effects:

Human Toxicity Excerpts:

/HUMAN EXPOSURE STUDIES/
...Workers exposed to formic /acid/ ... in a textile plant complained
of nausea. Air tests in the area revealed concentrations
... averaging 15 ppm.
[American Conference of Governmental Industrial Hygienists.
Documentation of the Threshold Limit Values
and Biological Exposure Indices. 5th ed.
Cincinnati, OH:
American Conference of Governmental Industrial Hygienists,
1986., p. 279]**PEER REVIEWED**

. . . SIGNS AND SYMPTOMS/
Formic acid produced by bees, wasps, and ants
will cause tissue irritation upon contact or injection.
[Doull, J., C.D. Klaassen, and M. D. Amdur (eds.).
Casarett and Doull's Toxicology. 2nd ed. New York:
Macmillan Publishing Co., 1980., p. 558]**PEER REVIEWED**

. . . /CASE REPORTS/ In a human case of formaldehyde poisoning,
toxic concentrations of formate (7-8 mm) were detected within 30 min
of ingestion, confirming rapid metabolism of formaldehyde to formate
in humans.
[WHO; Environ Health Criteria 196: Methanol p.62 (1997).
Available from:
http://www.inchem.org/documents/ehc/ehc/ehc196.htm
as of July 14, 2005. ]**PEER REVIEWED**

/CASE REPORTS/ Two patients were studied who presented
with methanol poisoning.
Formate accumulation was marked with initial blood levels ranging
from 11.1-26.0 meq/L.
Decrease in blood bicarbonate concentration of similar
magnitude coincided with the increase in formate accumulation.
Accumulation of formic acid thus plays a major part in the acidosis
observed in human subjects poisoned with methanol.
[McMartin KE et al; Am J Med 68 (3): 414-8 (1980) ]
**PEER REVIEWED**

. . . /LABORATORY ANIMALS:
Developmental or Reproductive Toxicity/
Sprague-Dawley rat embryo cultures (9th day of gestation)
were treated with sodium formate or formic acid at concentrations
of 200, 400, 800, 1200, 1600, 2000 ug/mL (sodium formate)
or 140, 270, 540, 810, 1080 ug/mL (formic acid).
The pH of the medium was no longer corrected after addition of the
test substance.
Both after 24- and after 48-h incubation with sodium formate,
there was a significant and concentration-dependent reduction of
the developmental parameters yolk sac diameter (YSD),
crown-rump length (CRL), head length (HL), somite number (SN)
and developmental score (DEVSC).
Embryolethality was significantly increased only in the highest
concentration after 48-h incubation.
The number of anomalies (mainly CNS: open anterior and posterior
neuropores and erratic neurorrhaphy)
was significantly increased
at 1.6 and 2.0 mg/mL after 24 h and at 0.8 and 2.0 mg/mL
after 48-h incubation.
The protein and DNA levels showed a significant
and concentration-dependent reduction.
Incubations with formic acid also showed a significant
and concentration-dependent reduction of
YSD, CRL, HL, SN and DEVSC after 24-h incubation
and of CRL, HL, SOM and DEVSC after 48 h.
Embryolethality was significantly increased in the highest
concentration
after 24 h and in the two highest concentrations after 48 h.
Protein and DNA concentrations showed significant and concentration
dependent decreases in both cases.
The number of anomalies (open anterior and posterior neuropores,
rotatory defects and enlarged maxillary process) showed a significant
increase only at 0.81 mg/mL after 48-h incubation.
To sum up, concentration-dependent embryotoxic and dysmorphic
changes were detected in the culture both using formate and formic acid
in this test system.
[EPA/Office of Pollution Prevention and Toxics;
High Production Volume (HPV)
Challenge Program's Robust Summaries and Test Plans.
Available from:
http://www.epa.gov/chemrtk/viewsrch.htm
on Formates (December 2001) as of July 12, 2005. ]
**PEER REVIEWED**

Food Survey Values:

Formic acid is a natural constituent
of some fruits, nuts, and dairy products(1).
Fruit wine, desert wine, and brandies contain formic acid(2).
Formic acid concns in wine and brandies produced from apples, pears,
plums, and apricots ranged from 2.7-87 mg/L(2).
Formic acid has been identified as a meat volatile(3).
[(1) Bingham E et al, eds; Patty's Industrial Hygiene
and Toxicology 5th ed,
NY, NY: John Wiley Sons. 5: 693 (2001)
(2) Sponholz WR et al;
Deutche-Lebensmittel-Rundshaw 85: 247-51 (1989)
(3) Shahidi F et al; CRC
Crit Rev Food Sci Nature 24: 141-243 (1986) ]
**PEER REVIEWED**

. . . Indirect food substance additives affirmed as generally
recognized
as safe.
(a) Formic acid (CH2O2, CAS Reg. No. 64?18?6)
is also referred to as methanoic acid or hydrogen carboxylic acid.
It occurs naturally in some insects and is contained in the free acid
state in a number of plants.
Formic acid is prepared by the reaction of sodium formate
with sulfuric acid and is isolated by distillation.
(b) Formic acid is used as a constituent of paper and paperboard
used for food packaging.
(c) The ingredient is used at levels not to exceed good manufacturing
practice in accordance with ?186.1(b)(1).
(d) Prior sanctions for formic acid different from the uses
established in this section do not exist or have been waived.
[21 CFR 186.1316; U.S. National Archives and Records
Administration's Electronic Code of Federal Regulations.
Available from:
http://www.gpoaccess.gov/ecfr as of June 1, 2005 ]
**PEER REVIEWED**

State Drinking Water Guidelines:

(FL) FLORIDA 14,000 ug/L

[ 14.0 mg/L gives 28 mg in 2 L daily drinking water ]
[USEPA/Office of Water; Federal-State Toxicology
and Risk Analysis Committee (FSTRAC).
Summary of State and Federal Drinking Water Standards and
Guidelines (11/93), p. ]**PEER REVIEWED**
*******************************************************

http://groups.yahoo.com/group/aspartameNM/message/1106
hangover research relevant to toxicity of 11% methanol in aspartame
(formaldehyde, formic acid): Calder I (full text): Jones AW:
Murray 2004.08.05 rmforall

Since no adaquate data has ever been published on the exact disposition
of toxic metabolites in specific tissues in humans of the 11% methanol
component of aspartame, the many studies on morning-after hangover
from the methanol impurity in alcohol drinks are the main available
resource to date.

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%,
one part in ten thousand).

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

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/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@catholic.ac.kr
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).

[ So, the normal methanol level was 2.62 mg per liter,
and increasing that by 50% = 1.3 mg per liter to 3.88 mg per liter
caused hangover symptoms. The human body has about
5.6 liters blood, so adding 1.3 mg per liter gives an estimate
of 7.3 mg added methanol, as much as 4 oz diet soda.

Diet soda is about 200 mg aspartame per 12 oz can,
which is 22 mg (11% methanol), 1.83 mg methnol per ounce.

This suggests that alcohol drinkers are more sensitive to methanol
than the average diet soda drinker, some of whom find symptoms
from a third of a diet soda.]

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.]

http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984: Monte:
Murray 2002.09.23

Humans suffer "toxic syndrome" (54) at a minimum lethal dose
of <1 gm/kg, much less than that of monkeys, 3-6 g/kg (42, 59).

The minimum lethal dose of methanol
in the rat, rabbit, and dog is 9.5, 7.0 , and 8.0 g/kg, respectively
(43);
ethyl alcohol is more toxic than methanol to these test animals (43)."

As a medical layman, I suggest that evidence mandates immediate
exploration of the role of these ubiquitious, potent formaldehyde
sources as co-factors in epidemiology, research, diagnosis,
and treatment in a wide variety of disorders.

Folic acid, from fruits and vegetables, plays a role by powerfully
protecting against methanol (formaldehyde) toxicity.

Many common drugs, such as aspirin, interfere with folic acid,
as do some mutations in relevant enzymes.

The majority of aspartame reactors are female.

http://groups.yahoo.com/group/aspartameNM/message/1291
European Food Safety Authority to decide aspartame safety by May:
caffeine diet drinks cause female hypertension, WC Winkelmayer et al,
JAMA 2005.11.09: PubMed lists 50 items for "diet soft drinks" since
2004 Oct.: Murray 2006.01.24

http://groups.yahoo.com/group/aspartameNM/message/1279
all three aspartame metabolites harm human erythrocyte [red blood cell]
membrane enzyme activity, KH Schulpis et al, two studies in 2005,
Athens, Greece, 2005.12.14: 2004 research review, RL Blaylock:
Murray 2006.01.14

http://groups.yahoo.com/group/aspartameNM/message/939
aspartame (aspartic acid, phenylalanine) binding to DNA:
Karikas July 1998: Murray 2003.01.05 rmforall
Karikas GA, Schulpis KH, Reclos GJ, Kokotos G
Measurement of molecular interaction of aspartame and
its metabolites with DNA. Clin Biochem 1998 Jul; 31(5): 405-7.
Dept. of Chemistry, University of Athens, Greece
http://www.chem.uoa.gr gkokotos@atlas.uoa.gr;
K.H. Schulpis inchildh@otenet.gr; G.J. Reclos reklos@otenet.gr;

http://groups.yahoo.com/group/aspartameNM/message/1271
combining aspartame and quinoline yellow, or MSG and brilliant blue,
harms nerve cells, eminent C. Vyvyan Howard et al, 2005
education.guardian.co.uk, Felicity Lawrence: Murray 2005.12.21

http://groups.yahoo.com/group/aspartameNM/message/1329
aspartame or MSG affects circadian rhythms in rats, two studies,
P. Subramanian, T. Manivasagam et al 2004:
Murray 2006.04.27

http://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text Trocho & Alemany 1998.06.26
Universitat Autònoma de Barcelona : Murray 2002.12.22

http://groups.yahoo.com/group/aspartameNM/message/1316
PubMed abstract: aspartame (methanol becoming formaldehyde) causes
many cancers in rats, Ramazzini Foundation, M Soffritti et al:
Murray 2006.03.06

http://www.ehponline.org/members/2005/8711/8711.html free full text

Environ Health Perspect. 2006 Mar; 114(3): 379-85.
First experimental demonstration of the multipotential carcinogenic
effects of aspartame administered in the feed to sprague-dawley rats.
Soffritti M, Belpoggi F, Esposti DD,
Lambertini L, Tibaldi E, Rigano A.
Cesare Maltoni Cancer Research Center, European Ramazzini
Foundation of Oncology and Environmental Sciences, Bologna, Italy.

The Cesare Maltoni Cancer Research Center of the European
Ramazzini Foundation has conducted a long-term bioassay on
aspartame (APM), a widely used artificial sweetener.

APM was administered with feed to 8-week-old Sprague-Dawley rats
(100-150/sex/group), at concentrations of
100,000, 50,000, 10,000, 2,000, 400, 80, or 0 ppm.

The treatment lasted until natural death, at which time
all deceased animals underwent complete necropsy.

Histopathologic evaluation of all pathologic lesions and of all organs
and tissues collected was routinely performed
on each animal of all experimental groups.

The results of the study show for the first time that APM,
in our experimental conditions, causes
a) an increased incidence of malignant-tumor-bearing animals
with a positive significant trend in males (p 0.05)
and in females (p 0.01),
in particular those females treated at 50,000 ppm (p 0.01);

b) an increase in lymphomas and leukemias
with a positive significant trend in both males (p 0.05)
and females (p 0.01),
in particular in females treated at doses of
100,000 (p 0.01), 50,000 (p 0.01), 10,000 (p 0.05),
2,000 (p 0.05), or 400 ppm (p 0.01);

c) a statistically significant increased incidence,
with a positive significant trend (p 0.01),
of transitional cell carcinomas of the renal pelvis and ureter and
their
precursors (dysplasias) in females treated at
100,000 (p 0.01), 50,000 (p 0.01), 10,000 (p 0.01),
2,000 (p 0.05), or 400 ppm (p 0.05);

and d) an increased incidence of malignant schwannomas
of peripheral nerves with a positive trend (p 0.05) in males.

The results of this mega-experiment indicate that APM
is a multipotential carcinogenic agent,
even at a daily dose of 20 mg/kg body weight,
much less than the current acceptable daily intake. [ 50 mg/kg bw ]

On the basis of these results,
a reevaluation of the present guidelines
on the use and consumption of APM is urgent
and cannot be delayed.

Key words: artificial sweetener, aspartame, carcinogenicity,
lymphomas, malignant schwannomas, rats, renal pelvis carcinomas.
PMID: 16507461 Feb 24 2006 04:49:50

Address correspondence to M. Soffritti, 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@ramazzini.it
We thank the U.S. National Toxicology Program for convening a group
of pathologists at the
National Institute of Environmental Health Sciences
to provide a second opinion for a set of malignant lesions and their
precursors related to aspartame treatment, and for their help in
statistical analysis.
We also thank all of the staff involved in the project.
This research was supported by the European Ramazzini Foundation of
Oncology and Environmental Sciences.
The authors declare they have no competing financial interests.
Received 3 October 2005; accepted 16 November 2005.

http://www.ehponline.org/members/2005/8711/tab1.jpg
[ transcribed to plain text ]
Table 1. Beverages and diet products studied at the CMCRC/ERF:
status of studies.

Study---------------------------No. of bioassays
---Products-------------------------Species---------No. Study status

1 Water in
polyvinyl chloride bottles---------2 rat a--------------2,200 P b

2 Coca-Cola---------------------4 rat a--------------1,999 RP

3 Pepsi Cola----------------------1 rat-----------------400 E

4 Ethyl alcohol--------------------4 rat, mouse a------1,458 P c

5 Sucrose-------------------------1 rat-----------------400 E

6 Aspartame (APM)--------------6 rat, mouse a------4,460 BO, PP d

7 Sucralose (Splenda)-------------1 mouse *-----------760 BO

8 Caffeine-------------------------1 rat-----------------800 E

9 Vitamin A-----------------------5 rat----------------5,100 E

10 Vitamin C----------------------5 rat----------------3,680 E

11 Vitamin E----------------------5 rat----------------3,680 E

12 Feed sterilized by--------------1 rat a---------------2,000 E
gamma radiation

Total-----------------------------36-------------------26,937

Abbreviations:
BO, biophase ongoing
E, in elaboration
P, published
PP, partially published
RP, ready for publication
a, treatment started from embryonic life
b, data from Maltoni et al. (1997)
c, data from Soffritti et al. (2002a)
d, data from Soffritti et al. (2005).
*, data from Soffritti et al. (1992)

Investigations into the metabolism of APM have shown that,
in rodents, nonhuman primates, and humans,
it is metabolized in the gastrointestinal tract
into three constituents --
aspartic acid, phenylalanine, and methanol --
which are absorbed into the systemic circulation (Ranney et al. 1976).

For each molecule of APM,
one molecule of each constituent is produced.

After absorption, they are then used, metabolized, and/or excreted by
the body following the same metabolic pathways
as when consumed through the ordinary diet:

aspartate is transformed into alanine plus oxaloacetate (Stegink 1984);

phenylalanine is transformed mainly into tyrosine and, to a smaller
extent, phenylethylamine and phenylpyruvate (Harper 1984);

and methanol is transformed into formaldehyde and then to formic acid
(Opperman 1984).
*******************************************************

Morando Soffritti 1, Fiorella Belpoggi 1, Davide Degli Esposti 1, Luca
Lambertini 1, Eva Tibaldi 1,
and Anna Rigano 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@ramazzini.it

Address correspondence to
Dr. M. Soffritti, M.D., Scientific Director of the 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@ramazzini.it

Acknowledgements: A special thanks to the
US National Toxicology Program (NTP)
for convening a group of pathologists at NIEHS
in order to provide a second opinion
for a set of lesions of malignancies and their precursors
related to the APM treatment, and for the help in statistical analysis.

http://groups.yahoo.com/group/aspartameNM/message/1250
aspartame causes cancer in rats at levels approved for humans,
Morando Soffritti et al, Ramazzini Foundation, Italy &
National Toxicology Program
of National Institute of Environmental Health Sciences
2005.11.17 Env. Health Pers. 35 pages: Murray

http://groups.yahoo.com/group/aspartameNM/message/1226
USA National Institutes of Health National Toxicology
Program aids eminent Ramazzini Foundation, Bologna, Italy,
in more results on cancers in rats from lifetime low levels
of aspartame (methanol, formaldehyde), Felicity Lawrence,
www.guardian.co.uk: Murray 2005.09.30

http://groups.yahoo.com/group/aspartameNM/message/1186
aspartame induces lymphomas and leukaemias in rats, full plain text,
M Soffritti, F Belpoggi, DD Esposti, L Lambertini: Ramazzini
Foundation study 2005.07.14: main results agree with their previous
methanol and formaldehyde studies: Murray 2005.09.03

http://groups.yahoo.com/group/aspartameNM/message/1189
Michael F Jacobson of CSPI now and in 1985 re aspartame
toxicity, letter to FDA Commissioner Lester Crawford;
California OEHHA aspartame critique 2004.03.12; Center for
Consumer Freedom denounces CSPI: Murray 2005.07.27

http://groups.yahoo.com/group/aspartameNM/message/1016
President Bush & formaldehyde (aspartame) toxicity:
Ramazzini Foundation carcinogenicity results Dec 2002:
Soffritti: Murray 2003.08.03 rmforall

p. 88 "The sweetening agent aspartame hydrolyzes in the
gastrointestinal tract to become free methyl alcohol,
which is metabolized in the liver
to formaldehyde, formic acid, and CO2. (11)"
Medinsky MA & Dorman DC. 1994; Assessing risks of low-level
methanol exposure. CIIT Act. 14: 1-7.

Ann N Y Acad Sci. 2002 Dec; 982: 87-105.
Results of long-term experimental studies on the carcinogenicity of
formaldehyde and acetaldehyde in rats.
Soffritti M, Belpoggi F, Lambertin L,
Lauriola M, Padovani M, Maltoni C.
Cancer Research Center, European Ramazzini Foundation for Oncology
and Environmental Sciences, Bologna, Italy. crcfr@ramazzini.it
Formaldehyde was administered for 104 weeks in drinking water
supplied ad libitum at concentrations of
1500, 1000, 500, 100, 50, 10, or 0 mg/L
to groups of 50 male and 50 female Sprague-Dawley rats beginning at
seven weeks of age.
Control animals (100 males and 100 females) received tap water only.
Acetaldehyde was administered to 50 male and 50 female
Sprague-Dawley rats beginning at six weeks of age at concentrations of
2,500, 1,500, 500, 250, 50, or 0 mg/L.
Animals were kept under observation until spontaneous death.
Formaldehyde and acetaldehyde were found to produce an increase
in total malignant tumors in the treated groups
and showed specific carcinogenic effects on various organs and tissues.
PMID: 12562630

Ann N Y Acad Sci. 2002 Dec; 982: 46-69.

Results of long-term experimental studies on the carcinogenicity of
methyl alcohol and ethyl alcohol in rats.
Soffritti M, Belpoggi F, Cevolani D,
Guarino M, Padovani M, Maltoni C.
Cancer Research Center, European Ramazzini Foundation for Oncology
and Environmental Sciences, Bologna, Italy. crcfr@ramazzini.it
Methyl alcohol was administered in drinking water
supplied ad libitum at doses of
20,000, 5,000, 500, or 0 ppm to groups of male and female
Sprague-Dawley rats 8 weeks old at the start of the experiment.
Animals were kept under observation until spontaneous death.
Ethyl alcohol was administered by ingestion in drinking water at a
concentration of 10% or 0% supplied ad libitum to groups of male and
female Sprague-Dawley rats; breeders and offspring were included in
the experiment.
Treatment started at 39 weeks of age (breeders), 7 days before mating,
or from embryo life (offspring)
and lasted until their spontaneous death.
Under tested experimental conditions, methyl alcohol and ethyl alcohol
were demonstrated to be carcinogenic for various organs and tissues.
They must also be considered multipotential carcinogenic agents.
In addition to causing other tumors, ethyl alcohol induced malignant
tumors of the oral cavity, tongue, and lips.
These sites have been shown to be target organs in man by
epidemiologic studies.
Publication Types: Review Review, Tutorial PMID: 12562628
*******************************************************

The Comet assay can quickly show whether aspartame or its body
products (methanol, formaldehyde, formic acid -- the same as in
hangovers from dark wines and liquors) are genotoxic:
Murray 2006.05.09

http://groups.yahoo.com/group/aspartameNM/message/1337
Comet assay finds DNA damage from sucralose, cyclamate, saccharin,
aspartame in mice: Sasaki YF & Tsuda S Aug 2002:
Murray 2006.05.08

[ Borderline evidence, in this pilot study of 39 food additives,
using test groups of 4 mice, for DNA damage from for stomach, colon,
liver, bladder, and lung 3 hr after oral dose of 2000 mg/kg
aspartame -- a very high dose.
Methanol is the only component of aspartame that
can lead to DNA damage. ]

http://groups.yahoo.com/group/aspartameNM/message/934
24 recent formaldehyde toxicity [Comet assay] reports:
Murray 2002.12.31

http://groups.yahoo.com/group/aspartameNM/message/961
genotoxins, Comet assay in mice: Ace-K, stevia fine; aspartame poor;
sucralose, cyclamate, saccharin bad: Y.F. Sasaki Aug 2002:
Murray 2003.01.27 [A detailed look at the data] ]
*******************************************************

http://groups.yahoo.com/group/aspartameNM/message/1345
EFSA, European Food Safety Authority says Ramazzini aspartame
cancer study is flawed, while Soffritti is half way through second huge
study, Felicity Lawrence, www.guardian.co.uk: Murray 2006.05.15

http://groups.yahoo.com/group/aspartameNM/message/1339
Obfuscation of the iatrogenic autism epidemic re mercury in kid
vaccines, Kenneth P. Stoller, Pediatrics 2006.05.06;
aspartame toxicity 2005.11.10: Comet assay can test genotoxicity,
EFSA admits ignorance re methanol residues, Murray 2006.05.10

http://groups.yahoo.com/group/aspartameNM/message/1335
Morando Soffritti of Ramazzini Foundation rebuts EFSA AFC critique,
www.laleva.org: Murray 2006.05.05

http://groups.yahoo.com/group/aspartameNM/message/1334
European Food Safety Authority discounts Ramazzini study re many
cancers in 1800 rats fed lifetime doses of aspartame:
Calorie Control Council press release: Murray 2006.05.05

http://www.efsa.eu.int/press_room/press_release/1472_en.html

http://www.efsa.eu.int/science/afc/afc_opinions/1471_en.html

http://www.efsa.eu.int/press_room/media_events/catindex_en.html

http://www.flyonthewall.com/FlyBroadcast/efsa.eu.int/AspartamePressConference/

http://www.efsa.eu.int/science/afc/afc_opinions/1471/afc_op_ej356_aspartame_en1.pdf

http://groups.yahoo.com/group/aspartameNM/message/1338
Aspartame: The healthy option? Richard A. Lovett, The New Scientist
2006.05.04: Murray 2006.05.08

http://groups.yahoo.com/group/aspartameNM/message/957
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
Murray 2003.01.12 rmforall EU Scientific Committee on Food,
a whitewash

http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame ( 2002.12.04 ):
59 pages, 230 references
*******************************************************