As School Doors Open, Food and Beverage Industries Rush In

Ah, the sounds of School Year 2006-2007: the clatter of coins going down the pop machines to let loose a POWERade or an aspartame-sweetened diet soda -- maybe even a bottle of juice or milk. The rip of a new box of "reduced-sugar" Fruit Loops (or Frosted Flakes or Apple Jacks) at breakfast.

PR firms got in the door ahead of most school bells. As a result, parents are especially likely to see signs of the American Beverage Association's (ABA) and Kellogg's promotional efforts to brand their children's eating and drinking habits this year.

Many massively-sugared soft drinks, but not their makers, have been suspended from school in 2006, the outcome of a national deal between Big Soda and the Clinton Foundation.

Kellogg's PR firm, Summit Marketing, has just announced "Morning Jump-Start Breakfast Kits," headlining them: "New, Convenient Pre-Packaged Breakfast is Win-Win for Kids and Schools." Here, Kellogg's PR flack apparently means "win-win" because the schools not only get cheap vitaminized junk food, but also "vibrant, primary-colored" educational materials which feature Tony the Tiger and Toucan Sam teaching math, science, and, guess what, nutrition and fitness. (There's a healthy PR confession in that sentence, since "win-win" usually refers to "wins" by the contracting parties -- Kellogg's and the schools.)

Certainly many obesity researchers (see here, here, and here) have promoted putting other tigers in our kids' tanks, including higher fibers, more fruit, lower calories and real vitamins. Perhaps it's time that "No Child Left Behind" testing include these questions: 1) Approximate the U.S. increase in overweight children since 1980 (tripled); 2) Guess the child obesity increase over the past 10 years? (one third); 3) Estimate the risk level of obese versus nonobese children in reaching insulin levels linked to Type 2 diabetes? (twelve times).

Both the ABA and Kellogg's strategies offer the pretense of addressing health issues. But what's really at stake?

In the ABA case, my thoughts wind back to this summer and... the NBA. In a post-championship game interview, watched by approximately nine million American households, Miami Heat Coach Pat Riley prominently reminded star Dwyane Wade to turn his Gatorade label out to the masses -- a comment that sports reporter Darrell Rovell (author of a blog and book on Gatorade) promoted in a column. During his own live post-game comments, Wade awkwardly declared to a handler -- "don't want water, give me the Gatorade."

Where did that come from? Maybe Wade himself, or, more likely, Gatorade's marketers, who know soft drink sales have been falling, sports drinks climbing, and the youth niche a crucial product entry point (for example, who would guess that teenage girls are among the largest consumers of sports drinks, perhaps because, along with all the sodium and potassium, they contain somewhat less sugar than other beverages.) So the beverage industry shifted its products into a growth niche while former President Clinton's foundation helped preserve the promotional deals many beverage makers have with schools.

Only one state, Connecticut, has banned soft drinks AND sports drinks from vending machines. Not that I have anything against my son drinking blue or green liquids with ingredient lists like chemistry sets, but limiting school purchases to water, juice and milk would help end the PR sell to kids and set the table for a healthier mindset about snacking and meals.

For the record, here's who's ringing the first PR bells this school year: BBDO Worldwide has created the $10 million national school-opening campaign to promote the beverage association's self-congratulatory campaign on "voluntary" limits on types of school beverages. The ads that just ran in Wisconsin feature a teenage football player saying "Dude, It's all about the food pyramid" with the ad copy: "We all know the importance of raising healthy children. We also know that parents can't do it alone. That's why we at America's beverage companies are proud to announce we're taking a major step to help..." One ad ends: "[W]e hope to help American's current and future schoolchildren grow up healthier than ever." (Than ever? Please see draft obesity test questions Nos. 1-3, above.) The ads are paid for jointly by Coke, Pepsi, and Cadbury Schweppes and are running in the Wall Street Journal, Parade, Real Simple, Woman's Day, major national news magazines, and newspapers across the country.

Summit, in turn, has offered schools the one-two punch of a Kellogg's food scientist and a manager for "Cereal Product Innovations" as contacts, perhaps to help explain how the Pop Tarts included in "Jump Starts" fit into a healthy, balanced diet. Another possible motive for the promotion: low-sugar remakes of popular sugared cereals haven't always fared well on supermarket shelves. Summit's press release calls the menu a "turnkey solution to serve breakfast" in school.

Turnkey? Student councils, or someone with a big school ID, need to put Tony the Tiger, not to mention Gatorade, on the other side of a locked door.


Arsenic in Ground Water of the Willamette Basin, Oregon "The Global Failure to Disclose Carcinogenic Contaminants in Bottled Drinks Consumed By Children" I ran for Lane Community College in 2003 against Jay Boziviech. He used the flag in all his yard signs and fliers.. He was spreading rumors to smear me.. He did every thing to profile me.. In May 2005, I ran for the Eugene, Oregon School Board , against the executive of Pepsi cola Eric Forrest. I was followed, stalked, telephone harassment, hate emails, more than 5 a day on my blog, and ran over several times on my way home. I was almost going to be killed. Just because of the corruption of Corporate Power and some of our elected officials! The previous superintendent David Piercy and his wife Mayor Kitty Piercy, had played a bigger role in destroying me. KEZI our local TV station paraded me with the help of Chamber of Commerce. They picked up a Jewish woman Aria Seligmann to run against me, to spilt the progressive community. So, all the Zionists came after me. I had to file a stalking order to stop Aria and her campaign manager "Green Party chair" William Maxwell. My two legislators' Sen. Vicki Walker -defended Pepsi executive: By blaming the obesity of the children on their family. Vicki said the "the children come to school obese. It is not the soda in the school to be blamed"- Rep. Bob Ackerman who had forged my family's signature and defrauded us, sold my family's condo, that worth $150, 000.00 by giving us only $41,000.00!- Then Mr. Ackerman listed the condo by a higher price than he actually sold it! My commissioner Bobby Green, my councilman Gray Pape, and three other Councilors endorsed Eric Forrest. And the so called, progressive Commissioner Pete Sorenson "The REAL Democrat" & Councilors Bonny Bettman, Andréa Ortiz and "Mayor for all Eugene", -but not the Arabs or Muslims- Kitty Piercy endorsed the other candidate who was not even democrat or qualified! And of course the previous Mayor Jim Torrey, who's running now for legislature seat,. Jim Torrey headed the kids Sport to hide his agenda of supporting junk food in the schools ! All the elected members of the Eugene school Board endorsed and appointed Eric Forrest to the Board. The 4J Superintendent George Russell, with our Superintendent Susan Castillo too were very much supportive of Eric Forrest and Soda in the Schools. Even Stand for the Children & all the Oregon School Association OSSA & Eugene, EESA , did not endorse me.They ended up endorsing & giving Erik Forrest the money.. My life was in peril & still is, just, because of $320.000.00 contribution from the soda executives. This contribution was not even invested in a good healthy food! We must put stop to this kind of abuse and corruption. We need to hold our elected official accountable for their misconduct and greed. PS: 25 applicants were interviewed for this position on Jan. 2005. When were asked if we're going to file on May 2005 election. All of us said YES. However, none had filed for this position but "ME". All the rest of the applicants were informed & warned NOT to file against the Pepsi executive Eric Forrest! I was set to be killed!! Suit Claims Coca-Cola's School Soda Contracts Illegal The Organic Consumers Association website:

unexamined diet research cofactors: formaldehyde from tobacco and wood smoke, it also forms from methanol in dark wines and liquors and 11% methanol part of aspartame: Murray 2006.09.16 aspartame groups and books: updated research review of 2004.07.16: Murray 2006.05.11 toxicity in rat brains from aspartame, Vences-Mejia A, Espinosa-Aguirre JJ et al 2006 Aug: Murray 2006.09.06 Connecticut bans artificial sweeteners in schools, Nancy Barnes, New Milford Times: Murray 2006.05.25 carcinogenic effect of inhaled formaldehyde, Federal Institute of Risk Assessment, Germany -- same safe level as for Canada: Murray 2006.06.02 Home sickness -- indoor air often worse, as our homes seal in pollutants [one is formaldehyde, also from the 11% methanol part of aspartame], Megan Gillis, Murray 2006.06.01 "Of course, everyone chooses, as a natural priority, to actively find, quickly share, and positively act upon the facts about healthy and safe food, drink, and environment." Rich Murray, MA Room For All 505-501-2298 1943 Otowi Road Santa Fe, New Mexico 87505 group with 77 members, 1,368 posts in a public, searchable archive methanol (formaldehyde, formic acid) disposition: Bouchard M et al, full plain text, 2001: substantial sources are degradation of fruit pectins, liquors, aspartame, smoke: Murray 2005.04.02 NIH NLM ToxNet HSDB Hazardous Substances Data Bank inadequate re aspartame (methanol, formaldehyde, formic acid): Murray 2006.08.19 HSDB Hazardous Substances Data Bank: Aspartame ASPARTAME CASRN: 22839-47-0 METHANOL CASRN: 67-56-1 FORMALDEHYDE CASRN: 50-00-0 FORMIC ACID CASRN: 64-18-6 formaldehyde from 11% methanol part of aspartame or from red wine causes same toxicity (hangover) harm: Murray 2006.05.24 Dark wines and liquors, as well as aspartame, provide similar levels of methanol, above 120 mg daily, for long-term heavy users, 2 L daily, about 6 cans. Within hours, methanol is inevitably largely turned into formaldehyde, and thence largely into formic acid -- the major causes of the dreaded symptoms of "next morning" hangover. Fully 11% of aspartame is methanol -- 1,120 mg aspartame in 2 L diet soda, almost six 12-oz cans, gives 123 mg methanol (wood alcohol). If 30% of the methanol is turned into formaldehyde, the amount of formaldehyde, 37 mg, is 18.5 times the USA EPA limit for daily formaldehyde in drinking water, 2.0 mg in 2 L average daily drinking water. Any unsuspected source of methanol, which the body always quickly and largely turns into formaldehyde and then formic acid, must be monitored, especially for high responsibility occupations, often with night shifts, such as pilots and nuclear reactor operators. Aspartame Toxicity Information Center Mark D. Gold 12 East Side Drive #2-18 Concord, NH 03301 603-225-2100 "Scientific Abuse in Aspartame Research" ******************************************************* ASPARTAME CASRN: 22839-47-0 Human Health Effects: Human Toxicity Excerpts: . . . Adverse effects: urticaria, angiodema, granulomatous panniculitis, cross-reactivity with sulfonamides, renal tubular acidosis (with large amounts) /From table/ [Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 996] **PEER REVIEWED** METHANOL CASRN: 67-56-1 Human Health Effects: Toxicity Summary: Methanol occurs naturally in humans, animals and plants. It is a natural constituent in blood, urine, saliva and expired air. ... The two most important sources of background body burdens for methanol and formate are diet and metabolic processes. Methanol is available in the diet principally from fresh fruits and vegetables, fruit juices ... fermented beverages ... and diet foods (principally soft drinks). The artificial sweetner aspartame is widely used and, on hydrolysis, 10% (by weight) of the molecule is converted to free methanol, which is available for absorption. ... Exposures to methanol can occur in occupational settings through inhalation or dermal contact. ... Methanol is readily absorbed by inhalation, ingestion and dermal exposure, and it is rapidly distributed to tissues according to the distribution of body water. A small amount of methanol is excreted unchanged by the lungs and kidneys. [ Alcohol Clin Exp Res. 1997 Aug; 21(5): 939-43. Endogenous production of methanol after the consumption of fruit. Lindinger W, Taucher J, Jordan A, Hansel A, Vogel W. Institut fur Ionenphysik, Leopold Franzens Universitat Innsbruck, Austria. After the consumption of fruit, the concentration of methanol in the human body increases by as much as an order of magnitude. This is due to the degradation of natural pectin (which is esterified with methyl alcohol) in the human colon. [ by bacteria ] In vivo tests performed by means of proton-transfer-reaction mass spectrometry show that consumed pectin in either a pure form (10 to 15 g) or a natural form (in 1 kg of apples) induces a significant increase of methanol in the breath (and by inference in the blood) of humans. The amount generated from pectin (0.4 to 1.4 g) [ 400 to 1400 mg ] is approximately equivalent to the total daily endogenous production (measured to be 0.3 to 0.6 g/day) [ 300 to 600 mg ] or that obtained from 0.3 liters of 80-proof brandy (calculated to be 0.5 g). [ 500 mg ] This dietary pectin may contribute to the development of nonalcoholic cirrhosis of the liver. PMID: 9267548 Alcohol Clin Exp Res. 1995 Oct; 19(5): 1147-50. Methanol in human breath. Taucher J, Lagg A, Hansel A, Vogel W, Lindinger W. Institut fur Ionenphysik, Universitat Innsbruck, Austria. Using proton transfer reaction-mass spectrometry for trace gas analysis of the human breath, the concentrations of methanol and ethanol have been measured for various test persons consuming alcoholic beverages and various amounts of fruits, respectively. The methanol concentrations increased from a natural (physiological) level of approximately 0.4 ppm up to approximately 2 ppm a few hours after eating about 1/2 kg of fruits, and about the same concentration was reached after drinking of 100 ml brandy containing 24% volume of ethanol and 0.19% volume of methanol. PMID: 8561283 [ My earlier errors were corrected 2005.07.11: 24 ml means 19 g ethanol, and 0.19 ml means 0.15 g = 150 mg methanol. One L diet soda has 61.5 mg methanol in the aspartame molecule, so 100 ml diet soda has 6.15 mg methanol, so the brandy has 24.4 times more methanol than diet soda. A pound of fruit gives about as much methanol as 2 L (nearly 6 cans) diet soda. ] ] ... Methanol is metabolized primarily in the liver by sequential oxidative steps to formaldehyde, formic acid and carbon dioxide. The initial step involves oxidation to formaldehyde by hepatic alcohol dehydrogenase ... In step 2, formaldehyde is oxidized by formaldehyde dehydrogenase to formic acid/or formate depending on the pH. In step 3, formic acid is detoxified to carbon dioxide by folate-dependent reactions. Elimination of methanol from the blood via the urine and exhaled air and by metabolism appears to be slow in all species, especially when compared to ethanol. ... It is the rate of metabolic detoxification, or removal of formate that is vastly different between rodents and primates and is the basis for the dramatic differences in methanol toxicity observed between rodents and primates. The acute and short term toxicity of methanol varies greatly between different species, toxicity being highest in species with a relatively poor ability to metabolize formate. In such cases of poor metabolism of formate, fatal methanol poisoning occurs as a result of metabolic acidosis and neuronal toxicity, whereas, in animals that readily metabolize formate, consequences of CNS depression (coma, respiratory failure, etc.) are usually the cause of death. Sensitive primate species (humans and monkeys) develop increased blood formate concentrations following methanol exposure, while resistant rodents, rabbits and dogs do not. Humans and non-human primates are uniquely sensitive to the toxic effects of methanol. Overall methanol has a low acute toxicity to non-primate animals. ... In the rabbit, methanol is a moderate irritant to the eye. It was not skin sensitizing ... There is no evidence from animal studies to suggest that methanol is a carcinogen ... The inhalation of methanol by pregnant rodents throughout the period of embryogenesis induces a wide range of concentration-dependent teratogenic and embryolethal effects. Treatment-related malformations, primarily extra or rudimentary cervical ribs and urinary or cardiovascular defects, were found in fetuses of rats ... Increased incidences of exencephaly and cleft palate were found in the offspring of ... mice ... There was increased embryo/fetal death ... and an increasing incidence of full litter resorptions. Reduced fetal weight was observed ... Fetal malformations ... included neural and ocular defects, cleft palate, hydronephrosis and limb anomalies. Humans (and non-human primates) are uniquely sensitive to methanol poisoning and the toxic effects in these species are characterized by formic acidemia, metabolic acidosis, ocular toxicity, nervous system depression, blindness, coma and death. Nearly all of the available information on methanol toxicity in humans relates to the consequences of acute rather than chronic exposures. A vast majority of poisonings involving methanol have occurred from drinking adulterated beverages and from methanol-containing products. Although ingestion dominates as the most frequent route of poisoning, inhalation of high concentrations of methanol vapor and percutaneous absorption of methanolic liquids are as effective as the oral route in producing acute toxic effects. The most noted health consequences of longer term exposure to lower levels of methanol is a broad range of ocular effects. ... The toxicity is manifest if formate generation continues at a rate that exceeds its rate of metabolism. ... The minimum lethal dose of methanol in the absence of medical treatment is between 0.3 and 1 g/kg. The minimum dose causing permanent visual defects is unknown. ... Wide interindividual variability of the toxic dose is a prominent feature in acute methanol poisoning. Two important determinants of human susceptibility to methanol toxicity appear to be (1) concurrent ingestion of ethanol, which slows the entrance of methanol into the metabolic pathway, and (2) hepatic folate status, which governs the rate of formate detoxification. The symptoms and signs of methanol poisoning, which may not appear until after an asymptomatic period ... include visual disturbances, nausea, abdominal and muscle pain, dizziness, weakness and disturbances of consciousness ranging from coma to clonic seizures. Visual disturbances ... range from mild photophobia and misty or blurred vision to markedly reduced visual acuity and complete blindness. In extreme cases death results. The principal clinical feature is severe metabolic acidosis of the anion-gap type. The acidosis is largely attributed to the formic acid produced when methanol is metabolized. ... Visual disturbances of several types (blurring, constriction of the visible field, changes in color perception, and temporary or permanent blindness) have been reported in workers ... No other adverse effects of methanol have been reported in humans except minor skin and eye irritation. ... Methanol is of low toxicity to aquatic organisms, and effects due to environmental exposure to methanol are unlikely to be observed, except in the case of a spill. [Environmental Health Criteria 196: Methanol pp. 1-9 (1997) by the International Programme on Chemical Safety (IPCS) under the joint sponsorship of the United Nations Environment Programme, the International Labour Organisation and the World Health Organization.]**PEER REVIEWED** Human Toxicity Excerpts: /HUMAN EXPOSURE STUDIES/ ...Teacher aides who worked at or near spirit duplicators that used a 99% methanol duplicator fluid /were studied/. The exposures ranged from 1 hr/day for 1 day/wk to 8 hr/day for 5 days/wk and had occurred for 3 years. Since the introduction of the equipment, the aides began to experience headaches, dizziness and eye irritation, blurred vision and nausea/upset stomach while working near the machines. Fifteen-minute breathing zone samples near 21 operating machines contained between 475 and 4000 mg/cu m of methanol vapor. Fifteen of these samples exceeded the NIOSH recommended 15-min standard of 1050 mg/cu m (800 ppm). The aides were also exposed while collating and stapling papers impregnated with the fluid up to 3 hr earlier and these exposures ranged from 235-1140 mg/cu m . The results suggested that chronic effects may occur when methanol concentrations exceed the threshold limit value (TLV) of 260 mg/cu m (200 ppm). The effects reported in the study ... were similar in nature but appeared less severe than those reported from acute poisoning by methanol [WHO; Environ Health Criteria 196: Methanol p.111 (1997). Available from: as of July 19, 2005. ]**PEER REVIEWED** FORMALDEHYDE CASRN: 50-00-0 Human Health Effects: Evidence for Carcinogenicity: CLASSIFICATION: B1; probable human carcinogen. BASIS FOR CLASSIFICATION: Based on limited evidence in humans, and sufficient evidence in animals. Human data include nine studies that show statistically significant associations between site-specific respiratory neoplasms and exposure to formaldehyde or formaldehyde-containing products. An increased incidence of nasal squamous cell carcinomas as observed in long-term inhalation studies in rats and in mice. The classification is supported by in vitro genotoxicity data and formaldehyde's structural relationships to other carcinogenic aldehydes such as acetaldehyde. HUMAN CARCINOGENICITY DATA: Limited. ANIMAL CARCINOGENICITY DATA: Sufficient. [U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Formaldehyde (50-00-0) Available from: on the Substance File List as of March 15, 2000]**PEER REVIEWED** ... SYMPTOMATOLOGY: A. Inhalation: 1. Irritation of mucous membranes, especially of eyes, nose & upper respiratory tract. 2. With higher concn, cough, dysphagia, bronchitis, pneumonia, edema or spasm of the larynx. Pulmonary edema is uncommon. B. Ingestion. 1. Immediate intense pain in mouth, pharynx & stomach. 2. Nausea, vomiting, hematemesis, abdominal pain & occasionally diarrhea (which may be bloody). 3. Pale, clammy skin & other signs of shock. 4. Difficult micturition, hematuria, anuria. 5. Vertigo, convulsions, stupor, & coma. 6. Death due to respiratory failure. C. Skin contact: 1. Irritation & hardening of skin. Strong solutions produce coagulation necrosis. 2. Dermatitis & hypersensitivity from prolonged or repeated exposure. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-197] **PEER REVIEWED** . . . The effect of formaldehyde exposure on medical students conducting dissections in the gross anatomy laboratory course /was evaluated using/ self-administered questionnaires designed to assess the frequency of occurrence of various symptoms indicating the acute effects of formaldehyde exposure. The questionnaires were given to a cohort of 1st-yr medical students on completion of the gross anatomy lab course. Air sampling of formaldehyde levels in the anatomy labs was carried out on one day during the time in which these students were conducting dissections. ... Although the results of the air sampling showed formaldehyde levels to be well below current occupational standards, significant numbers of students reported experiencing symptoms associated with formaldehyde exposure. Estimates of the relative risk of experiencing formaldehyde-related symptoms in the anatomy laboratories compared to the control laboratories ranged from 2.0-19.0, depending on the particular symptom. In addn, it was found that female students were 3 times more likely to report formaldehyde-related symptoms than male students. [Fleischer JM; NY J Med 87 (7): 385-8 (1987)] **PEER REVIEWED** . . . Symptoms: Local: Conjunctivitis, corneal burns; brownish discoloration of skin; dermatitis, urticaria (hives), pustulovesicular eruption. Inhalation: rhinitis & anosmia (loss of sense of smell); pharyngitis, laryngospasm; tracheitis & bronchitis; pulmonary edema, cough, constriction in chest; dypsnea (difficult breathing), headache, weakness, palpitation (rapid heart beat), gastro enteritis (inflammation of the stomach & intestines). Ingestion: Burning in mouth & esophagus; nausea & vomiting; abdominal pain, diarrhea, vertigo (dizziness), unconsciousness, jaundice, albuminuria, hematuria, anuria, acidosis, convulsions. [ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988., p. 249] **PEER REVIEWED** . . . Four groups of patients with long-term inhalation exposure to formaldehyde were compared with controls who had short-term periodic exposure to formaldehyde. The following were determined for all groups: total white cell, lymphocyte, and T cell counts; helper/suppressor ratios; total Ta1+, IL2+, and B cell counts; antibodies to formaldehyde-human serum albumin conjugate and autoantibodies. When compared with the controls, the patients had significantly higer antibody titers to formaldehyde-human serum albumin. In addition, significant increases in Ta1+, IL2+, and B cells and autoantibodies were observed. Immune activation, autoantibodies, and anti formaldehyde-human erum albumin antibodies are associated with long-term formaldehyde inhalation. [Thrasher JD et al; Arch Environ Health 45 (4): 217-23 (1990)] **PEER REVIEWED** [ formaldehyde toxicity: Thrasher & Kilburn: Shaham: EPA: Gold: Wilson: CIIN: Murray 2002.12.12 rmforall Thrasher (2001): "The major difference is that the Japanese demonstrated the incorporation of FA and its metabolites into the placenta and fetus. The quantity of radioactivity remaining in maternal and fetal tissues at 48 hours was 26.9% of the administered dose." [ Ref. 14-16 ] Arch Environ Health 2001 Jul-Aug; 56(4): 300-11. Embryo toxicity and teratogenicity of formaldehyde. [100 references] Thrasher JD, Kilburn KH. Sam-1 Trust, Alto, New Mexico, USA. full text full text Jack Dwayne Thrasher, Alan Broughton, Roberta Madison. Immune activation and autoantibodies in humans with long-term inhalation exposure to formaldehyde. Archives of Environmental Health. 1990; 45: 217-223. PMID: 2400243 ] ... measured the formation of DNA-protein cross links in peripheral white blood cells of occupationally exposed workers (n=12) & unexposed controls (n=8). The avg length of ... exposure was 13 yr. ... Venous blood samples were collected ... . Personal & room concn of formaldehyde were collected at various periods during the working day among the exposed subjects, with formaldehyde room concn ranging from 1.38-1.6 ppm. Personal monitoring devices indicated formaldehyde concn of 2.8-3.1 ppm during peak work & an avg concn of 1.46 ppm at times when work was usually completed. Exposure to formaldehyde resulted in a significant incr in the incidence of DNA-protein cross links. Mean ... incidences in exposed & nonexposed workers were 28 + or - 6 & 22 + or - 6%, respectively. Within the exposed workers group, technicians had significantly greater levels of DNA-protein cross links than physicians (32.3 + or - 4.3 & 26.3 + or - 4.4%, respectively). A linear relationship between yr of exposure & DNA-protein cross links formation was also detected. When the data were analyzed considering worker smoking habits, DNA-protein cross links was consistently elevated among formaldehyde-exposed versus corresponding controls (p=0.03). [DHHS/ATSDR; Toxicological Profile for Formaldehyde p. 86 (1999)] **PEER REVIEWED** . . . No biologic monitoring techniques exist at present, either for the reliable determineation of formaldehyde levels in tissue or for the determination of formaldehyde adducts formed with macromolecules. Techniques are under development for nonspecific monitoring of exposure through periodic assessment of chromosome damage (micronucleus formation or sister chromatid exchange frequency) in workers exposed to formaldehyde. [Rom, W.N. (ed.). Environmental and Occupational Medicine. 2nd ed. Boston, MA: Little, Brown and Company, 1992., p. 868] **PEER REVIEWED** . . . The assessment of formaldehyde exposure can be accomplished through measurement of the metabolite formic acid. Formic acid is also an endogenously produced substance formed by the degradation of glycine. There was no information in the literature that showed a correlation between urinary formic acid levels & formaldehyde exposure levels. This measurement is also a poor indicator of the extent of formaldehyde absorption, due to the high endogenous levels of formic acid. Urine Reference Ranges: Normal-normal population level: 21 mg/l (endogenously produced formic acid); Exposed- not established; Toxic- not established. [Ryan, R.P., C.E. Terry, S.S. Leffingwell (eds.) Toxicology Desk Reference 5th ed. Volumes 1-2. Taylor & Francis Philadelphia, PA. 2000, p. 714] **PEER REVIEWED** . . . Release of /formaldehyde/ vapors in mobile homes has been associated with headache & pulmonary & dermal irritation. /Occupants of mobile homes are possibly exposed/. [Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1214] **PEER REVIEWED** . . . Smokers and persons who live in a home with a cigarette smoker also may be exposed to higher levels of formaldehyde. Environmental tobacco smoke, which is a combination of diluted sidestream smoke released form a cigarette's burning end and mainstream smoke exhaled by an active smoker, can contribute 10-25% (0.1-1 mg/day) of the total average indoor exposure to formadehyde ... . [DHHS/ATSDR; Toxicological Profile for Formaldehye p. 311 (1999)] [ faults in 1999 July EPA 468-page formaldehyde profile: Elzbieta Skrzydlewska PhD, Assc. Prof., Medical U. of Bialystok, Poland, abstracts -- ethanol, methanol, formaldehyde, formic acid, acetaldehyde, lipid peroxidation, green tea, aging, Lyme disease: Murray 2004.08.08 ] **PEER REVIEWED** . . . Cigarette smoke and products of combustion contain formaldehyde(1). Cigarette smoke contains 15 to 20 mg formaldehyde per cigarette(1). Avg formaldehyde exposure from passive smoking is between 0.23 to 0.27 ppm(1). A 'pack-a-day' smoker may inhale as much as 0.4-2.0 mg formaldehyde(1). [ See below for Federal Drinking Water Guidelines: EPA 1000 ug/l [ 1.0 mg/l gives 2 mg for daily 2 l drinking water ]] [(1) Bingham E et al, eds; Patty's Toxicology. 5th ed. NY, NY: John Wiley & Sons Inc. 5: 980-3 (2001)] **PEER REVIEWED** Food Survey Values: Formaldehyde occurs naturally in foods, and foods may be contaminated as a result of fumigation (of e.g. grain), cooking (as a combustion product) and release from formaldehyde resin-based tableware(1). It has been used as a bacteriostatic agent in some foods, such as cheese(1). Fruits and vegetables typically contain 3-60 mg/kg, and meat and fish, 6-20 mg/kg(1). [(1) IARC; Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva, Switzerland: WHO 62: 243 (1995)]**PEER REVIEWED** Federal Drinking Water Guidelines: EPA 1000 ug/l [ 1.0 mg/l gives 2 mg for daily 2 l drinking water ] [USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines (11/93), p. ]**QC REVIEWED** FORMIC ACID CASRN: 64-18-6 Human Health Effects: Human Toxicity Excerpts: /HUMAN EXPOSURE STUDIES/ ...Workers exposed to formic /acid/ ... in a textile plant complained of nausea. Air tests in the area revealed concentrations ... averaging 15 ppm. [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 279]**PEER REVIEWED** . . . SIGNS AND SYMPTOMS/ Formic acid produced by bees, wasps, and ants will cause tissue irritation upon contact or injection. [Doull, J., C.D. Klaassen, and M. D. Amdur (eds.). Casarett and Doull's Toxicology. 2nd ed. New York: Macmillan Publishing Co., 1980., p. 558]**PEER REVIEWED** . . . /CASE REPORTS/ In a human case of formaldehyde poisoning, toxic concentrations of formate (7-8 mm) were detected within 30 min of ingestion, confirming rapid metabolism of formaldehyde to formate in humans. [WHO; Environ Health Criteria 196: Methanol p.62 (1997). Available from: as of July 14, 2005. ]**PEER REVIEWED** /CASE REPORTS/ Two patients were studied who presented with methanol poisoning. Formate accumulation was marked with initial blood levels ranging from 11.1-26.0 meq/L. Decrease in blood bicarbonate concentration of similar magnitude coincided with the increase in formate accumulation. Accumulation of formic acid thus plays a major part in the acidosis observed in human subjects poisoned with methanol. [McMartin KE et al; Am J Med 68 (3): 414-8 (1980) ] **PEER REVIEWED** . . . /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Sprague-Dawley rat embryo cultures (9th day of gestation) were treated with sodium formate or formic acid at concentrations of 200, 400, 800, 1200, 1600, 2000 ug/mL (sodium formate) or 140, 270, 540, 810, 1080 ug/mL (formic acid). The pH of the medium was no longer corrected after addition of the test substance. Both after 24- and after 48-h incubation with sodium formate, there was a significant and concentration-dependent reduction of the developmental parameters yolk sac diameter (YSD), crown-rump length (CRL), head length (HL), somite number (SN) and developmental score (DEVSC). Embryolethality was significantly increased only in the highest concentration after 48-h incubation. The number of anomalies (mainly CNS: open anterior and posterior neuropores and erratic neurorrhaphy) was significantly increased at 1.6 and 2.0 mg/mL after 24 h and at 0.8 and 2.0 mg/mL after 48-h incubation. The protein and DNA levels showed a significant and concentration-dependent reduction. Incubations with formic acid also showed a significant and concentration-dependent reduction of YSD, CRL, HL, SN and DEVSC after 24-h incubation and of CRL, HL, SOM and DEVSC after 48 h. Embryolethality was significantly increased in the highest concentration after 24 h and in the two highest concentrations after 48 h. Protein and DNA concentrations showed significant and concentration dependent decreases in both cases. The number of anomalies (open anterior and posterior neuropores, rotatory defects and enlarged maxillary process) showed a significant increase only at 0.81 mg/mL after 48-h incubation. To sum up, concentration-dependent embryotoxic and dysmorphic changes were detected in the culture both using formate and formic acid in this test system. [EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) Challenge Program's Robust Summaries and Test Plans. Available from: on Formates (December 2001) as of July 12, 2005. ] **PEER REVIEWED** Food Survey Values: Formic acid is a natural constituent of some fruits, nuts, and dairy products(1). Fruit wine, desert wine, and brandies contain formic acid(2). Formic acid concns in wine and brandies produced from apples, pears, plums, and apricots ranged from 2.7-87 mg/L(2). Formic acid has been identified as a meat volatile(3). [(1) Bingham E et al, eds; Patty's Industrial Hygiene and Toxicology 5th ed, NY, NY: John Wiley Sons. 5: 693 (2001) (2) Sponholz WR et al; Deutche-Lebensmittel-Rundshaw 85: 247-51 (1989) (3) Shahidi F et al; CRC Crit Rev Food Sci Nature 24: 141-243 (1986) ] **PEER REVIEWED** . . . Indirect food substance additives affirmed as generally recognized as safe. (a) Formic acid (CH2O2, CAS Reg. No. 64?18?6) is also referred to as methanoic acid or hydrogen carboxylic acid. It occurs naturally in some insects and is contained in the free acid state in a number of plants. Formic acid is prepared by the reaction of sodium formate with sulfuric acid and is isolated by distillation. (b) Formic acid is used as a constituent of paper and paperboard used for food packaging. (c) The ingredient is used at levels not to exceed good manufacturing practice in accordance with ?186.1(b)(1). (d) Prior sanctions for formic acid different from the uses established in this section do not exist or have been waived. [21 CFR 186.1316; U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from: as of June 1, 2005 ] **PEER REVIEWED** State Drinking Water Guidelines: (FL) FLORIDA 14,000 ug/L [ 14.0 mg/L gives 28 mg in 2 L daily drinking water ] [USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines (11/93), p. ]**PEER REVIEWED** ******************************************************* hangover research relevant to toxicity of 11% methanol in aspartame (formaldehyde, formic acid): Calder I (full text): Jones AW: Murray 2004.08.05 rmforall Since no adaquate data has ever been published on the exact disposition of toxic metabolites in specific tissues in humans of the 11% methanol component of aspartame, the many studies on morning-after hangover from the methanol impurity in alcohol drinks are the main available resource to date. Jones AW (1987) found next-morning hangover from red wine with 100 to 150 mg methanol (9.5% w/v ethanol, 100 mg/l methanol, 0.01%, one part in ten thousand). Pharmacol Toxicol. 1987 Mar; 60(3): 217-20. Elimination half-life of methanol during hangover. Jones AW. Department of Forensic Toxicology, University Hospital, SE-581 85 Linkoping, Sweden. This paper reports the elimination half-life of methanol in human volunteers. Experiments were made during the morning after the subjects had consumed 1000-1500 ml red wine (9.5% w/v ethanol, 100 mg/l methanol) the previous evening. [ 100 to 150 mg methanol ] The washout of methanol from the body coincided with the onset of hangover. The concentrations of ethanol and methanol in blood were determined indirectly by analysis of end-expired alveolar air. In the morning when blood-ethanol dropped below the Km of liver alcohol dehydrogenase (ADH) of about 100 mg/l (2.2 mM), the disappearance half-life of ethanol was 21, 22, 18 and 15 min. in 4 test subjects respectively. The corresponding elimination half-lives of methanol were 213, 110, 133 and 142 min. in these same individuals. The experimental design outlined in this paper can be used to obtain useful data on elimination kinetics of methanol in human volunteers without undue ethical limitations. Circumstantial evidence is presented to link methanol or its toxic metabolic products, formaldehyde and formic acid, with the pathogenesis of hangover. PMID: 3588516 methanol products (formaldehyde and formic acid) are main cause of alcohol hangover symptoms [same as from similar amounts of methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec: Murray 2006.01.20 Addict Biol. 2005 Dec;10(4): 351-5. Concentration changes of methanol in blood samples during an experimentally induced alcohol hangover state. Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ. Chuncheon National Hospital, Department of Psychiatry, The Catholic University of Korea, Seoul, Korea. Songsin Campus: 02-740-9714 Songsim Campus: 02-2164-4116 Songeui Campus: 02-2164-4114 eight hospitals [ Han-Kyu Lee ] A hangover is characterized by the unpleasant physical and mental symptoms that occur between 8 and 16 hours after drinking alcohol. After inducing experimental hangover in normal individuals, we measured the methanol concentration prior to and after alcohol consumption and we assessed the association between the hangover condition and the blood methanol level. A total of 18 normal adult males participated in this study. They did not have any previous histories of psychiatric or medical disorders. The blood ethanol concentration prior to the alcohol intake (2.26+/-2.08) was not significantly different from that 13 hours after the alcohol consumption (3.12+/-2.38). However, the difference of methanol concentration between the day of experiment (prior to the alcohol intake) and the next day (13 hours after the alcohol intake) was significant (2.62+/-1.33/l vs. 3.88+/-2.10/l, respectively). [ So, the normal methanol level was 2.62 mg per liter, and increasing that by 50% = 1.3 mg per liter to 3.88 mg per liter caused hangover symptoms. The human body has about 5.6 liters blood, so adding 1.3 mg per liter gives an estimate of 7.3 mg added methanol, as much as 4 oz diet soda. Diet soda is about 200 mg aspartame per 12 oz can, which is 22 mg (11% methanol), 1.83 mg methnol per ounce. This suggests that alcohol drinkers are more sensitive to methanol than the average diet soda drinker, some of whom find symptoms from a third of a diet soda.] A significant positive correlation was observed between the changes of blood methanol concentration and hangover subjective scale score increment when covarying for the changes of blood ethanol level (r=0.498, p<0.05). This result suggests the possible correlation of methanol as well as its toxic metabolite to hangover. PMID: 16318957 [ The "toxic metabolite" of methanol is formaldehyde, which in turn partially becomes formic acid -- both potent cumulative toxins that are the actual cause of the toxicity of methanol.] Aspartame: Methanol and the Public Interest 1984: Monte: Murray 2002.09.23 Humans suffer "toxic syndrome" (54) at a minimum lethal dose of <1 gm/kg, much less than that of monkeys, 3-6 g/kg (42, 59). The minimum lethal dose of methanol in the rat, rabbit, and dog is 9.5, 7.0 , and 8.0 g/kg, respectively (43); ethyl alcohol is more toxic than methanol to these test animals (43)." As a medical layman, I suggest that evidence mandates immediate exploration of the role of these ubiquitious, potent formaldehyde sources as co-factors in epidemiology, research, diagnosis, and treatment in a wide variety of disorders. Folic acid, from fruits and vegetables, plays a role by powerfully protecting against methanol (formaldehyde) toxicity. Many common drugs, such as aspirin, interfere with folic acid, as do some mutations in relevant enzymes. The majority of aspartame reactors are female. European Food Safety Authority to decide aspartame safety by May: caffeine diet drinks cause female hypertension, WC Winkelmayer et al, JAMA 2005.11.09: PubMed lists 50 items for "diet soft drinks" since 2004 Oct.: Murray 2006.01.24 all three aspartame metabolites harm human erythrocyte [red blood cell] membrane enzyme activity, KH Schulpis et al, two studies in 2005, Athens, Greece, 2005.12.14: 2004 research review, RL Blaylock: Murray 2006.01.14 aspartame (aspartic acid, phenylalanine) binding to DNA: Karikas July 1998: Murray 2003.01.05 rmforall Karikas GA, Schulpis KH, Reclos GJ, Kokotos G Measurement of molecular interaction of aspartame and its metabolites with DNA. Clin Biochem 1998 Jul; 31(5): 405-7. Dept. of Chemistry, University of Athens, Greece; K.H. Schulpis; G.J. Reclos; combining aspartame and quinoline yellow, or MSG and brilliant blue, harms nerve cells, eminent C. Vyvyan Howard et al, 2005, Felicity Lawrence: Murray 2005.12.21 aspartame or MSG affects circadian rhythms in rats, two studies, P. Subramanian, T. Manivasagam et al 2004: Murray 2006.04.27 aspartame puts formaldehyde adducts into tissues, Part 1/2 full text Trocho & Alemany 1998.06.26 Universitat Autònoma de Barcelona : Murray 2002.12.22 PubMed abstract: aspartame (methanol becoming formaldehyde) causes many cancers in rats, Ramazzini Foundation, M Soffritti et al: Murray 2006.03.06 free full text Environ Health Perspect. 2006 Mar; 114(3): 379-85. First experimental demonstration of the multipotential carcinogenic effects of aspartame administered in the feed to sprague-dawley rats. Soffritti M, Belpoggi F, Esposti DD, Lambertini L, Tibaldi E, Rigano A. Cesare Maltoni Cancer Research Center, European Ramazzini Foundation of Oncology and Environmental Sciences, Bologna, Italy. The Cesare Maltoni Cancer Research Center of the European Ramazzini Foundation has conducted a long-term bioassay on aspartame (APM), a widely used artificial sweetener. APM was administered with feed to 8-week-old Sprague-Dawley rats (100-150/sex/group), at concentrations of 100,000, 50,000, 10,000, 2,000, 400, 80, or 0 ppm. The treatment lasted until natural death, at which time all deceased animals underwent complete necropsy. Histopathologic evaluation of all pathologic lesions and of all organs and tissues collected was routinely performed on each animal of all experimental groups. The results of the study show for the first time that APM, in our experimental conditions, causes a) an increased incidence of malignant-tumor-bearing animals with a positive significant trend in males (p 0.05) and in females (p 0.01), in particular those females treated at 50,000 ppm (p 0.01); b) an increase in lymphomas and leukemias with a positive significant trend in both males (p 0.05) and females (p 0.01), in particular in females treated at doses of 100,000 (p 0.01), 50,000 (p 0.01), 10,000 (p 0.05), 2,000 (p 0.05), or 400 ppm (p 0.01); c) a statistically significant increased incidence, with a positive significant trend (p 0.01), of transitional cell carcinomas of the renal pelvis and ureter and their precursors (dysplasias) in females treated at 100,000 (p 0.01), 50,000 (p 0.01), 10,000 (p 0.01), 2,000 (p 0.05), or 400 ppm (p 0.05); and d) an increased incidence of malignant schwannomas of peripheral nerves with a positive trend (p 0.05) in males. The results of this mega-experiment indicate that APM is a multipotential carcinogenic agent, even at a daily dose of 20 mg/kg body weight, much less than the current acceptable daily intake. [ 50 mg/kg bw ] On the basis of these results, a reevaluation of the present guidelines on the use and consumption of APM is urgent and cannot be delayed. Key words: artificial sweetener, aspartame, carcinogenicity, lymphomas, malignant schwannomas, rats, renal pelvis carcinomas. PMID: 16507461 Feb 24 2006 04:49:50 Address correspondence to M. Soffritti, Cesare Maltoni Cancer Research Center, European Ramazzini Foundation of Oncology and Environmental Sciences, Castello di Bentivoglio, Via Saliceto, 3, 40010 Bentivoglio, Bologna, Italy. 39-051-6640460 Fax: 39-051-6640223 We thank the U.S. National Toxicology Program for convening a group of pathologists at the National Institute of Environmental Health Sciences to provide a second opinion for a set of malignant lesions and their precursors related to aspartame treatment, and for their help in statistical analysis. We also thank all of the staff involved in the project. This research was supported by the European Ramazzini Foundation of Oncology and Environmental Sciences. The authors declare they have no competing financial interests. Received 3 October 2005; accepted 16 November 2005. [ transcribed to plain text ] Table 1. Beverages and diet products studied at the CMCRC/ERF: status of studies. Study---------------------------No. of bioassays ---Products-------------------------Species---------No. Study status 1 Water in polyvinyl chloride bottles---------2 rat a--------------2,200 P b 2 Coca-Cola---------------------4 rat a--------------1,999 RP 3 Pepsi Cola----------------------1 rat-----------------400 E 4 Ethyl alcohol--------------------4 rat, mouse a------1,458 P c 5 Sucrose-------------------------1 rat-----------------400 E 6 Aspartame (APM)--------------6 rat, mouse a------4,460 BO, PP d 7 Sucralose (Splenda)-------------1 mouse *-----------760 BO 8 Caffeine-------------------------1 rat-----------------800 E 9 Vitamin A-----------------------5 rat----------------5,100 E 10 Vitamin C----------------------5 rat----------------3,680 E 11 Vitamin E----------------------5 rat----------------3,680 E 12 Feed sterilized by--------------1 rat a---------------2,000 E gamma radiation Total-----------------------------36-------------------26,937 Abbreviations: BO, biophase ongoing E, in elaboration P, published PP, partially published RP, ready for publication a, treatment started from embryonic life b, data from Maltoni et al. (1997) c, data from Soffritti et al. (2002a) d, data from Soffritti et al. (2005). *, data from Soffritti et al. (1992) Investigations into the metabolism of APM have shown that, in rodents, nonhuman primates, and humans, it is metabolized in the gastrointestinal tract into three constituents -- aspartic acid, phenylalanine, and methanol -- which are absorbed into the systemic circulation (Ranney et al. 1976). For each molecule of APM, one molecule of each constituent is produced. After absorption, they are then used, metabolized, and/or excreted by the body following the same metabolic pathways as when consumed through the ordinary diet: aspartate is transformed into alanine plus oxaloacetate (Stegink 1984); phenylalanine is transformed mainly into tyrosine and, to a smaller extent, phenylethylamine and phenylpyruvate (Harper 1984); and methanol is transformed into formaldehyde and then to formic acid (Opperman 1984). ******************************************************* Morando Soffritti 1, Fiorella Belpoggi 1, Davide Degli Esposti 1, Luca Lambertini 1, Eva Tibaldi 1, and Anna Rigano 1 1 Cesare Maltoni Cancer Research Center, European Ramazzini Foundation of Oncology and Environmental Sciences, Bologna, Italy Address of the institution: Cesare Maltoni Cancer Research Center, European Ramazzini Foundation of Oncology and Environmental Sciences. Castello di Bentivoglio, Via Saliceto, 3, 40010 Bentivoglio, Bologna, Italy +39/051/6640460 Fax +39/051/6640223 Address correspondence to Dr. M. Soffritti, M.D., Scientific Director of the Cesare Maltoni Cancer Research Center, European Ramazzini Foundation of Oncology and Environmental Sciences. Castello di Bentivoglio, Via Saliceto, 3, 40010 Bentivoglio, Bologna, Italy +39/051/6640460 Fax +39/051/6640223 Acknowledgements: A special thanks to the US National Toxicology Program (NTP) for convening a group of pathologists at NIEHS in order to provide a second opinion for a set of lesions of malignancies and their precursors related to the APM treatment, and for the help in statistical analysis. aspartame causes cancer in rats at levels approved for humans, Morando Soffritti et al, Ramazzini Foundation, Italy & National Toxicology Program of National Institute of Environmental Health Sciences 2005.11.17 Env. Health Pers. 35 pages: Murray USA National Institutes of Health National Toxicology Program aids eminent Ramazzini Foundation, Bologna, Italy, in more results on cancers in rats from lifetime low levels of aspartame (methanol, formaldehyde), Felicity Lawrence, Murray 2005.09.30 aspartame induces lymphomas and leukaemias in rats, full plain text, M Soffritti, F Belpoggi, DD Esposti, L Lambertini: Ramazzini Foundation study 2005.07.14: main results agree with their previous methanol and formaldehyde studies: Murray 2005.09.03 Michael F Jacobson of CSPI now and in 1985 re aspartame toxicity, letter to FDA Commissioner Lester Crawford; California OEHHA aspartame critique 2004.03.12; Center for Consumer Freedom denounces CSPI: Murray 2005.07.27 President Bush & formaldehyde (aspartame) toxicity: Ramazzini Foundation carcinogenicity results Dec 2002: Soffritti: Murray 2003.08.03 rmforall p. 88 "The sweetening agent aspartame hydrolyzes in the gastrointestinal tract to become free methyl alcohol, which is metabolized in the liver to formaldehyde, formic acid, and CO2. (11)" Medinsky MA & Dorman DC. 1994; Assessing risks of low-level methanol exposure. CIIT Act. 14: 1-7. Ann N Y Acad Sci. 2002 Dec; 982: 87-105. Results of long-term experimental studies on the carcinogenicity of formaldehyde and acetaldehyde in rats. Soffritti M, Belpoggi F, Lambertin L, Lauriola M, Padovani M, Maltoni C. Cancer Research Center, European Ramazzini Foundation for Oncology and Environmental Sciences, Bologna, Italy. Formaldehyde was administered for 104 weeks in drinking water supplied ad libitum at concentrations of 1500, 1000, 500, 100, 50, 10, or 0 mg/L to groups of 50 male and 50 female Sprague-Dawley rats beginning at seven weeks of age. Control animals (100 males and 100 females) received tap water only. Acetaldehyde was administered to 50 male and 50 female Sprague-Dawley rats beginning at six weeks of age at concentrations of 2,500, 1,500, 500, 250, 50, or 0 mg/L. Animals were kept under observation until spontaneous death. Formaldehyde and acetaldehyde were found to produce an increase in total malignant tumors in the treated groups and showed specific carcinogenic effects on various organs and tissues. PMID: 12562630 Ann N Y Acad Sci. 2002 Dec; 982: 46-69. Results of long-term experimental studies on the carcinogenicity of methyl alcohol and ethyl alcohol in rats. Soffritti M, Belpoggi F, Cevolani D, Guarino M, Padovani M, Maltoni C. Cancer Research Center, European Ramazzini Foundation for Oncology and Environmental Sciences, Bologna, Italy. Methyl alcohol was administered in drinking water supplied ad libitum at doses of 20,000, 5,000, 500, or 0 ppm to groups of male and female Sprague-Dawley rats 8 weeks old at the start of the experiment. Animals were kept under observation until spontaneous death. Ethyl alcohol was administered by ingestion in drinking water at a concentration of 10% or 0% supplied ad libitum to groups of male and female Sprague-Dawley rats; breeders and offspring were included in the experiment. Treatment started at 39 weeks of age (breeders), 7 days before mating, or from embryo life (offspring) and lasted until their spontaneous death. Under tested experimental conditions, methyl alcohol and ethyl alcohol were demonstrated to be carcinogenic for various organs and tissues. They must also be considered multipotential carcinogenic agents. In addition to causing other tumors, ethyl alcohol induced malignant tumors of the oral cavity, tongue, and lips. These sites have been shown to be target organs in man by epidemiologic studies. Publication Types: Review Review, Tutorial PMID: 12562628 ******************************************************* The Comet assay can quickly show whether aspartame or its body products (methanol, formaldehyde, formic acid -- the same as in hangovers from dark wines and liquors) are genotoxic: Murray 2006.05.09 Comet assay finds DNA damage from sucralose, cyclamate, saccharin, aspartame in mice: Sasaki YF & Tsuda S Aug 2002: Murray 2006.05.08 [ Borderline evidence, in this pilot study of 39 food additives, using test groups of 4 mice, for DNA damage from for stomach, colon, liver, bladder, and lung 3 hr after oral dose of 2000 mg/kg aspartame -- a very high dose. Methanol is the only component of aspartame that can lead to DNA damage. ] 24 recent formaldehyde toxicity [Comet assay] reports: Murray 2002.12.31 genotoxins, Comet assay in mice: Ace-K, stevia fine; aspartame poor; sucralose, cyclamate, saccharin bad: Y.F. Sasaki Aug 2002: Murray 2003.01.27 [A detailed look at the data] ] ******************************************************* EFSA, European Food Safety Authority says Ramazzini aspartame cancer study is flawed, while Soffritti is half way through second huge study, Felicity Lawrence, Murray 2006.05.15 Obfuscation of the iatrogenic autism epidemic re mercury in kid vaccines, Kenneth P. Stoller, Pediatrics 2006.05.06; aspartame toxicity 2005.11.10: Comet assay can test genotoxicity, EFSA admits ignorance re methanol residues, Murray 2006.05.10 Morando Soffritti of Ramazzini Foundation rebuts EFSA AFC critique, Murray 2006.05.05 European Food Safety Authority discounts Ramazzini study re many cancers in 1800 rats fed lifetime doses of aspartame: Calorie Control Council press release: Murray 2006.05.05 Aspartame: The healthy option? Richard A. Lovett, The New Scientist 2006.05.04: Murray 2006.05.08 safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF: Murray 2003.01.12 rmforall EU Scientific Committee on Food, a whitewash Mark Gold exhaustively critiques European Commission Scientific Committee on Food re aspartame ( 2002.12.04 ): 59 pages, 230 references *******************************************************