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vinyl acetate, ethyl alcohol, or aspartame in womb increases later cancers in adults with lifetime exposure in many studies, M Soffritti et al, Ramazzini Foundation, Basic Clin. Pharm. Toxicol. 2008 Feb.: Rich Murray 2008.02.07

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  • Rich Murray
    vinyl acetate, ethyl alcohol, or aspartame in womb increases later cancers in adults with lifetime exposure in many studies, M Soffritti et al, Ramazzini
    Message 1 of 1 , Feb 7, 2008
      vinyl acetate, ethyl alcohol, or aspartame in womb increases later
      cancers in adults with lifetime exposure in many studies,
      M Soffritti et al, Ramazzini Foundation, Basic Clin. Pharm. Toxicol.
      2008 Feb.: Rich Murray 2008.02.07
      http://rmforall.blogspot.com/2008_02_01_archive.htm
      Thursday, February 7, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1511
      ____________________________________________________


      See also:

      need to find safe levels for aspartame (methanol, formaldehyde,
      formic acid) via rapid, safe, low-cost, highly accurate and sensitive modern
      breath gas analysis: Claire Turner et al, Foundation for Innovative New
      Diagnostics: Rich Murray 2008.02.07
      http://rmforall.blogspot.com/2008_02_01_archive.htm
      Thursday, February 7, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1512


      "The results, reported in table 6, show that aspartame
      causes a significant,
      dose-related increase of lymphomas/leukaemias
      and malignant tumours of the renal pelvis and ureter in females
      and malignant tumours of peripheral nerves in males.

      These results demonstrate for the first time that aspartame is a
      carcinogenic agent, capable of inducing malignancies
      at various dose levels,
      including those lower than the current acceptable daily intake
      for humans (50 mg/kg of body weight in the USA,
      40 mg/kg of body weight in the European Union)."

      "Based on the results of long-term carcinogenicity bio-assays testing
      chemical and physical agents using rodents, there is ample evidence
      demonstrating that developmental, in conjunction with adult exposure
      to carcinogenic risks, produces an overall increase in the incidence of
      malignant tumours and an increased incidence of specific neoplasms related
      to exposures to specific carcinogens.

      Moreover, when comparing prenatal and postnatal exposure, the development of
      certain tumours may appear earlier in life.

      We must take into serious consideration the warnings provided by
      long-term carcinogenicity studies and take adequate action today.

      Based on the evidence presented, increased attention must be given
      to developmental exposures to diffuse carcinogens.

      It is only in this way that in the future we can hope to avoid a passive
      registration of a worsening epidemiological situation."


      www.blackwell-synergy.com/action/showFullText?submitFullText=Full+Text+HTML&doi=10.1111%2Fj.1742-7843.2007.00200.x
      free full text

      Basic & Clinical Pharmacology & Toxicology
      Volume 102 Issue 2 Page 118-124, February 2008

      To cite this article:
      Morando Soffritti, Fiorella Belpoggi, Davide Degli Esposti,
      Laura Falcioni, Luciano Bua (2008)
      Consequences of Exposure to Carcinogens
      Beginning During Developmental Life
      Basic & Clinical Pharmacology & Toxicology 102 (2), 118-124.
      doi:10.1111/j.1742-7843.2007.00200.x

      Free Content
      Full Text

      MiniReview

      Consequences of Exposure to Carcinogens
      Beginning During Developmental Life
      Morando Soffritti,
      Fiorella Belpoggi,
      Davide Degli Esposti,
      Laura Falcioni and
      Luciano Bua
      Cesare Maltoni Cancer Research Center,
      European Ramazzini Foundation of Oncology and Environmental Sciences,
      Bologna, Italy

      Author for correspondence: Morando Soffritti,
      Cesare Maltoni Cancer Research Center,
      European Ramazzini Foundation of Oncology and Environmental Sciences,
      Castello di Bentivoglio, Via Saliceto 3,
      40010 Bentivoglio, Bologna, Italy
      fax +39 051 6640223, e-mail crcfr@...

      Abstract:

      The increased incidence of cancer over the last 50-60 years may be largely
      attributed to two factors:
      the ageing of the population
      and the diffusion of agents and situations
      presenting carcinogenic risks.

      Today, we have entered into a new era in which populations are
      ever-increasingly exposed to diffuse carcinogenic risks,
      present not only in the occupational,
      but also in the general environment.

      We must now also consider an additional factor in the carcinogenic process,
      that is, the age in which exposure to carcinogenic risks begins.

      Apart from the paradigmatic cases of diethylstilboestrol and ionizing
      radiation, the available epidemiological data concerning the adult
      consequences of developmental exposure to carcinogens
      is very limited.

      However, important data have been provided by long-term
      experimental carcinogenicity bioassays conducted using rodents.

      This paper reports a selection of studies conducted in the
      laboratories of the Cesare Maltoni Cancer Research Center
      of the European Ramazzini Foundation
      in which exposure to the chemical agents vinyl acetate monomer,
      ethyl alcohol and aspartame was started
      during developmental life and continued into adulthood.

      The results of these studies provide supporting evidence that
      lifespan exposure to carcinogenic agents
      beginning during developmental life produces
      an overall increase in the carcinogenic effects observed.

      Moreover, when comparing prenatal and postnatal exposure,
      the data demonstrate that the development of cancers
      may appear earlier in life.

      Cancer represents one of the most important issues in public health today,
      both in the industrialized and developing worlds.

      The epidemiological dimension of the disease is epidemic,
      with one out of two males and one out of three females
      destined to become ill with cancer during their lifetimes [1].

      Above all, cancer affects the oldest segment of the population,
      from 60-84 years of age.

      Data from the Nominative Mortality Register
      of European Ramazzini Foundation
      from the period 1982-2002 show that more than 30%
      of the mortality in the province of Bologna, Italy, is cancer-related.

      Of these deaths, 80% occurred after the age of 60-65 years [2].

      If we consider the estimates that in 25 years,
      the number of persons over
      than the age of 70 years will have doubled,
      it is necessary to prepare for a
      dramatic increase in the number of tumours.

      In the USA alone, it is predicted that the number of cancers
      will indeed double by 2050 [1].

      Although the scientific effort and economic resources dedicated to cancer
      have increased over the last 30 years
      (directed especially towards the
      discovery of effective cancer drug therapies),
      in the USA, the 5-year relative survival rates
      based on patient follow-up from 1976-2000 have not
      substantially improved (table 1),
      with the exception of female breast,
      prostate and colon-rectal cancer,
      for which early diagnosis has certainly played an important role.

      Other exceptions are cancers of the lung and bronchus in males
      that reflects the decrease in smoking more than the past 30 years.

      The increased incidence of cancer over the last 50-60 years may be
      attributed to two increasing trends:
      (i) the increase in life expectancy (about 10 years for males
      and 15 years for females);
      and (ii) the increase in the diffusion of agents and situations
      presenting carcinogenic risks in both the occupational and general
      environment.
      A third factor in the carcinogenetic process is genetic predisposition;
      however, it is unlikely that this factor has changed significantly
      over the last decades.

      In addition, a fourth factor must also be considered; that is,
      the age in which exposure to carcinogenic risks begins.

      In this context, the present epidemiological dimension of cancer
      is undoubtedly a sign of the previous era in which the majority of the
      population had been exposed to carcinogenic risks either in the occupational
      environment as adolescents or adults.

      Today, however, we are facing an era characterized
      by two new trends:
      (i) lifetime exposure to carcinogenic risks beginning during
      developmental life (prenatally or postnatally).

      This exposure during early development, when cell mutiplication and
      differentiation make an organism more vulnerable, may cause an increase in
      carcinogenic effects later in life;

      and (ii) exposure to 'diffuse carcinogenic risks'.
      This term is used to describe carcinogenic risks of low potency,
      but to which almost the entire population of the planet
      may be exposed.

      Examples of diffuse carcinogenic risks include:
      (i) agents that are slightly carcinogenic at any dose;
      (ii) low or extremely low doses of strong carcinogenic agents;
      or (iii) mixtures of small doses of any carcinogenic agent [3].

      Apart from the paradigmatic cases of diethylstilboestrol and ionizing
      radiation, the available epidemiological data concerning the adult
      consequences of developmental exposure to carcinogenic agents
      are very limited.

      We now know much more about the effects of this early exposure thanks to
      experimental long-term bioassays.

      If adequately designed and conducted, these bioassays can produce data that
      can be effectively used to identify/predict carcinogenic risks and,
      consequently, to make decisions to protect public health.

      Numerous long-term carcinogenicity studies have been conducted
      at the Cesare Maltoni Cancer Research Center
      of the European Ramazzini Foundation (CMCRC/ERF)
      that demonstrate the life-time consequences of chemical/physical
      exposures beginning during developmental life and lasting for life.

      This paper presents a selection of these exemplary cases
      including vinyl acetate, ethyl alcohol and aspartame.

      The case of vinyl acetate monomer

      Vinyl acetate monomer is an important compound used in the
      plastics industry.

      It is also used in the production of resin in chewing gum.

      The limited available epidemiological data on vinyl acetate monomer
      do not allow for an evaluation of its potential carcinogenic risks
      in human beings.

      Carcinogenicity studies on rats and mice,
      conducted prior to the most recent
      International Agency for Research on Cancer evaluation [4],
      have been in one way or another inadequate
      to evaluate the carcinogenic potential of vinyl acetate monomer.

      In the 1980s, a series of experiments were simultaneously
      conducted at the CMCRC/ERF using Sprague-Dawley rats,
      Wistar rats and Swiss mice.

      A similar protocol was applied for all three experiments.

      Vinyl acetate monomer was administered by ingestion
      in drinking water supplied ad libitum at the concentrations of
      5000, 1000 or 0 p.p.m. to
      17-week-old males and females (breeders)
      and 12-day-old embryos (offspring).

      The treatment lasted 104 weeks in rats and 78 weeks in mice.

      All animals were monitored until natural death (130-150 weeks).

      The plan of each experiment and the significant carcinogenic
      results are reported in tables 2-4.

      In the tested conditions, vinyl acetate monomer was demonstrated
      to be a multipotent carcinogenic agent, inducing malignant tumours
      of the oral cavity, tongue, oesophagus and forestomach
      in both strains of rats and mice.

      A slight increase of the incidence of adenomas/carcinomas of the lung and of
      malignant tumours of the uterus in mice
      was also observed [5-7].

      Furthermore, the carcinogenic effects were strongly increased when exposure
      began during foetal life.

      The case of ethyl alcohol

      Various epidemiological studies have shown a positive relationship between
      consumption of alcoholic beverages and the increase of
      cancer risks of the
      oral cavity, pharynx, larynx, oesophagus and liver.

      However, as reported in the most recent
      International Agency for Research on Cancer monograph
      on this agent [8], many experimental studies conducted on
      rats and mice exposed to various concentrations of ethyl alcohol
      administered in drinking water did not show the same effects.

      In an experiment performed at the CMCRC/ERF laboratories,
      ethyl alcohol was administered by ingestion in
      drinking water at the concentration of
      10% or 0% and supplied ad libitum
      to male and female Sprague-Dawley rats,
      both breeders and offspring.

      In order to detect carcinogenic risk when exposure
      begins during adult life,
      treatment of breeders started at 39 weeks of age,
      7 days before mating.

      Treatment of offspring began during embryonic life.

      Treatment of all rodents lasted for 104 weeks
      and all animals were observed until spontaneous death.

      The plan of the experiment and the significant carcinogenic
      results are reported in table 5.

      In contrast with previous studies,
      in the test conditions of the CMCRC
      ethyl alcohol was indeed demonstrated to be carcinogenic
      for various organs and tissues,
      in particular inducing malignant tumours of oral cavity, tongue and
      lips, and oesophagus, the same sites that were shown to be target organs in
      the aforementioned epidemiological studies [9].

      Importantly, the incidence of malignant tumours of the oral cavity
      was higher when exposure began during embryonic life.

      The case of aspartame

      Aspartame is an artificial sweetener consumed
      by hundreds of millions of people worldwide.

      It is used in over 6000 products, including soft drinks,
      chewing gum, candy, desserts and yogurt,
      as well as in more than 500 pharmaceutical products,
      in particular, syrups and antibiotics for children.

      Prior to the commercialization of aspartame in the 1970s,
      the manufacturers of the compound conducted various experimental studies on
      rats and mice to test its carcinogenicity.

      When taken together, the results of these studies were considered negative
      with regard to the carcinogenicity of aspartame.

      Doubts were, however, raised
      by some in the scientific community about the
      conduct of the experiments
      and the fact that some cases of malignant brain
      tumours were found among animals treated with aspartame
      while none were found among the control group.

      Given the limitations of these studies
      due to the number of animals per sex and group,
      the duration of the experiment,
      and the ever growing use of aspartame throughout the years,
      the CMCRC/ERF decided in the late 1990s to
      plan and perform an experiment that would provide an adequate evaluation of
      the potential carcinogenic effects of aspartame.

      The first CMCRC/ERF study [10-12] was conducted on 1800 Sprague-Dawley rats
      (100-150/per sex/per group).

      Aspartame was added to the standard rat diet in quantities of
      100,000; 50,000; 10,000; 2000; 400; 80 or 0 p.p.m.
      in order to simulate daily intake of
      5000, 2500, 500, 100, 20, 4 or 0 mg/kg of body weight.

      Treatment of the animals began at 8 weeks of age
      and continued until spontaneous death.

      The results, reported in table 6, show that aspartame
      causes a significant, dose-related increase
      of lymphomas/leukaemias
      and malignant tumours of the renal pelvis and ureter in females
      and malignant tumours of peripheral nerves in males.

      These results demonstrate for the first time that aspartame is a
      carcinogenic agent, capable of inducing malignancies
      at various dose levels,
      including those lower than the current acceptable daily intake
      for humans (50 mg/kg of body weight in the USA,
      40 mg/kg of body weight in the European Union).

      As soon as we perceived the carcinogenic effects of aspartame
      during the elaboration of the data in our first mega-experiment,
      we planned an integrated programme of long-term bioassays,
      beginning treatment from prenatal life,
      on an additional 1500 rats and mice in order to better
      quantify the carcinogenic risks of aspartame.

      The second CMCRC/ERF study [13] was conducted on
      400 Sprague-Dawley rats (70-95/per sex/per group).

      Aspartame was added to the standard rat diet in quantities of
      2000, 400 or 0 p.p.m. in order to simulate daily intake of
      100, 20 and 0 mg/kg of body weight.

      Treatment of the animals began on the 12th day of foetal life
      and lasted until natural death.

      The results of the second study show an increased incidence of
      lymphomas/leukaemias in female rats with respect to the first study.

      Moreover, the study shows that when lifespan exposure to
      aspartame begins during foetal life,
      the age at which lymphomas/leukaemias develop in females
      is anticipated (fig. 1).

      In addition, for the first time, a significant increase
      in mammary cancers in females was also observed.

      The results of this second study confirm the first experimental
      demonstration of aspartame's multipotential carcinogenicity and demonstrate
      that developmental exposure
      aggravates the carcinogenic effects (tables 7 and 8).

      Conclusions

      It is well known that the latency time of most cancers
      (i.e. the time elapsing between the start of exposure
      to carcinogenic risks and the
      clinical manifestation of cancers)
      may span from 20 to 40 years [14].

      In light of the fact that 80% of cancers are diagnosed
      over the age of 55-60 years,
      we may attribute the present epidemiological dimension of cancer
      to exposure beginning during adolescence or adulthood.

      Nowadays, we are facing a new era in which exposure
      to carcinogenic risks
      begins during developmental life (prenatal and postnatal)
      and continues into adulthood.

      Based on the results of long-term carcinogenicity bio-assays testing
      chemical and physical agents using rodents, there is ample evidence
      demonstrating that developmental, in conjunction with adult exposure
      to carcinogenic risks, produces an overall increase in the incidence of
      malignant tumours and an increased incidence of specific neoplasms related
      to exposures to specific carcinogens.

      Moreover, when comparing prenatal and postnatal exposure,
      the development of certain tumours may appear earlier in life.

      We must take into serious consideration the warnings provided by
      long-term carcinogenicity studies and take adequate action today.

      Based on the evidence presented, increased attention must be given
      to developmental exposures to diffuse carcinogens.

      It is only in this way that in the future we can hope to avoid a passive
      registration of a worsening epidemiological situation.

      References

      1
      American Cancer Society. Cancer Statistics 2006.
      Available from: http://www.cancer.org Accessed 28 May 2007.
      2
      Soffritti M, Vrahulaki C, Belpoggi F et al.
      Resoconti del registro tumori di Bologna e provincia 1982-2002.
      Eur J Oncol; in press.
      3
      Soffritti M, Belpoggi F, Minardi F, Bua L, Maltoni C.
      Megaexperiments to identify and assess diffuse carcinogenic risks.
      Ann N Y Acad Sci 1999; 895: 34-55.
      Synergy, Medline, ISI, Chemport, CSA
      4
      International Agency for Research on Cancer.
      IARC Monographs on the Evaluation of
      Carcinogenic Risks to Humans,
      Wood Dust and Formaldehyde,
      vol. 62. IARC, Lyon, France, 1995.
      5
      Minardi F, Belpoggi F, Soffritti M et al.
      Results of long-term carcinogenicity bioassay
      on vinyl acetate monomer in Sprague-Dawley rats.
      Ann N Y Acad Sci 2002; 982: 106-22.
      Synergy, Medline, ISI, Chemport, CSA
      6
      Belpoggi F, Soffritti M, Minardi F et al.
      Results of a long-term carcinogenicity bioassay
      on vinyl acetate monomer in Wistar rats.
      Eur J Oncol 2002; 7: 279-93.
      7
      Maltoni C, Ciliberti A, Lefemine G, Soffritti M.
      Results of a long-term experimental study on the carcinogenicity
      of vinyl acetate monomer in mice.
      Ann N Y Acad Sci 1997; 837: 209-38.
      Synergy, Medline, ISI, Chemport, CSA
      8
      International Agency for Research on Cancer.
      IARC Monographs on the Evaluation
      of Carcinogenic Risks to Humans,
      Alcohol Drinking,
      vol. 44. IARC, Lyon, France, 1998.
      9
      Soffritti M, Belpoggi F, Cevolani D, Guarino M,
      Padovani M, Maltoni C.
      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.
      Synergy, Medline, ISI, Chemport, CSA
      10
      Soffritti M, Belpoggi F, Degli Esposti D, Lambertini L.
      Aspartame induces lymphomas and leukaemias in rats.
      Eur J Oncol 2005; 10: 107-16.
      11
      Belpoggi F, Soffritti M, Padovani M, Degli Esposti D,
      Lauriola M, Minardi F.
      Results of long term carcinogenicity bioassay
      on Sprague-Dawley rats exposed
      to aspartame administered in feed.
      Ann N Y Acad Sci 2006; 1076: 559-77.
      Synergy, Medline, ISI, Chemport
      12
      Soffritti M, Belpoggi F, Degli Esposti D, Lambertini L,
      Tibaldi E, Rigano A.
      First experimental demonstration of the
      multipotential carcinogenic effects
      of aspartame administered in the feed to Sprague-Dawley Rats.
      Environ Health Perspect 2006; 114: 379-85.
      Medline, ISI, Chemport
      13
      Soffritti M, Belpoggi F, Degli Esposti D, Tibaldi E, Lauriola M.
      Lifespan exposure to low doses of aspartame
      beginning during prenatal life increases cancer effects in rats.
      Environ Health Perspect 2007; 115: 1293-7.
      Medline, ISI, Chemport
      14
      Owen WG.
      Diffuse mesothelioma and exposure to
      asbestos dust in the merseyside area.
      Br Med J 1964; 2: 214-8.
      Medline, Chemport

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      www.ehponline.org/members/2007/10271/10271.pdf
      free full text 24 pages
      National Institutes of Health
      U.S. Department of Health and Human Services
      ENVIRONMENTAL HEALTH PERSPECTIVES
      Lifespan Exposure to Low Doses of Aspartame
      Beginning During Prenatal Life Increases Cancer Effects in Rats
      doi:10.1289/ehp.10271 (available at http://dx.doi.org/)
      Online 13 June 2007
      Morando Soffritti 1,
      Fiorella Belpoggi 1,
      Eva Tibaldi 1,
      Davide Degli Esposti 1,
      Michela Lauriola 1
      1 Cesare Maltoni Cancer Research Center,
      European Ramazzini Foundation
      of Oncology and Environmental Sciences, Bologna Italy
      Address of the institution: Cesare Maltoni Cancer Research Center,
      European Ramazzini Foundation
      of Oncology and Environmental Sciences
      Castello di Bentivoglio, Via Saliceto, 3, 40010 Bentivoglio, Bologna,
      Italy +39 051 6640460 fax +39 051 6640223
      crcfr@..., www.ramazzini.it
      Address correspondence to: M. Soffritti
      Acknowledgements:
      This research was supported entirely by the
      European Ramazzini Foundation Environmental Sciences.
      The authors declare that they have no competing financial interests.
      http://groups.yahoo.com/group/aspartameNM/message/1441


      www.ramazzini.it/fondazione/docs/NYAS_Aspartame_Ramazzini.pdf
      Results of Long-Term Carcinogenicity Bioassay
      on Sprague-Dawley Rats
      Exposed to Aspartame Administered in Feed
      Ann. N.Y. Acad. Sci. 2006 Sep; 1076: 559-577.
      Fiorella Belpoggi,
      Morando Soffritti,
      Michela Padovani,
      Davide Degli Esposti,
      Michelina Lauriola, and
      Franco Minardi.
      The end judges everything --
      HERODOTUS (480-425 B.C.) The History
      Cesare Maltoni Cancer Research Center,
      European Foundation of Oncology and Environmental Sciences
      'B. Ramazzini', 40010 Bentivoglio, Bologna, Italy
      http://groups.yahoo.com/group/aspartameNM/message/1382
      [ and, previously ]
      First experimental demonstration of the multipotential
      carcinogenic effects of aspartame
      administered in the feed to Sprague-Dawley rats.
      Environ. Health Perspect. 2006 Mar; 114: 379-385.
      PMID: 16507461
      Soffritti M, Belpoggi F, Degli Esposti D, Lambertini L,
      Tibaldi E, Rigano A.
      Environmental Health Perspectives Volume 113, Number 11
      November 2005 Current print issue
      The full version of this article is available for free in PDF format.
      http://ehp.niehs.nih.gov/members/2005/8711/8711.pdf 35 pages
      First Experimental Demonstration of the
      Multipotential Carcinogenic Effects of Aspartame
      Administered in the Feed to Sprague-Dawley Rats.
      Morando Soffritti, Fiorella Belpoggi, Davide Degli Esposti,
      Luca Lambertini, Eva Tibaldi, and Anna Rigano.
      doi:10.1289/ehp.8711 (available at http://dx.doi.org/)
      Online 17 November 2005
      The National Institute of Environmental Health Sciences
      National Institutes of Health
      U.S. Department of Health and Human Services
      http://www.ehponline.org/
      Cesare Maltoni Cancer Research Center,
      European Ramazzini Foundation of Oncology and
      Environmental Sciences
      Sofritti, M. et al. 2005.
      Aspartame induces lymphomas and leukaemias in rats.
      Eur. J. Oncol. 2005; 10: 107-116.
      http://groups.yahoo.com/group/aspartameNM/message/1250

      formaldehyde in FEMA trailers and other sources
      (aspartame, dark wines and liquors, tobacco smoke):
      Murray 2008.01.30
      http://rmforall.blogspot.com/2008_01_01_archive.htm
      Wednesday, January 30, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1508

      Dark wines and liquors, as well as aspartame, provide
      similar levels of methanol, above 100 mg daily, for
      long-term heavy users, 2 L daily, about 6 cans.

      Methanol is inevitably largely turned into formaldehyde,
      and thence largely into formic acid.
      It is the major cause 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,

      185 times the New Jersey limit,
      615 times the California and Maine limits,
      1850 times the Maryland limit.


      For instance, hangover researchers claim that it is the ~150 mg/L methanol
      impurity, about one part in 10,000,
      twice the level from aspartame in diet sodas,
      in dark wines and liquors that,
      turned into formaldehyde and then formic acid,
      is the major cause of the dreadful symptoms
      of "morning after" hangover:

      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 rmforall

      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

      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@...
      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@...
      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/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

      Here I have combined fairly equivalent data from
      their aspartame, methanol, and formaldehyde studies.
      Aspartame groups were 100-150 rats each,
      methanol 100 rats each,
      and formaldehyde 50 rats each
      (formaldehyde control groups 100 rats each).

      Aspartame and methanol are directly comparable,
      since the 11% methanol component of aspartame upon ingestion
      is immediately and fully released into the GI tract,
      and then much of that quickly turned into formaldehyde and
      then formic acid, both of which account for the toxicity of methanol.

      aspartame dose a
      -----------------equivalent methanol dose
      ---------------- (11% of aspartame)
      ------------------------------roughly equivalent formaldehyde dose
      ----------------------------- (30% of methanol)

      Males
      Females
      Males + Females

      Animals with lymphomas and leukaemias [hemolymphoreticular
      neoplasias] % of each group of animals

      Group
      100 rats each


      --------------------20,000-40.0
      ----------------------------28.0 #^
      --------------------------- 34.0

      I-100,000-29.0
      ------------25.0**
      ------------27.0

      II--50,000-20.0-----5,000-36.0--1,500-46.0 **
      ------------25.0**---------24.0---------20.0*
      ------------22.5------------30.0---------33.0

      -----------------------------------1,000-22.0*
      ------------------------------------------22.0*
      ------------------------------------------22.0

      -------------------------------------500-24.0*
      ------------------------------------------14.0
      ------------------------------------------19.0

      III-10,000-15.0
      ------------19.0*
      ------------17.0

      -----------------------500-35.0
      ----------------------------24.0
      ----------------------------29.5

      -----------------------100-26.0**
      ----------------------------16.0
      ----------------------------21.0

      ---------------------------------------50-20.0
      -------------------------------------------14.0
      -------------------------------------------17.0

      IV-2,000--22.0
      ------------18.7*
      ------------20.3

      V----400--16.7
      ------------20.0**
      ------------18.3
      ---------------------------------------10--8.0
      ------------------------------------------10.0
      --------------------------------------------9.0

      ------------------------15-20.0 [-50 rats ]
      ----------------------------10.0 [-50 rats ]
      ----------------------------15.0 [100 rats ]

      VI------80-15.3
      ------------14.7
      ------------15.0

      VII------0-20.7----------0-28.0---------0-8.0 [ control groups ]
      -------------8.7------------13.0------------7.0
      ------------14.7------------20.5------------7.5

      a Considering the life-span average weight
      of a rat (male and female) as 400 g
      and the average consumption of food as 20 g per day

      * aspartame, statistically significant p= 0.05;
      ** aspartame, statistically significant p= 0.01
      using poly-k test (k = 3)

      # methanol, p<0.05 using X2 test
      ^ methanol, p<0.05 using Cochrane-Armitage test
      for dose-response relationship

      * formaldehyde, p<0.05 using X2 test
      ** formaldehyde, p<0.01 using X2 test

      We can grasp the main picture by studying the results at a high level of
      exposure:

      II--50,000-20.0-----5,000-36.0----1,500-46.0 **
      ------------25.0**---------24.0-----------20.0*
      ------------12.5------------30.0-----------33.0

      The results amount to 1.3 to 5.75 times their control group levels.
      Aspartame, methanol, and formaldehyde results broadly agree.
      Unknown factors are causing differences between males and females.

      The control groups vary widely,
      with the percentage of rats with these most common cancers,
      present at natural death, ranging from 7.0% to 28.0%.
      A layman can only speculate as to the possible causes in a uniform
      population of rats in the same huge laboratory facility for decades,
      such as various viruses, bacteria, or molds,
      or variable impurities in the tap water.

      Formaldehyde at 50 ppm shows a doubling of the percentage
      of rats with these cancers, for groups of just 50 rats.
      It is a safe bet that studies using groups of 100 to 200 rats
      would establish significance at this 50 ppm level,
      which in turn would mandate the reduction
      of the present USA EPA level (1999) from 1 ppm
      for lifetime exposure to formaldehyde in drinking water to 0.05 ppm, since
      the human limit is estimated by dividing
      the lowest harmful animal level by 1000.

      www.finddiagnostics.org/
      FIND Foundation for Innovative New Diagnostics
      71, av. Louis-Casaï
      Case postale 93
      1216 Cointrin/Geneva, Switzerland
      Tel: + 41 (22) 710 05 90 Fax: + 41 (22) 710 05 99
      info@...;
      _____________________________________________________


      formaldehyde in FEMA trailers and other sources
      (aspartame, dark wines and liquors, tobacco smoke):
      Murray 2008.01.30
      http://rmforall.blogspot.com/2008_01_01_archive.htm
      Wednesday, January 30, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1508

      The FEMA trailers give about the same amount of formaldehyde daily
      as from a quart of dark wine or liquor, or two quarts (6 12-oz cans)
      of aspartame diet soda, from their over 1 tenth gram methanol impurity
      (one part in 10,000), which the body quickly makes into
      formaldehyde -- enough to be the major cause of "morning after"
      alcohol hangovers.

      Methanol and formaldehyde also result from many fruits and
      vegetables, tobacco and wood smoke, heater and vehicle exhaust,
      household chemicals and cleaners, cosmetics, and new cars, drapes,
      carpets, furniture, particleboard, mobile homes, buildings, leather...
      so all these sources add up and interact with many other toxic
      chemicals.

      BN Ames and LS Gold, 1998, have presented detailed information
      that there is no increase in recent decades for most cancers, and that
      common carcinogens do not result in significant exposures to the
      average human population.

      However, individuals are not average -- each person has a unique
      genetic makeup, resulting in a huge range of variation of vulnerability
      to specific chemicals, as is well evidenced in the case of methanol,
      formaldehyde, and formic acid, especially with regard to behavioral
      effects.

      Each is subject to very wide ranges of exposure levels.

      Many are in especially vulnerable groups, depending on diet,
      obesity, sex, exercise, life stress, age from conception to very old,
      severe toxic exposures, injuries, and diseases.

      It is clear that a variety of multiple chemical sensitivity syndromes
      do exist, often with remarkable hypersensitivity.

      Methanol, formaldehyde, and formic acid toxicity are unusual, in
      that humans are far more vulnerable than any other mammal,
      as much as ten to sixty-fold, which complicates the utility of animal
      data.

      The unusally long human life span also increases the role
      of long-term chronic low-level exposure.

      http://groups.yahoo.com/group/aspartameNM/message/1455
      FEMA slow to safety test Katrina toxic trailers, Charles Babington,
      Associated Press -- 1 ppm formaldehyde in air is about half the
      daily dose from 3 cans aspartame diet soda and ten times the
      1999 EPA alarm level for drinking water: Murray 2007.07.23
      http://groups.yahoo.com/group/aspartameNM/message/1455

      "Paulison said FEMA received "just over 200 complaints of strange
      odors including formaldehyde" in trailers and that 58 trailers were
      replaced "because of formaldehyde concerns."

      Occupants of five other trailers were moved to apartments, he said.

      Several lawmakers said FEMA should have seen the 200 complaints
      as a sign of a much wider problem. "


      1 ppm formaldehyde in air is half the daily dose
      from 3 cans aspartame diet soda
      and ten times the 1999 EPA alarm level for drinking water.

      J. D. Trasher et al in 1990 found many symptoms
      in 19 mobile home residents,
      living with 0.05 to 0.5 ppm formaldehyde.

      http://www.drthrasher.org/formaldehyde_1990.html full text
      Jack Dwayne Thrasher, Alan Broughton, Roberta Madison.
      Immune activation and autoantibodies in humans
      with long-term inhalation exposure to formaldehyde.
      Archives of Environmental Health. 1990; 45: 217-223.
      "Immune activation, autoantibodies, and anti-HCHO-HAS
      antibodies are associated with long-term formaldehyde inhalation."
      PMID: 2400243

      FEMA found 1.2 ppm formaldehyde in April 2005
      in one of over 120,000 mobile homes
      supplied for recent hurricane victims --
      75 times more than the
      0.016 level set for 8-hour working days
      by the National Institute for Occupational Safety and Health
      for workers to be required to wear respirators.

      http://www.arb.ca.gov/toxics/tac/appendxc.htm

      1 ppm FA in air = 1.23 mg/cubic meter, so breathing 20 cubic
      meters would retain about 20 mg FA daily, ten times the 1999 EPA
      alarm level for drinking water.

      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 EP
      limit for daily formaldehyde in drinking water,
      2.0 mg in 2 L average daily drinking water.

      Medicine has to consider that the many sources of methanol and
      formaldehyde are additive co-factors.

      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


      "... aspartame. It's perfectly safe," eminent diabetes MD S. Kalani
      Brady -- er, Doctor, RX for ignorance, 3 days earnest study of
      recent 2 years of mainstream research by groups independent of
      vested interests: Murray 2008.01.27
      http://rmforall.blogspot.com/2008_01_01_archive.htm
      Sunday, January 27, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1507

      details on 6 epidemiological studies since 2004 on diet soda (mainly
      aspartame) correlations, as well as 14 other mainstream studies on
      aspartame toxicity since summer 2005: Murray 2007.11.27
      http://rmforall.blogspot.com/2007_11_01_archive.htm
      Wednesday, November 14, 2007
      http://groups.yahoo.com/group/aspartameNM/message/1490

      Hawaiian aspartame ban bills in House and Senate challenge
      corporate clout, Sen. J. Kalani English & Suzanne Chun Oakland,
      Rep. Calvin K.Y. Say & Mele Carroll: Murray 2008.01.25
      http://rmforall.blogspot.com/2008_01_01_archive.htm
      Friday, January 25, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1505

      www.capitol.hawaii.gov/site1/house/members/rep13.asp

      Mele Carroll
      13th Representative District
      Hawaii State Capitol, Room 405
      415 South Beretania Street
      Honolulu, HI 96813
      Phone 808-586-6790; fax 808-586-6779
      From Maui, toll free 984-2400 + 66790
      From Molokai and Lanai,
      toll free 1-800-468-4644 + 66790
      E-mail repcarroll@...;

      http://groups.yahoo.com/group/aspartameNM/message/1426
      ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
      will join Tesco and also Sainsbury to ban and limit
      aspartame, MSG, artificial flavors dyes preservatives additives,
      trans fats, salt "nasties" to protect kids from ADHD:
      leading UK media: Murray 2007.05.15

      http://groups.yahoo.com/group/aspartameNMmessage/1451
      Artificial sweeteners (aspartame, sucralose) and coloring
      agents will be banned from use in newly-born and baby foods,
      the European Parliament decided: Latvia ban in schools 2006:
      Murray 2007.07.12
      ____________________________________________________


      Seizures and hyponatremia after excessive intake of diet coke, LJ
      Mortelmans, M Van Loo, HG De Cauwer, K Merlevede, Klina
      General Hospital, Brasschaat, Belgium, EJEM 2008 Feb:
      Mark D. Gold critique: Murray 2008.01.10
      http://rmforall.blogspot.com/2008_01_01_archive.htm
      Thursday, January 10, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1502


      See also:
      possible neurologic effects of aspartame, TJ Maher, RJ Wurtman,
      Environ. Health Persp. 1987 Nov, full text: other seizure reports re
      aspartame, methanol, formaldehyde, formic acid:
      Murray 2008.01.10
      http://rmforall.blogspot.com/2008_01_01_archive.htm
      Thursday, January 10, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1501


      Eur J Emerg Med. 2008 Feb; 15(1): 51.
      Seizures and hyponatremia after excessive intake of diet coke.
      Mortelmans LJ, Luc.mortelmans@...,
      Van Loo M,
      De Cauwer HG, haralddecauwer@...,
      Merlevede K. Karen.Merlevede@...,
      Departments of
      a Emergency Medicine
      b Neurology,
      Klina General Hospital, Brasschaat, Belgium.

      We describe a case of epileptic seizures after a massive intake of
      diet coke.

      Apart from the hyponatremia due to water intoxication the
      convulsions can be potentiated by the high dose of caffeine and
      aspartame from the diet coke.

      To our knowledge this is the first report of seizures due to
      excessive diet coke intake. PMID: 18180668


      Methyl alcohol ingestion as a model etiologic agent in multiple
      sclerosis, WC Monte, D Glanzman, C Johnston;
      Methanol induced neuropathology in the mammalian central
      nervous system, Woodrow C. Monte, Renee Ann Zeising,
      both reports 1989.12.04: Murray 2007.12.28
      http://rmforall.blogspot.com/2007_12_01_archive.htm
      Friday, December 28 2007
      http://groups.yahoo.com/group/aspartameNM/message/1499

      [ These seminal 1989 studies by Prof. Woodrow C. Monte are
      also given in this previous post, along his two recent comprehensive
      reviews:

      role of formaldehyde, made by body from methanol from foods and
      aspartame, in steep increases in fetal alcohol syndrome, autism,
      multiple sclerosis, lupus, teen suicide, breast cancer, Nutrition
      Prof. Woodrow C. Monte, retired, Arizona State U., two reviews,
      190 references supplied, Fitness Life, New Zealand
      2007 Nov, Dec: Murray 2007.12.26
      http://rmforall.blogspot.com/2007_12_01_archive.htm
      Wednesday, December 26 2007
      http://groups.yahoo.com/group/aspartameNM/message/1498 ]

      folic acid prevents neurotoxicity from formic acid, made by body
      from methanol impurity in alcohol drinks [ also 11 % of aspartame ], BM
      Kapur, PL Carlen, DC Lehotay, AC Vandenbroucke,
      Y Adamchik, U. of Toronto,
      2007 Dec., Alcoholism Cl. Exp. Res.:
      Murray 2007.11.27
      http://rmforall.blogspot.com/2007_11_01_archive.htm
      Wednesday, November 27, 2007
      http://groups.yahoo.com/group/aspartameNM/message/1495

      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/1453
      Souring on fake sugar (aspartame), Jennifer Couzin,
      Science 2007.07.06: 4 page letter to FDA from 12 eminent
      USA toxicologists re two Ramazzini Foundation
      cancer studies 2007.06.25: Murray 2007.07.18

      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/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

      Devra Lee Davis, U. Pittsburgh Cancer Institute, rejects
      aspartame -- Luke Ravenstahl, Mayor, drinks 12 cans Diet Pepsi
      daily: accurate warning by Ronald K. Frazer: Murray 2008.01.13
      http://rmforall.blogspot.com/2008_01_01_archive.htm
      Sunday, January 13, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1503

      http://groups.yahoo.com/group/aspartameNM/message/1141
      Nurses Health Study can quickly reveal the
      extent of aspartame (methanol, formaldehyde, formic acid) toxicity: Murray
      2004.11.21

      The Nurses Health Study is a bonanza of information about the
      health of probably hundreds of nurses who use 6 or more cans daily
      of diet soft drinks -- they have also stored
      blood and tissue samples from their immense pool of subjects.

      http://en.wikipedia.org/wiki/Aspartame_controversy
      ____________________________________________________


      "Of course, everyone chooses, as a natural priority, to enjoy peace,
      joy, and love by helping to find, quickly share, and positively act
      upon evidence about healthy and safe food, drink, and environment."

      Rich Murray, MA Room For All rmforall@...
      505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

      http://groups.yahoo.com/group/aspartameNM/message/1469
      highly toxic formaldehyde, the cause of alcohol hangovers, is
      made by the body from 100 mg doses of methanol from dark wines
      and liquors, dimethyl dicarbonate, and aspartame:
      Murray 2007.08.31

      http://RMForAll.blogspot.com new primary archive

      http://groups.yahoo.com/group/aspartameNM/messages
      group with 119 members, 1,512 posts in a public archive
      ____________________________________________________
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