http://groups.yahoo.com/group/aspartameNM/message/872
immune system reactions due to formaldehyde from the 11% methanol in
aspartame: Thatcher: Tephly: Monte: Murray 9.27.2 rmforall

Life Sci 1991;48(11):1031-41
The toxicity of methanol.
Tephly TR.
Department of Pharmacology, University of Iowa, Iowa City 52242.

Methanol toxicity in humans and monkeys is characterized by a latent
period of many hours followed by a metabolic acidosis and
ocular toxicity. This is not observed in most lower animals. The
metabolic acidosis and blindness is apparently due to formic acid
accumulation in humans and monkeys, a feature not seen in lower animals.

The accumulation of formate is due to a deficiency in
formate metabolism which is, in turn, related, in part, to low hepatic
tetrahydrofolate (H4 folate). An excellent correlation between
hepatic H4 folate and formate oxidation rates has been shown within and
across species. Thus, humans and monkeys possess low
hepatic H4 folate levels, low rates of formate oxidation and
accumulation of formate after methanol. Formate, itself, produces
blindness in monkeys in the absence of metabolic acidosis. In addition
to low hepatic H4 folate concentrations, monkeys and humans
also have low hepatic 10-formyl H4 folate dehydrogenase levels, the
enzyme which is the ultimate catalyst for conversion of formate
to carbon dioxide. This review presents the basis for the role of folic
acid-dependent reactions in the regulation of methanol toxicity.
Publication Types: Review Review, Academic PMID: 1997785

page 1035 "In the past, formaldehyde has often been suggested as the
methanol metabolite which produces toxicity (34,35). Today, a great
deal of information is available concerning its lack of such a role.
The presence of elevated formaldehyde levels in body fluids or tissues
following methanol administration has not been observed.
No formaldehyde has been detected in blood, urine or tissues obtained
from methanol-treated animals (36,37) and, in methanol-poisoned humans,
formaldehyde increases have not been observed....
About 85% of a low dose of 14C-formaldehyde [radioactive label] is
excreted as pulmonary 14CO2 (49,50)....."

This suggests that 15% of the formaldehyde is indeed retained in the
body, a very significant result, considering its extreme and complex
toxicity.

49. W.B. Neely, Biochem. Pharmacol. 13: 1137-1142 (1964)

50. Xenobiotica 1982 Feb;12(2):119-24
Formaldehyde metabolism by the rat: a re-appraisal.
Mashford PM, Jones AR.

1. The metabolism of [14C]formaldehyde
has been investigated in the male Sprague-Dawley rat.
It is extensively oxidized to CO2
and formate, which is excreted in the urine. 2. Two radioactive
compounds isolated from the urine of rats dosed with
[14C]formaldehyde have been identified as N-hydroxymethylurea and
N,N'-bis-(hydroxymethyl)urea, and shown to be urinary
artefacts. 3. Previous studies of the metabolism
of formaldehyde by rats have been re-appraised.
Differences in the rate of oxidation
of formaldehyde in various strains of rats result in the excretion of
different urinary metabolites and, in some cases, formaldehyde.
Excretion of formaldehyde leads to the formation of several artefacts
depending on the components present in the urine. PMID: 6806997

http://www.drthrasher.org/formaldehyde_1990.html
J. D. Thatcher study (1990):

"The patients in our study had symptoms and complaints
related to several organs, as described previously, (4,5,9)
which were similar to symptoms
of workers with multiple chemical sensitivity,(11) cacosmia,(12) and
other chemical exposures. (13-15) We report on the differences in
humoral and cell-mediated immunity in humans with long-term inhalation
exposure to HCHO vs. asymptomaticstudents (controls) who experienced
short-term, periodic exposure to the chemical.

[ http://lassesen.com/cfids/cacosmia.htm
Cacosmia (a.k.a. Multiple Chemical Sensitivity) Details:
* Chemical odour intolerance induced headache, itching eyes, irritated
or congested nose, dry and/or sore throat, cough, dizziness,
and itching or rash.
* Cacosmics reported increased prevalence of physician-diagnosed
nasal allergies, breast cysts, hypothyroidism, sinusitis,
food sensitivities, irritable bowel, and migraine headache.
Resource: http://www.mcsrr.org ]"

"Symptoms. All patients in this study had sought continuous medical
attention because of multiple organ symptoms involving the central
nervous system (CNS) (headaches, memory loss, difficulty completing
tasks, dizziness), upper- and lower-respiratory symptoms,
skeletal-muscle complaints, and gastroenteritis. Three common symptoms
were expressed:
[1.] and initial flu-like illness from which they had not fully
recovered;
[2.] chronic fatigue; and [3.] an olfactory sensitivity to ambient
conditions containing low concentrations of chemicals. (4,9,11)"

"It is recognized that chemicals and therapeutic drugs are associated
with a Lupus-like syndrome. (28,29 ) The observations made on the
patients in this study support this concept."

Aspartame reactors have often asked about whether there exist medical
tests for their vulnerability.

I want to assemble funding and a team to replicate Thatcher's study,
testing aspartame reactors for immune system reactions, triggered by
exposure to formaldehyde. Any aspartame reactor can probably get these
tests prescribed by their doctors, and insurance may well pay for them.
The results, along with their case histories, can be immediately posted
on the Net. This will be of immense interest to patients, medical
professionals, and lawyers.

We should find that aspartame reactors also react to formaldehyde and
to methanol exposures, while people with Multiple Chemical Sensitivity
and the like also react to aspartame and methanol.

Many sources agree that it is possible to use a lot of
aspartame daily, particularly from diet soda, and that the methanol
component, exactly 11% by weight, is quickly released in the GI tract,
metabolized into the about same weight of formaldehyde, then
subsequently and quickly into formic acid,
and thence to carbon dioxide and water.

The question is: how much of this formaldehyde, a deadly, potent,
cumulative toxin with complex multiple effects, as much as 20 mg from
the 200 mg aspartame in a 12-oz can of diet soda, results in various
toxic processes in humans?

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
RTM: ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999
5.30.2 rmforall

http://www.atsdr.cdc.gov/tfacts111.html
[excerpts]

Agency for Toxic Substances and Disease Registry
Division of Toxicology
1600 Clifton Road NE, Mailstop E-29
Atlanta, GA 30333 888-422-8737 FAX: (404)498-0057
ATSDRIC@...
http://www.atsdr.cdc.gov/contacts.html

Dr. Christopher T. De Rosa, Director, Division of Toxicology
(404) 498-0160 Fax: (404) 498-0094 cyd0@...

Spengler, Robert, Sc.D., Associate Administrator for Science
(404) 498-0003 FAX: (404) 498-0081 : RSpengler@...

http://www.atsdr.cdc.gov/science/bscroster01.html
Board of Scientific Counselors Roster June 2001

http://www.atsdr.cdc.gov/COM/omweb.html
Mr. Ronnie D. Wilson, the ATSDR Ombudsman
(404) 498 0004 (888) 422 8737] Fax (404) 498 0083 RWilson2@...
When all routine avenues have been
exhausted, the ATSDR ombudsman can be
called to impartially investigate, mediate,
and assist in areas where the "system" has
failed. In doing so, this office is not an
advocate for the interests of ATSDR, nor is
it an advocate for business, nor industry,
nor private citizens, nor any other
government entity. It is an advocate for
problem resolution.

ToxFAQsTM for Formaldehyde CAS# 50-00-0 July 1999

Has the federal government made recommendations to protect human health?

The EPA recommends that an adult should not drink water containing more
than 1 milligram of formaldehyde per liter of water (1 mg/L) [equals 1
ppm] 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."

The Occupational Safety and Health Administration (OSHA) has set a
permissable exposure limit for formaldehyde of 0.75 parts per million
(ppm) for an 8-hour workday, 40-hour workweek. [in air]

The National Institute for Occupational Safety and Health (NIOSH)
recommends an exposure limit of 0.016 ppm. [in air]

Source of Information:
Agency for Toxic Substances and Disease Registry (ATSDR). 1999.
Toxicological profile for formaldehyde. Atlanta, GA: U.S. Department of
Health and Human Services, Public Health Service.
http://www.atsdr.cdc.gov/toxprofiles/tp111.html July 1999

http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984:
Monte: Murray 9.23.2 rmforall

Rereading this prescient classic review from 1984, I find its findings
are supported in much recent research, so I am again making the full
text widely available.
[I have put my comments or corrections in square brackets, and spaced
the text to ease the reader's task]

For instance, I had forgotten this, which answers the industry PR
"science" that fruits and vegetables
supply much more methanol than does aspartame:

"Fruit and vegetables contain pectin with variable methyl ester content.

However, the human has no digestive enzymes for pectin (6, 25)
particularly the pectin esterase required
for its hydrolysis to methanol (26).

Fermentation in the gut may cause disappearance of pectin (6) but the
production of free methanol is not guaranteed by fermentation (3). In
fact, bacteria in the colon probably reduce methanol directly to formic
acid or carbon dioxide (6) (aspartame is completely absorbed before
reaching the colon). Heating of pectins has been shown to cause
virtually no demethoxylation; even temperatures of 120 deg C produced
only traces of methanol (3). Methanol evolved during cooking of high
pectin foods (7) has been accounted for in the volatile fraction during
boiling and is quickly lost to the atmosphere (49).
Entrapment of these volatiles probably accounts for the elevation in
methanol levels of certain fruit and vegetable products
during canning (31, 33)."

Recent research [see links at end of post] supports his focus on the
methanol to formaldehyde toxic process:

"The United States Environmental Protection Agency in their Multimedia
Environmental Goals for Environmental Assessment recommends a minimum
acute toxicity concentration of methanol in drinking water at 3.9 parts
per million, with a recommended limit of consumption below 7.8 mg/day
(8). This report clearly indicates that methanol:

"is considered a cumulative poison
due to the low rate of excretion once it is absorbed.
In the body, methanol is oxidized to formaldehyde and
formic acid; both of these metabolites are toxic." (8)....

Recently the toxic role of formaldehyde (in methanol toxicity) has been
questioned (34). No skeptic can overlook the fact that, metabolically,
formaldehyde must be formed as an intermediate to formic acid
production (54).

Formaldehyde has a high reactivity which may be why it
has not been found in humans or other primates during methanol
poisioning (59)....

If formaldehyde is produced from methanol and does have a reasonable
half life within certain cells in the poisoned organism the chronic
toxicological ramifications could be grave.

Formaldehyde is a known
carcinogen (57) producing squamous-cell carcinomas by inhalation
exposure in experimental animals (22). The available epidemiological
studies do not provide adequate data for assessing the carcinogenicity
of formaldehyde in man (22, 24, 57).

However, reaction of formaldehyde
with deoxyribonucleic acid (DNA) has resulted in irreversible
denaturation that could interfere with DNA replication and result in
mutation (37)...."

http://www.dorway.com/wmonte.txt
Dr. Woodrow C. Monte Aspartame: methanol, and the public health.
Journal of Applied Nutrition 1984; 36 (1): 42-54.
(62 references) Professsor of Food Science
Director of the Food Science and Nutrition Laboratory
Arizona State University, Tempe, Arizona 85287
6411 South River Drive #61 Tempe, Arizona 85283-3337
602-965-6938 woody.monte@...
The methanol from 2 L of diet soda, 5.6 12-oz cans, 20 mg/can, is
112 mg, 10% of the aspartame. The EPA limit for water is 7.8 mg daily
for methanol (wood alcohol), a deadly cumulative poison. Many users
drink 1-2 L daily. The reported symptoms are entirely consistent
with chronic methanol toxicity. (Fresh orange juice has 34 mg/L, but,
like all juices, has 16 times more ethanol, which strongly protects
against methanol.) [Monte has retired to New Zealand.]

Note that if 15% of the EPA daily limit for methanol in drinking water,
7.8 mg, is retained in the body as formaldehyde, that is 1.17 mg, about
half of the EPA daily limit for formaldehye in drinking water, 2 mg.
However, if only 15% of that 2 mg from drinking water
is retained in the body, that is 0.3 mg--
so the formaldehye limit is actualy 3.9 times larger, in terms of the
formaldehyde actually retained in the body, according to this chain of
reasonable estimates. This suggests a lack of harmony between the EPA
limits for methanol and formaldehyde, which in turn suggests that this
important topic is not as yet well understood scientifically.

Thatcher's report about symptoms from long-term, low-level exposure to
formaldehyde gives much the same litany of complex symptoms as
aspartame reactors, who often report using 2-4 L daily of diet soda,
providing 112-224 mg methanol, resulting in some probable chronic
formaldehyde toxicity-- 15% gives 16.8-33.6 mg daily formaldehyde
retention. This is 56-112 times the EPA limit of 2 mg formaldehyde in
drinking water, if 15%, 0.3 mg, is retained in the body.

Therefore, we can expect to find signs and symptoms of chronic toxicity
from long-term, low-dose formaldehyde exposure in heavy users of
aspartame, such as a daily drinking level of 2-4 L diet soda--
of course there are many other dietary sources.

The most common symptoms are, in rough order of
occurence, considering hundreds of case reports: * headaches
* many body and joint pains (or burning, tingling, tremors, twitching,
spasms, cramps, or numbness) * fever, fatigue
* "mind fog", "feel unreal", poor memory, confusion, anxiety,
irritability, depression, mania, insomnia, dizziness, slurred speech,
ringing in ears, sexual problems, poor vision, hearing, or taste
* red face, itching, rashes, burning eyes or throat,
dry mouth or eyes, mouth sores * hair loss
* obesity, bloating, edema, anorexia,
poor or excessive hunger or thirst * breathing problems
* nausea, diarrhea or constipation * coldness * sweating
* racing heart, high blood pressure, erratic blood sugar levels
* seizures * birth defects * brain cancers * addiction
* aggrivates diabetes, autism, ADHD, allergies,
and interstitial cystitis (bladder pain).

http://www.drthrasher.org/formaldehyde_1990.html
Arch Environ Health 1990 Jul-Aug;45(4):217-23
Immune activation and autoantibodies in humans
with long-term inhalation exposure to formaldehyde.
Thrasher JD, Broughton A, Madison R.
Thrasher & Associates, Northridge, California.

Four groups of patients with long-term inhalation exposure to
formaldehyde (HCHO) were compared with controls who had short-term
periodic exposure to HCHO. The following were determined for all
groups: total white cell, lymphocyte, and T cell counts; T
helper/suppressor ratios; total Ta1+, IL2+, and B cell counts;
antibodies to
formaldehyde-human serum albumin (HCHO-HSA) conjugate and
autoantibodies.
When compared with the controls, the patients had
significantly higher antibody titers to HCHO-HSA.
In addition, significant increases in Ta1+, IL2+, and B cells and
autoantibodies were observed.
Immune activation, autoantibodies, and anti-HCHO-HSA
antibodies are associated with long-term formaldehyde inhalation.
PMID: 2400243

[Extracts}
Inhalation exposure to formaldehyde (HCHO)
is associated with symptoms of irritation to mucous membranes, (1,2)
chronic health problems (e.g., asthma, (2) nasopharyngeal cancer, (3)
and multiple subjective health complaints. (4,5) )
Recent observations have shown that both humoral-and cell-mediated
immunologic mechanisms occur in humans with long-term
HCHO exposure. Antibodies of all isotypes to HCHO conjugated human
serum albumin (HCHO-HSA) are demonstrable in HCHO anaphylaxis, (6)
hemodialysis patients, (7) mobile home residents, (4) persons with
occupational exposures, (5,8) office workers, (9) and in persons in
other environments. (4)
In addition, changes in cell-mediated immunity include increases in
eosinophils, basophils, and T-suppressor cells
following acute exposure of patients with HCHO asthma. (10) Moreover,
individuals with multiple subjective health complaints associated with
long-term HCHO inhalation have evidence of immune activation and the
presence of autoantibodies. (4,5)

The patients in our study had symptoms and complaints
related to several organs, as described previously, (4,5,9)
which were similar to symptoms
of workers with multiple chemical sensitivity,(11) cacosmia,(12) and
other chemical exposures. (13-15) We report on the differences in
humoral and cell-mediated immunity in humans with long-term inhalation
exposure to HCHO vs. asymptomaticstudents (controls) who experienced
short-term, periodic exposure to the chemical.

[ http://lassesen.com/cfids/cacosmia.htm
Cacosmia (a.k.a. Multiple Chemical Sensitivity) Details:
* Chemical odour intolerance induced headache, itching eyes, irritated
or congested nose, dry and/or sore throat, cough, dizziness,
and itching or rash.
* Cacosmics reported increased prevalence of physician-diagnosed
nasal allergies, breast cysts, hypothyroidism, sinusitis,
food sensitivities, irritable bowel, and migraine headache.
Resource: http://www.mcsrr.org ]

Materials and Methods

Controls and patients.
Five groups of subjects exposed to HCHO,
who gave informed consent, were included in this study. (1)
Controls consisted
of students of chiropractic medicine (16 males, 12 females), mean age =
29 +- 9 y) exposed to HCHO for 13 h/wk for 28 wk while studying human
anatomy. Immunologic tests were performed 12 mo following the last
classroom exposure.
No measurements of HCHO concentrations were made.
It is assumed that classroom ambient concentrations were at least 0.43
ppm. [1.] The students stated that during exposure they experienced
eye, nose and throat irritation and that there was a pungent odor of
HCHO. They did not have residual health complaints (symptoms), and
they were asymptomatic at the time blood was taken. [2.] Mobile home
residents consisted of 19 patients (6 males, 13 females), mean age 41
+-20 y) who currently lived in mobile homes. The patients had lived in
their environments for 2-7 y and reported multiple symptoms. (4,9)
Measured HCHO concentrations ranged from 0.05 to 0.5 ppm at the time
blood samples were taken.
[3.] Office workers included 21 patients (5 males,
16 females, mean age of 40 +-10 y) who worked in new office buildings
where there was inadequate ventilation (closed buildings).
The patients had multiple health complaints. (9)
It was determined from medical histories that their symptoms commenced
with employment, waned when away from work (i.e., weekends, holidays,
vacations) and became worse upon return to work.
No HCO measurements were done; however, closed
buildings have ambient concentrations ranging from 0.01 to 0.77 ppm.
(1,16) [4.] This group included 21 patients (10 males, 11 females,
mean age of 35 + -17 y) who had multiple symptoms and who had been
removed from their original sources of HCHO exposure (mobile homes
and/or particleboard subflooring) for at least 1 y. The HCHO
concentrations measured during their exposures ranged from 0.14 to 0.81
ppm. [5.] Occupationally exposed patients
(6 males, 2 females, mean age of 45 + -11 y)
had HCHO exposures from the following: biology and human
anatomy classes, mortuary, pathology, physical therapy, formica
furniture (particleboard), and carbonless copy paper. Information on
six of these patients was previously published. (5)

Symptoms. All patients in this study had sought continuous medical
attention because of multiple organ symptoms involving the central
nervous system (CNS) (headaches, memory loss, difficulty completing
tasks, dizziness), upper- and lower-respiratory symptoms,
skeletal-muscle complaints, and gastroenteritis. Three common symptoms
were expressed:
[1.] and initial flu-like illness from which they had not fully
recovered;
[2.] chronic fatigue; and [3.] an olfactory sensitivity to ambient
conditions containing low concentrations of chemicals. (4,9,11)

One of the students smoked cigarettes (1 pack/d), whereas the remainder
and all patients were nonsmokers. No attempt was made to correlate the
immunological data with histories of allergies and/or atopy. Previous
efforts to make this correlation have led to negative findings.
(4,5,9)....

Higher anti-HCHO-HSA isotypes (i.e, 1:16 or greater) are present in the
patients v. controls.
One explanation for this difference is simply
the lag time between the last exposure v. the time of antibody
detection. However, the higher titers
of IgE and IgM isotypes in the patients suggests that a more recent
exposure has occurred, particularly if the
higher IgG titers are considered also. In this vein, the patients
complain of a sensitivity (both olfactory and respiratory) to
environments containing low concentrations of HCHO and other chemicals.
Thus, the higher titers may indicate that their immune systems are on
constant alert, undergoing continuous activation upon encountering and
recognizing environmental haptens. (4-6,8,9)
It would be of interest to examine for other haptens to which the
patients may be responding. (9)

The higher antibody titers and the larger proportion
of individuals with anti-HCHO isotypes in the
removed patients v. controls merit comment.
Both groups were at least 1 y removed from their original source of
exposure. However, the controls were asymptomatic,
whereas the patients experienced ongoing
health problems associated with environmental exposures,
e.g. new carpets, fresh paints, new furnishings, diesel
exhaust, and perfumes. Thus, it appears that long-term low-level
exposure to HCHO, and possibly other haptens, lead to immunological
recognition and immune activation in sensitized individuals.
Apparently, shorter periodic exposure to HCHO
may lead to recognition but not necessarily immune activation.
Moreover, chronic low-level exposures to
HCHO appear to effect a sensitivity to environmental chemicals.(4-6,
8,9) Perhaps the anti-HCHO-HSA isotypes in these patients is but one
aspect of a multiple immunologic response to environmental exposures as
observed in building-related illness. (9)

It is recognized that chemicals and therapeutic drugs are associated
with a Lupus-like syndrome. (28,29 ) The observations made on the
patients in this study support this concept.
The percentage of specific autoantibodies
(e.g., ASS, APC, ANA, etc.) are consistently higher in
the patients vs. controls (Table 4). Moreover, the odds ratios for the
presence of at least 1, 2 or 3 autoantibodies are greater in the
residents of mobile homes and office workers (p <.05) relative to
controls (Table 5).

Presently, autoimmune disorders have not been diagnosed clinically in
these patients.
However, current investigations in progress appear to
correlate the presence of APC autoantibodies with gastritis complaints
and antimyelin autantibodies with CNS and PNS symptoms.

In conclusion, measurements of changes in WBCs, T cells, and H/S ratios
in individuals with apparent chemical sensitivities appear to be
inadequate immune parameters to examine. If one assumes that these
individuals respond immunogically to environmental chemicals,
investigations into autoimmunity
and immune activation and perturbations in the interleukins,
luekotreines, prostglandins, and other immunologic mediators
appear to be fruitful areas for further research. (29-32)
Thus, it appears that HCHO sensitivity is a real phenomenon
and requires further research. (4,27-32 ) [End of report]
http://www.drthrasher.org
Jack D. Thrasher, Ph.D. toxicology@...
Sam-1 Trust, P.O. Box 874, Alto, New Mexico 88312
(505) 336-8312 fax (425) 675-7379

http://www.aal.xohost.com/allabout.htm
Alan Broughton, MD, PhD inquire@...
AAL Reference Laboratories, Inc.[formerly Antibody Assay Laboratories]
1715 E. Wilshire #715 Santa Ana, Ca 92705
(714)972-9979 Fax: (714)543-2034
(800)522-2611(US and Canada) - Physicians Only Please

Roberta Madison, D.P.H. roberta.madison@...
Dept. Health Science, California State University
Northridge, California
(818)-677-2969 fax (818) 677-3977

References

1.Breysse P. The immediate and long-term effects of formaldehyde.
Comments Toxicol 1988; 2: 135-53.

2. Nordman H, Keskinen H, Tuppurainen M. Formaldehyde asthma -
rare or overlooked? J Allergy Clin Immunol 1985; 75: 81-99.

3. Vaughn TL, Strader C, Davis S, Dling JR. Formaldehyde and cancers of
the pharynx, sinus and nasal cavity. II. Residential exposure. Cancer
1987: 28: 685-88.

4. Broughton A, Thrasher JD. Antibodies and altered cell mediated
immunity in formaldehyde exposed humans. Comments Toxicol 1988; 2:
155-70.

5. Thrasher JD, Broughton A, Micevich P. Antibodies and immune profiles
of individuals occupationally exposed to formaldehyde: six case reports.
Am J Ind Med 1988; 14: 479-88.

6. Maurice F, Rivory J-P, Larsson PH, Johansson SGO, Bousquet J.
Anaphylactic shock caused by formaldehyde in a patient undergoing
long-term hemodialysis.
J Allergy Clin Immunol 1987; 77: 594-97.

7. Patterson R, Patera V, Grammar IC, Harris K. Human antibodies against
formaldehyde-human serum albumin or human serum albumin in individuals
exposed to formaldehyde. Int Arch Allergy Appl Immunol 1986; 79: 53-59.

8. Wilhelmsson G, Holmstrom M. Positive formaldehyde-RAST after
prolonged formaldehyde exposure by inhalation. Lancet II(8851): 54.

9. Thrasher, JD, Madison R, Broughton A, Gard Z. Building-related
illness and antibodies to albumin conjugates of formaldehyde, toluene
diisocyanate and trimellitic anhydride. Am J Ind Med 1989; 15: 187-195.

10. Pross H.F., Day JH, Clark RH, Lees REM. Immunologic studies of
subjects with asthma exposed to formaldehyde and ureaformalehyde (UFFI)
off-products. J Allergy Clin Immunol 187; 79: 787-810.

11. Cullen MR. Workers with multiple chemical sensitivities: an
overview. Occup Med:State of the Art Rev 1987; 2: 655-61.

12. Ryan CM, Morrow LA, Hodgson M. Cascosmia and neurobehavioral
dysfunction associated with occupational exposure to mixtures of organic
solvents. Am J Psychol 1988; 1442-45.

13. Broughton A, Thrasher JD, Gard Z. Immunological evaluation of four
arc welders exposed to fumes from ignited polyurethane (isocyanate)
foam: antibodies and immune profiles. Am J Ind Med 1988; 13: 463-72.

14. Bekesi JG, Roboz J, Fischblein A, et al. Immunological, biochemical
and clinical consequences of exposure to polybrominated biphenyls. In:
Immunotoxicology and Immunopharmacology, Dean J et al, eds. New York:
Raven Press, 1985; pp. 3393-406.

15. Zeiss CR. Lung disease induced by reactive chemicals. Clin Rev
Allergy 1985; 3: 217-26.

16. Konopinski VH. Forrmaldehyde in office and commercial environments.
Am Ind Hyg Assoc J 1985; 46: 65-68.

17. Voller A. Heterogeneous enzyme-immuno assays and their applications.

In: Enzyme Imunnoassay, Maggie ET, ed. Boca Raton:
CRC Press, 1979; pp. 181-96.

18. Boyuma A. Isolation of mononuclear and granuloyctes from human
blood. Scand J Clin Lab Invest. 1968; 21(Suppl 97): 77-89.

19. Englemane EG, Warnke F, Fox FI, Levy R. Studies of a human
lymphocyte-T antigen recognized by monoclonal antibody.
PNAS 19981; 78: 791-95.

20. Fox DA, Hussey RE, Fitzgerald KA, et al. Ta1,
a noval 105 KD human T cell activation antigen defined by a monoclonal
antibody. J Immunol 1984; 133: 351-54.

21. Nakamura RM, Tucker ES. Anitbodies as reagent. In: Diagnosis and
management by laboratory methods, Henry JD, ed. Philadelphia: WB
Saunders, 1979; p. 1184.

22. Schlesselman JJ. Case control studies design conduct and analysis.
New York: Oxford University Press, 1982; pp. 122-177.

23. Hafler DA, Fox DA, Benjamin D, Winer HL. Antigen reactive cells are
defined by Ta1. J Immunol 1985; 137: 414-18.

24. Hafler DA, Box DA, Manning ME, et al. In vivo activated lymphocytes
in the peripheral blood and cerebrospinal fluid of patients with
multiple sclerosis. New Eng J Med 1985; 312: 1404-11.

25. Mitzutani H, Tsubakio T, Tomiyana Y, et al. Increased circulating
1a-positive T cells in patients with idiopathic thrombocytopenia
purpura. Clin Exp Immunol 1987; 67: 191-97.

26. Jackson RA, Morris MA, Haynes BF, Eisenbarth GS. Increased
1a-antigen-bearing T cells in Type I diabetes mellitus. New Eng J Med
1981; 306: 785-88.

27. Nossal GJV. Current concepts in immunology: basic components of the
immune system. New J Med 287; 316: 1320-25.

28, Amos HE, Park BK. Understanding immunotoxic drug reactions. In:
Immunotoxicology and Immunopharmacology, Dean J, et al, eds. New York:
Raven Press, 1986; pp. 207-28.

29. Bigazzi PE. Autoimmunity induced by chemicals.
Clin Toxicol 1988; 26: 125-56.

30. Marks JG, Traullelin JJ, Zwillich CW, Demers LM. Contact urticaria
and airway obstruction from carbonless copy paper.
JAMA 1984; 252; 1046-40.

31. LaMarte FP, Merchant JA, Casale T. Acute systemic reactions to
carbonless copy paper associated with histamine release.
JAMA 1988; 260: 242-43.

32. Stanworth DR. Current concepts in hypersensitivity. In:
Immunotoxicology and Immunopharmacology, Dean J, et al, eds. New York:
Raven Press, 1985; pp. 91-98.
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http://www.california.com/~hawk/DrThrasherFormaldehyde1987.htm
Thrasher JD; Wojdani, Aristo; Heuser, Gunnar 28 references
Evidence for Formaldehyde Antibodies and Altered Cellular Immunity in
Subjects Exposed to Formaldehyde in Mobile Homes
Archives of Environmental Health, Vol. 42, pp. 347-350, 1987

http://www.drthrasher.org/formaldehyde_embryo_toxicity.html
Thrasher JD, Kilburn KH. 100 references
Embryo toxicity and teratogenicity of formaldehyde.
Arch Environ Health 2001 Jul-Aug; 56(4): 300-11
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Rich Murray, MA Room For All rmforall@...
1943 Otowi Road, Santa Fe NM 87505 USA 505-986-9103

http://groups.yahoo.com/group/aspartameNM/message/871
aspartame toxicity brief review: Murray 9.23.2 rmforall

http://groups.yahoo.com/group/aspartameNM/messages
for 871 posts in a public searchable archive

http://groups.yahoo.com/group/aspartameNM/message/862 long review

http://groups.yahoo.com/group/aspartameNM/message/860
RTM: FDA: objections to neotame approval 8.3.2 rmforall 38 pages

http://groups.yahoo.com/group/aspartameNM/message/868
Murray: submit complaints and papers to FDA Docket 02P-0317
by Jan 12 2003: Recall Aspartame as a Neurotoxic Drug 9.20.2 rmforall

http://www.dorway.com/tldaddic.html 5-page review
Roberts HJ Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan; HJRobertsMD@...
http://www.sunsentpress.com/ sunsentpress@...
Sunshine Sentinel Press P.O.Box 17799 West Palm Beach, FL 33416
800-814-9800 561-588-7628 561-547-8008 fax

http://groups.yahoo.com/group/aspartameNM/message/669
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 85.00 postpaid data from 1200 cases
available at http://www.amazon.com
over 600 references from standard medical research
http://www.aspartameispoison.com/contents.html 34 chapters

http://groups.yahoo.com/group/aspartameNM/message/859
RTM: Roberts: the life work of a brilliant clinician:
aspartame toxicity 8.2.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/790
RTM: Moseley:
review Roberts "Aspartame Disease: An Ignored Epidemic" 2.7.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/782
RTM: Smith, Terpening, Schmidt, Gums:
full text: aspartame, MSG, fibromyalgia 1.17.2 rmforall
Jerry D Smith, Chris M Terpening, Siegfried OF Schmidt, and John G Gums
Relief of Fibromyalgia Symptoms Following
Discontinuation of Dietary Excitotoxins.
The Annals of Pharmacotherapy 2001; 35(6): 702–706.
Malcolm Randall Veterans Affairs Medical Center, Gainesville, FL, USA.
BACKGROUND: Fibromyalgia is a common rheumatologic disorder that is
often difficult to treat effectively.
CASE SUMMARY: Four patients diagnosed with fibromyalgia syndrome
for two to 17 years are described.
All had undergone multiple treatment
modalities with limited success. All had complete, or nearly complete,
resolution of their symptoms within months after eliminating monosodium
glutamate (MSG) or MSG plus aspartame from their diet.
All patients were women with multiple comorbidities
prior to elimination of MSG.
All have had recurrence of symptoms whenever MSG is ingested.

Siegfried O. Schmidt, MD Asst. Clinical Prof. siggy@...
Community Health and Family Medicine, U. Florida, Gainesville, FL
Shands Hospital
West Oak Clinic Gainesville, FL 32608-3629 352-376-5071

Debbie J. Hypes painfreeliving@... 304-872-4141 (Case # 1 of 4)
P.O Box 25 Lookout, WV 25868-0025 She has about 1,000 on her local
mailing list, and has been a volunteer activist since 1997. Her guide
first came out in 1997: http://www.Pain-Free-Living.net
"The Food Plan: How To Do It" $ 5 by mail, free by email.
Her sister Darlene, now 47, cured her own severe fibromyalgia in 1995
by using an elimination diet, and then Debbie also cured herself by
1997. Their doctor, Siegfried Schmidt, paying attention, tried it on
two selected women, who got well, and are his third and fourth cases.

http://groups.yahoo.com/group/aspartameNM/message/846
RTM: aspartame in Merck Maxalt-MLT worsens migraine,
AstraZeneca Zomig, Eli Lilly Zyprexa,
J&J Merck Pepcid AC (Famotidine 10mg) Chewable Tab,
Pfizer Cool Mint Listerine Pocketpaks 7.16.2 rmforall
Migraine MLT-Down: an unusual presentation of migraine
in patients with aspartame-triggered headaches.
Newman LC, Lipton RB Headache 2001 Oct; 41(9): 899-901.
[Merck 10-mg Maxalt-MLT, for migraine, has 3.75 mg aspartame,
while 12 oz diet soda has 200 mg.]
Headache Institute, St. Lukes-Roosevelt Hospital Center, New York, NY
Department of Neurology newmanache@...
Albert Einstein College of Medicine, Bronx, NY
Innovative Medical Research RLipton@...

http://groups.yahoo.com/group/aspartameNM/message/855
RTM: Blumenthall & Vance:
aspartame chewing gum headaches Nov 1997 7.28.2 rmforall
Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches.
Headache 1997 Nov-Dec; 37(10): 665-6.
Department of Neurology, University of Oklahoma College of Medicine,
Tulsa, USA. neurotulsa@...
Aspartame, a popular dietetic sweetener, may provoke headache in some
susceptible individuals. Herein, we describe three cases of young women
with migraine who reported their headaches could be provoked by chewing
gum sweetened with aspartame. [6-8 mg aspartame per stick chewing gum]

http://ww.presidiotex.com/barcelona/index.html
Trocho C, Pardo R, Rafecas I, Virgili J, Remesar X,
Fernandez-Lopez JA, Alemany M ["Trok-ho"]
Formaldehyde derived from dietary aspartame binds to tissue
components in vivo. Life Sci 1998 Jun 26; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular, Facultat de Biologia,
Universitat de Barcelona, Spain.
http://www.presidiotex.com/barcelona/index.html
Maria Alemany, PhD (male) alemany@...

http://groups.yahoo.com/group/aspartameNM/message/864
Murray: Butchko, Tephly, McMartin: Alemany: aspartame formaldehyde
adducts in rats 9.8.2 rmforall
Prof. Alemany vigorously affirms the validity of the Trocho study
against criticism:
Butchko, HH et al [24 authors], Aspartame: review of safety.
Regul. Toxicol. Pharmacol. 2002 April 1; 35 (2 Pt 2): S1-93, review
available for $35, [an industry paid organ]. Butchko:
"When all the research on aspartame, including evaluations in both the
premarketing and postmarketing periods, is examined as a whole, it is
clear that aspartame is safe, and there are no unresolved questions
regarding its safety under conditions of intended use."

http://groups.yahoo.com/group/aspartameNM/message/873
MCS, aspartame, formaldehyde, other toxicants:
Kerns: Murray 9.27.2 rmforall [excellent overview]

http://groups.yahoo.com/group/aspartameNM/message/867
Murray: Thatcher:
simple tests for immune system reactions due to formaldehyde from the
11% methanol in aspartame: Tholen 9.17.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/628
Rich Murray: Professional House Doctors: Singer: EPA: CPSC:
formaldehyde toxicity 6.10.1 rmforall

http://groups.yahoo.com/group/aspartameNM/message/863
Murray: Wilson: CIIN: EPA: Gold: Thrasher & Kilburn: Shaham:
formaldehyde toxicity 8.22.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/645
Rich Murray: 18 recent formaldehyde toxicity [Comet assay] abstracts
6.25.1 rmforall

http://groups.yahoo.com/group/aspartameNM/message/622
Rich Murray: Gold: Koehler: Walton: Van Den Eeden: Leon:
aspartame toxicity 6.4.1 rmforall

http://groups.yahoo.com/group/aspartameNM/message/623
Rich Murray: Simmons: Gold: Schiffman: Spiers:
aspartame toxicity 6.4.1 rmforall

http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984:
Monte: Murray 9.23.2 rmforall
Dr. Woodrow C. Monte Aspartame: methanol, and the public health.
Journal of Applied Nutrition 1984; 36 (1): 42-54.
(62 references) Professsor of Food Science
Director of the Food Science and Nutrition Laboratory
Arizona State University, Tempe, Arizona 85287
6411 South River Drive #61 Tempe, Arizona 85283-3337
602-965-6938 woody.monte@...
The methanol from 2 L of diet soda, 5.6 12-oz cans, 20 mg/can, is
112 mg, 10% of the aspartame. The EPA limit for water is 7.8 mg daily
for methanol (wood alcohol), a deadly cumulative poison. Many users
drink 1-2 L daily. The reported symptoms are entirely consistent
with chronic methanol toxicity. (Fresh orange juice has 34 mg/L, but,
like all juices, has 16 times more ethanol, which strongly protects
against methanol.)

"Fruit and vegetables contain pectin
with variable methyl ester content.
However, the human has no digestive enzymes for pectin (6, 25)
particularly the pectin esterase required
for its hydrolysis to methanol (26).

Fermentation in the gut may cause disappearance of pectin (6) but the
production of free methanol is not guaranteed by fermentation (3). In
fact, bacteria in the colon probably reduce methanol directly to formic
acid or carbon dioxide (6) (aspartame is completely absorbed before
reaching the colon). Heating of pectins has been shown to cause
virtually no demethoxylation; even temperatures of 120 deg C produced
only traces of methanol (3). Methanol evolved during cooking of high
pectin foods (7) has been accounted for in the volatile fraction during
boiling and is quickly lost to the atmosphere (49).
Entrapment of these volatiles probably accounts for the elevation in
methanol levels of certain fruit and vegetable products
during canning (31, 33)."

Recent research [see links at end of post] supports his focus on the
methanol to formaldehyde toxic process:

"The United States Environmental Protection Agency in their Multimedia
Environmental Goals for Environmental Assessment recommends a minimum
acute toxicity concentration of methanol in drinking water at 3.9 parts
per million, with a recommended limit of consumption below 7.8 mg/day
(8). This report clearly indicates that methanol:

"is considered a cumulative poison
due to the low rate of excretion once it is absorbed.
In the body, methanol is oxidized to formaldehyde and
formic acid; both of these metabolites are toxic." (8)....

Recently the toxic role of formaldehyde (in methanol toxicity) has been
questioned (34). No skeptic can overlook the fact that, metabolically,
formaldehyde must be formed as an intermediate to formic acid
production (54).

Formaldehyde has a high reactivity which may be why it
has not been found in humans or other primates during methanol
poisioning (59)....

If formaldehyde is produced from methanol and does have a reasonable
half life within certain cells in the poisoned organism the chronic
toxicological ramifications could be grave.

Formaldehyde is a known
carcinogen (57) producing squamous-cell carcinomas by inhalation
exposure in experimental animals (22). The available epidemiological
studies do not provide adequate data for assessing the carcinogenicity
of formaldehyde in man (22, 24, 57).

However, reaction of formaldehyde
with deoxyribonucleic acid (DNA) has resulted in irreversible
denaturation that could interfere with DNA replication and result in
mutation (37)...."
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