3 Common Responses...

Whenever "people that don't care" or either skeptics hear something like, "Aspartame is not good for you", there are common responses that they will have. These individuals will usually respond with the information from the corporation that created the ingredient/product and that information has been generated by big money to "scientifically" explain that there is no causes for concern.

 

3 Common Responses

 

In my recent browsing, for information on Methanol/Aspartame, I came across a webpage that was text only and it was a response to someone's points on Methanol not being bad for you. I am not sure who wrote it, but they get a big thumbs up from Magnesoothe.

 

 

 

 

Here is what it had to say:

         Chronic Methanol/Formaldehyde Poisoning From Aspartame
         ------------------------------------------------------

Q.  I have been told that methanol in aspartame is not a problem for 
    several reasons:

    1.  The dose of methanol from aspartame is far below what causes
        methanol poisoning.

    2.  The methanol from aspartame does not show up in the 
        bloodstream unless huge amount of aspartame are given.

    3.  Methanol is found in higher doses in alcoholic beverages, fruit 
        and juices and therefore methanol in aspartame must be safe.


Answer
------
You are a victim of Monsanto's public relations (PR) campaign.  This 
PR campaign is often propogated by organizations that are given large 
sums of money and "scientific" assistance by Monsanto (e.g., IFIC, 
ADA).  Unfortunately some individuals on the Internet have begun to 
spread this PR even though they have absolutely no familiarity with 
the scientific literature.

==> 1.  The dose of methanol from aspartame is far below what causes
==>     methanol poisoning.

I think that every sane scientist would agree that it would be 
criminal to expose the human population to small doses of an 
exceptionally toxic poison without extensive testing of the effects 
of chronic, long-term exposure.  Methanol certainly qualifies as an 
exceptionally toxic substance, even at extremely low doses (Bennett
1953, Posner 1975, Roe 1982).  Kavet (1990) states that the minimum 
*single* dose needed for methanol to cause death (without medical 
treatment) is 300 - 1000 mg/kg.  This is equivalent to only
0.85 ounces to 2.85 ounces for a 154 lbs (70 kg) man (or much less 
for a child).

The amount of methanol needed to cause acute toxicity varies widely 
from person to person (Kavet 1990).  The nutritional status of the 
individual, co-ingestion of protective substances (e.g., ethanol), 
and presence of food in the stomach may effect the toxicity of 
methanol (Posner 1975).  It is interesting to note that since the 
presence of food in the stomach may slightly lower toxicity, the 
ingestion of aspartame with food or especially in capsules (as it is 
often given in double-blind experiments) may lower toxicity to some
unknown extent.  In addition, the interaction of methanol exposure 
with exposure to other chemicals or drugs may increase methanol 
toxicity (Posner 1975).

There are *no* controlled, long-term human studies of low-level
methanol exposure (Kavet 1990).  No ethical company would dose 
millions of people with low doses of an exceptionally toxic poison 
without conducting long-term research on a small number of human
beings.  Yet that is exactly what the aspartame manufacturer did.
Many of the *short-term* human studies have shown slight adverse
changes after an extreme low dose of methanol exposure (Chao 1959,
Ubaydullayev 1963, Cook 1991).  The doses of methanol given in these
studies are equivalent to the one can of aspartame-containing soda to
slightly above the U.S. FDA's "Acceptable Daily Intake" for aspartame.
One study (Chuwers 1995) found no adverse changes from a single, 
one-hour, low-level exposure to methanol.  These very short studies are 
not definitive.  We are essentially concerned with the effects of 
long-term chronic methanol exposure.

Clinically, chronic exposure to methanol has been seen to produced
headaches, dizziness, nausea, ear buzzing, GI distiurbances,
weakness, vertigo, chills, memory lapses, numbness & shooting
pains, behavioral disturbances, neuritis, misty vision, vision
tunneling, blurring of vision, conjunctivitis, insomnia, vision
loss, depression, heart problems (including disease of the heart 
muscle), pancreatic inflammation (Kavet 1990, Monte 1984, Posner 
1975).

The methanol from aspartame is converted to formaldehyde and then 
formic acid (DHHS 1993, Liesivuori 1991).  Chronic formaldehyde
exposure at *very* low doses has been shown to cause immune system
and neurological damage and changes as well as headaches, general poor
health, permanent genetic damage, and a number of other serious 
health problems (Fujimaki 1992, John 1994, Liu 1993, Main 1983,
Molhave 1986, National Research Council 1981, Shaham 1996, Srivastava
1992, Vojdani 1992, Wantke 1996).  One experiment (Wantke 1996) showed
that chronic exposure to formaldehyde caused systemic health problems
(i.e., poor health) in children at an air concentration of *only*
0.043 - 0.070 parts per million!  Clearly, chronic exposure to an
extremely small amount of formaldehyde is to be avoided.

It is important to understand that extremely low-level methanol and
formaldehyde exposure from other sources add to the health problems
seen from this extremely toxic poison.  The toxic load of chemicals 
including methanol and formaldehyde has increased tremendously over 
the last 15 years.  Methanol is used as a fuel on a small scale
(EPA 1994). It is also used in paint strippers, duplicator fluid,
model airplane fuel and dry gas (EPA 1994). Formaldehyde can be
found in carpeting, clothing, glues, adhesives, cements, paste,
resins, urea-foam insulation, particle board, plywood, cellulose
esters, paint, primer, paint stripping agents, paper, polishes, waxes,
disinfectants, cleansers, fumigators, cosmetics, preservatives, 
medication, mouthwash, inks, sealers, and many other products
(Remington 1987, page 89).  However, aspartame is likely the biggest 
source for formaldehyde exposure for most individuals.

On October 24, 1996, Richard Nelson from the Monsanto PR department
put a scientifically indefensible PR statement on the Internet 
about methanol from aspartame.  He pointed to an industry 
experiment of infant non-human primates where the primates were
given the equivalent of 300 mg/kg of methanol per day for 270
days (in the form of 3000 mg/kg day of aspartame).  According to
Mr. Nelson, the non-human primates showed absolutely no adverse
effects.  (This post can be found by doing a "Power Search" at the
Deja News web page:  http://www.dejanews.com/ )

What he did not say was that the minimum *single* dose of methanol 
that would cause *death* in a human being when untreated is
between 300 mg/kg - 1000 mg/kg (Kavet 1990).  Taking 300 mg/kg of
methanol per day for *270* days (not just a single, near-lethal 
dose) would almost certainly cause death or severe permanent 
damage in most human beings in such an experiment.  The reason 
why such a dose would be so deadly to humans is that human beings
are, by far, much more sensitive to methanol toxicity than any
other animal (Roe 1982).  Other aspartame metabolites are as much
as 20 times more toxic in humans than in non-human primates (to be
discussed in a separate FAQ).  

In addition, Mr. Nelson neglected to mention that the first
pre-approval experiment of aspartame on non-human primates did not 
turn out so well.  Out of the seven monkeys receiving medium or high 
doses of aspartame, six suffered grand mal seizures and one died 
(Graves 1984).  This information came out at U.S. Congressional 
Hearings.

This is just one of many cases of company PR put out that sounds
convincing until the statement is carefully analyzed by
*independent* and knowledgable persons.

The accumulation of formic acid has been shown in a recent animal
study (Eells 1996a) at methanol doses lower than that which would 
cause acute health effects.  Formic acid accumunlation in organs
has been suggested as a possibility by a well-known researcher
(Liesivuori 1986):

     "The data indicated that formic acid may have a
     long biological half-life possibly causing an
     accumulation of the acid in the body. This might
     constitute a hitherto unappreciated toxicological
     hazard, as the acid is an inhibitor of oxygen
     metabolism."

Liesivuori later points out that formic acid may accumulate
in the brain, kidneys, spinal fluid, and other organs
because of the slow excretion from the body (Liesivuori
1991).  Such an accumulation could have very serious, long-
term health consequences.  Even if there is no accumulation,
however, the damage from regular exposure to methanol metabolites
such as formaldehyde can be cumulative.

Methanol may also break down into fatty acid methyl esters 
(Kaphalia 1995).  The safety of such chronic exposure to 
increased amounts of fatty acid methyl esters over many years
has never been addressed by independent research.

Finally, it is extremely important that when one considers the
toxicity of chronic long-term exposure to methanol-->
formaldehyde-->formic acid, one has to consider *synergistic
effects*.   Synergistic effects of food additives have been
seen in scientific literature (e.g., Ershoff 1976).  For example,
some people have considered that aspartic acid, the excitotoxic
amino acid, obtained in free form from aspartame can significantly
increase the changes or damage caused by the formadehyde or formic
acid formed from the methanol in aspartame. 

Eells (1996a) points out that chronic methanol exposure in rats led 
to the "inhibition of retinal mitochondrial function and energy 
production by formic acid."  It appears that the methanol may have 
been converted to formic acid in the retina.  There was a buildup
of formic acid in the retina and vitreous humour as well as a
reduction of electroretinogram (ERG) wave amplitudes in the high
and *low* methanol-exposed rats.  Liesivuori (1991) described formic
acid's effects at the cellular level:

     "Exposure to either methanol or formic acid leads
     to accumulation of acid in the body. Formic acid
     inhibits cytochrome oxidase, causing decreased
     synthesis of ATP. This is followed by anaerobic
     glycolysis and lactic acidosis. At the same time,
     and also because of acidosis, the generation of
     superoxide anions and hydroxyl radicals is
     enhanced leading to membrane damage, lipid
     peroxidation and mitochondrial damage. This, and
     the decreased pH in acidosis, allows the influx of
     calcium into the cells. Although the mitochondrial
     dysfunction may be secondary to calcium overload
     in the mitochondria, the final consequence is cell
     death."

Eells (1996b) points out that excitatory amino acid toxicity may be 
the "mediators of retinal damage secondary to formate induced energy 
depletion in methanol-intoxication."  Formic acid inhibits
cytochrome oxidase, an important component of ATP synthesis (as 
described above).  Cell damage or death can occur when certain cells
are exposed to excess levels of excitotoxic amino acids (e.g., 
glutamic acid (MSG), aspartic acid, cysteine, etc.) (Blaylock 1994, 
Lipton 1994).  In fact, Olney (1969) showed that retinal damage 
can be seen in mice exposed to a dose of a free (i.e., unbound to 
protein) excitotoxic amino acid.  In order to remove excess
excitotoxic amino acid from extracellular space, glial cells
surround the neuron and supply them with energy (Blaylock 1994,
page 39, Lipton 1994).  This takes large amounts of ATP.
Therefore, increases in formic acid in the retina and/or
increases in excitotoxic amino acid concentration in the retina 
could cause gradual retinal damage as suggested by the Eells (1996a) 
experiment.  

Aspartame gives a person increase methanol==>formic acid exposure 
*as well as* an exposure to increased levels of an excitotoxic amino
acid, aspartic acid (Stegink 1987).  There is no reason to limit the
possibility of gradual damage from dangerous syndergistic reactions
of formic acid + an excitotoxic amino acid to only the retina.
These problems may occur anywhere the increased formic acid from
aspartame happens to temporarily or permanently accumulate in a
particular individual and excitatory damage can occur.  (Excitotory 
amino acid damage will be discussed in more detail in the aspartic 
acid FAQ.)

In conclusion, while it seems clear that long-term, low-level 
exposure to methanol==>formaldehyde==>formic acid from aspartame may 
cause cumulative toxicity damage in individuals, it is very important 
to consider methanol metabolite toxicity from aspartame in the light 
of possible synergetic reactions with other aspartame breakdown 
products (e.g., excitotoxic amino acids). Such a synergistic reaction
could increase methanol toxicity many-fold.

==> 2.  The methanol from aspartame does not show up in the 
==>     bloodstream unless huge amount of aspartame are given.

The methanol from aspartame causes a significant rise in the plasma
methanol levels at doses of *less* than one can of soda in a 66 lbs
(30 kg) child (and possibly at much lower doses) (Davoli 1986).
One would expect that the small but significant rise in methanol
levels seen in this study would lead to an increased formaldehyde
exposure since methanol from aspartame has been shown to convert to
formaldehyde and formic acid (Stegink 1981).  From the earlier
discussion we can see how dangerous chronic, low-level exposure to
formaldehyde can be.

For over 15 years, the aspartame manufacturer, Monsanto, has been 
using methanol testing procedures that are badly flawed.  They either
measured at a time when the methanol would have already be converted
to formaldehyde (e.g., after 24 hours) and/or used a measuring
technique that was capable of registering only huge increases in the
methanol levels (e.g., > 4 mg/l plasma levels).  Serious researchers 
who study methanol levels use tests (which were developed many years
ago) that can measure smaller (e.g., 0.25 mg/l to 4 mg/l) but still
quite large increases in plasma methanol levels (Cook 1991, 
d'Alessandro 1994).  The Davoli (1986) experiment is the only plasma
methanol measurement from aspartame ingestion that was conducted at
a proper time and used a proper measuring technique.  Even after the 
Davoli (1986) experiment these industry researchers continued to use 
these flawed tests which guaranteed that no plasma methanol increases 
would be seen.  How anyone could trust manufacturer-sponsored
"research" after this nonsense is beyond me!

The urine and blood formate measurements by in manufacturer-funded 
"research" are equally suspicious.  Measurements were often taken 
hours before the peak level would be expected at 12 to 16 hours 
(McMartin 1975, Liesivuori 1987).  Average baseline measurements of 
formate in these experiments (e.g., Stegink 1981) were two to three
times higher than formate measurements in experiments conducted by
real methanol/formate researchers (d'Alessandro 1994, Baumann 1979, 
Heinrich 1982, Buttery 1988, Osterloh 1986).  A prominent 
methanol/formate researcher has stated that the type of formate 
testing procedures used are "notoriously inaccurate" (Liesivuori 
1986).  Triebig (1989) and Heinzow (1992) point out that urine 
formate measurements are not an appropriate parameter for 
biological-monitoring of low-level formaldehyde exposure.

The problems with industry-conducted methanol and formate 
measurements are only the tip of the iceberg as far as non-obvious, 
yet serious experimental flaws go.  Even though there has been so
much ridiculous, unscientific behavior seen in the industry-
sponsored research, some scientists and researchers continue to be
fooled and repeat the same argument that "methanol from aspartame
dose not raise plasma methanol levels."  In 1984, the U.S. FDA 
Commissioner believed this bordering-on-fraudulent research when he 
stated that "dry uses of aspartame showed no detectable levels of 
methanol in the blood of human subjects following the ingestion of 
aspartame at 34 [mg/kg] body weight...." (Federal Register 1984).
A recent study by U.K. scientists also made similar mistakes by 
trusting aspartame industry research relating to methanol 
(Puthrasingam 1996).

==>3.  Methanol is found in higher doses in alcoholic beverages, fruit 
==>    and juices and therefore methanol in aspartame must be safe.

Knowledgable scientists know that methanol conversion to the toxic 
formaldehyde and formic acid metabolites is blocked when it is 
co-ingested with significant amounts of ethanol in alcoholic 
beverages.  This is because the ethanol acts as a protective factor 
which allows the elimination of methanol through the breath and 
urine before it is converted to formaldehyde (Liesivuori 1991, 
Roe 1982). So this proves that it would be ludicrous to 
automatically assume that methanol in fruits and juices is converted 
to formaldehyde.  There is strong evidence showing that it is not 
converted to formaldehyde to any significant extent (like methanol
from alcoholic beverages) and/or there is a protective factor 
preventing toxicity.

It has been shown that the ingestion of a moderate amount of fruit 
such as a 3-5 apples or oranges causes approximately 0.75 grams of 
methanol to be released into the body (Lindinger 1997).  Such a daily 
intake throughout the day (or equivalent amount from juices) is 
approximately equivalent to the amount of methanol absorption seen in
workplace exposure that has lead to the development of methanol 
toxicity symptoms (Frederick 1984, Kingsley 1954-55, Kavet 1990).
In other words it is approximately equivalent to working five days 
per week in air with a methanol concentration of 260 mg/m3.  This 
methanol air concentration is higher than found in a methanol-laden 
chemical plant (120 mg/m3) (Heinrich 1982) and a methanol-laden 
printing shop (~140 mg/m3) (Baumann 1979).

  Absorbed Methanol From 1.5 kg Fruit (or juice equiv)  During Day
  ----------------------------------------------------------------
  750 mg of methanol (from fruit) * 7 days / 70 kg

     = 75 mg/kg/week of methanol absorption.

  Absorbed Methanol From 260 mg/m3 Air Exposure During Workweek
  -------------------------------------------------------------
  The formula used to calculate methanol inhaled in the
  Baumann (1979) study was discussed by Kavet (1990):

  (260 mg/m3 * 6.67 m3/workday * 5 workdays * 60 absorption
                        rate) / 70 kg

     = 74 mg/kg/week of methanol absorption.

0.75 grams (750 mg) of methanol obtained from fruit is equivalent to 
the amount of methanol obtained from drinking 0.45 liters of brandy 
(40% ethanol) containing 0.5% methanol (Lindinger 1997). This amount 
of methanol without a protective factor such as ethanol would qualify 
as a "significantly methanol-contaminated beverage" (Lindinger 1997).

In order to believe that methanol from fruit juice is metabolized 
like that from aspartame, one has to believe that the a moderate 
to high daily intake of fruit is equivalent to drinking almost half a 
liter of methanol-contaminated brandy every day and is equivalent to
working in a methanol contaminated workplace 5 days per week. 
Obviously, there must be some protective factor in 
methanol-containing foods (as there are in traditionally-ingested 
alcoholic beverages).  If there weren't a protective factor, then we 
would be seeing widespread low-level methanol poisoning in persons
who ingest fruit regularly.

An interesting note:  A child ingesting the equivalent of the
FDA's "Acceptable" Daily Intake of aspartame is getting the equivalent
amount of methanol as is obtained by an adult working 33.0 hours in a
methanol-laden printing shop or approximately 40 hours in a methanol-
laden chemical plant (Kavet 1990).  Such an regular level of 
aspartame intake by children has already been seen as possible in
industry research (Frey 1976)).

----------------------

Persons who are acutely sensitive to formaldehyde exposure (such
as described in "Formaldehyde and Other Aldehydes" by the National
Research Council (1981)) often report that they are similarly
sensitive to aspartame, but not fruit juices.

  "The only other thing that has ever given me a migrane was
   inhaling formaldehyde."

  "I am very sensitive to formaldehyde--new carpets and 
   Nutrasweet/aspartame give me serious headaches)."

I get many comments from formaldehyde-sensitive people that they 
experience acute toxicity from aspartame ingestion.

Given that huge and quickly growing numbers of health problems
being reported from chronic, long-term aspartame use (Stoddard
1995, DHHS 1995) and the evidence that people are being chronically
exposed to formaldehyde (among the several potentially dangerous
breakdown products), and given that almost all independent human
studies (including double-blind studies) and animal studies have
shown problems with aspartame, one cannot possibly fathom
recommending long-term use without extensive and long-term 
*independent* research.

Here is a quote from an Ophthalmologist and a scientist who was one
of the few experts of methanol toxicity and eye damage in the U.S.:

---------------

  Dr. Morgan Raiford, Ophthal. [deceased]
  Facts About Aspartame
  May 20, 1987

  The above product is also manufactured as NutraSweet.  This 
  pharmological spin-off is a highly profitable item, with a growing 
  market.  These products are used as a sweetener, some 200 times as 
  sweet as regular can sugar.

  This product has some highly toxic reactions in the human visual 
  pathway, and we are beginning to observe the tragic damage to the 
  optic nerve, such as blindness, partial to total optic nerve atrophy. 
  Once this destructive process has developed there is no return of 
  visual restoration.  We are beginning to see and observe another 
  toxic reaction which affects the central nervous system which is 
  related to phenylalanine levels in the central nervous system.  These 
  observations are more vague, however, it stimulates the damaging to 
  the brain and the central nervous system, having the manifestations 
  as PKU Neuro Damage.  Over 3,000 cases have been reported, and the 
  FDA to date has ignored this existence.

  Human Visual Pathway Damage

  The human visual pathway admists ninety percent of our intellectual 
  input to the brain and central nervous system.  All of the learning 
  processes are centered during ones life time.  The mechanism of this 
  tragic damage to the human visual system from this product is and has 
  been known for over a decade that visual loss takes place.  When this 
  drug enters the digestive tract, largely the upper portion, this 
  aspartame molecule spins off a by product known as methanol or 
  methyl-alcohol.  This product enters the bloodstream and when these 
  portions reach the highly metabolic region of the optic nerve and 
  retina, partial atrophy can and does take place.  The vision can not 
  do without oxygen and nutrition for more than ninety seconds without 
  revealing some damage.  Total loss of vision is present and there is 
  no return.  In the very early stages in which is referred to as the 
  "wet stage", treatment can be given and will reserve the destructive 
  pathology to the optic nerve and retina.  This must be in the mind of 
  the physician and he must understand the chemical ongoing process.  
  The writer has seen many cases where the patient was allowed to go to 
  the degrees of blindness, as this diagnosis of optic neuritis was 
  rendered, as the term idiopathic neuritis of optic nerve was given, 
  usually steriods until systemic gross body and facial moon developed. 
  This therapy has demonstrated the total lack of understanding of the 
  basic lack of biochemical physiology at the molecular level.
  
  The variability or onset of the optic nerve atrophy is of a type that 
  one must first think of this pathology, and it requires a certain 
  amount of listening to the patient.  The quantity of symptoms vary 
  with each patient.

  Over the past year the writer has observed the fact that any portion 
  of the central nervous system can and is affected.  Since the 
  chemical phenylalanine is mixed up with some metabolic mess, we have 
  seen symptoms of varying hue in the extremities, sensations of 
  dullness of the intellect, visual shadows, evidence of word structure 
  reversing and some hearing impairment is noted by the individual.  
  This can and will in time cause problems in learning.  The medical 
  community must alert itself that we have a problem that has surfaced 
  due to the factor of the drug industry.  Parents must be alerted to 
  the side reactions of this toxic product and its reactions.

---------------

As one writer recently stated when referring to the fact that a
significant dose of formaldehyde is obtained from aspartame breakdown
and that formaldehyde is used in embalming:

   "Chemically speaking, it's as if image-conscious dieters, in 
    their quest for weight loss, were sucking on the toe of a
    corpse 'just for the taste of it.'"
    (Rauer 1996)    

More detailed information about chronic methanol/formaldehyde poisoning 
from aspartame can be found in the draft scientific/historic review 
document listed on:

            http://www.holisticmed.com/aspartame/

Please contact me, mgold@tiac.net , if you have any questions and I 
will either answer the question if possible or refer you to the 
appropriate scientific expert.

---------------

                     References Cited

Baumann, K., J. Angerer, 1979. "Occupational Chronic
  Exposure to Organic Solvents. VI. Formic Acid
  Concentration in Blood and Urine as an Indicator of
  Methanol Exposure," International Archives of
  Occupational and Environmental Health, Volume 42, page
  241.

Bennett, I.L., et al., 1953. "Acute Methyl Alcohol
  Poisoning: A Review Based on Experiences in an Outbreak
  of 323 Cases," Medicine, Volume 32, page 431-463.

Blaylock, Russell L., 1994. "Excitotoxins: The Taste That
  Kills," Health Press, Santa Fe, New Mexico, c1994.

Buttery, J.E., B.R. Chamberlain, 1988. "A Simple Enzymatic
  Method for the Measurement of Abnormal Levels of Formate
  in Plasma," Journal of Analytical Toxicology, Volume 12,
  page 292-294.

Chao, C.T., 1959. "Material on the Hygeinic Standardization of the 
  Maximally Permissible Concentration of Methanol Vapors in the 
  Atmosphere," Gig. Sanit., 24:7.

Chuwers, P., J. Osterloh, T. Kelly, A. D'Alessandro, P. Quinlan,
  C. Becker, 1995. "Neurobehavioral effects of low-level methanol 
  vapor exposure in healthy human volunteers," Environmental
  Research, Volume 71, No. 2, pages 141-150.

Cook, M.R., F.J. Bergman, et al., 1991. "Effects of Methanol
  Vapor on Human Neurobehavioral Measures," Research Report
  No. 42, Health Effects Institute, 141 Portland Street,
  Suite 7300, Cambridge, MA 02139, (617) 621-0266, August
  1991.

d'Alessandro, Alessandra, et al., 1994, "Formate in Serum
  and Urine after Controlled Methanol Exposure at the
  Threshold Limit Value," Environmental Health
  Perspectives, Volume 102, No. 2, February, 1994, page 178-
  181.

Davoli, E., et al., 1986. "Serum Methanol Concentrations in
  Rats and in Men After a Single Dose of Aspartame," Food
  and Chemical Toxicology, Volume 24, No. 3, page 187-189.

DHHS 1993. "Methanol Toxicity," American Family Physician,
  Volume 71(1):163-171, January 1993. Adapted from Case
  Studies in Environmental Medicine published by the Agency
  For Toxic Substances and Disease Registry, U.S.
  Department of Helath and Human Services.

DHHS 1995. Department of Health and Human Services. "Report
  on All Adverse Reactions in the Adverse Reaction
  Monitoring System." (April 20, 1995).

Eells, Janis T., et al., 1996a. "Formate-Induced Alterations in 
  Retinal Function in Methanol-Intoxicated Rats," Toxicology and 
  Applied Pharmacology, Volume 140, page 58-69.

Eells, Janis T., 1996b.  "Mechanism of Methanol-Induced Retinal 
  Alterations," NIH Grant Application, Project No. 5 R01 ES06648-03,
  FY96, NIH CRISP Database:  gopher://gopher.nih.gov:70/11/res/crisp

EPA 1994. "Methanol Basics," Fact Sheet OMS-7. EPA 400-F-92-
  009.

Ershoff, Benjamin H., 1976. "Synergistic Toxicity of Food
  Additives in Rats Fed a Diet Low in Dietary Fiber,"
  Journal of Food Science, Volume 41, page 949-951.

Federal Register 1984. "Food Additives Permitted for Direct
  Addition to Food for Human Consumption; Aspartame,"
  Volume 49, No. 36, February 22, 1984, page 6672-6682.

Frederick, Linda J., et al., 1984. "Investigation and
  Control of Occupational Hazards Associated with the Use
  of Spirit Duplicators," American Industrial Hygiene
  Association Journal, Volume 45, No. 1, page 51-55.

Frey, Gunther H., 1976. "Use of Aspartame By Apparently
  Healthy Children and Adolescents," Journal of Toxicology
  and Environmental Health, Volume 2, page 401-415.

Fujimaki, H., et al., 1992. "Mast Cell Response to
  Formadehyde," International Archives of Allergy &
  Immunology, Volume 98, No. 4, page 324-331.

Graves, Florence, 1984. "How Safe is Your Diet Soft Drink,"
  Common Cause Magazine, July/August 1984. Reprinted in
  Congressional Record (1985a, pages S5497-S5506)

Heinrich, R., J. Angerer, 1982. "Occupational Chronic
  Exposure to Organic Solvents. X. Biological Monitoring
  Parameters for Methanol Exposure," International Archives
  of Occupational and Environmental Health, Volume 50, page
  341.

Heinzow, B., T. Ellrott 1992. "Formic Acid in Urine -- A
  Significant Parameter in Environmental Diagnosis?"
  Zentralbl Hyg Umweltmed, Volume 192, No. 5, page 455-461.

John, E.M., et al., 1994. "Spontaneous Abortion Among
  Cosmetologists," Epidemiology, Volume 5, No. 2, page 147-
  155.

Kaphalia, Bhupendra S., James B. Carr, G.A.S. Ansari, 1995. 
  "Increased Endobiotic Fatty Acid Methyl Esters Following Exposure to 
  Methanol," Fundamental and Applied Toxicology, Volume 28, Page 
  264-273.

Kavet, Robert, Kathleen M. Nauss, 1990. "The Toxicity of
  Inhaled Methanol Vapors," Critical Reviews in Toxicology,
  Volume 21, Issue 1, page 21-50.

Kingsley, W.H., F.G. Hirsch, 1954-1955. "Toxicological
  Considerations in Direct Process Spirit Duplication
  Machines," Compen. Medicine, Volume 40, page 7-8.

Liesivuori, Jyrik, 1986. "Slow Urinary Elimination of Formic
  Acid in Occupationally Exposed Farmers," Annals of
  Occupational Hygiene, Volume 30, No. 3, page 329-333.

Liesivuori, Jyrik, H. Savolainen, 1987. "Urinary Formic Acid
  as an Indicator of Occupational Exposure to Formic Acid
  and Methanol," American Industrial Hygiene Association
  Journal, Volume 48, page 32-34.

Liesivuori, Jyrki, Heikki Savolainen, 1991. "Methanol and
  Formic Acid Toxicity: Biochemical Mechanisms,"
  Pharmacology & Toxicology, Volume 69, page 157-163.

Lindinger, W., J. Taucher, A. Jordan, A. Hansel, W. Vogel, 1997. 
  "Endogenous Production of Methanol after the Consumption of 
  Fruit," Alcoholism: Clinical and Experimental Research, 
  Volume 21, No. 5, pages 939-943.

Lipton, Stuart A., Paul A. Rosenberg, 1994. "Excitatory
  Amino Acids as a Final Common Pathway for Neurologic
  Disorders," New England Journal of Medicine, Volume 300,
  No. 9, page 613-622.

Liu, Kai-Shen, et al., 1993. "Irritant Effects of Formaldehyde
  Exposure in Mobile Homes," Environmental Health
  Perspectives, Volume 94, page 91-94.

Main, D.M., T.J. Hogan, 1983. "Health Effect of Low-Level
  Exposure to Formaldehyde," Journal of Occupational
  Medicine, Volume 25, page 896-900.

McMartin, Kenneth E., et al., 1975. "Methanol Poisoning: I.
  The Role of Formic Acid in the Development of Metabolic
  Acidosis in the Monkey and Reversal by 4-Methylpyrazole,"
  Biochemical Medicine, Volume 13, page 319-333.

Molhave, L., et al., 1986. "Dose-Response Relation of
  Volitile Organic Compounds in the Sick Building
  Syndrome," Clinical Ecology, Volume 4, No. 2, page 52-56.

Monte, Woodrow C., 1984. "Aspartame: Methanol and the Public
  Health," Journal of Applied Nutrition, Volume 36, No. 1,
  page 42-54.

National Research Council 1981. "Formaldehyde and Other
  Aldehydes," National Research Council, National Academy
  Press, Washington, D.C., c1981.

Olney, John W., 1969. "Glutamate-Induced Retinal Degeneration in 
  Neonatal Mice. Electron Microscopy of the Acutely Evolving Lesion," 
  Journal of Neuropathology and Experimental Neurology, Volume 28, 
  pages 455-474.

Osterloh, J., 1986. "The Utility of Tetrabromophenophthalein
  Methyl Ester (TBPME) Spot Test for the Identification of
  Drug Positive Urines," Journal of Analytical Toxicology,
  Volume 10, page 255.

Posner, Herbert S., 1975. "Biohazards of Methanol in
  Proposed New Uses," Journal of Toxicology and
  Environmental Helath, Volume 1, page 153-171.

Puthrasingam S., et al., 1996. "Aspartame Pharmacokinetics - The 
  Effect of Ageing," Age and Ageing, Volume 25, Number 3, pages 
  217-220.

Rauer, Julie, 1996. Spy Magazine, December 1996, page 29.

Remington, Dennis W., Barbara W. Higa, 1987. "The Bitter
  Truth About Artificial Sweeteners," Published by Vitality
  House International, Inc., 3707 North Canyon Road #8-C,
  Provo, Utah 84604, (801) 224-9214.

Roe, O., 1982. "Species Differences in Mehtanol Poisoning,"
  CRC Critical Reviews In Toxicology, October 1982, page
  275-286.

Shaham, J., Y. Bomstein, A. Meltzer, Z. Kaufman, E. Palma, J. Ribak, 
  1996. "DNA--protein Crosslinks, a Biomarker of Exposure to 
  Formaldehyde--in vitro and in vivo Studies," Carcinogenesis, Volume 
  17, No. 1, page 121-125.

Srivastava, A.K., et al., 1992. "Clinical studies of
  employees in a sheet-forming process at a paper mill,"
  Veterinary and Human Toxicology, Volume 34, No. 6, page
  525-527.

Stegink, Lewis D., et al., 1981. "Blood Methanol
  Concentrations in Normal Adult Subject Administered Abuse
  Doses of Aspartame," Journal of Toxicology and
  Environmental Health, Volume 7, page 281-290.

Stegink, Lewis D., et al. 1987. "Plasma Amino Acid
  Concentrations in Normal Adults Administered Aspartame in
  Capsules or Solution: Lack of Bioequivalence,"
  Metabolism, Volume 36, No. 5, page 507-512.

Stoddard, Mary Nash, 1995. Conversations between Mary Nash
  Stoddard of the Aspartame Consumer Safety Network and
  Mark D. Gold.

Triebig, G., et al., 1989. "Formaldehyde exposure at various
  workplaces," Science of the Total Envirnment, Volume 79,
  No. 2, page 191-195.

Ubaydullayev, R., 1963. "A Study of Hygienic Properties of Methanol 
  as an Atmospheric Air Pollutant," USSR Li. Air Pollut. Relat. Occup. 
  Dis. -- A Survey, 17:39.

Vojdani, A., 1992. "Immune Alteration Associated With
  Exposure to Toxic Chemicals," Toxicol Ind Health, Volume
  8, No. 5, page 239-254.

Wantke, F., C.M. Demmer, P. Tappler, M. Gotz, R. Jarisch, 1996. 
  "Exposure to Gaseous Formaldehyde Induces IgE-Mediated Sensitization 
  To Formaldehyde in School-Children," Clinical and Experimental 
  Allergy, Volume 26, pages 276-280.
Sale

Unavailable

Sold Out