Posted: 29 June 2010
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 2010.06.27
64 KB truncated version 2010.06.27
Sunday, June 27, 2010 full text
205 KB full text
Herein I offer abstracts and three full texts of dozens of studies by a world-class biochemist and her associates, mostly experiments with rats, on ethanol toxicity since 1984 and methanol toxicity since 1993. Enough details are provided to show the competency and credibility of E. Skrzydlewska and her colleagues over two decades, and to make access to their literature more convenient for professionals.
For instance, anyone can click on this post at the above URL, and in Outlook Express, use Control F to search the text for any word. Yahoo Groups also includes a fine search function.
A conscientious, responsible review of any reseach that affects the interests of vast commercial vested interests has to provide justified criticism of dubious studies, reviews, and conclusions, that are characteristically the main sources for private and professional information. My experience since I first started investigating toxicity issues in 1999 is, count on it, wolves guard the sheep.
To be effective, this criticism has to be calm, civil, detailed, specific, reasonable, founded on evidence, focused on issues and not on persons, and based on easily accessed public sources, so that anyone interested in basing their conclusions on facts can start the laborous process of deciding for themselves.
25 rules of disinformation , Sweeney 1997: Murray 2001.07.04 rmforall
As a medical layman, age 68, after two decades as a home health care giver, my volunteer public service for toxicity issues on the Net since January 1999 depends entirely on earning credibility by deserving it.
146 members, 1,607 posts in a public searchable archive
I regret that I almost never receive negative feedback based on any specifics of this work, for this would enable me, in the finest tradition of science, to either reverse, amend, or clarify my positions, to the benefit of humanity, as well as deepening my own satisfaction and confidence in a long-term effort.
However, it is indubitable that the best disinformation strategy is to simply ignore any inconvenient researchers and their work, or, if that becomes problematic due to the quality of the worker and his work, to firmly repeat the exact opposite of truth, for example, "Aspartame is the most tested food additive in history," while using ad hominen statements to dismiss, ridicule, and marginalize the opposition. Fanning a "flame war" of escalating incivility is a virtually infallible strategy for muddying the waters, preventing any real examination of actual facts.
I should also here assert that, so far, I have not ever received a penny of support for my toxicity service, save for about $ 300 of free books, from both sides of the debate. Furthermore, when the happy day ensues when I receive payment of any sort, I will immediately and forever make this clearly and completely known on the Net, along with full details for contacting the sources, who must agree to respond responsibly, immediately, and publicly to all inquiries. All my financial information about this work will be immediately, clearly, and forever public. I cannot be bought, bent, or borrowed. I don't deal in secret.
A persistent, consistent campaign that provides facts about an actual toxin can only succeed.
Fact is, the 11% methanol component of aspartame, readily released into the G.I. tract, is within hours converted into potent amounts of formaldehyde and formic acid, in amounts scores of times higher than that allowed by the EPA for daily drinking water.
I have recently summarized mainstream evidence that the similar amounts of methanol impurity, about one part in ten thousand, in dark wines and liquors, are largely responsible for the famed "morning after" hangover:
Hangover research relevant to toxicity of 11% methanol in aspartame (formaldehyde, formic acid): Calder I (full text): Jones AW: Murray 2004.08.06 rmforall
Similar potent levels of methanol, and its inevitable products in the human
body, formaldehyde and formic acid, can also ensue from fermentation of
fruits by certain yeast and bacteria in the colon:
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. 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 -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
[Methanol has a blood half-life of about 2.5 hours, so after 13 hours, its blood level is reduced to about 3 %, which would be 12 to 42 mg for the whole body, if the degradation of pectin by bacteria in the GI tract is fast, while slower production of methanol from pectin would produce lower peak methanol levels.
The ADH enzyme does not start to convert methanol into formaldehyde until blood levels of ethanol have become very low -- then the resulting conversion of the residual methanol into formaldehyde in specific tissues is the main cause of "morning after" hangover symptoms.
High levels of folic acid protect many people from this toxic production of formaldehyde, but not for the brain or retina.]
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. [24 ml = 64 mg ethanol and 0.19 ml = 0.33 mg methanol] PMID: 8561283
These three potent dietary sources of methanol, formaldehyde, and formic acid, which impact many people, and cause the same symptoms in vulnerable and sensitized people, are ignored in the following prestigious, official source:
[Extract ] [My comments are in square brackets.]
[I saved this document as 4 plain text files of 250 to 289 KB each: http://health.groups.yahoo.com/group/aspartameNM/files]
TOXICOLOGICAL PROFILE FOR FORMALDEHYDE
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Public Health Service Agency for Toxic Substances and Disease Registry July 1999
[http://www.atsdr.cdc.gov firstname.lastname@example.org 888-42-ATSDR
404-498-0110 fax 404-498-0093
Agency for Toxic Substances and Disease Registry Division of Toxicology
1600 Clifton Road NE, Mailstop E-29 Atlanta, GA 30333
* Information line and technical assistance Phone: (800) 447-1544 Fax: (404) 639-6359
* To order toxicological profiles, contact
National Technical Information Service 5285 Port Royal Road Springfield
VA 22161 Phone: (800) 553-6847 or (703) 487-4650
The National Center for Environmental Health (NCEH) focuses on preventing or controlling disease, injury, and disability related to the interactions between people and their environment outside the workplace.
Contact: NCEH, Mailstop F-29, 4770 Buford Highway, NE, Atlanta, GA 30341-3724 . Phone: 770-488-7000 . FAX: 770-488-7015.
The National Institute for Occupational Safety and Health (NIOSH) conducts research on occupational diseases and injuries, responds to requests for assistance by investigating problems of health and safety in the workplace, recommends standards to the Occupational Safety and Health Administration (OSHA) and the Mine Safety and Health Administration (MSHA), and trains professionals in occupational safety and health.
Contact: NIOSH, 200 Independence Avenue, SW, Washington, DC 20201 . Phone: 513-533-8328 800-356-4674 or NIOSH Technical Information Branch, Robert A. Taft Laboratory, Mailstop C-19, 4676 Columbia Parkway, Cincinnati, OH 45226-1998 Phone: 800-35-NIOSH fax 513-533-8573
The National Institute of Environmental Health Sciences (NIEHS) is the principal federal agency for biomedical research on the effects of chemical, physical, and biologic environmental agents on human health and well-being.
Contact: NIEHS, PO Box 12233, 104 T.W. Alexander Drive, Research Triangle Park, NC 27709 Phone: 919-541-3212.
Office of Communications 919-541-3345 TTY 919-541-0731
The Association of Occupational and Environmental Clinics (AOEC) has developed a network of clinics in the United States to provide expertise in occupational and environmental issues. Contact: AOEC, 1010 Vermont Avenue, NW, #513, Washington, DC 20005 Phone: 202-347-4976 FAX: 202-347-4950 Web Page: http://www.aoec.org/ e-mail: AOEC@AOEC.ORG
AOEC Clinic Director: http://occ-envmed.mc.duke.edu/oem/aoec.htm
The American College of Occupational and Environmental Medicine (ACOEM) is an association of physicians and other health care providers specializing in the field of occupational and environmental medicine.
http://www.acoem.org http://www.acoem.org/feedback email contact Contact: ACOEM, 55 West Seegers Road, Arlington Heights, IL 60005 Phone: 847-818-1800 FAX: 847-818-9266.] FORMALDEHYDE page iii UPDATE STATEMENT
Toxicological profiles are revised and republished as necessary, but no less than once every three years. [I could not locate any more recent updates than July 1999 via Google.]
Sharon Wilbur, M.A. [Not a PhD level degree]
[Environmental Health Scientist]
ATSDR, Division of Toxicology, Atlanta, GA
M. Olivia Harris, M.A. [ Not a PhD level degree]
ATSDR, Division of Toxicology, Atlanta, GA
[Environmental Health Scientist
1600 Clifton Road NE, E29 Atlanta, GA 30333
P: 404-639-5091 F: 404-639-6315 email@example.com]
Peter R. McClure, Ph.D., DABT [Veterinarian]
Syracuse Research Corporation, North Syracuse, NY
[Syracuse Research Corporation Environmental Science Center
301 Plainfield Road Suite 350 Syracuse, New York 13212 (315) 452 8420 firstname.lastname@example.org ]
Wayne Spoo, DVM, DABT, DABVT [Veterinarian]
Research Triangle Institute, Research Triangle Park, NC
[Jerry Wayne Spoo Operations Director, Life Sciences and Toxicology 919-541-6000 email@example.com http://www.rti.org http://www.abvt.org
CPT Spoo, HHC, USACAPOC, AOCP-MS, 910-432-2209.
A peer review panel was assembled for formaldehyde. The panel consisted of the following members:
1. Carson Conaway, Research Scientist, American Health Foundation, Valhalla, New York 10595; [http://www.ahf.org/contact
1 Dana Road Valhalla, NY 10595
300 E. 42nd. Street New York, NY 10017
Carson Clifford Conaway, Ph. D., DABT [Veterinarian]
Research Scientist phone: (914) 789-7210 email: firstname.lastname@example.org
Institute for Cancer Prevention
In addition to his research work, Dr. Conaway is an Adjunct Associate Professor in the Department of Pharmacology, New York Medical College. In that capacity, he is called upon to present lectures in toxicology to graduate students in the College of Basic Medical Sciences and in the School of Public Health.
2. John Egle, Jr., Professor, Department of Pharmacology and Toxicology, Medical College of Virginia, Smith Bldg., Room 656, Richmond, VA 23219; and [http://www.medschool.vcu.edu John L. Egle, Jr no longer listed. Last PubMed study in 1995. Studies on formaldehyde, 2 in 1974, 1 in 1972, no PubMed abstracts for these.]
3. Vincent Garry, Director, Environmental Medicine, University of Minnesota, 421 29th Ave., SE Minneapolis, MN 55414.
Vincent F Garry Title: Professor
Department: Lab Medicine/Pathology (office: Lab Med/Pathology Department)
Dept Campus: UMN Twin Cities
E-mail Address: email@example.com
Office Address: Lab Med/Pathology Department
225 Mayo 8609 420 Delaware St SE Minneapolis, MN 55455
Campus Mail: Lab Medicine and Pathology
MMC 609 Mayo 8609 420 Delaware St SE Minneapolis, MN 55455
Office Phone:+1 612-626-3354 Fax:+1 612-626-3380
Address: 4829 Girard Ave So Minneapolis, MN 55409
Toxicol Appl Pharmacol. 2004 Jul 15; 198(2): 152-63.
Pesticides and children.
Department of Laboratory Medicine and Pathology and Program in Toxicology, University of Minnesota School of Medicine, Minneapolis, MN 55455, USA.
Prevention and control of damage to health, crops, and property by insects, fungi, and noxious weeds are the major goals of pesticide applications. As with use of any biologically active agent, pesticides have unwanted side-effects. In this review, we will examine the thesis that adverse pesticide effects are more likely to occur in children who are at special developmental and behavioral risk. Children's exposures to pesticides in the rural and urban settings and differences in their exposure patterns are discussed. The relative frequency of pesticide poisoning in children is examined. In this connection, most reported acute pesticide poisonings occur in children younger than age 5. The possible epidemiological relationships between parental pesticide use or exposure and the risk of adverse reproductive outcomes and childhood cancer are discussed. The level of consensus among these studies is examined. Current concerns regarding neurobehavioral toxicity and endocrine disruption in juxtaposition to the relative paucity of toxicant mechanism-based studies of children are explored. PMID: 15236951]
These experts collectively have knowledge of formaldehyde's physical and chemical properties, toxicokinetics, key health end points, mechanisms of action, human and animal exposure, and quantification of risk to humans.
All reviewers were selected in conformity with the conditions for peer review specified in Section 104(I)(13) of the Comprehensive Environmental Response, Compensation, and Liability Act, as amended.
Scientists from the Agency for Toxic Substances and Disease Registry (ATSDR) have reviewed the peer reviewers' comments and determined which comments will be included in the profile.
A listing of the peer reviewers' comments not incorporated in the profile, with a brief explanation of the rationale for their exclusion, exists as part of the administrative record for this compound. [Not easily accessible by public]
A list of databases reviewed and a list of unpublished documents cited are also included in the administrative record. [Not easily accessible by public]
The citation of the peer review panel should not be understood to imply its approval of the profile's final content. The responsibility for the content of this profile lies with the ATSDR.... [Apparently, the peer review panel's opinions carry little weight.]
1. PUBLIC HEALTH STATEMENT
This public health statement tells you about formaldehyde and the effects of exposure....
1.2 WHAT HAPPENS TO FORMALDEHYDE WHEN IT ENTERS THE ENVIRONMENT?
Most of the formaldehyde you are exposed to in the environment is in the air.... [A very misleading statement, as already pointed out above]
There is usually more formaldehyde present indoors than outdoors. [Ignores the issue of dietary sources]
Formaldehyde is released to the air from many home products and you may breath in formaldehyde while using these products.
Latex paint, fingernail hardener, and fingernail polish release a large amount of formaldehyde to the air. [Bound to be much less than the potent amounts in dietary sources, which have immediate strong effects on sensitive and sensitivized persons and other vulnerable groups]
Plywood and particle board, as well as furniture and cabinets made from them, fiberglass products, new carpets, decorative laminates, and some permanent press fabrics give off a moderate amount of formaldehyde. [This shows why new buildings, and especially mobile homes and RVs are toxic for many people.]
Some paper products, such as grocery bags and paper towels, give off small amounts of formaldehyde.
Because these products contain formaldehyde, you may also be exposed on the skin by touching or coming in direct contact with them.
You may also be exposed to small amounts of formaldehyde in the food you eat. [The amounts in dietary sources are the most potent sources for most people.]
You are not likely to be exposed to formaldehyde in the water you drink because it does not last a long time in water. [This ignores the fact that methanol, always turned into formaldehyde and formic acid in humans, does indeed last a very long time in water and dietary sources.]
Many other home products contain and give off formaldehyde although the amount has not been carefully measured. [Potent dietary sources have been systematically ignored for decades ]
These products include household cleaners, carpet cleaners, disinfectants, cosmetics, medicines, fabric softeners, glues, lacquers, and antiseptics. [Notice "cosmetics", "medicines", "disinfectants", "antiseptics" -- to this list of direct skin contact items, we can add hair care products, shoe leather, and some permanent press clothes.]
You may also breath formaldehyde if you use unvented gas or kerosene heaters indoors or if you or someone else smokes a cigar, cigarette, or pipe indoors.
The amount of formaldehyde in mobile homes is usually higher than it is in conventional homes because of their lower air turnover. [Evades the issue that particleboard and other materials common in mobile homes are strong formaldehyde sources, which this study showed caused symptoms and immune system signs:
http://www.drthrasher.org/formaldehyde_1990.html full text Jack Dwayne Thrasher, Alan Broughton, Roberta Madison. Immune activation and autoantibodies in humans with long-term inhalation exposure to formaldehyde. Archives of Environmental Health. 1990; 45: 217-223. "Immune activation, autoantibodies, and anti-HCHO-HSA antibodies are associated with long-term formaldehyde inhalation." PMID: 2400243 firstname.lastname@example.org]
People who work at or near chemical plants that make or use formaldehyde can be exposed to higher than normal amounts of formaldehyde.
Doctors, nurses, dentists, veterinarians, pathologists, embalmers, workers in the clothing industry or in furniture factories, and teachers and students who handle preserved specimens in laboratories also might be exposed to higher amounts of formaldehyde.
FORMALDEHYDE 4 1. PUBLIC HEALTH STATEMENT
Institute for Occupational Safety and Health (NIOSH) estimates that 1,329,332 individuals in the United States have had the potential for occupational exposure to formaldehyde. [Common sense suggests that health professionals who have been exposed to formaldehyde and have become sensitized and symptomatic naturally will have a prejudice against discovering the real extent of the danger.]
1.4 HOW CAN FORMALDEHYDE ENTER AND LEAVE MY BODY?
Formaldehyde can enter your body after you breath it in, drink or eat it, or when it comes in contact with your skin....
Once absorbed, formaldehyde is very quickly broken down. [Notice the phrase "very quickly broken down", which skirts the issue that potent levels of formaldehyde and formic acid are inevitably produced in humans, and retained in complex, unresearch amounts.]
Almost every tissue in the body has the ability to break down formaldehyde. [Again the dangers are waved away by definition. The correct way to say this is that formaldehyde and formic acid toxicity affects every tissue in the body.]
It is usually converted to a non-toxic chemical called formate, which is excreted in the urine. [This is an astonishing, brazen deceit, defining formic acid as "non-toxic". Notice the qualification "usually".]
Formaldehyde can also be converted to carbon dioxide and breathed out of the body. [Notice the qualification "can".]
It can also be broken down so the body can use it to make larger molecules needed in your tissues, or it can attach to deoxyribonucleic acid (DNA) or to protein in your body.... [In one sentence, formaldehyde is portrayed as a useful food, while the very serious and complex issue of formaldehyde adducts to DNA and proteins in all tissues and cells is minimalized:
C. Trocho (1998 July 26): [ Not cited in this lengthy tome. ] "In all, the rats retained, 6 hours after administration, about 5% of the label, half of it in the liver." They used a very low level of aspartame ingestion, 10 mg/kg, for rats, which have a much greater tolerance for aspartame than humans. So, the corresponding level for humans would be about 1 or 2 mg/kg. [60 to 120 mg aspartame for a 60-kg person, of which 11% is methanol, 6.6 to 13.2 mg] Many headache studies in humans used doses of about 30 mg/kg daily. [1800 mg aspartame for a 60-kg person, of which 11% is methanol, 198 mg]
Aspartame puts formaldehyde adducts into tissues, Part 1/2
full text, Trocho & Alemany 1998.06.26: Murray 2002.12.22 rmforall
Formaldehyde derived from dietary aspartame binds to tissue components in vivo.
Life Sci June 26 1998; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Spain.
http://www.bq.ub.es/cindex.html LÝnies de Recerca: Toxicitat de l'aspartame http://www.bq.ub.es/grupno/grup-no.html
Sra. Carme Trocho, Sra. Rosario Pardo, Dra. Immaculada Rafecas, Sr. Jordi Virgili, Dr. Xavier Remesar, Dr. Jose Antonio Fernandez-Lopez, Dr. MariÓ Alemany [male]
Fac. Biologia Tel.: (93)4021521, FAX: (93)4021559
Sra. Carme Trocho "Trok-ho" Fac. Biologia Tel.: (93)4021544
FAX: (93)4021559 email@example.com ; firstname.lastname@example.org
Adult male rats were given an oral dose of 10 mg/kg aspartame, 14C-labeled in the methanol carbon. At timed intervals of up to 6 hours, the radioactivity in plasma and several organs was investigated. Most of the radioactivity found (>98% in plasma, >75% in liver) was bound to protein. Label present in liver, plasma and kidney was in the range of 1-2% of total radioactivity administered per g or mL, changing little with time. Other organs (brown and white adipose tissues, muscle, brain, cornea and retina) contained levels of label in the range of 1/12th to 1/10th of that of liver. In all, the rats retained, 6 hours after administration, about 5% of the label, half of it in the liver.
The specific radioactivity of tissue protein, RNA and DNA was quite uniform. The protein label was concentrated in amino acids, different from methionine, and largely coincident with the result of protein exposure to labeled formaldehyde. DNA radioactivity was essentially in a single different adduct base, different from the normal bases present in DNA. The nature of the tissue label accumulated was, thus, a direct consequence of formaldehyde binding to tissue structures.
The administration of labeled aspartame to a group of cirrhotic rats resulted in comparable label retention by tissue components, which suggests that liver function (or its defect) has little effect on formaldehyde formation from aspartame and binding to biological components.
The chronic treatment of a series of rats with 200 mg/kg of non-labeled aspartame during 10 days results in the accumulation of even more label when given the radioactive bolus, suggesting that the amount of formaldehyde adducts coming from aspartame in tissue proteins and nucleic acids may be cumulative.
It is concluded that aspartame consumption may constitute a hazard because of its contribution to the formation of formaldehyde adducts. PMID: 9714421
"The high label presence in plasma and liver is in agreement with the carriage of the label from the intestine to the liver via the portal vein. The high label levels in kidney and, to a minor extent, in brown adipose tissue and brain are probably a consequence of their high blood flows (45). Even in white adipose tissue, the levels of radioactivity found 6 hours after oral administration were 1/25th those of liver. Cornea and retina, both tissues known to metabolize actively methanol (21,28) showed low levels of retained label. In any case, the binding of methanol-derived carbon to tissue proteins was widespread, affecting all systems, fully reaching even sensitive targets such as the brain and retina....
The amount of label recovered in tissue components was quite high in all the groups, but especially in the NA rats. In them, the liver alone retained, for a long time, more than 2 % of the methanol carbon given in a single oral dose of aspartame, and the rest of the body stored an additional 2 % or more. These are indeed extremely high levels for adducts of formaldehyde, a substance responsible of chronic deleterious effects (33), that has also been considered carcinogenic (34,47). The repeated occurrence of claims that aspartame produces headache and other neurological and psychological secondary effects-- more often than not challenged by careful analysis-- (5, 9, 10, 15, 48) may eventually find at least a partial explanation in the permanence of the formaldehyde label, since formaldehyde intoxication can induce similar effects (49).
The cumulative effects derived from the incorporation of label in the chronic administration model suggests that regular intake of aspartame may result in the progressive accumulation of formaldehyde adducts.
It may be further speculated that the formation of adducts can help to explain the chronic effects aspartame consumption may induce on sensitive tissues such as brain (6, 9, 19, 50).
In any case, the possible negative effects that the accumulation of formaldehyde adducts can induce is, obviously, long-term.
The alteration of protein integrity and function may needs some time to induce substantial effects.
The damage to nucleic acids, mainly to DNA, may eventually induce cell death and/or mutations.
The results presented suggest that the conversion of aspartame methanol into formaldehyde adducts in significant amounts in vivo should to be taken into account because of the widespread utilization of this sweetener.
Further epidemiological and long-term studies are needed to determine the extent of the hazard that aspartame consumption poses for humans."]
Some people are more sensitive to the effects of formaldehyde than others.... [Again a very significant, complex, and problematic issue is mentioned and minimalized in one sentence-- notice the phrase "some people".]
The Department of Health and Human Services (DHHS) has determined that formaldehyde may reasonably be anticipated to be a human carcinogen (NTP).
The International Agency for Research on Cancer (IARC) has determined that formaldehyde is probably carcinogenic to humans.
This determination was based on specific judgements that there is limited evidence in humans and sufficient evidence in laboratory animals that formaldehyde can cause cancer.
The Environmental Protection Agency (EPA) has determined that formaldehyde is a probable human carcinogen based on limited evidence in humans and sufficient evidence in laboratory animals.... [These extremely alarming admissions ought to be emphasized and used to support calls for urgent research, action, and public warning.]
The most common way for children to be exposed to formaldehyde is by breathing it. [ Again, kids are kept at risk with this policy of denial of the potent role of dietary sources. ] Children may also be exposed by wearing some types of new clothes or cosmetics.
A small number of studies have looked at the health effects of formaldehyde in children. [Notice the term "small number", which serves to both mention and minimalize the problem of a dire shortage of adaquate research.]
It is very likely that breathing formaldehyde will result in nose and eye irritation (burning feeling, itchy, tearing, and sore throat). [The focus is placed on the most unimportant symptoms.]
We do not know if the irritation would occur at lower concentrations in children than in adults. [Research that could threaten vested interests somehow just doesn't get funded.]
Studies in animals suggest that formaldehyde will not cause birth defects in humans. [Notice the qualification "suggest".]
Inhaled formaldehyde or formaldehyde applied to the skin is not likely to be ntransferred from mother to child in breast milk or to reach the developing fetus.... [Notice the qualification "not likely".
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. email@example.com
Sam-1 Trust, Alto, New Mexico, USA.
http://www.drthrasher.org/formaldehyde_embryo_toxicity.html full text ]
Formaldehyde is usually found in the air.
Formaldehyde levels are also higher indoors than outdoors.
Opening windows or using a fan to bring in fresh air is the easiest way to lower formaldehyde levels in the home and reduce the risk of exposure to your family. [This reassuring, simple advice is dangerous, since the potent dietary sources are ignored.]
Removing formaldehyde sources from the house will also reduce the risk of exposure.
Since formaldehyde is found in tobacco smoke, not smoking or smoking outside will reduce exposure to formaldehyde.
Unvented heaters, such as portable kerosene heaters, also produce formaldehyde. If you do not use these heaters in your home or shop, you help to prevent the build up of formaldehyde indoors.
Formaldehyde is found in small amounts in many consumer products including antiseptics, medicines, dish-washing liquids, fabric softeners, shoe-care agents, carpet cleaners, glues, adhesives, and lacquers.
If you or a member of your family uses these products, providing fresh outdoor air when you use them, this will reduce your exposure to formaldehyde.
Some cosmetics, such as nail hardeners, have very high levels of formaldehyde.
If you do not use these products in a small room, or if you have plenty of ventilation when you use them, you will reduce your exposure to formaldehyde.
If your children are not in the room when you use these products, you will also reduce their exposure to formaldehyde.
Formaldehyde is emitted from some wood products such as plywood and particle board, especially when they are new.
The amount of formaldehyde released from them decreases slowly over a few months. [Notice "slowly over a few months".]
If you put these materials in your house, or buy furniture or cabinets made from them, opening a window will lower formaldehyde in the house. [What happens in winter?]
The amount of formaldehyde emitted to the house will be less if the wood product is covered with plastic laminate or coated on all sides.
If it is not, sealing the unfinished sides will help to lower the amount of formaldehyde that is given off. Some permanent press fabrics emit formaldehyde. [Why aren't there warning labels?]
Washing these new clothes before use will usually lower the amount of formaldehyde and reduce your family's risk of exposure.
FORMALDEHYDE 7 1. PUBLIC HEALTH STATEMENT
1.8 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN EXPOSED TO FORMALDEHYDE?
We have no reliable test to determine how much formaldehyde you have been exposed to or whether you will experience any harmful health effects....
[Another casual mention of an alarming reality]
1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO PROTECT HUMAN HEALTH?
The federal government develops regulations and recommendations to protect public health.
Regulations can be enforced by law.
Federal agencies that develop regulations for toxic substances include the EPA, the Occupational Safety and Health Administration (OSHA), and the Food and Drug Administration (FDA).
Recommendations provide valuable guidelines to protect public health but cannot be enforced by law. [Not reassuring...]
Federal organizations that develop recommendations for toxic substances include the Agency for Toxic Substances and Disease Registry (ATSDR) and the NIOSH. [ATSDR and NIOSH cannot enforce their recommendations.]
Regulations and recommendations can be expressed in not-to-exceed levels in air, water, soil, or food that are usually based on levels that affect animals, then they are adjusted to help protect people. [This bypasses the issue that the reseach on humans is very inadequate to determine the actual, complex toxicity of methanol, formaldehyde, and formic acid.]
Sometimes these not-to-exceed levels differ among federal organizations because of different exposure times (an 8-hour workday or a 24-hour day), the use of different animal studies, or other factors.... [An outstanding example of disharmony in the EPA is the fact that the 1998.05.05 EPA IRIS level for oral methanol in humans (Oral Rfd) is 0.5 mg/kg/day, or 30 mg oral methanol daily for a 60 kg human. The animal study used was:
U.S. EPA. 1986. Rat oral subchronic toxicity study with methanol. Office of Solid Waste, Washington, DC.
I have not found on the Net any information as to the authors, institution, abstract, or full text of this study.
But the EPA ATSDR limit for formaldehyde in drinking water is 1 ppm, or 2 mg daily for a typical daily consumption of 2 L of water:
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999: Murray 2002.05.30 rmforall
Agency for Toxic Substances and Disease Registry Division of Toxicology
1600 Clifton Road NE, Mailstop E-29Atlanta, GA 30333 888-422-8737 FAX: (404)498-0057 ATSDRIC@cdc.gov http://www.atsdr.cdc.gov/contacts.html
"The EPA recommends that an adult should not drink water containing more than 1 milligram of formaldehyde per liter of water (1 mg/L) for a lifetime exposure, and a child should not drink water containing more than 10 mg/L for 1 day or 5 mg/L for 10 days."
This stringent limit means that if over 13% of the oral methanol limit results in production of formaldehyde in the human body by the liver, then the formaldehyde limit would be exceeded. This is cutting things pretty close.
http://www.epa.gov/iris/subst/0305.htm also http://www.china-pops.net/enwww/IRIS-Mirror/subst/0305.htm 1998.05.05
USA Environmental Protection Agency EPA
Integrated Risk Information System IRIS
This site explains that the harmful rat dose of 500 mg/kg body weight per day was divided by 10 for "interspecies extrapolation" (the higher vulnerability of humans than rats), by 10 for "range of sensitivity" (the variation of individual human vulnerability), and by 10 for "subchronic to chronic exposure" (the increased danger from lifetime as compared to the 3 month exposure in the rat test), giving a total reduction of 10x10x10 = 1000 for the UF = Uncertainty Factor.
The human Oral RfD is the rat Oral RfD divided by 1000, so 500 mg/kg/day is reduced to 0.5 mg/kg/day , so that the allowed dose for a 60 kg human is 30 mg oral methanol daily.
Moreover, a recent study found that after 4 months of moderate oral aspartame, rats took four times longer to finish a simple, one-turn maze-- an alarming level of neurotoxicity:
Murray, full plain text & critique: chronic aspartame in rats affects memory, brain cholinergic receptors, and brain chemistry, Christian B, McConnaughey M et al, 2004 May: 2004.06.05
"Control and treated rats were trained in a T-maze to a particular side and then periodically tested to see how well they retained the learned response.
Rats that had received aspartame (250 mg/kg/day) in the drinking water for 3 or 4 months showed a significant increase in time to reach the reward in the T-maze, suggesting a possible effect on memory due to the artificial sweetener."
The 11% methanol component of aspartame is immediately released in the GI tract, so these rats were being exposed to only 27.5 mg/kg/day methanol.
The EPA IRIS on 1998.05.05 used a 1986 90 day rat study to find a No-Observed-Effect Level (NOEL) value of 500 mg/kg/day, which, divided by 1000, became their human long-term safe methanol level of 0.5 mg per kg body weight per day, which for a 60 kg average person is 30 mg methanol daily, for oral exposure.
However, the rat level is 18 times greater than that for the level of dramatic memory loss and clear-cut brain changes found by McConnaughey M, May 2004.
This suggests reducing the human long-term safe level twenty times to .025 mg/kg/day = 25 micrograms per kg body weight per day, which for a 60 kg average person is 1.5 mg oral methanol per day.
It is certain that high levels of aspartame use, above 2 liters daily for months and years, must lead to chronic formaldehyde-formic acid toxicity.
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), about 22 mg methanol per can.
If only 10% of the methanol accumulates daily as formaldehyde, that would give 12 mg daily formaldehyde accumulation -- about 60 times more than the 0.2 mg from 10% retention of the 2 mg EPA daily limit for formaldehyde in drinking water.
If about 30% of oral methanol is retained as formaldehyde and formic acid, then this EPA ATSDR formaldehyde limit of 2 mg daily for 2 L drinking water suggests a corresponding methanol limit of 6.7 mg daily, about 4.5 times the safe limit based on the McConnaughey data. This is much closer than the 1998 EPA IRIS limit of 30 mg daily oral methanol, which is 20 times the McConnaughey data limit. ]
Returning to the voluminous work of Elzbieta Skrzydlewska, it is important that many of her studies suggest that many safe substances may prevent or treat toxicity from methanol and its inevitable toxic human body products, formaldehyde and formic acid:
N-acetylcysteine (2000); U-83836E containing a trolox ring (1997); green tea (2004); vitamins E, C, A, and beta-carotene (2004); glutathione (2001); N-Acetylcysteine (NAC) (2001); melatonin (2001); low and medium levels of cysteine (1990).
"Methanol, when introduced into all mammals, is oxidized into formaldehyde and then into formate, mainly in the liver.
Such metabolism is accompanied by the formation of free radicals....
The consequences of methanol metabolism and toxicity distinguish the human and monkey from lower animals.
Formic acid is likely to be the cause of the metabolic acidosis and ocular toxicity in humans and monkeys, which is not observed in most lower animals.
Nevertheless, chemically reactive formaldehyde and free radicals may damage most of the components of the cells of all animal species, mainly proteins and lipids...."
Toxicology Mechanisms and Methods
Publisher: Taylor & Francis Health Sciences, part of the Taylor & Francis
Group Issue: Volume 13, Number 4 / Oct-Dec 2003 Pages: 277 - 293
Toxicological and Metabolic Consequences of Methanol Poisoning
Elzbieta Skrzydlewska, Assoc. Professor, MSc, PhD, Deputy Dean of Faculty of Pharmacy, Head of Department of Analytical Chemistry, Medical University of Bialystok, Mickiewicza 2A 15-230 Bialystok 8, P.O. Box 14, Poland
Kilinskiego 1 15-089 Bialystok, Poland fax (48 85)7485408
Methanol, when introduced into all mammals, is oxidized into formaldehyde and then into formate, mainly in the liver.
Such metabolism is accompanied by the formation of free radicals.
In all animals, methanol oxidation, which is relatively slow, proceeds via the same intermediary stages, usually in the liver, and various metabolic systems are involved in the process, depending on the animal species.
In nonprimates, methanol is oxidized by the catalase-peroxidase system, whereas in primates, the alcohol dehydrogenase system takes the main role in methanol oxidation.
The first metabolite (formaldehyde is rapidly oxidized by formaldehyde dehydrogenase) is the reduced glutathione (GSH)-dependent enzyme.
Generated formic acid is metabolized into carbon dioxide with the participation of H4folate and two enzymes, 10-formyl H4folate synthetase and dehydrogenase, whereas nonprimates oxidize formate efficiently.
Humans and monkeys possess low hepatic H4folate and 10-formyl H4folate dehydrogenase levels and are characterized by the accumulation of formate after methanol intoxication.
The consequences of methanol metabolism and toxicity distinguish the human and monkey from lower animals.
Formic acid is likely to be the cause of the metabolic acidosis and ocular toxicity in humans and monkeys, which is not observed in most lower animals.
Nevertheless, chemically reactive formaldehyde and free radicals may damage most of the components of the cells of all animal species, mainly proteins and lipids.
The modification of cell components results in changes in their functions.
Methanol intoxication provokes a decrease in the activity and concentration of antioxidant enzymatic as well as nonenzymatic parameters, causing enhanced membrane peroxidation of phospholipids.
The modification of protein structure by formaldehyde as well as by free radicals results changes in their functions, especially in the activity of proteolytic enzymes and their inhibitors, which causes disturbances in the proteolytic-antiproteolytic balance toward the proteolytics and enhances the generation of free radicals.
Such a situation can lead to destructive processes because components of the proteolytic-antiproteolytic system during enhanced membrane lipid peroxidation may penetrate from blood into extracellular space, and an uncontrolled proteolysis can occur.
This applies particularly to extracellular matrix proteins.
Free Radicals, Methanol Metabolism, Methanol Poisoning, Proteases, Protease Inhibitors
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J Pharm Pharmacol. 2000 May; 52(5): 547-52.
Protective effect of N-acetylcysteine on rat liver cell membrane during methanol intoxication. firstname.lastname@example.org
Dobrzynska I, Skrzydlewska E, Kasacka I, Figaszewski Z.
Institute of Chemistry, University in Bialystok, Poland.
Methanol is oxidized in vivo to formaldehyde and then to formate, and these processes are accompanied by the generation of free radicals. We have studied the effect of N-acetylcysteine on liver cell membrane from rats intoxicated with methanol (3.0 g kg(-1)). Evaluation of the effect was achieved by several methods. Lipid peroxidation and surface charge density were measured. An ultrastructural study of the liver cells was undertaken. The concentration of marker enzymes of liver damage (alanine aminotransferase and aspartate aminotransferase) in blood serum was measured. Methanol administration caused an increase in lipid peroxidation products (approximately 30%) as well as in surface charge density (approximately 60%). This might have resulted in the membrane liver cell damage visible under electron microscopy and a leak of alanine aminotransferase and aspartate aminotransferase into the blood (increase of approximately 70 and 50%, respectively). Ingestion of N-acetylcysteine with methanol partially prevented these methanol-induced changes. Compared with the control group, lipid peroxidation was increased by approximately 3% and surface charge density by approximately 30%. Alanine aminotransferase and aspartate aminotransferase activity increased by 9 and 8%, respectively, compared with the control group. The results suggested that N-acetylcysteine was an effective antioxidant in methanol intoxication. It may have efficacy in protecting free radical damage to liver cells following methanol intoxication. PMID: 10864143
"Changes in protein structure resulted both from free radical action and formaldehyde generation during methanol intoxication."
J Appl Toxicol. 2000 May-Jun; 20(3): 239-43.
Effect of methanol intoxication on free-radical induced protein oxidation.
Skrzydlewska E, Elas M, Farbiszewski R, Roszkowska A.
Department of Analytical Chemistry, Medical University, 15-230 Bialystok 8, Poland.
Oxygen free radicals are generated during methanol-induced liver injury, as was shown for ethanol. The effect of methanol intoxication (6 g kg(-1) body wt.) on protein modification in the liver of rats was investigated. Electron spin resonance determination indicated an increase in the free radical signal 6 and 12 h after intoxication. After 7 days of treatment, the contents of malondialdehyde and carbonyl groups in proteins were significantly increased. The level of amino groups and sulphydryl groups and the amount of tryptophan in proteins were decreased, whereas the amount of bi-tyrosine was increased significantly. Changes in protein structure resulted both from free radical action and formaldehyde generation during methanol intoxication.
Copyright 2000 John Wiley & Sons, Ltd. PMID: 10797478
Toxicology. 2000 Dec 7; 156(1): 47-55.
N-acetylcysteine or trolox derivative mitigate the toxic effects of methanol on the antioxidant system of rat brain.
Farbiszewski R, Witek A, Skrzydlewska E.
Department of Analytical Chemistry, Bialystok Medical Academy, Mickiewicza Str 2, P.O. Box 14, 15-230 Bialystok 8, Poland.
The effect of two compounds: N-acetylcysteine (NAC) and trolox derivative (U-83836E) on the methanol induced impairment of the antioxidant system of the rat brain was studied in male Wistar rats (approx. 250 g body weight). The animals were divided into six main groups: control group (0.5 ml of physiological saline intragastrically), NAC group (150 mg/kg intraperitoneally-i.p), U-83836E group (10 mg/kg i.p.), methanol group (3 g/kg intragastrically), NAC+methanol and U-83836E+methanol groups. In these particular groups the changes in antioxidant parameters were observed for 6,12,24,48 h and 5 and 7 days. The results proved that the use of methanol and N-acetylcysteine increased the activities of Cu,Zn-superoxide dismutase, glutathione peroxidase and glutathione reductase by about 15,15 and 41%, respectively, in comparison to the group of rats receiving methanol alone. Similarly, the level of GSH increased by about 17%, the concentration of ascorbate by 20%, while the thiobarbituric acid-reactive substances (TBA-rs) diminished to the values as in control group. The use of new antioxidant U8383E and methanol showed less beneficial effect in the measured parameters however, it serves as a better protector for the methanol induced decrease in GSH-content. These data suggest that NAC and U-83836E mitigate the toxic effects of methanol on the antioxidant system of the rat brain. PMID: 11162875
Rocz Akad Med Bialymst. 1999; 44: 89-101.
Morphological changes in the liver of rats intoxicated with methanol.
Kasacka I, Skrzydlewska E.
Department of Histology and Embryology, Medical Academy of Bialystok.
On the basis of morphological examinations in light and electron microscope, the evaluation of methanol influence on the liver of rats was conducted. The examination was carried out in the group of 36 rats that were given a single dose of methanol (1.5 g/kg b.w.) into the stomach through a gastric tube. The liver was taken from rats under the ether anaesthesia after 6, 12, and 24 hours as well as after 2, 5, and 7 days of methanol administration. Results showed that methanol intoxication caused visible changes in the examined organ. Only 6 h after intoxication, lobular peripheral hepatocytes presented characteristic features of vacuolar degradation persisting up to 48 h. Since the second day of intoxication, many cells with double nuclei were found more frequently than in controls. Single hepatocytes or small hepatocytic clusters with the features of deliquescent necrosis could be seen after 5 and 7 days of examination. All animals intoxicated with methanol showed distinct weakness of glycogen reaction. The loss of glycogen resources was highest at 24 h after methanol administration. The results indicate, that methanol causes morphological changes in the rat liver and that intensification of these changes depends on the time after intoxication. PMID: 10697423
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). 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) -- the same amount that produces hangover from red wine.
The expert review by Monte WC (1984) states: "An alcoholic consuming 1500 calories a day from alcoholic sources alone may consume between 0 and 600 mg of methanol each day depending on his choice of beverages (Table 1)...." Table 1 lists red wine as having 128 mg/l methanol, about one part in ten thousand.
Aspartame: Methanol and the Public Interest 1984: Monte: Murray 2002.09.23 rmforall
Dr. Woodrow C. Monte Aspartame: methanol, and the public health.
Journal of Applied Nutrition 1984; 36 (1): 42-54.
(62 references) Professsor of Food Science [retired 1992]
Arizona State University, Tempe, Arizona 85287 email@example.com
The methanol from 2 L of diet soda, 5.6 12-oz cans, 20 mg/can, is 112 mg, 10% of the aspartame. The EPA limit for water is 7.8 mg daily for methanol (wood alcohol), a deadly cumulative poison. Many users drink 1-2 L daily. The reported symptoms are entirely consistent with chronic methanol toxicity. (Fresh orange juice has 34 mg/L, but, like all juices, has 16 times more ethanol, which strongly protects against methanol.)
"The greater toxicity of methanol to man is deeply rooted in the limited biochemical pathways available to humans for detoxification. The loss of uricase (EC 22.214.171.124.), formyl-tetrahydrofolate synthetase (EC 126.96.36.199.) (42) and other enzymes (18) during evolution sets man apart from all laboratory animals including the monkey (42).
There is no generally accepted animal model for methanol toxicity (42, 59).
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)."
"Fruit and vegetables contain pectin with variable methyl ester content. However, the human has no digestive enzymes for pectin (6, 25) particularly the pectin esterase required for its hydrolysis to methanol (26).
Fermentation in the gut may cause disappearance of pectin (6) but the production of free methanol is not guaranteed by fermentation (3). In fact, bacteria in the colon probably reduce methanol directly to formic acid or carbon dioxide (6) (aspartame is completely absorbed before reaching the colon). Heating of pectins has been shown to cause virtually no demethoxylation; even temperatures of 120 deg C produced only traces of methanol (3). Methanol evolved during cooking of high pectin foods (7) has been accounted for in the volatile fraction during boiling and is quickly lost to the atmosphere (49). Entrapment of these volatiles probably accounts for the elevation in methanol levels of certain fruits and vegetable products during canning (31, 33)."
Rich Murray, MA
Boston University Graduate School 1967 psychology
BS MIT 1964, history and physics
1943 Otowi Road
Santa Fe, New Mexico 87505
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