Friday, May 4, 2007

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Cancer Update from John Hopkins


1. Every person has cancer cells in the body. These cancer cells do not show up in the standard tests until they have multiplied to a few billion. When doctors tell cancer patients that there are no
more cancer cells in their bodies after treatment, it just means the tests are unable to detect the cancer cells because they have not reached the detectable size.

2. Cancer cells occur between 6 to more than 10 times in a person's lifetime.

3. When the person's immune system is strong the cancer cells will be destroyed and prevented from multiplying and forming tumors.

4. When a person has cancer it indicates the person has multiple nutritional deficiencies. These could be due to genetic, environmental, food and lifestyle factors.

5. To overcome the multiple nutritional deficiencies, changing diet and including supplements will strengthen the immune system.

6. Chemotherapy involves poisoning the rapidly-growing cancer cells and also destroys rapidly-growing healthy cells in the bone marrow, gastro-intestinal tract etc, and can cause organ damage, like liver,
Kidneys, heart, lungs etc.

7. Radiation while destroying cancer cells also burns, scars and damages healthy cells, tissues and organs.

8. Initial treatment with chemotherapy and radiation will often reduce tumor size. However prolonged use of chemotherapy and radiation do not result in more tumor destruction.

9. When the body has too much toxic burden from chemotherapy and radiation the immune system is either compromised or destroyed, hence the person can succumb to various kinds of infections and complications.

10. Chemotherapy and radiation can cause cancer cells to mutate and become resistant and difficult to destroy. Surgery can also cause cancer cells to spread to other sites.

11. An effective way to battle cancer is to starve the cancer cells by not feeding it with the foods it needs to multiply.

CANCER CELLS FEED ON:

a. Sugar is a cancer-feeder. By cutting off sugar it cuts off one important food supply to the cancer cells. Sugar substitutes like NutraSweet, Equal,Spoonful, etc are made with Aspartame and it is harmful. A better natural substitute would be Manuka honey or molasses but only in very small amounts. Table salt has a chemical added to make it white in colour. Better alternative is Bragg's aminos or sea salt.

b. Milk causes the body to produce mucus, especially in the gastro-intestinal tract. Cancer feeds on mucus. By cutting off milk and substituting with unsweetened soya milk cancer cells are being starved.

c. Cancer cells thrive in an acid environment. A meat-based diet is acidic and it is best to eat fish, and a little chicken rather than beef or pork. Meat also contains livestock antibiotics, growth hormones and parasites, which are all harmful, especially to people with cancer.

d. A diet made of 80% fresh vegetables and juice, whole grains,seeds, nuts and a little fruits help put the body into an alkaline environment.About 20% can be from cooked food including beans. Fresh vegetable juices provide live enzymes that are easily absorbed and reach down to cellular levels within 15 minutes to nourish and enhance growth of healthy cells. To obtain live enzymes for building healthy cells try and drink fresh vegetable juice (most vegetables including bean sprouts)and eat some raw vegetables 2 or 3 times a day. Enzymes are destroyed at temperatures of 104 degrees F (40 degrees C).

e. Avoid coffee, tea, and chocolate, which have high caffeine.Green tea is a better alternative and has cancer-fighting properties. Water-best to drink purified water, or filtered, to avoid known toxins and heavy metals in tap water. Distilled water is acidic, avoid it.

12. Meat protein is difficult to digest and requires a lot of digestive enzymes. Undigested meat remaining in the intestines become putrified and leads to more toxic buildup.

13. Cancer cell walls have a tough protein covering. By refraining from or eating less meat it frees more enzymes to attack the protein walls of cancer cells and allows the body's killer cells to destroy the cancer cells.

14. Some supplements build up the immune system (IP6, Flor-ssence,Essiac, anti-oxidants, vitamins, minerals, EFAs etc.) to enable the body's own killer cells to destroy cancer cells. Other supplements like vitamin E are known to cause apoptosis, or programmed cell death, the body's normal method of disposing of damaged, unwanted, or unneeded cells.

15. Cancer is a disease of the mind, body, and spirit. A proactive and positive spirit will help the cancer warrior be a survivor. Anger, unforgiveness and bitterness put the body into a stressful and acidic environment. Learn to have a loving and forgiving spirit. Learn to relax and enjoy life.

16. Cancer cells cannot thrive in an oxygenated environment. Exercising daily, and deep breathing help to get more oxygen down to the cellular level. Oxygen therapy is another means employed to destroy cancer cells.

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1 comment:

  1. formaldehyde as a potent unexamined cofactor in cancer research --
    sources include methanol, dark wines and liquors, aspartame, wood and
    tobacco smoke: IARC Monographs on the Evaluation of Carcinogenic Risks
    to Humans implicate formaldehyde in #88 and alcohol drinks in #96:
    some related abstracts: Murray 2007.04.30
    http://groups.yahoo.com/group/aspartameNM/message/1417

    [ See also:

    http://groups.yahoo.com/group/aspartameNM/message/1286
    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


    http://groups.yahoo.com/group/aspartameNM/message/1143
    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 ]


    " Absorbed formaldehyde can be oxidized to formate and carbon dioxide
    or can be incorporated into biologic macromolecules. "

    [ References include: Soffritti M, Belpoggi F, Lambertini L, Lauriola
    M, Padovani M, Maltoni C. 2002. Results of long-term experimental
    studies on the carcinogenicity of formaldehyde and acetaldehyde in
    rats. Ann NY Acad Sci 982:87-105.

    Soffritti M, Maltoni C, Maffei F, Biagi R. 1989. Formaldehyde: an
    experimental multipotential carcinogen. Toxicol Ind Health 5:699-730.
    "

    Morando Soffritti is a member of the Working Group. ]


    http://www.ehponline.org/members/2005/7542/7542.html free full text

    After a thorough discussion of the epidemiologic, experimental, and
    other relevant data, the working group concluded that formaldehyde is
    carcinogenic to humans, based on sufficient evidence in humans and in
    experimental animals.

    In the epidemiologic studies, there was sufficient evidence that
    formaldehyde causes nasopharyngeal cancer, "strong but not sufficient"
    evidence of leukemia, and limited evidence of sinonasal cancer.

    The working group also concluded that 2-butoxyethanol and 1-tert-
    butoxy-2-propanol are not classifiable as to their carcinogenicity to
    humans, each having limited evidence in experimental animals and
    inadequate evidence in humans.

    These three evaluations and the supporting data will be published as
    Volume 88 of the IARC Monographs. PMID: 16140628


    Environ Health Perspect. 2005 Sep; 113(9): 1205-8.
    Meeting report: summary of IARC monographs on formaldehyde, 2-
    butoxyethanol, and 1-tert-butoxy-2-propanol.

    * Cogliano VJ, Vincent James Cogliano cogliano@iarc.fr,
    * Grosse Y, Yann Grosse grosse@iarc.fr,
    * Baan RA, Robert A. Baan baan@iarc.fr,
    * Straif K, Kurt Straif, straif@iarc.fr,
    * Secretan MB, Marie Béatrice Secretan secretan@iarc.fr,
    * El Ghissassi F, Fatiha El Ghissassi elghissassi@iarc.fr,
    * Working Group for Volume 88.


    http://monographs.iarc.fr/ENG/Staff/index.php
    photo of Carcinogen Identification and Evaluation Group - Staff

    Secretariat: Tel. +33 (0)4 72 73 85 07 Fax +33 (0)4 72 73 83 19

    Head of Programme, Vincent James Cogliano

    Secretary, Helene Lorenzen-Augros

    Scientists:
    Robert Baan (genetic toxicology)
    Fatiha El Ghissassi (biochemistry/genetic toxicology)
    Yann Grosse (carcinogenesis/bioassays)
    Béatrice Secretan (molecular toxicology)
    Kurt Straif (epidemiology)

    Technical Assistants:
    Sandrine Egraz
    Martine Lézère
    Jane Mitchell

    IARC, 150 Cours Albert Thomas, 69372 Lyon CEDEX 08, France
    Tel: +33 (0)4 72 73 84 85 - Fax: +33 (0)4 72 73 85 75
    © IARC 2004 - All Rights Reserved
    http://monographs.iarc.fr cie@iarc.fr,

    Monographs Recently Published

    IARC Monographs Vol 88
    Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol

    December 2006
    478 pages
    ISBN 92 832 1288 6
    US$ 40

    This volume re-evaluates the available evidence on the carcinogenic
    potential of formaldehyde, a substance that is found in the workplace
    and in the environment.
    Formaldehyde is widely used in resins that bind wood products, pulp
    and paper; in glasswool and rockwool insulation; in plastics and
    coatings, textile finishing, chemical manufacture; and as a
    disinfectant and preservative. Also evaluated are two glycol ethers, 2-
    butoxyethanol and 1-tert-butoxypropan-2-ol, which are widely used as
    solvents in paints and paint thinners, coatings, glass and surface
    cleaners, inks, adhesives, personal-care products, and as chemical
    intermediates.
    As for formaldehyde, there is sufficient evidence in epidemiological
    studies for nasopharyngeal cancer, strong but not sufficient evidence
    for leukaemia, and limited evidence for sinonasal cancer.
    The extensive scientific database on the mechanisms by which
    formaldehyde can induce nasal-tract cancer in humans is considered.
    These data provide strong support for the empirical observation of
    nasopharyngeal cancer in humans.
    In contrast, the lack of information on possible mechanisms by which
    formaldehyde might increase the risk for leukaemia in humans tempered
    the interpretation of the epidemiological data on that cancer.
    Although this volume focuses on a qualitative assessment of the
    carcinogenic potential of formaldehyde, subsequent predictions of the
    risks for nasopharyngeal cancer should consider pertinent information
    on mechanisms of carcinogenesis, including genotoxicity and dose-
    dependent cytoxicity.
    A theme common to the three evaluations is the consideration of
    mechanistic information to develop and evaluate hypotheses on the
    sequence of steps that lead to the induction of tumours in
    experimental animals.
    The hypothesized mechanisms described provide an interesting set of
    cases that range from a vast literature on respiratory tract tumours
    in rats induced by the inhalation of formaldehyde to some more
    tentative hypotheses on the various tumours observed in animals
    following exposure to both glycol ethers.
    Recurring issues were the criteria that characterize a rare tumour or
    how to introduce additional information to resolve difficult
    questions; for example, how to consider the results of historical
    controls.

    International Agency for Research on Cancer, Lyon, France.

    An international, interdisciplinary working group of expert
    scientists met in June 2004 to develop IARC Monographs on the
    Evaluation of the Carcinogenic Risk of Chemicals to Humans (IARC
    Monographs) on formaldehyde, 2-butoxyethanol, and 1-tert-butoxy-2-
    propanol.

    Each IARC Monograph includes a critical review of the pertinent
    scientific literature and an evaluation of an agent's potential to
    cause cancer in humans.

    Key words: 1-tert-butoxy-2-propanol, 2-butoxyethanol, carcinogen,
    formaldehyde, glycol ethers, hazard identification, IARC Monographs,
    leukemia, nasopharyngeal cancer, sinonasal cancer. Environ Health
    Perspect 113: 1205-1208 (2005) . doi:10.1289/ehp.7542 available via
    http://dx.doi.org/ [Online 12 May 2005]

    Address correspondence to V.J. Cogliano, Carcinogen Identification
    and Evaluation, International Agency for Research on Cancer, 150 cours
    Albert Thomas, 69372 Lyon cedex 08, France.
    Telephone: 33-4-72-73-84-76. Fax: 33-4-72-73-83-19. E-mail:
    cogliano@iarc.fr,

    The Working Group for Volume 88 of the IARC Monographs includes:
    Ulrich Andrae (Germany) , andrae@gsf.de, Dr. Ulrich Andrae, GSF-
    Institut für Toxikologie,. Postfach 1129, D-85758 Neuherberg, Germany
    Fax: 149-089-3187-3449
    Sherwood Burge (UK) ,
    Rajendra S Chhabra (USA) , http://dir.niehs.nih.gov/dirtob/chhabra.htm
    chhabrar@niehs.nih.gov, General Toxicology Group, TOB, ETP, DIR
    John Cocker (UK) , Health and Safety Laboratory, Buxton, UK
    john.cocker@hsl.gov.uk,
    David N Coggon (UK) , MRC Environmental Epidemiology Unit at the
    University of Southampton, UK dnc@mrc.soton.ac.uk,
    Rory Conolly (USA) , Rconolly@ciit.org, Senior Research Biologist,
    National Center for Computational Toxicology, Office of Research and
    Development, U.S. Environmental Protection Agency
    Paul Demers (Canada) , pdemers@unixg.ubc.ca, Occupational Hygiene
    Institute, University of British Columbia
    David A Eastmond (USA) , david.eastmond@ucr.edu, Enviromental
    Toxicology Graduate Program, University of California Riverside, CA
    92521 (951) 827-4497 (Voice) (951) 827-3087 (Fax)
    Elaine Faustman (USA) , faustman@u.washington.edu, Professor, Env. and
    Occ. Health Sciences, Adjunct Professor, Evans School 206-685-2269
    Victor J Feron (the Netherlands) , TNO Nutrition and Food Research
    (retired), The Netherlands TNO-CIVO TOXICOLOGY AND NUTRITION INSTITUTE
    Utrechtseweg 48 3704 HE Zeist The Netherlands (31)-3404 44 144
    Michel Gérin (Canada, Chair) , gerinm@ere.umontreal.ca, Departement
    de medecine du travail et d'hygiene du milieu, Universite de Montreal,
    Quebec, Canada.
    Marcel Goldberg (France) , marcel.goldberg@st-maurice.inserm.fr,
    France -- National Institute of Health and Medical Research INSERM
    Unite 88, HNSM 14 Rue de Val d'Osne F-94410 St. Maurice France [33]
    1-451-83859 [33] 1-451-83889
    Departement Sante Travail, Institut de Veille Sanitaire, 12, rue du
    Val d'Osne, 94410 Saint Maurice, France
    Bernard D Goldstein (USA) , bdgold@pitt.edu, Director of the
    Environmental and Occupational Health Sciences Institute and Professor
    and Chair of the Department of Environmental and Community Medicine at
    UMDNJ - Robert Wood Johnson Medical School. Dean's Office, University
    of Pittsburgh Graduate School of Public Health, A624 Crabtree Hall,
    130 DeSoto St., Pittsburgh, PA 15261, USA.
    Roland C Grafström (Sweden) , roland.grafstrom@imm.ki.se, Roland C
    Grafström, Institute of Environmental Medicine, Karolinska Institutet,
    Box 210, S−17177 Stockholm, Sweden
    Telefax: +46-8−329402
    Johnni Hansen (Denmark) , johnni@cancer.dk, PhD, Senior researcher,
    Danish Cancer Registry , Institute of Cancer Epidemiology, Danish
    Cancer Society, Strandboulevarden 49, DK-2100, Copenhagen, Denmark.
    Michael Hauptmann (USA) , The National Cancer Institute
    Kathy Hughes (Canada) , Head, Existing Substances Section 1, Health
    Canada,
    Ted Junghans (USA) , tjunghans@tech-res.com, Technical Resources
    International, Inc., 6500 Rock Spring Drive, Suite 650, Bethesda, MD
    20817, USA.
    Dan Krewski (Canada) , MHA, MSc, PhD dkrewski@uottawa.ca, Professor
    Director, R. Samuel McLaughlin Centre for Population Health Risk
    Assessment, Institute of Population Healt, 1 Stewart Street, Room 320,
    Phone: (613) 562-5381 Fax: (613) 562-5380
    Steve Olin (USA) , solin@ilsi.org, ILSI International Life Sciences
    Institute
    Martine Reynier (France) , martine.reynier@inrs.fr, Mme Martine
    REYNIER, Institut National de Recherche et de Sécurité (INRS), 30, rue
    Olivier Noyer, 75680 Paris Cedex 14 (France) Tel : +33 (0)1 40 44 30
    81 Fax : +33 (0)1 40 44 30 54
    Judith Shaham (Israel) , yshaham@bezeqint.net, Occupational Cancer
    Department, National Institute of Occupational and Environmental
    Health, Raanana, Israel. MD, Occupational Cancer Unit, Occupational
    Health & Rehabilitation Institute, P.O. Box 3, Raanana 43100, ISRAEL

    Morando Soffritti (Italy) , crcfr@ramazzini.it, European Foundation
    of Oncology and Environmental Sciences "B. Ramazzini", Cesare Maltoni
    Cancer Research Center, Bologna, Italy

    Leslie Stayner (USA) , lstayner@uic.edu, Division of Epidemiology and
    Biostatistics, University of Illinois at Chicago School of Public
    Health (M/C 923), 1603 West Taylor Street, Room 971, Chicago, IL
    60612. E-mail:
    Patricia Stewart (USA) , National Food Safety and Toxicology
    Center, 165 Food Safety and Toxicology Building, Michigan State
    University, East Lansing, MI 48824; fax (517) 432-2310
    Douglas Wolf (USA) , wolf.doug@epa.gov, DVM, PhD, USEPA,
    (Toxicology)

    We gratefully acknowledge the important contributions of the
    administrative staff of the IARC Monographs: S. Egraz, M. Lézère, J.
    Mitchell, and E. Perez.

    The IARC Monographs are supported, in part, by grants from the
    U.S. National Cancer Institute, the European Commission, the U.S.
    National Institute of Environmental Health Sciences, and the U.S.
    Environmental Protection Agency.

    The authors declare they have no competing financial interests.

    Received 31 August 2004 ; accepted 12 May 2005.

    Introduction

    Twenty-six scientists from 10 countries met at the International
    Agency for Research on Cancer (IARC) in June 2004 to develop IARC
    Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to
    Humans (IARC Monographs) on formaldehyde, 2-butoxyethanol, and 1-tert-
    butoxy-2-propanol (IARC, in press). This is the fourth IARC evaluation
    of formaldehyde and the first of the glycol ethers.

    Formaldehyde is widely used in resins that bind wood products, pulp
    and paper, and glasswool and rockwool insulation. It is also used in
    plastics and coatings, textile finishing, and chemical manufacturing
    and as a disinfectant and preservative. High concentrations can be
    found in some work environments, and much lower concentrations in
    homes.

    2-Butoxyethanol is a glycol ether widely used as a solvent in paints,
    paint thinners, glass-cleaning and surface-cleaning products
    (especially in the printing and silk-screening industries), and
    personal-care and other personal products and as a chemical
    intermediate. General-population exposure can occur through the use of
    consumer products, particularly cleaning agents.

    1-tert-Butoxy-2-propanol is a glycol ether that has found increasing
    use as a solvent in coatings, glass-cleaning and surface-cleaning
    products, inks, adhesives, and nail-polish lacquers.

    Materials and Methods

    IARC convenes an international, interdisciplinary working group of
    expert scientists to develop each volume of the IARC Monographs. The
    working group writes a critical review of the pertinent scientific
    literature (published articles, articles accepted for publication, and
    publicly available documents from government agencies) and a consensus
    evaluation of each agent's potential to cause cancer in humans.

    The IARC Monographs are developed during an 8-day meeting whose
    objectives are review and consensus. Before the meeting, each member
    of the working group writes a portion of the critical review. At the
    meeting, four subgroups (exposure, cancer in humans, cancer in
    experimental animals, and mechanistic and other relevant data) review
    these drafts and develop consensus subgroup drafts. Then the working
    group meets in plenary session to review the subgroup drafts and
    develop a consensus evaluation. After the meeting, IARC scientists
    review the final draft for accuracy and clarity before publication.

    The evaluation is developed in steps (IARC 2005). The subgroup of
    epidemiologists proposes an evaluation of the evidence of cancer in
    humans as sufficient evidence, limited evidence, inadequate evidence,
    or evidence suggesting lack of carcinogenicity. A subgroup of
    toxicologists and pathologists proposes an evaluation of the evidence
    of cancer in experimental animals, choosing one of the same
    descriptors. Combination of these two partial evaluations yields a
    preliminary default evaluation that the agent is one of the following:
    group 1, carcinogenic to humans;
    group 2A, probably carcinogenic to humans;
    group 2B, possibly carcinogenic to humans;
    group 3, not classifiable as to its carcinogenicity to humans; or
    group 4, probably not carcinogenic to humans.

    When the epidemiologic evidence is sufficient, the final evaluation is
    carcinogenic to humans, regardless of the experimental evidence. In
    other cases, the mechanistic and other relevant data are considered to
    determine whether the default evaluation should be modified upward or
    downward. A subgroup of experts in cancer mechanisms assesses the
    strength of the mechanistic data and whether the mechanisms of tumor
    formation in experimental animals can operate in humans. The overall
    evaluation is a matter of scientific judgment, reflecting the combined
    weight of the evidence.

    Working groups are selected to invite the best-qualified experts and
    to avoid real or apparent conflicts of interests. Consideration is
    given also to demographic diversity and a balanced representation of
    all scientific views. Each potential participant submits a Declaration
    of Interests [World Health Organization (WHO) 2005], which IARC
    assesses to determine whether there is a conflict that warrants some
    limitation on participation. An expert with a real or apparent
    conflict of interest may not serve as chairperson, draft text
    discussing cancer data, or participate in the evaluations. IARC
    strives to ensure that the working group is free from all attempts at
    interference, before and during the meeting. This includes lobbying,
    written materials, and meals or other favors offered by interested
    parties. Working group members are asked not to discuss the subject
    matter with anyone outside the meeting and to report all attempts at
    interference (Cogliano et al. 2004).

    Results

    Formaldehyde.

    There was a statistically significant excess of deaths from
    nasopharyngeal cancer in the largest and most informative cohort study
    of industrial workers (Hauptmann et al. 2004), with statistically
    significant exposure-response relationships for peak and cumulative
    exposure.

    An excess of deaths from nasopharyngeal cancer was also observed in a
    proportionate mortality analysis of the largest U.S. cohort of
    embalmers (Hayes et al. 1990),
    and an excess of cases of nasopharyngeal cancer was observed in a
    Danish study of proportionate cancer incidence among workers at
    companies that manufactured or used formaldehyde (Hansen and Olsen
    1995).

    Although other cohort studies reported fewer cases of nasopharyngeal
    cancer than expected (Coggon et al. 2003; Pinkerton et al. 2004;
    Walrath and Fraumeni 1983), the working group noted that the deficits
    were small and the studies had low power to detect an effect on
    nasopharyngeal cancer.

    Of seven case-control studies of nasopharyngeal cancer (Armstrong et
    al. 2000; Hildesheim et al. 2001; Olsen et al. 1984; Roush et al.
    1987; Vaughan et al. 1986, 2000; West et al. 1993), five found
    elevations of risk for exposure to formaldehyde.

    The working group considered it "improbable that all of the positive
    findings for nasopharyngeal cancer that were reported from the
    epidemiologic studies, and particularly from the large study of
    industrial workers in the United States, could be explained by bias or
    unrecognized confounding effects." The working group concluded that
    these studies provide "sufficient epidemiological evidence that
    formaldehyde causes nasopharyngeal cancer in humans."

    Excess mortality from leukemia, primarily of the myeloid type, has
    been observed relatively consistently in six of seven studies of
    embalmers, funeral parlor workers, pathologists, and anatomists (Hall
    et al. 1991; Hayes et al. 1990; Levine et al. 1984; Logue et al. 1986;
    Stroup et al. 1986; Walrath and Fraumeni 1983, 1984).

    A recent meta-analysis found that, overall, the relative risk for
    leukemia in these workers was increased and did not vary significantly
    among studies (Collins and Lineker 2004).

    There had been speculation that these findings might be explained by
    viruses; however, the working group found little evidence that these
    occupations have a higher incidence of viral infections or that
    viruses have a causal role in myeloid leukemia.

    Until recently, these leukemia findings received little attention
    because excess leukemia had not been observed in the studies of
    industrial workers.

    There is now, however, some evidence for an association between
    formaldehyde exposure and leukemia in the recent updates of two of the
    three major industrial cohorts. A statistically significant exposure-
    response relationship was observed for leukemia and, particularly, for
    myeloid leukemia in the study of industrial workers in the United
    States, based on peak exposure and, to a lesser degree, on average
    intensity of exposure to formaldehyde (Hauptmann et al. 2003).

    There was no excess mortality from leukemia when the industrial
    workers were compared with the general U.S. population, but a
    comparison with the general population may be biased.

    In another study, excess mortality from leukemia was found in the
    recent update of garment workers in the United States (Pinkerton et
    al. 2004). This excess was statistically significant among workers
    with a longer duration of exposure and follow-up.

    In contrast, the updated study of industrial workers in the United
    Kingdom did not find excess mortality from leukemia (Coggon et al.
    2003). This high-quality study had sufficient size and follow-up to
    have reasonable power for detecting an excess of leukemia, but it did
    not report on peak exposures or the risk of myeloid leukemia
    specifically.

    The working group concluded, "In summary, there is strong but not
    sufficient evidence for a causal association between leukaemia and
    occupational exposure to formaldehyde." This conclusion, falling
    between sufficient and limited evidence, was based on a consistently
    increased risk in studies of embalmers, funeral parlor workers,
    pathologists, and anatomists and was present in two of the three most
    informative studies of industrial workers.

    Several case-control studies have investigated the relationship
    between formaldehyde exposure and sinonasal cancer. A pooled analysis
    of 12 studies showed an increased risk of adenocarcinoma in men and
    women thought never to have been exposed to wood dust or leather dust,
    with an exposure-response trend for an index of cumulative exposure
    (Luce et al. 2002).

    One other case-control study (Olsen and Asnaes 1986) and a
    proportionate incidence study (Hansen and Olsen 1995) showed an
    increased risk of sinonasal cancer, particularly squamous cell
    carcinoma.

    Against these largely positive findings, the three most informative
    cohort studies of industrial workers showed no excesses of sinonasal
    cancer (Coggon et al. 2003; Hauptmann et al. 2004; Pinkerton et al.
    2004).

    The working group noted that most studies did not distinguish tumors
    as originating in the nose or sinuses; thus, an increased risk of
    nasal cancer would be diluted if there were no corresponding effect on
    the sinuses.

    In the case-control studies, the working group also noted the
    potential for confounding by wood dust exposure, which is associated
    with adenocarcinoma.

    The working group concluded that there is limited evidence that
    formaldehyde causes sinonasal cancer in humans.

    In experimental animals, several studies have shown that inhalation
    exposure induces squamous cell carcinomas of the nasal cavities in
    rats (Albert et al. 1982; Feron et al. 1988; Gibson 1984; Kamata et
    al. 1997; Kerns et al. 1983; Monticello et al. 1996; Morgan et al.
    1986; Sellakumar et al. 1985; Woutersen et al. 1989), although single
    studies in mice (Kerns et al. 1983) and hamsters (Dalbey 1982) showed
    no carcinogenic effects.

    Four studies of formaldehyde administered to rats in drinking water
    gave varying results:
    One showed an increased incidence of forestomach papillomas in male
    rats (Takahashi et al. 1986);
    a second showed an increased incidence of gastrointestinal
    leiomyosarcomas in female rats and in both sexes combined (Soffritti
    et al. 1989);
    a third showed increased incidences of total malignant tumors,
    lymphomas and leukemias, and testicular interstitial-cell adenomas in
    male rats (Soffritti et al. 2002);
    whereas a fourth did not show a carcinogenic effect (Til et al.
    1989).

    Formaldehyde also showed co-carcinogenic effects by inhalation,
    ingestion, and dermal exposure (Dalbey 1982; Iverson 1986; Takahashi
    et al. 1986).

    The toxicokinetics of inhaled formaldehyde have been well studied
    (Agency for Toxic Substances and Disease Registry 1999).

    More than 90% of inhaled formaldehyde is absorbed in the upper
    respiratory tract (Heck et al. 1985).

    Absorbed formaldehyde can be oxidized to formate and carbon dioxide or
    can be incorporated into biologic macromolecules.

    Formaldehyde has a half-life of about 1 min in rat plasma (Rietbrock
    1965).

    Inhalation exposure has not been found to alter the endogenous
    concentration of formaldehyde in the blood of rats, monkeys, or humans
    (Casanova et al. 1988; Heck et al. 1983, 1985).

    Oral exposure to 14C-formaldehyde resulted in some excretion in urine
    and feces within 12 hr (Galli et al. 1983).

    Dermal application of 14C-formaldehyde resulted in some urinary
    excretion in rats and monkeys (Jeffcoat et al. 1983).

    Evidence shows that formaldehyde is genotoxic in multiple in vitro
    models and in exposed humans and laboratory animals.

    Human studies reported increased DNA-protein crosslinks in workers
    exposed to formaldehyde (Shaham et al. 1996, 2003), and this is
    consistent with studies in laboratory rats and monkeys.

    Cellular proliferation increases considerably at concentrations > 6
    ppm and amplifies the genotoxic effects of formaldehyde.

    The working group concluded, "The current data indicate that both
    genotoxicity and cytotoxicity play important roles in the
    carcinogenesis of formaldehyde in nasal tissues."

    On the other hand, with respect to the potential for formaldehyde to
    induce leukemia, the working group was not aware of any good rodent
    models for acute myeloid leukemia in humans.

    Several possible mechanisms were considered, such as clastogenic
    damage to circulating stem cells.

    There is a single study reporting cytogenetic abnormalities in the
    bone marrow of rats inhaling formaldehyde (Kitaeva et al. 1990).

    The working group concluded, "Based on the data available at this
    time, it was not possible to identify a mechanism for the induction of
    myeloid leukaemia in humans." This is an area needing more research.

    The working group concluded that formaldehyde is carcinogenic to
    humans (group 1), based on sufficient evidence in humans and
    sufficient evidence in experimental animals.

    Based on the information now available, this classification is higher
    than those of previous IARC evaluations (IARC 1982, 1987, 1995).

    2-Butoxyethanol.

    2-Butoxyethanol was tested for carcinogenicity by inhalation exposure
    in male and female mice and rats [National Toxicology Program (NTP)
    2000]. Clear increases in tumor incidence were observed only in mice.
    In male mice exposed to 2-butoxyethanol, there was a dose-related
    increase in the incidence of hemangiosarcomas of the liver. In female
    mice, there was a dose-related increase in the incidences of combined
    forestomach squamous-cell papillomas and carcinomas (mainly
    papillomas). In female rats, there was a positive trend in the
    occurrence of benign or malignant pheochromocytomas (mainly benign) of
    the adrenal medulla, but this equivocal result could not be attributed
    with confidence to exposure to 2-butoxyethanol. No increases were
    observed in male rats. The epidemiologic data were inadequate for this
    compound.

    Regarding mechanisms of carcinogenesis, the working group considered
    that hemolysis and associated oxidative stress in the liver have been
    proposed to be linked to the induction of mouse liver neoplasia. They
    also considered that, in view of lower sensitivity to hemolysis of
    human erythrocytes and higher human liver concentrations of the
    antioxidant vitamin E, the induction of liver tumors in humans would
    be improbable through this pathway, but it was noted that other
    potential mechanisms have not been investigated. The working group
    observed that the mouse forestomach tumors are associated with high
    local exposure to 2-butoxyethanol and high local concentrations of the
    toxic metabolite 2-butoxyacetic acid.

    The working group concluded that 2-butoxyethanol is not classifiable
    as to its carcinogenicity to humans (group 3), with limited evidence
    in experimental animals and inadequate evidence in humans.

    1-tert-Butoxy-2-propanol.

    1-tert-Butoxy-2-propanol was tested for carcinogenicity by inhalation
    exposure in male and female mice and rats (Doi et al. 2004; NTP 2003).
    In a single study in both male and female mice, a dose-related
    increase in the combined incidence of liver tumors (hepatocellular
    adenomas and carcinomas), including hepatoblastomas, was observed.
    When hepatocellular carcinomas and hepatoblastomas were combined,
    there was a significant trend for the increase in malignant tumors in
    females. In male rats, there were marginal, nonsignificant increases
    in the incidences of renal tubule adenomas (with one carcinoma at the
    highest dose) and hepatocellular adenomas, but these findings were
    considered to be equivocal. In female rats, there were no dose-related
    increases in tumor incidence. No epidemiologic data were available for
    this compound.

    With regard to mechanisms of carcinogenesis, the working group found
    the available data inadequate to elucidate a potential mechanism for
    the mouse liver tumors. They found the renal effects largely
    consistent with the alpha2u-globulin-associated nephropathy that
    occurs in male rats, but concluded that the available evidence
    satisfies only some, but not all, of the IARC criteria for the
    mechanism associated with accumulation of alpha2u-globulin. Regarding
    the potential for genotoxic effects, the working group was not able to
    draw any meaningful conclusion in view of the scarcity of the data
    available.

    The working group concluded that 1-tert-butoxy-2-propanol is not
    classifiable as to its carcinogenicity to humans (group 3), with
    limited evidence in experimental animals and inadequate evidence in
    humans.

    Discussion

    A theme common to these three evaluations is the consideration of
    mechanistic information to develop and evaluate hypotheses about the
    sequence of steps leading to the induction of tumors in experimental
    animals.

    The hypothesized mechanisms described in these evaluations provide an
    interesting set of cases that range from a vast literature on
    respiratory-tract tumors in rats induced by inhalation of formaldehyde
    to some more tentative hypotheses about the various tumors observed in
    animals after exposure to glycol ethers.

    Both types of mechanistic data sets were of use in the evaluation
    process.

    The evaluation of formaldehyde as carcinogenic to humans shows the
    importance of mechanistic information in the classification of
    carcinogens.

    For the nasopharyngeal tumors, the working group discussed the
    convergence of the epidemiologic, experimental, and mechanistic
    evidence.

    If the evidence in humans had been less than sufficient, the strong
    mechanistic evidence in exposed humans and sufficient evidence in
    experimental animals might still have led to classification as
    group 1.

    The extensive mechanistic data for formaldehyde-induced respiratory
    cancer provide strong support for the empirical observation of
    nasopharyngeal cancer in humans, although computer models that predict
    an anterior-to-posterior gradient of formaldehyde deposition in the
    upper respiratory tract would predict that formaldehyde would cause
    cancer in the nose as well as the nasopharynx in humans.

    On the other hand, the lack of information on possible mechanisms by
    which formaldehyde might increase the risk of leukemia in humans
    tempered the interpretation of the epidemiologic data on that cancer
    type.

    The entire working group discussed at length this divergence between
    the epidemiologic and mechanistic conclusions for leukemia.

    Information to support a biologically plausible mechanism could have
    supported a stronger conclusion about the evidence of leukemia in
    humans.

    In the evaluations of the glycol ethers, the working group grappled
    with questions of interpretation and scientific judgment.

    A recurring issue was the criterion for characterizing a rare tumor or
    an unusual set of observations that can carry greater weight than a
    typical bioassay result.

    A related matter was how to bring in additional information to resolve
    difficult questions -- or example, how to consider the results of
    historical controls or alternative statistical tests.

    When the working group tried to, but could not, reach consensus on a
    question of interpretation or scientific judgment, the evaluation
    presented the differing positions favored by its members.

    For instance, dose-related induction of hepatoblastoma in male and
    female mice, considering hepatoblastoma as a rare neoplasm with low
    spontaneous incidence in mice, especially in females.

    Most of the working group, nevertheless, considered the evidence to be
    limited, based on the interpretation of hepatoblastoma being a variant
    of hepatocellular carcinoma.

    It is important to note that the evaluation of an agent as not
    classifiable as to its carcinogenicity to humans is not a
    determination of safety, with respect to both cancer and effects other
    than cancer.

    It indicates that the data did not meet the minimum standards
    developed by the IARC for sufficient evidence in experimental animals
    and suggests that further testing is needed, particularly when there
    is widespread human exposure or another reason for public health
    concern.

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    Last Updated: August 5, 2005

    http://www.iarc.fr/
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    Group 1 carcinogenic to humans (87);
    Group 2A probably carcinogenic to humans (63);
    Group 2B possibly carcinogenic to humans (234);
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    Lancet Oncol. 2007 Apr; 8(4): 292-3.
    Carcinogenicity of alcoholic beverages.

    * Baan R,
    * Straif K,
    * Grosse Y,
    * Secretan B,
    * El Ghissassi F,
    * Bouvard V,
    * Altieri A,
    * Cogliano V;
    * WHO International Agency for Research on Cancer Monograph
    Working Group.

    PMID: 17431955


    [ Their Monograph #96 on alcohol references Morando Soffritti:

    " 18 Soffritti M, Belpoggi F, Cevolani D, et al. Results
    of long-term experimental studies on the
    carcinogenicity of methyl alcohol and ethyl
    alcohol in rats. Ann N Y Acad Sci 2002; 982: 46-69. " ]

    http://genomics.unc.edu/news_events/96_Baan_alcohol.pdf

    page 292 http://oncology.thelancet.com Vol 8 April 2007
    Policy Watch

    Carcinogenicity of alcoholic beverages http://monographs.iarc.fr/

    Robert Baan,
    Kurt Straif,
    Yann Grosse,
    Béatrice Secretan,
    Fatiha El Ghissassi,
    Véronique Bouvard,
    Andrea Altieri,
    Vincent Cogliano,
    on behalf of the WHO International Agency for Research on Cancer
    Monograph Working Group

    In February, 2007, 26 scientists from 15 countries met at the
    International
    Agency for Research on Cancer (IARC) in Lyon, France, to reassess the
    carcinogenicity
    of alcoholic beverages and of ethyl carbamate (urethane), a frequent
    contaminant of fermented foods and beverages.

    These assessments will be published as volume 96 of the IARC
    Monographs.1

    This paper reports on the assessment of alcoholic beverages.

    Details on the assessment of ethyl carbamate can be found at
    http://monographs.iarc.fr/

    Although moderate alcohol consumption has some health benefits,2
    the WHO identified the consumption of alcohol as one of the top-10
    risks
    for worldwide burden of disease.3

    In 2002, more than 1.9 billion adults (over 15 years of age) around
    the
    world were estimated to be regular consumers of alcoholic beverages,
    with an average daily consumption
    of 13 g of ethanol (about one drink).4

    In general, men drink alcohol more often and in larger quantities than
    women.

    On the basis of production data, per-capita consumption
    is highest in eastern Europe and the Russian Federation.

    In Africa, South America, and Asia, alcohol consumption is
    comparatively lower,
    but a large proportion of alcohol is produced locally and remains
    unrecorded.

    Over the past 40 years, alcohol consumption has remained stable in
    most regions of
    the world, except in the western Pacific region -- predominantly China
    --
    where it has increased by about five times.

    In addition to ethanol and water, alcoholic beverages can contain many
    different substances derived from fermentation,
    contamination, and from the use of additives or flavours.

    The Working Group reviewed the epidemiological published work on the
    possible association between alcohol consumption and cancer at 27
    anatomical
    sites.

    Many studies of different design and in different populations
    around the world have consistently shown that regular alcohol
    consumption
    is associated with an increased risk for cancers
    of the oral cavity, pharynx, larynx, and oesophagus.5-7

    Daily consumption of around 50 g of alcohol increases the risk for
    these cancers by
    two to three times, compared with the risk in non-drinkers.

    Additionally, the effects of drinking and smoking seem to be
    multiplicative.

    Furthermore, in populations that are deficient in the activity of
    aldehyde dehydrogenase,
    an enzyme involved in the catabolism of ethanol,
    much higher risks for oesophageal cancer after alcohol consumption
    have
    been reported than in populations with a fully active enzyme.8

    A large number of cohort and case-control studies provide strong
    evidence
    that the consumption of alcohol is an independent risk factor
    for primary liver cancer.

    Cirrhosis and other liver diseases often occur before the cancer
    becomes manifest
    and patients with these disorders generally reduce their alcohol
    intake.

    Therefore, the effect of alcohol consumption on the risk for liver
    cancer is difficult to quantify.9

    More than 100 epidemiological studies that assessed the association
    between alcohol consumption and breast cancer in women consistently
    found an increased risk with increasing alcohol intake.

    A pooled analysis of 53 studies on more than 58,000 women with breast
    cancer
    showed that daily consumption of about 50 g of alcohol is associated
    with a relative risk of about 1.5 (95% confidence interval 1.3 --
    1.6),
    compared with that in non-drinkers.10

    For regular consumption of even 18 g of alcohol per day the relative
    risk is
    significantly increased.10

    The association between alcohol consumption and colorectal cancer
    has been reported on by more than 50 prospective and case-control
    studies.

    Pooled results from eight cohort studies11 and data from recent meta-
    analyses
    provide evidence for an increased relative risk of about 1.4
    for colorectal cancer with regular consumption of about 50 g of
    alcohol per day,
    compared with that in nondrinkers.

    This association seems to be similar for colon cancer and for rectal
    cancer.11,12

    By contrast, both cohort and case-control studies provide consistent
    evidence
    of no increase in risk for renal-cell cancer with increasing alcohol
    consumption.

    In several studies, increasing alcohol intake was associated
    with a significantly lower risk for renal-cell cancer.

    This inverse trend was seen in both men and women.13,14

    Furthermore, two prospective cohort studies and several large case-
    control studies
    showed an inverse association or no association between alcohol
    consumption
    and non-Hodgkin lymphoma;
    most studies showed a lower risk in drinkers than in non-drinkers.
    15,16

    For cancers of the lung and stomach, there were suggestions that
    alcohol
    consumption might be associated with an increased risk,
    but confounding by smoking and dietary habits could not be ruled out.

    For other cancers, the evidence of an association between alcohol
    consumption
    and cancer risk was generally sparse or inconsistent.

    In animals, administration of ethanol in drinking-water caused a dose
    related
    increase in the incidence of hepatocellular adenomas and carcinomas
    in male mice,17 an increased incidence of head and neck carcinomas
    in male and female rats, an increased incidence of fore-stomach
    carcinomas,
    testicular interstitial-cell adenomas, and osteosarcomas
    of the head, neck, and other sites in male rats,18
    and of

    Policy Watch http://oncology.thelancet.com Vol 8 April 2007 page 293

    mammary adenocarcinomas in female rats.19

    In most of the studies in which ethanol was co-administered with
    known carcinogens, it enhanced the carcinogenic effect.

    The Working Group concluded that there is "sufficient evidence" for
    the carcinogenicity of
    ethanol in animals.20

    The major alcohol-metabolising enzymes in humans are the
    alcohol dehydrogenases (ADH) that oxidise alcohol (ethanol) to
    acetaldehyde,
    and the aldehyde dehydrogenases (ALDH) that detoxify acetaldehyde to
    acetate.

    The variant allele ALDH2*2, which encodes an inactive subunit of the
    enzyme ALDH2,
    is dominant and highly prevalent in certain populations of Asian
    ethnicity (28-45%),
    but rare in other ethnic groups.21

    Most homozygous carriers of this allele (ALDH2*2/*2) are abstainers or
    infrequent drinkers,
    because the enzyme deficiency would cause a strong facial flushing
    response,
    physical discomfort, and severe toxic reactions.

    In heterozygous carriers (ALDH2*1/*2, with about 10% residual ALDH2
    activity)
    these acute adverse effects are less severe, but when alcohol is
    consumed
    these carriers are at high risk for several alcohol-related
    aerodigestive cancers.

    For example, genetic epidemiological studies provide strong evidence
    that the heterozygous genotype contributes substantially to the
    development
    of oesophageal cancer related to alcohol consumption,
    with relative risks -- compared with carriers of the homozygous
    ALDH2*1/*1
    genotype, which encodes the active enzyme -- of up to 12 for heavy
    drinkers.22

    Compared with those with the ALDH2*1/*1 genotype,
    the heterozygous carriers have higher levels of acetaldehyde in blood
    and saliva
    after alcohol drinking, and in a recent study higher levels of
    acetaldehyde-related
    DNA adducts have been measured in their lymphocytes.23

    Overall, the Working Group confirmed that alcoholic beverages are
    "carcinogenic to humans" (Group 1),20
    and concluded that the occurrence of malignant tumours of the oral
    cavity,
    pharynx, larynx, oesophagus, liver, colorectum, and female breast
    is causally related to alcohol consumption.

    For renal-cell cancer and non-Hodgkin lymphoma
    the Working Group concluded that there is "evidence suggesting lack of
    carcinogenicity"
    for alcohol drinking.20

    The addition of breast cancer and colorectal cancer,
    two of the most common cancers worldwide, to the list of cancers
    causally related to alcohol consumption suggests that the proportion
    of cancers
    attributable to alcohol consumption is higher than previously
    estimated.

    Because these associations were generally noted with different types
    of alcoholic beverage, and in view of the carcinogenicity of ethanol
    in animals,
    the Working Group also classified ethanol in alcoholic beverages
    as "carcinogenic to humans" (Group 1).20

    The Working Group agreed that the substantial mechanistic evidence
    in humans deficient in aldehyde dehydrogenase indicates that
    acetaldehyde
    derived from the metabolism of ethanol in alcoholic beverages
    contributes to causing malignant oesophageal tumours.

    The IARC authors declared no conflicts of interest.

    1 IARC. IARC monographs on the evaluation of carcinogenic risks to
    humans. Volume 96.
    Alcoholic beverage consumption and ethylcarbamate (urethane).
    Lyon: International Agency for Research on Cancer (in press).

    2 WHO. WHO Global Status Report on Alcohol
    2004. Geneva: World Health Organization,
    Department of Mental Health and Substance Abuse.

    3 Ezzati M, Rodgers A, Lopez AD, et al. Mortality
    and burden of disease attributable to
    individual risk factors. In: Ezzati M, Lopez AD,
    Rodgers A, Murray CJL, eds. Comparative
    quantifi cation of health risks. Global and
    regional burden of disease attributable to
    selected major risk factors. Volume 2. Geneva:
    World Health Organization, 2004: 2141-66.

    4 WHO. WHO Global Alcohol Database.
    http://www.who.int/globalatlas/default.asp
    (accessed March 2, 2007).

    5 Boeing H. Alcohol and risk of cancer of the upper
    gastrointestinal tract: first analysis of the EPIC
    data. In: Riboli E, Lambert R, eds. Nutrition and
    lifestyle: opportunities for cancer prevention.
    IARC Sci Publ 156. Lyon: International Agency
    for Research on Cancer, 2002: 151-54.

    6 Talamini R, Bosetti C, La Vecchia C, et al.
    Combined eff ect of tobacco and alcohol on
    laryngeal cancer risk: a case-control study.
    Cancer Causes Control 2002; 13: 957-64.

    7 Znaor A, Brennan P, Gajalakshmi V, et al.
    Independent and combined eff ects of tobacco
    smoking, chewing and alcohol drinking on the
    risk of oral, pharyngeal and esophageal cancers
    in Indian men. Int J Cancer 2003; 105: 681-86.

    8 Yokoyama A, Omori T. Genetic polymorphisms
    of alcohol and aldehyde dehydrogenases and
    risk for esophageal and head and neck cancers.
    Alcohol 2005; 35: 175-85.

    9 Bagnardi V, Blangiardo M, La Vecchia C, et al.
    A meta-analysis of alcohol drinking and cancer
    risk. Br J Cancer 2001; 85: 1700-05.

    10 Hamajima N, Hirose K, Tajima K, et al. Alcohol,
    tobacco and breast cancer - collaborative
    reanalysis of individual data from 53
    epidemiological studies, including 58,515 women
    with breast cancer and 95,067 women without
    the disease. Br J Cancer 2002; 87: 1234-45.

    11 Cho E, Smith-Warner SA, Ritz J, et al. Alcohol
    intake and colorectal cancer: a pooled analysis
    of 8 cohort studies. Ann Intern Med 2004;
    140: 603-13.

    12 Moskal A, Norat T, Ferrari P, Riboli E. Alcohol
    intake and colorectal cancer risk: a dose response
    meta-analysis of published cohort
    studies. Int J Cancer 2007; 120: 664-71.

    13 Hu J, Mao Y, White K. Diet and vitamin or
    mineral supplements and risk of renal cell
    carcinoma in Canada. Cancer Causes Control
    2003; 14: 705-14.

    14 Hsu CC, Chow WH, Boff etta P, et al. Dietary risk
    factors of kidney cancer in eastern and central
    Europe. Am J Epidemiol 2007 (in press).

    15 Morton LM, Zheng T, Holford TR, et al.
    Alcohol consumption and risk of non-Hodgkin
    lymphoma: a pooled analysis. Lancet Oncol
    2005; 6: 469-76.

    16 Besson H, Brennan P, Becker N, et al. Tobacco
    smoking, alcohol drinking and non-Hodgkin's
    lymphoma: a European multicenter casecontrol
    study (Epilymph). Int J Cancer 2006; 119: 901-08.

    17 US National Toxicology Program. Toxicology
    and Carcinogenesis Studies of Urethane +
    Ethanol (CAS Nos. 51-79-6 & 64-17-5) in
    F344/N Rats and B6C3F1 Mice (drinking-water
    studies). NTP Technical Report No. 510.
    Bethesda: National Institutes of Health, 2004.

    18 Soffritti M, Belpoggi F, Cevolani D, et al. Results
    of long-term experimental studies on the
    carcinogenicity of methyl alcohol and ethyl
    alcohol in rats. Ann N Y Acad Sci 2002; 982: 46-69.

    19 Watabiki T, Okii Y, Tokiyasu T, et al. Long-term
    ethanol consumption in ICR mice causes
    mammary tumor in females and liver fibrosis
    in males. Alcohol Clin Exp Res 2000; 24: 117S-22S.

    20 IARC. Preamble to the IARC monographs on
    the evaluation of carcinogenic risks to humans.
    http://monographs.iarc.fr/ENG/Preamble/
    CurrentPreamble.pdf (accessed March 2, 2007).

    21 Goedde HW, Agarwal DP, Fritze G, et al.
    Distribution of ADH2 and ALDH2 genotypes in
    diff erent populations. Hum Genet 1992; 88: 344-46.

    22 Lewis SJ, Smith GD. Alcohol, ALDH2, and
    esophageal cancer: a meta-analysis which
    illustrates the potentials and limitations of a
    Mendelian randomization approach. Cancer
    Epidemiol Biomarkers Prev 2005; 14: 1967-71.

    23 Matsuda T, Yabushita H, Kanaly RA, et al.
    Increased DNA damage in ALDH2-deficient
    alcoholics. Chem Res Toxicol 2006; 19: 1374-78.

    Monograph Working Group Members

    WC Willett -- Chair (USA); WWillett@hsph.harvard.edu,
    AB Miller, ab.miller@sympatico.ca,
    J Rehm (Canada); jtrehm@aol.com, Centre for Addiction and Mental
    Health, Toronto, Ontario Canada
    L Cai (China); l0cai001@louisville.edu, Dr. Lu Cai, Department of
    Medicine, University of Louisville School of Medicine, 511 South Floyd
    St., MDR 533, Louisville, KY 40202 l0cai001@louisville.edu
    Department of Medicine, University of Louisville, School of Medicine,
    Louisville, Kentucky
    Department of Pharmacology and Toxicology, University of Louisville,
    School of Medicine, Louisville, Kentucky
    K Bloomfield (Denmark); Kim Bloomfield kbl@health.sdu.dk, Unit of
    Health Promotion Research, University of Southern Denmark, Niels Bohrs
    Vej 9, 6700 Esbjerg, Denmark. Tel: +45-6550 4111; Fax: +45-6550 4283
    P Eriksson (Finland); per.eriksson@ebc.uu.se, Department of
    Environmental Toxicology, Uppsala University, Norbyvagen 18A, S-752 36
    Uppsala, Sweden
    J Bénichou (France, unable to attend); jacques.benichou@chu-rouen.fr,
    University of Rouen School of Medicine and Rouen University Hospital,
    Department of Biostatistics, Rouen, France
    DW Lachenmeier, Lachenmeier@web.de, Chemisches und
    Veterinaruntersuchungsamt (CVUA) Karlsruhe, Weissenburger Str. 3,
    D-76187, Karlsruhe, Germany, Institut fur Rechtsmedizin, Technische
    Universitat Dresden, Fetscherstr. 74, D-01307 Dresden, Germany
    HK Seitz (Germany); helmut_karl.seitz@urz.uni-heidelberg.de,
    Laboratory of Alcohol Research, Liver Disease and Nutrition and
    Department of Medicine, Salem Medical Center, Heidelberg, Germany
    C La Vecchia (Italy);
    S Kono, skono@phealth.med.kyushu-u.ac.jp, Department of Preventive
    Medicine, Faculty of Medical Sciences, Kyushu University, Fukuoka,
    Japan
    A Yokoyama (Japan); National Hospital Organization Kurihama
    Alcoholism Center, Kanagawa, Japan
    S-I Cho (Republic of Korea); Department of Environmental Health,
    School of Public Health, Seoul National University, 28 YeonKeon-Dong,
    Jongro-Gu, Seoul 110-799, Republic of Korea.
    Sung-il Cho, MD; Department of Environmental Health, Harvard School
    of Public Health, 665 Huntington Avenue, FXB-101, Boston, MA
    02115-6096
    Sung-il Cho, scho@snu.ac.kr, Department of Epidemiology, School of
    Public Health and Institute of Health and Environment, Seoul National
    University, Jongno-gu Yeongun-dong 28, Seoul 110-460, Republic of
    Korea
    L-L Griciute (Lithuania);
    E Weiderpass (Norway); ewv@kreftregisteret.no, Department of
    Etiological Research, The Cancer Registry of Norway, N-0310 Oslo,
    Norway
    M Marques (Portugal);
    N Rehn-Mendoza (Singapore);
    G Gmel (Switzerland); gerhard.gmel@chuv.ch, Alcohol Treatment
    Center, Lausanne University Hospital, CH-1011 Lausanne, Switzerland
    NE Allen, naomi.allen@cancer.org.uk, Cancer Research UK Epidemiology
    Unit, University of Oxford, Radcliffe Infirmary, Oxford OX2 6HE, UK
    V Beral (UK); beralv@icrf.icnet.uk, Cancer Research UK Epidemiology
    Unit, University of Oxford, Radcliffe Infirmary, Oxford OX2 6HE, UK
    LM Anderson, Andersol@mail.ncifcrf.gov, Laboratory of Comparative
    Carcinogenesis, National Cancer Institute at Frederick, Frederick, MD
    21702, USA
    FA Beland, fbeland@nctr.fda.gov, Division of Biochemical
    Toxicology, National Center for Toxicological Research, Jefferson,
    Arkansas 72079, USA
    PJ Brooks, pjbrooks@mail.nih.gov, Section on Molecular Neurobiology,
    Laboratory of Neurogenetics, National Institute on Alcohol Abuse and
    Alcoholism, 5625 Fishers Lane, Room 3S32, MSC 9412, Rockville, MD
    20852, USA
    DW Crabb, dcrabb@iupui.edu, Indiana Alcohol Research Center,
    Division of Gastroenterology and Hepatology, Department of Medicine,
    Indiana University School of Medicine, Indianapolis, USA
    SM Gapstur, sgapstur@northwestern.edu, Department of Preventive
    Medicine, Feinberg School of Medicine, Northwestern University,
    Chicago, IL 60611, USA
    I Rusyn, iir@unc.edu, Department of Environmental Sciences and
    Engineering, University of North Carolina at Chapel Hill, Chapel Hill,
    NC 27599, USA
    Z-F Zhang (USA) ZFZHANG@UCLA.EDU, ZUO-FENG ZHANG
    Department of Epidemiology, UCLA School of Public Health, 71-225 CHS,
    Box 951772, 650 Charles E. Young Drive, South Los Angeles, CA
    90095-1772 (310) 825-8418 (Office) (310) 206-6039 (Fax)

    Conflicts of interests
    DWC is a member of the Medical Advisory Council of the Alcoholic
    Beverages Medical Research Foundation. www.abmrf.org/
    1122 Kenilworth Drive, Suite 407, Baltimore, Maryland 21204
    410.821.7066 Fax: 410.821.7065 info@abmrf.org,

    All other members of the Working Group declared no conflicts of
    interests.

    Invited Specialists None

    Representatives A Huici-Montagud (European Commission, Luxembourg)

    Observers None
    ///////////////////////////////////////////////////////////


    BMC Gastroenterol. 2006 Dec 4;6: 41.
    Time trends in socioeconomic differences in incidence rates of
    cancers of gastro-intestinal tract in Finland.

    * Weiderpass E,
    * Pukkala E.

    Department of Etiological Research, The Cancer Registry of Norway,
    N-0310 Oslo, Norway. ewv@kreftregisteret.no,

    BACKGROUND: The magnitude of socioeconomic differences in health
    varies between societies, and over time within a given society.
    We studied the association between social class and incidence of
    cancers of the gastro-intestinal tract over time in a large cohort in
    Finland.
    METHODS: We studied social class variation among 45-69 year-old Finns
    during 1971-95 in incidence of cancers of the gastro-intestinal tract
    by means of a computerized record linkage of the Finnish Cancer
    Registry and the 1970 Population Census, which included social class
    data.
    RESULTS: There were 2.3 million individuals in the cohort under follow-
    up, with 1622 cases of cancer of the esophagus, 8069 stomach (non-
    cardia), 1116 cardia, 408 small intestine, 6361 colon, 5274 rectum,
    1616 liver, 1756 gallbladder, and 5084 pancreas during 1971-1995.
    Cancers of the esophagus, stomach, cardia, gallbladder and pancreas
    were most common among persons belonging to a low social class.
    Cancers of the small intestine in males only, colon in both genders,
    and rectum in females were most common in the higher social classes.
    Incidence of stomach cancer decreased and incidence of colon cancer
    increased over time in both genders in all social classes, and the
    large differences between social classes remained unchanged over time.
    Incidence rates of cardia cancer did not change substantially over
    time.
    CONCLUSION: There is a large variation in incidence of cancer of the
    gastrointestinal tract by social class in Finland.

    Although much of the observed social class differences probably could
    be explained by known etiological factors such as diet, physical
    exercise, alcohol consumption, smoking and exogenous hormone use,
    part of the variation is apparently attributable to largely unknown
    factors.
    PMID: 17144908


    Int J Cancer. 2004 Feb 20; 108(5): 741-9.
    The role of type of tobacco and type of alcoholic beverage in oral
    carcinogenesis.

    * Castellsague X,
    * Quintana MJ,
    * Martinez MC,
    * Nieto A,
    * Sanchez MJ,
    * Juan A,
    * Monner A,
    * Carrera M,
    * Agudo A,
    * Quer M,
    * Munoz N,
    * Herrero R,
    * Franceschi S,
    * Bosch FX.

    Institut Catala d'Oncologia, Servei d'Epidemiologia i Registre del
    Cancer, L'Hospitalet de Llobregat, Barcelona, Spain.
    xcastellsague@ico.scs.es,

    Incidence rates of oral and oropharyngeal cancers (oral cancer) in
    Spain are among the highest in Europe.
    Spain has a population heavily exposed to various types of tobacco and
    alcoholic beverages but the role and impact of tobacco type and
    beverage type in oral carcinogenesis remain controversial.
    To estimate the independent and joint effects of tobacco smoking and
    alcohol drinking habits on the risk of developing oral cancer, we
    carried out a multicenter, hospital-based, case-control study in
    Spain. Data from 375 patients newly diagnosed with cancer of the oral
    cavity or oropharynx and 375 matched control subjects were analyzed
    using multivariate logistic regression procedures.
    All exposure characteristics of amount, duration and cessation of both
    tobacco smoking and alcohol drinking were strongly associated with
    cancer risk following a dose-dependent relationship.
    At equal intake or duration levels, black-tobacco smoking and drinking
    of spirits were both associated with a 2- to 4-fold increase in cancer
    risk compared to blond tobacco smoking or drinking of wine or beer,
    respectively.
    While ever exposure to smoking only or drinking only was associated
    with a moderate and nonsignificant increase in cancer risk, a history
    of simultaneous exposure to both habits was associated with a 13-fold
    increase that was compatible with a synergistic effect model (p-value
    for interaction: 0.008).
    Exposure to black tobacco smoking and/or drinking of spirits may
    account for up to 77% of oral cancer occurrence in Spain.
    Both black tobacco smoking and drinking of spirits place individuals
    at a very high risk of developing oral cancer.

    Simultaneous exposure to tobacco and alcohol consumption increases
    oral cancer risk in a synergistic fashion, even when consumption
    levels are moderate.

    These results underline the importance of type of tobacco and alcohol
    concentration in oral carcinogenesis.
    Copyright 2003 Wiley-Liss, Inc. PMID: 14696101


    http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=2817164
    free full text pdf

    Am J Public Health. 1989 Nov; 79(11): 1516-20.
    Carcinogenicity of dark liquor.

    * Rothman KJ,
    * Cann CI,
    * Fried MP.
    Department of Medicine, Boston University Medical Center, MA.
    KENNETH J. ROTHMAN, DRPH, krothman@rti.org, Epidemiology Research,
    RTI Health Solutions, RTI International, Research Triangle Park, North
    Carolina, USA
    CRISTINA I. CANN, Former Associate Editor, Epidemiology; Boston
    University School of Public Health
    MARVIN P. FRIED, MD mfried@montefiore.org, Montefiore Medical
    Center, Medical Arts Pavilion, 3400 Bainbridge Avenue, MAP, Room 3rd
    floor, Bronx, NY 10467 (718) 920-2991 Fax: (718) 882-2463
    Professor, Department of Otorhinolaryngology - Head & Neck Surgery
    Chair, Department of Otorhinolaryngology - Head & Neck Surgery


    To investigate whether the non-alcohol content of distilled
    alcoholic beverages affects the carcinogenicity of the beverage, we
    conducted an epidemiologic study of laryngeal and hypopharyngeal
    cancer.
    We interviewed 384 cases (or spouses, for deceased cases), and
    compared their responses with those of 876 controls.
    We classed distilled liquors as dark or light, a rough division
    according to content of potentially carcinogenic compounds in the
    beverages.
    The relative effect on hypopharyngeal cancer risk was much stronger
    for those who reported high consumption of dark liquor (relative risk
    = 4.4, 90% confidence interval = 2.9, 6.8) than for those reporting
    comparable consumption of light liquor (relative risk = 1.3, 90% CI =
    0.8, 2.1).
    For laryngeal cancer, consumption of dark liquor had a smaller effect,
    and there was little distinction between the effects of dark and light
    liquor.
    The data appear consistent with the theory that the non-alcoholic
    content of distilled alcoholic beverages is a determinant of cancer
    risk, and that alcoholic beverages act topically rather than
    systemically in their carcinogenic action.

    PMID: 2817164


    J Agric Food Chem. 2006 May 31; 54(11): 3911-5.
    Quantification of selected volatile constituents and anions in
    Mexican Agave spirits (Tequila, Mezcal, Sotol, Bacanora).

    * Lachenmeier DW,
    * Sohnius EM,
    * Attig R,
    * Lopez MG.

    Chemisches und Veterinaruntersuchungsamt (CVUA) Karlsruhe,
    Weissenburger Strasse 3, 76187 Karlsruhe, Germany Lachenmeier@web.de

    A large collection (n = 95) of Mexican Agave spirits with
    protected appellations of origin (Tequila, Mezcal, Sotol, and
    Bacanora) was analyzed using ion and gas chromatography
    Because of their production from oxalate-containing plant material,
    all Agave spirits contained significant concentrations of oxalate
    (0.1-9.7 mg/L).
    The two Tequila categories ("100% Agave" and "mixed") showed
    differences in the methanol, 2-/3-methyl-1-butanol, and 2-
    phenylethanol concentrations with lower concentrations in the mixed
    category.
    Mezcal showed no significant differences in any of the evaluated
    parameters that would allow a classification.
    Sotol showed higher nitrate concentrations and lower 2-/3-methyl-1-
    butanol concentrations.
    Bacanora was characterized by exceptionally high acetaldehyde
    concentrations and a relatively low ethyl lactate content.

    The methanol content was the most problematic compound regarding the
    Mexican standards:
    two Tequilas (4%), five Sotols (31%), and six Bacanoras (46%) had
    levels above the maximum methanol content of 300 g/hL of alcohol.

    In conclusion, the composition of Mexican Agave spirits was found to
    vary over a relatively large range.
    PMID: 16719514


    J Agric Food Chem. 2005 Mar 23; 53(6): 2151-7.
    Multivariate analysis of FTIR and ion chromatographic data for the
    quality control of tequila.

    * Lachenmeier DW,
    * Richling E,
    * Lopez MG,
    * Frank W,
    * Schreier P.

    Chemisches und Veterinaruntersuchungsamt (CVUA) Karlsruhe,
    Weissenburger Strasse 3, 76187 Karlsruhe, Germany. Lachenmeier@web.de,

    Principal component analysis (PCA) was applied to the
    chromatographic and spectroscopic data of authentic Mexican tequilas
    (n = 14) and commercially available samples purchased in Mexico and
    Germany (n = 24).
    The scores scatter plot of the first two principal components (PC) of
    the anions chloride, nitrate, sulfate, acetate, and oxalate accounting
    for 78% of the variability allowed a classification between tequilas
    bottled in Mexico and overseas;
    however, no discrimination between tequila categories was possible.
    Mexican products had a significantly (p = 0.0014) lower inorganic
    anion concentration (range = 1.5-5.1 mg/L; mean = 2.5 mg/L) than the
    products bottled in the importing countries (range = 3.3-62.6 mg/L;
    mean = 26.3 mg/L).
    FTIR allowed a rapid screening of density and ethanol as well as the
    volatile compounds methanol, ethyl acetate, propanol-1, isobutanol,
    and 2-/3-methyl-1-butanol using partial least-squares regression
    (precisions = 5.3-29.3%).
    Using PCA of the volatile compounds, a differentiation between tequila
    derived from "100% agave" (Agave tequilana Weber var. azul, Agavaceae)
    and tequila produced with other fermentable sugars ("mixed"tequila)
    was possible.
    The first two PCs describe 89% of the total variability of the data.
    Methanol and isobutanol influenced the variability in PC1, which led
    to discrimination.

    The concentrations of methanol and isobutanol were significantly
    higher (methanol, p = 0.004; isobutanol, p = 0.005) in the 100% agave
    (methanol, 297.9 ± 49.5; isobutanol, 251.3 ± 34.9) than in the mixed
    tequilas (methanol, 197.8 ± 118.5; isobutanol, 151.4 ± 52.8).
    PMID: 15769149


    Int J Cancer. 1979 Apr 15; 23(4): 443-7.
    Oesophageal cancer and alcohol consumption; importance of type of
    beverage.

    * Tuyns AJ,
    * Pequignot G,
    * Abbatucci JS.

    The role of alcohol consumption in oesophageal cancer in Normandy
    has been studied by a retrospective study of 312 male cases and 869
    controls.
    The linear relationship between the logarithm of risk and overall
    daily alcohol consumption was confirmed after adjustment for tobacco.
    The role of each specific alcoholic beverage was further investigated
    by computing relative risks for individuals consuming a given beverage
    and for those drinking other beverages only, within each overall
    alcohol consumption category.
    It is concluded:
    (1) that there is a linear relationship between the logarithm of risk
    of oesophageal cancer and overall daily ethanol consumption, whatever
    the beverage
    (2) that the effect is more marked for strong beverages
    (3) that there is an additional risk related to apple brandy and
    cider.
    PMID: 437923
    ///////////////////////////////////////////////////////////


    second large Ramazzini study on low dose lifetime aspartame in rats
    confirms carcinogenicity -- Morando Soffritti will give data and get
    Selikoff award April 23 at Mount Sinai School of Medicine in NYC:
    Murray 2007.04.24
    http://groups.yahoo.com/group/aspartameNM/message/1415

    http://groups.yahoo.com/group/aspartameNM/message/1250
    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

    http://groups.yahoo.com/group/aspartameNM/message/1226
    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,
    www.guardian.co.uk: Murray 2005.09.30

    http://groups.yahoo.com/group/aspartameNM/message/1186
    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

    http://groups.yahoo.com/group/aspartameNM/message/1189
    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

    http://groups.yahoo.com/group/aspartameNM/message/1016
    President Bush & formaldehyde (aspartame) toxicity:
    Ramazzini Foundation carcinogenicity results Dec 2002:
    Soffritti: Murray 2003.08.03 rmforall

    http://www.ramazzini.it./fondazione/pdfUpload/Ann%20NY%20Acad%20Sci%20982%2087-105_2002.pdf
    19 page free full text pdf

    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. crcfr@ramazzini.it

    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. crcfr@ramazzini.it

    http://www.ramazzini.it./fondazione/pdfUpload/Ann%20NY%20Acad%20Sci%20982%2046-69_2002.pdf
    24 page free full text pdf

    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


    http://groups.yahoo.com/group/aspartameNM/message/1339
    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

    http://groups.yahoo.com/group/aspartameNM/message/1335
    Morando Soffritti of Ramazzini Foundation rebuts EFSA AFC critique,
    www.laleva.org: Murray 2006.05.05

    http://groups.yahoo.com/group/aspartameNM/message/1334
    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

    http://www.efsa.eu.int/press_room/press_release/1472_en.html

    http://www.efsa.eu.int/science/afc/afc_opinions/1471_en.html

    http://www.efsa.eu.int/press_room/media_events/catindex_en.html

    http://www.flyonthewall.com/FlyBroadcast/efsa.eu.int/AspartamePressConference/

    www.efsa.eu.int/science/afc/afc_opinions/1471/afc_op_ej356_aspartame_en1.\pdf

    http://groups.yahoo.com/group/aspartameNM/message/1338
    Aspartame: The healthy option? Richard A. Lovett, The New Scientist
    2006.05.04: Murray 2006.05.08

    http://groups.yahoo.com/group/aspartameNM/message/1302
    The Lowdown on Sweet? (Ramazzini Foundation, M Soffritti proof that
    aspartame causes cancers), Melanie Warner, The New York Times:
    sucralose: Prof. DL Katz: Murray 2006.02.12

    http://groups.yahoo.com/group/aspartameNM/message/1303
    David L. Katz MD comments briefly with Diane Sawyer on ABC
    Good Morning America re Ramazzini aspartame cancer study:
    excellent opus at Yale U: mainstream research on aspartame
    (methanol, formaldehyde, formic acid) toxicity: Murray 2006.02.14
    ///////////////////////////////////////////////////////////


    aspartame (methanol, formaldehyde) toxicity research summary: Rich
    Murray 2007.04.30
    http://groups.yahoo.com/group/aspartameNM/message/1404

    One liter aspartame diet soda, about 3 12-oz cans,
    gives 61.5 mg methanol,
    so if 30% is turned into formaldehyde, the formaldehyde
    dose of 18.5 mg is 37 times the recent EPA limit of
    0.5 mg per liter daily drinking water for a 10-kg child:
    www.epa.gov/teach/chem_summ/Formaldehyde_summary.pdf
    2007.01.05 [ does not discuss formaldehyde from methanol
    or aspartame ]
    http://www.epa.gov/teach/teachsurvey.html comments
    teach@environmentalhealthconsulting.com


    "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 rmforall@comcast.net
    505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

    http://groups.yahoo.com/group/aspartameNM/messages
    group with 74 members, 1,421 posts in a public, searchable archive
    http://RMForAll.blogspot.com

    http://groups.yahoo.com/group/aspartameNM/message/1340
    aspartame groups and books: updated research review of
    2004.07.16: Murray 2006.05.11


    http://groups.yahoo.com/group/aspartameNM/message/1395
    Aspartame Controversy, in Wikipedia democratic
    encyclopedia, 72 references (including AspartameNM # 864
    and 1173 by Murray), brief fair summary of much more
    research: Murray 2007.01.01


    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.

    http://groups.yahoo.com/group/aspartameNM/message/1286
    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


    http://groups.yahoo.com/group/aspartameNM/message/1143
    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

    "According to model predictions, congruent with the data in the
    literature [Dorman et al., 1994; Horton et al., 1992], a certain
    fraction of formaldehyde is readily oxidized to formate,
    a major fraction of which is rapidly converted to CO2 and exhaled,
    whereas a small fraction is excreted as formic acid in urine.

    However, fits to the available data in rats and monkeys of Horton et
    al. [1992] and Dorman et al. [1994] show that, once formed, a
    substantial fraction of formaldehyde is converted to unobserved forms.

    This pathway contributes to a long-term unobserved compartment.

    The latter, most plausibly, represents either the formaldehyde that
    [directly or after oxidation to formate] binds to various endogenous
    molecules [Heck et al., 1983; Røe, 1982] or is incorporated in the
    tetrahydrofolic-acid-dependent one-carbon pathway to become the
    building block of a number of synthetic pathways
    [Røe, 1982; Tephly and McMartin, 1984].

    That substantial amounts of methanol metabolites or by-products are
    retained for a long time is verified by Horton et al. [1992] who
    estimated that 18 h following an iv injection of 100 mg/kg of
    14C-methanol in male Fischer-344 rats,
    only 57% of the dose was eliminated from the body.

    >From the data of Dorman et al. [1994] and Medinsky et al. [1997],
    it can further be calculated that 48 h following the start
    of a 2-h inhalation exposure to 900 ppm of 14C-methanol vapors
    in female cynomolgus monkeys,
    only 23% of the absorbed 14C-methanol was eliminated from the body.

    These findings are corroborated by the data of Heck et al. [1983]
    showing that 40% of a 14C-formaldehyde inhalation dose remained
    in the body 70 h postexposure.

    In the present study, the model proposed rests on acute exposure
    data, where the time profiles of methanol and its metabolites were
    determined only over short time periods
    [a maximum of 6 h of exposure and a maximum of 48 h postexposure].

    This does not allow observation of the slow release from the long-term
    components.

    It is to be noted that most of the published studies on the detailed
    disposition kinetics of methanol regard controlled short-term
    [iv injection or continuous inhalation exposure over a few hours]
    methanol exposures in rats, primates, and humans
    [Batterman et al., 1998; Damian and Raabe, 1996;
    Dorman et al., 1994; Ferry et al., 1980; Fisher et al., 2000;
    Franzblau et al., 1995; Horton et al., 1992; Jacobsen et al., 1988;
    Osterloh et al., 1996; Pollack et al., 1993; Sedivec et al., 1981;
    Ward et al., 1995; Ward and Pollack, 1996].

    Experimental studies on the detailed time profiles following
    controlled repeated exposures to methanol are lacking."

    http://groups.yahoo.com/group/aspartameNM/message/1406
    brain cell tangles and neuron death similar to Alzheimers
    via low dose formaldehyde from methanol,
    Chunlai Nie, Rongqiao He et al, China, 2007.01.23 BMC
    Neuroscience 28 pages, 63 references: Murray 2007.01.24


    http://groups.yahoo.com/group/aspartameNM/message/1385
    Coca-Cola carcinogenicity in rats, Ramazzini Foundation,
    F Belpoggi, M Soffritti, Annals NY Academy Sciences
    2006 Sept, parts of 17 pages: Murray 2006.12.02

    http://groups.yahoo.com/group/aspartameNM/message/1382
    Fiorella Belpoggi & Morando Soffritti of Ramazzini
    Foundation prove lifetime carcinogenicity of Coca-Cola,
    aspartame, and arsenic, Annals of the NY Academy of
    Sciences: Murray 2006.11.28


    http://groups.yahoo.com/group/aspartameNM/message/1369
    Bristol, Connecticut, schools join state program to limit
    artificial sweeteners, sugar, fats for 8800 students,
    Johnny J Burnham, The Bristol Press: Murray 2006.09.22

    http://groups.yahoo.com/group/aspartameNM/message/1341
    Connecticut bans artificial sweeteners in schools,
    Nancy Barnes, New Milford Times: Murray 2006.05.25


    http://groups.yahoo.com/group/aspartameNM/message/1376
    soft drinks and adolescent hyperactivity, mental distress,
    conduct problems, Lars Lien, Nanna Lien, Sonja Heyerdahl,
    Mayne Thoresen, Espen Bjertness 2006 Oct., A J Pub Health:
    Murray 2006.10.21

    http://groups.yahoo.com/group/aspartameNM/message/1375
    healthy diet, vitamins, and fish oil help reduce
    depression and violence, studies by Joseph Hibbeln,
    Bernard Gesch, and Stephen Schoenthaler, articles by
    Felicity Lawrence in UK Guardian Unlimited and Pat
    Thomas in The Ecologist: Murray 2006.10.21

    http://groups.yahoo.com/group/aspartameNM/message/1353
    carcinogenic effect of inhaled formaldehyde, Federal
    Institute of Risk Assessment, Germany -- same safe level
    as for Canada: Murray 2006.06.02

    http://groups.yahoo.com/group/aspartameNM/message/1352
    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, WinnipegSun.com: Murray 2006.06.01


    http://groups.yahoo.com/group/aspartameNM/message/1414
    effect of aspartame on oncogene and suppressor gene expressions in
    mice, Katalin Gambos, Istvan Ember, et al, University of Pecs,
    Hungary, In Vivo 2007 Jan; scores of their relevant past studies since
    1977: Murray 2007.04.14

    http://groups.yahoo.com/group/aspartameNM/message/1366
    toxicity in rat brains from aspartame, Vences-Mejia A,
    Espinosa-Aguirre JJ et al 2006 Aug: Murray 2006.09.06

    http://groups.yahoo.com/group/aspartameNM/message/1373
    aspartame rat brain toxicity re cytochrome P450 enzymes,
    especially CYP2E1, Vences-Mejia A, Espinosa-Aguirre JJ
    et al, 2006 Aug, Hum Exp Toxicol: relevant abstracts re
    formaldehyde from methanol in alcohol drinks:
    Murray 2006.09.29

    http://groups.yahoo.com/group/aspartameNM/message/1271
    combining aspartame and quinoline yellow, or MSG and
    brilliant blue, harms nerve cells, eminent C. Vyvyan
    Howard et al, 2005 education.guardian.co.uk,
    Felicity Lawrence: Murray 2005.12.21

    http://groups.yahoo.com/group/aspartameNM/message/1277
    50% UK baby food is now organic -- aspartame or MSG
    with food dyes harm nerve cells, CV Howard 3 year study
    funded by Lizzy Vann, CEO, Organix Brands,
    Children's Food Advisory Service: Murray 2006.01.13

    http://groups.yahoo.com/group/aspartameNM/message/1279
    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


    http://groups.yahoo.com/group/aspartameNM/message/1349
    NIH NLM ToxNet HSDB Hazardous Substances Data Bank
    inadequate re aspartame (methanol, formaldehyde,
    formic acid): Murray 2006.08.19

    http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~HwoSfJ:1
    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


    http://groups.yahoo.com/group/aspartameNM/message/1052
    DMDC: Dimethyl dicarbonate 200mg/L in drinks adds methanol
    98 mg/L ( becomes formaldehyde in body ): EU Scientific
    Committee on Foods 2001.07.12: Murray 2004.01.22


    http://www.HolisticMed.com/aspartame mgold@holisticmed.com
    Aspartame Toxicity Information Center Mark D. Gold
    12 East Side Drive #2-18 Concord, NH 03301 603-225-2100

    http://www.holisticmed.com/aspartame/abuse/methanol.html
    "Scientific Abuse in Aspartame Research"

    http://groups.yahoo.com/group/aspartameNM/message/957
    safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
    Murray 2003.01.12 EU Scientific Committee on Food,
    a whitewash

    http://groups.yahoo.com/group/aspartameNM/message/1045
    http://www.holisticmed.com/aspartame/scf2002-response.htm
    Mark Gold exhaustively critiques European Commission
    Scientific Committee on Food re aspartame ( 2002.12.04 ):
    59 pages, 230 references
    ///////////////////////////////////////////////////////////


    http://groups.yahoo.com/group/aspartameNM/message/782
    RTM: Smith, Terpening, Schmidt, Gums:
    full text: aspartame, MSG, fibromyalgia 2002.01.17
    Jerry D Smith, Chris M Terpening,
    Siegfried OF Schmidt, and John G Gums
    Relief of Fibromyalgia Symptoms Following
    Discontinuation of Dietary Excitotoxins.
    The Annals of Pharmacotherapy 2001; 35(6): 702-706.
    Malcolm Randall Veterans Affairs Medical Center,
    Gainesville, FL, USA.
    BACKGROUND: Fibromyalgia is a common rheumatologic
    disorder that is often difficult to treat effectively.
    CASE SUMMARY: Four patients diagnosed with fibromyalgia
    syndrome for two to 17 years are described.
    All had undergone multiple treatment modalities with
    limited success.
    All had complete, or nearly complete,
    resolution of their symptoms within months after
    eliminating monosodium glutamate (MSG)
    or MSG plus aspartame from their diet.
    All patients were women with multiple comorbidities
    prior to elimination of MSG.
    All have had recurrence of symptoms whenever MSG
    is ingested.

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

    http://groups.yahoo.com/group/aspartameNM/message/915
    formaldehyde toxicity: Thrasher & Kilburn: Shaham: EPA:
    Gold: Wilson: CIIN: Murray 2002.12.12

    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. toxicology@drthrasher.org
    Sam-1 Trust, Alto, New Mexico, USA. full text
    http://www.drthrasher.org/formaldehyde_embryo_toxicity.html

    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.
    PMID: 2400243
    ///////////////////////////////////////////////////////////

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