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.
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, firstname.lastname@example.org , 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.