Guest guest Posted September 13, 2006 Report Share Posted September 13, 2006 "Our kind of science" explained in plain English. (1) There is no "zero" in chemistry, biology or microbiology. When no spore is observed in 75 L of air sample, the concentration is less than 13 spore/m3. It's never "zero". When no (less than 1) rat dies (or gets sick) in a group of 1000 rats in an scientific experiment, the mortality (or sickness) rate is less than 0.1%. It's never zero. At a concentration of 1000 fold lower, the rate for human could be less than 0.0001%, less than 0.0000001%, etc. Unless you can put millions of humans in cages and conduct the study, you will never know. Unfortunately, in the court room, you need to find out who is one of those sensitive individuals and who is one of the others that just tries to get some money, which is a difficult process. (2) Can medications make you sick? Does-response relationship is for the majority of the population. It's never about the individuals. Pharmaceutical companies spend a lot of money doing animal studies, human trials. Does that guarantee that no one ever got sick from taking their medications? Comparing to pharmaceutical studies, you need to determine the biomarker, dosage, exposure, etc. in environmental toxiclogy studies. And, that's very difficult. (3) Multiple toxicities of one chemical Many chemicals have toxicity in higher concentrations & carcinogenicity (or a different toxic effect) in lower concentrations. Can you say that no other toxicity can exist at concentrations below no-observed- adverse-effect levels (NOAELs) of pulmonary inflammation and hemorrhage caused by Stachy spores? No, you cannot. The difficulties in studying toxicity of chemicals in low concentrations is that you need a fairly large size of animals (maybe human) and long term of observation. Most of the time, it's not financially feasible. Maybe more funding will become available when the conscienceness level is raised. Sharon: I think it is important for everyone to find out who is the real victim and who is not. Yes, I believe mold (I didn't use "mycotoxins") can make people sick, but not everyone live in a house with some (or a lot of) mold is sickened by mold even if they are actually sick. The people who pretend (or ignorantly believed) to be sicken by mold is hurting the chance of the real victims to be compensated. Ok, I should stop now before I make too much health effects comments since I am just a microbiologist. (Greg, just joking.) Thank goodness, I did take some classes and almost majored in environmental toxicology at one time. Wei Tang, Ph.D. QLAB snk1955@... wrote: Greg, Wayne, Carl, Steve and Others, Thank you for speaking out about the science. And thank you for voicing your opinion that I, too, should have a right to speak. So you all understand, I do study science. I have a college degree in the science I study. It's just that the science I study, which is how a concept is marketed, is different than the science you all study. Unfortunately, the science of marketing is greatly impacting your science, and not in a positive manner. Medical and other trusted associations are being misused to promote schools of thought that are not scientific in foundation, yet are beneficial to those who have financial stakes in moldie buildings. This promotion of a wrong concept comes on the backs of those who have been made ill from moldie buildings. With that said, let me show you the fundamental flaw within the ACOEM Mold Statement that has been used as a weapon against the sick in order to limit financial liability within the courtroom. It has little to do with your science and much to do with marketing. The concept being promoted within the ACOEM Mold Statement is that they have been able to scientifically deduce it is implausible (highly unlikely at best, even for the most vulnerable of subpopulations) mycotoxin exposure within an indoor environment could ever reach a threshold level that would cause human illness. Yet, none of the 40 papers cited within the toxicity section make this conclusion.No other document before or since the ACOEM mold statement purports to be able to make this conclusion, except for one. It is also authored by the principals of the same litigation defense support corp,Veritox 2004, This paper is also based on other's work with math applied by the authors to make their conclusions. So, if none of the papers purportedly being reviewed, make the finding of implausibility of human illness, then where within the document is this conclusion made? There are six papers (that I have attached their abstracts at the end) referenced within the section of mathematical extrapolations in regard to human toxicity. They are all rodent studies and make no conclusions themselves regarding a human threshold level/dose response. They are: 74. Creasia DA, et al. Acute inhalation toxicity of T-2 mycotoxin in mice. Fundam Appl Toxicol. 1987;8:230-5. 75. Creasia DA, et al. Acute inhalation toxicity of T-2 mycotoxin in the rat and guinea pig. Fundam Appl Toxicol. 1990;14:54-9. 31.Nikulin M, et al. Experimental lung mycotoxicosis in mice induced by Stachybotrys atra. Int J Exp Pathol. 1996;77:213-8. 76 Rao CY, Brain JD, Burge HA. Reduction of pulmonary toxicity of Stachybotrys chartarum spores by methanol extraction of mycotoxins. Appl Environ Microbiol. 2000;66:2817-21. 77.Rao CY, Burge HA, Brain JD. The time course of responses to intratracheally instilled toxic Stachybotrys chartarum spores in rats. Mycopathologia. 2000;149:27-34. 79.Nikulin M, et al. Effects of intranasal exposure to spores of Stachybotrys atra in mice. Fundam Appl Toxicol. 1997;35:182-8. The authors chose to use the Rao study, River-Dawley rats, for the foundation upon which they based their mathematical extrapolations purported to be indicative of human exposure. The River-Dawley rats had high levels of S. chartarum spores intratracheally instilled into 10-week-old males for a minute amount of time, as is stated in the above cited reference #76. From the ACOEM Mold Statement, "High doses (30 x 106 spores/kg and higher) produced pulmonary inflammation and hemorrhage in both species. A range of doses were administered in the rat studies and multiple, sensitive indices of effect were monitored, demonstrating a graded dose response with 3 x 106 spores/kg being a clear no-effect dose"...."If the no-effect 3 x 106 spores/kg intratracheal bolus dose in rats is regarded as a 1-minute administration (3 x 106 spores/kg/min), achieving the same dose rate in humans (using the same default assumptions as previously) would require airborne concentrations of 3.0 x 109 spores/m3 for an infant, 9.5 x 109 spores/m3 for a child, or 22.0 x 109 spores/m3 for an adult." One could argue about the methol challenge, sensitivity of rats over mice, River-Dawley rats vs. Jarvis rats, NOAEL & LOAEL, varying mycotoxins produced by the same molds, and many aspects of the above cited mechanistic studies. But to argue these points would irrelevant in understanding the deceit of the paper. To argue these points would only be buying in to the smoke and mirrors of the marketing of the matter. It is not the studies themselves where the fundamental flaw of the paper lays. It is the mathematical calculations that took one high dose, acute rat study and applied extrapolated math to conclude the absence of human illness. This is the fundemental flaw of the paper. This is where the marketing lies lays. The false statement of the document is, "The preceding calculations suggest lower bound estimates of airborne S. chartarum spore concentrations corresponding to essentially no-effect acute and subchronic exposures." It is only the "preceding calculations" that support the statement of, "Except for a few studies on cancer, toxicologic studies of mycotoxins are acute or short-term studies that use high exposure concentrations to reveal immediate effects in small populations of animals. Chronic studies that use lower exposure concentrations and approximate human exposure more closely have not been done except for a small number of cancer studies." According to the IOM, Damp Indoor Spaces and Health Report, 2004, there is no legitimate science to support the above statements within the ACOEM Mold Statement. IOM, Chapter 4 Mycotoxins "In vitro studies, as explained below, are not suitable for human risk assessment. Risk can be extrapolated from animal studies to human health effects only if chronic animal exposures have produced sufficient information to establish no-observed-adverse-effect levels (NOAELs) and lowest-observed-adverse-effect levels (LOAELs). Extrapolation of risk exposure from animal experiments must always take into account species differences between animals and humans, sensitivities of vulnerable human populations, and gaps in animal data." "Except for a few studies on cancer, toxicologic studies of mycotoxins are acute or short-term studies that use high exposure concentrations to reveal immediate effects in small populations of animals. Chronic studies that use lower exposure concentrations and approximate human exposure more closely have not been done except for a small number of cancer studies.""Thus results of animal studies cannot be used by themselves to draw conclusions about human health effects." In addition, the ending sentence of the Rao, Burge et. al, that the ACOEM authors used as a foundation for their extrapolations, states: "The consequences of low-level chronic exposure remain to be investigated, as does the relevance of the rodent data to human exposure." [EMPHASIS ADDED.] It is commonly known, accepted science that one cannot take a rat study, add some math and deduce all human illness is not plausible from indoor mycotoxin exposure. And for one to do so is to knowingly promote Junk Science. Sharon Kramer BBA, Marketing 74. Creasia DA, et al. Acute inhalation toxicity of T-2 mycotoxin in mice. Fundam Appl Toxicol. 1987;8:230-5. Experiments were conducted to study the acute inhalation toxicity of T-2 mycotoxin in both young adult and mature mice. For a 10-min aerosol exposure, the 24-hr LC50 of T-2 mycotoxin in young adult mice was 0.08 ± 0.04 mg T-2/liter air and that for mature mice was 0.325 ± 0.1 mg T-2/liter air. Deaths among mice exposed to the higher aerosol concentrations used in this study (i.e., 1.5 to 2.4 mg T-2/liter air) occurred in less than 5 hr. General clinical symptoms in these animals immediately postexposure were tremors, lethargy, stilted gait, and, in some animals, prostration.[sound familiar?] In experiments separate from the concentration-response studies, total deposition of T-2 aerosol and selective retention of T-2 in the respiratory tract and nasal turbinates were determined analytically from 3H-labeled T-2. When total deposition of T-2 was quantitated, there was excellent agreement between that amount of T-2 deposited and that amount of T-2 predicted from calculations based on aerosol size and animal minute volume. Based on the aerosol deposition data, the LD50 values of T-2 mycotoxins was 0.24 mg/kg for young adult mice and 0.94 mg/kg for mature mice. For mice, inhalation of T-2 mycotoxin is at least 10 times more toxic than systemic administration (LD50 4.5 mg/kg) and at least 20 times more toxic than dermal administration (LD50 > 10 mg/kg). 75. Creasia DA, et al. Acute inhalation toxicity of T-2 mycotoxin in the rat and guinea pig. Fundam Appl Toxicol. 1990;14:54-9. In this study, concentration-response parameters were determined for rats and guinea pigs systematically exposed to an aerosol of T-2 toxin. The LC50 for a 10-min exposure to T-2 toxin aerosol was 0.02 mg T-2/liter air for rats and 0.21 mg T-2/liter air for guinea pigs. Data from total T-2 deposition in rats and guinea pigs exposed to their respective LC50 aerosol concentration gave an LD50 of 0.05 mg T-2/kg body weight for the rat and 0.4 mg T-2/kg body weight for the guinea pig. These data show that inhaled T-2 toxin is approximately 20 times more toxic to the rat (0.05 mg T-2/kg body wt inhaled vs 1.0 mg T-2/kg body wt ip) and at least twice as toxic to the guinea pig (0.4 mg T-2/kg body wt inhaled vs 1–2 mg T-2/kg body wt ip) than ip administered T-2 toxin. Histopathologic examination of major organs in both the rat and guinea pig after respiratory exposure to T-2 toxin indicated that lesions were similar to those described after systemic administration of the toxin. Gross and microscopic alterations of respiratory tract tissue after T-2 aerosol exposure were minimal and could not account for the increase in toxicity. 31.Nikulin M, et al. Experimental lung mycotoxicosis in mice induced by Stachybotrys atra. Int J Exp Pathol. 1996;77:213-8. Stachybotrys atra is often isolated from building materials in houses with moisture problems. Spores of S. atra can contain mycotoxins which may lead to various symptoms in exposed residents in damp houses. The pathogenesis of S. atra-induced lung diseases has not been elucidated. The purpose of the present study was to investigate lung mycotoxicosis experimentally in mice after an intranasal exposure to spores of S. atra-fungus. One group of mice received one intranasal injection of spores of a toxic strain of S. atra (1 x 10(6) spores) and the other group spores of a less toxic strain. Spores of both strains contained spirolactones and spirolactams while the highly toxic strain contained also trichothecene mycotoxins, satratoxins. The spores containing satratoxins caused severe intra-alveolar, bronchiolar and interstitial inflammation with haemorrhagic exudative processes in the alveolar and bronchiolar lumen. A significant difference was observed in the severity of the lung damage caused by the two strains of S. atra. The spores without satratoxins induced a milder inflammation, so that the toxic compounds of S. atra-spores are most likely responsible for the severity of the lung injury. 76 Rao CY, Brain JD, Burge HA. Reduction of pulmonary toxicity of Stachybotrys chartarum spores by methanol extraction of mycotoxins. Appl Environ Microbiol. 2000;66:2817-21. The fungus Stachybotrys chartarum has been implicated in cases of nonspecific indoor air quality complaints in adults and in cases of pulmonary hemorrhaging in infants. The effects that have been described have been attributed to mycotoxins. Previous dose-effect studies focused on exposure to a single mycotoxin in a solvent, a strategy which is unlikely to accurately characterize the effects of inhaled spores. In this study we examined the role of mycotoxins in the pulmonary effects caused by S. chartarum spores and the dose dependency of these effects.[sic in rats] S. chartarum spores were extracted in methanol to reduce the mycotoxin content of the spores. Then either untreated (toxin-containing) or methanol-extracted S. chartarum spores were intratracheally instilled into male 10-week-old River-Dawley rats. [Here is a topic for a whole nother day] After 24 h, the lungs were lavaged, and the bronchoalveolar lavage fluid was analyzed to determine differences in lactic dehydrogenase, albumin, hemoglobin, myeloperoxidase, and leukocyte differential counts. Weight change was also monitored. Our data show that methanol extraction dramatically reduced the toxicity of S. chartarum spores. No statistically significant effects were observed in the bronchoalveolar lavage fluids of the animals that were treated with methanol-extracted spores at any dose. Conversely, dose-dependent effects of the toxin-containing spores were observed when we examined the lactic dehydrogenase, albumin, and hemoglobin concentrations, the polymorphonuclear leukocyte counts, and weight loss. Our findings show that a single, intense exposure to toxin-containing S. chartarum spores results in pulmonary inflammation and injury in a dose-dependent manner. Importantly, the effects are related to methanol-soluble toxins in the spores. 77.Rao CY, Burge HA, Brain JD. The time course of responses to intratracheally instilled toxic Stachybotrys chartarum spores in rats. Mycopathologia. 2000;149:27-34. Stachybotrys chartarum is a fungal species that can produce mycotoxins, specifically trichothecenes.[and what else?] Exposures in the indoor environment have reportedly induced neurogenic symptoms in adults and hemosiderosis in infants. However, little evidence has linked measured exposures to any fungal agent with any health outcome. We present here a study that focuses on quantitatively assessing the health risks from fungal toxin exposure. [in rats] Male, 10 week old River-Dawley rats were intratracheally instilled with approximately 9.6 million Stachybotrys chartarum spores in a saline suspension. The lungs were lavaged 0 h (i.e., immediately post-instillation), 6, 24 or 72 h after instillation. Biochemical indicators (albumin, myeloperoxidase, lactic dehydrogenase, hemoglobin) and leukocyte differentials in the bronchoalveolar lavage fluid and weight change were measured. We have demonstrated that a single, acute pulmonary exposure to a large quantity of Stachybotrys chartarum spores by intratracheal instillation causes severe injury detectable by bronchoalveolar lavage.[in rats] The primary effect appears to be cytotoxicity and inflammation with hemorrhage. There is a measurable effect as early as 6 h after instillation, which may be attributable to mycotoxins in the fungal spores. The time course of responses supports early release of some toxins, with the most severe effects occurring between 6 and 24 h following exposure. By 72 h, recovery has begun, although macrophage concentrations remained elevated. [so how does this information even remotely relate to HUMAN, low dose, chronic exposure?} WR, Platts-Mills TAE. Aerobiology and Inhalant Allergens. In: Middleton E, Jr et al, eds. Allergy: Principles and Practice. St. Louis: Mosby Co.; 1998:367-403. Horner WE, et al. Fungal allergens. Clin Microbiol Rev. 1995;8:161-79. Billings CG, P. Damp housing and asthma. Monaldi Arch Chest Dis. 1998;53:43-9. Burr ML. Health effects of indoor molds. Rev Environ Health. 2001;16:97-103. Macher J. Health effects of bioaerosols. In: Macher J, ed. Bioaerosols: assessment and control. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1999:3-1 to -12. Purokivi MK, et al. Changes in pro-inflammatory cytokines in association with exposure to moisture-damaged building microbes. Eur Respir J. 2001;18:951-8. Roponen M, et al. Fungal spores as such do not cause nasal inflammation in mold exposure. Inhal Toxicol. 2002;14:541-9. Fink J, Zacharisen MC. Hypersensitivity Pneumonitis. In: Middleton E, Jr. et al, eds. Allergy: Principles and Practice. St. Louis: Mosby Co.; 1998:994-1004. Flaherty DK, et al. Multilaboratory comparison of three immunodiffusion methods used for the detection of precipitating antibodies in hypersensitivity pneumonitis. J Lab Clin Med. 1974;84:298-306. California Department of Health Services, Environmental Health Investigations Branch: Misinterpretatin of Stachybotrys serology, 2000.www.dhs.ca.gov/ps/deodc/ehib/ehib2/topics/serologyf2.htm, accessed 2002. Greenberger PA. Allergic bronchopulmonary aspergillosis, allergic fungal sinusitis, and hypersensitivity pneumonitis. Clin Allergy Immunol. 2002;16:449-68. Greenberger PA, R. Diagnosis and management of allergic bronchopulmonary aspergillosis. Ann Allergy. 1986;56:444-8. Cockrill BA, Hales CA. Allergic bronchopulmonary aspergillosis. Ann Rev Med. 1999;50:303-16. Zhaoming W, Lockey RF. A review of allergic bronchopulmonary aspergillosis. J Investig Allergol Clin Immunol. 1996;6:144-51. Slavin RG. Allergic bronchopulmonary aspergillosis. Clin Rev Allergy. 1985;3:167-82. Katzenstein AL, Sale SR, Greenberger PA. Allergic Aspergillus sinusitis: a newly recognized form of sinusitis. J Allergy Clin Immunol. 1983;72:89-93. deShazo RD, Swain RE. Diagnostic criteria for allergic fungal sinusitis. J Allergy Clin Immunol. 1995;96:24-35. Schubert MS, Goetz DW. Evaluation and treatment of allergic fungal sinusitis. I. Demographics and diagnosis. J Allergy Clin Immunol. 1998;102:387-94. Schubert MS. Fungal rhinosinusitis: diagnosis and therapy. Curr Allergy Asthma. Rep 2001;1:268-76. Blonz ER. Is there an epidemic of chronic candidiasis in our midst? JAMA. 1986;256:3138-9. Executive Committee of the American Academy of Allergy and Immunology. Clinical ecology. J Allergy Clin Immunol. 1986;78:269-71. Hawkins C, Armstrong D. Fungal infections in the immunocompromised host. Clin Haematol. 1984;13:599-630. Walsh TJ, Dixon DM. Nosocomial aspergillosis: environmental microbiology, hospital epidemiology, diagnosis and treatment. Eur J Epidemiol. 1989;5:131-42. Singh N. Trends in the epidemiology of opportunistic fungal infections: predisposing factors and the impact of antimicrobial use practices. Clin Infect Dis. 2001;33:1692-6. Munoz P, Burillo A, Bouza E. Environmental surveillance and other control measures in the prevention of nosocomial fungal infections. Clin Microbiol Infect. 2001;7 Suppl 2: 38-45. Ciegler A, et al. Mycotoxins: occurrence in the environment. In: Shank RC, ed. Mycotoxins and N-nitroso Compounds: Environmental Risks. Volume I. Boca Raton, FL: CRC Press, Inc.; 1981:1-50. Committee on Protection Against Mycotoxins. National Research Council. Protection against trichothecene mycotoxins. 1983. Washington, DC, National Academy Press. Hendry KM, Cole EC. A review of mycotoxins in indoor air. J Toxicol Environ Health. 1993;38:183-98. Nikulin M, et al. Stachybotrys atra growth and toxin production in some building materials and fodder under different relative humidities. Appl Environ Microbiol. 1994;60:3421-24. Rao CY. Toxigenic fungi in the indoor environment. In: Spengler JD, Samset JM, McCarthy JS, eds. Indoor Air Quality Handbook. McGraw Hill; 2001:46-2 and 46-4. Nikulin M, et al. Experimental lung mycotoxicosis in mice induced by Stachybotrys atra. Int J Exp Pathol. 1996;77:213-8. Jarvis BB, et al. Study of toxin production by isolates of Stachybotrys chartarum and Memnoniella echinata isolated during a study of pulmonary hemosiderosis in infants. Appl Environ Microbiol. 1998;64:3620-5. Vesper SJ, et al. Hemolysis, toxicity, and randomly amplified polymorphic DNA analysis of Stachybotrys chartarumstrains. Appl Environ Microbiol. 1999;65:3175-81. Andersen B, Nielsen KF, Jarvis BB. Characterization of Stachybotrys from water-damaged buildings based on morphology, growth, and metabolic production. Mycologia. 2002;94(3):392-403. Tobin RS, et al. Significance of fungi in indoor air: report of a working group. Can J Public Health. 1987;78:S1-S32. JE, et al. Cytotoxic fungal spores in the indoor atmosphere of the damp domestic environment. FEMS Microbiol Lett. 1992;79:337-43. Rao CY, Burge HA, Chang JC. Review of quantitative standards and guidelines for fungi in indoor air. J Air Waste Manag Assoc. 1996;46:899-908. Tuomi T, et al. Mycotoxins in crude building materials from water-damaged buildings. Appl Environ Microbiol. 2000;66:1899-904. Schiefer HB. Mycotoxins in indoor air: a critical toxicological viewpoint. Indoor air ’90: Proceedings of the fifth international conference on indoor air. 167-72. 1990. World Health Organization. Selected mycotoxins: ochratoxins, trichothecenes, ergot. Environmental Health Criteria 105. Geneva: 1990:30,77,169. Drobotko VG. stachybotryotoxicosis: a new disease of horses and humans. Am Rev Soviet Med. 1945;2:238-42. Kaminski E, Stawicki S, Wasowicz E. Volatile flavor compounds produced by molds of Aspergillus,. Pennicillium, and Fungi imperfecti. Appl Microbiol. 1974;27:1001-4. Pohland AE. Mycotoxins in review. Food Addit Contam. 1993;10:17-28. Forgacs J, Carll WT. Mycotoxicoses. Adv Vet Sci. 1962;7:273-382. Ciegler A, JW. Mycotoxins and mycotoxicoses. BioScience. 1980;30:512-15. Hudler GW. Magical Mushrooms, Mischievous Molds. Princeton University Press, 1998. Emanuel DA, Wenzel FJ, Lawton BR. Pulmonary mycotoxicosis. Chest. 1975;67:293-7. Di Paolo N, et al. Inhaled mycotoxins lead to acute renal failure. Nephrol Dial Transplant. 1994;9 Suppl 4:116-20. 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Clinical-epidemiological investigation of health effects caused by Stachybotrys atra building contamination. Proceedings of Indoor Air ’93: Health effects 1993;1:225-30. Johanning E, et al. Health and immunology study following exposure to toxigenic fungi (Stachybotrys chartarum ) in a water-damaged office environment. Int Arch Occup Environ Health. 1996;68:207-18. Hodgson MJ, et al. Building-associated pulmonary disease from exposure to Stachybotrys chartarum and Aspergillus versicolor. JOEM. 1998;40:241-9. Jarvis BB. Mycotoxins and indoor air quality. In: Morey PR, Feeley JC, Otten JA, eds. Biological Contaminants in Indoor Environments. Philadelphia: ASTM, 1990:201-14. Flannigan B, JD. Health implications of fungi in indoor environments: an overview. In: Samson RA, et al, eds. Health Implications of Fungi in Indoor Environments. Amsterdam: Elsevier, 1994:3-28. Menzies D, Bourbeau J. Building-related illnesses. N Engl J Med. 1997;337:1524-31. Fung F, R, S. Stachybotrys, a mycotoxin-producing fungus of increasing toxicologic importance. J Toxicol Clin Toxicol. 1998;36:79-86. Robbins CA, et al. Health effects of mycotoxins in indoor air: a critical review. Appl Occup Environ Hyg.2000;15:773-84. Sudakin DL. Stachybotrys chartarum: current knowledge of its role in disease. MedGenMed. 2000;E11. Page EH, Trout DB. The role of Stachybotrys mycotoxins in buildings related illness. Am Ind Hyg Assoc J. 2001;62:644-8. Terr AI. Stachybotrys: relevance to human disease. Ann Allergy Asthma Immunol. 2001;87:57-63. Burge HA. Fungi: toxic killers or unavoidable nuisances? Ann Allergy Asthma Immunol. 2001;87:52-6. Centers for Disease Control and Prevention (CDC). Acute pulmonary hemorrhage/hemosiderosis among infants – Cleveland, January 1993-November 1994. MMWR Morb Mortal Wkly Rep. 1994;43:881-83. Centers for Disease Control and Prevention (CDC). Update: pulmonary hemorrhage/hemosiderosis among infants – Cleveland, Ohio, 1993-1996. MMWR Morb Mortal Wkly Rep. 1997;46:33-5. Montaña E, et al. Environmental risk factors associated with pediatric idiopathic pulmonary hemorrhage and hemosiderosis in a Cleveland community. Pediatrics. 1997;99:e5. Etzel RA, et al. Acute pulmonary hemorrhage in infants associated with exposure to Stachybotrys atra and other fungi. Arch Pediatr Adolesc Med. 1998;152:757-62. Centers for Disease Control and Prevention (CDC). Availability of case definition for acute idiopathic pulmonary hemorrhage in infants. MMWR Morb Mortal Wkly Rep. 2001;50:494-95. Centers for Disease Control and Prevention (CDC). Update: pulmonary hemorrhage/hemosiderosis among infants – Cleveland, Ohio, 1993-1996. MMWR Morb Mortal Wkly Rep. 2000;49:180-84. Creasia DA, et al. Acute inhalation toxicity of T-2 mycotoxin in mice. Fundam Appl Toxicol. 1987;8:230-5. Creasia DA, et al. Acute inhalation toxicity of T-2 mycotoxin in the rat and guinea pig. Fundam Appl Toxicol. 1990;14:54-9. Rao CY, Brain JD, Burge HA. Reduction of pulmonary toxicity of Stachybotrys chartarum spores by methanol extraction of mycotoxins. Appl Environ Microbiol. 2000;66:2817-21. Rao CY, Burge HA, Brain JD. The time course of responses to intratracheally instilled toxic Stachybotrys chartarum spores in rats. Mycopathologia. 2000;149:27-34. EPA Office of Research and Development. Volume I: General Factors. Exposure Factors Handbook. 1997 Aug. Washington, DC, US Environmental Protection Agency. Nikulin M, et al. Effects of intranasal exposure to spores of Stachybotrys atra in mice. Fundam Appl Toxicol. 1997;35:182-8. Shelton BG, et al. Profiles of airborne fungi in buildings and outdoor environments in the United States. Appl Environ Microbiol. 2002;68:1743-53. Macher J. Bioaerosols: assessment and control. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1999. American Industrial Hygiene Association. Report of Microbial Growth Task Force. Fairfax, VA: AIHA Press, 2001. EPA Office of Air and Radiation, Indoor Air Division. Mold remediation in schools and commercial buildings. 2001 Mar. Washington DC, US Environmental Protection Agency. Wei Tang, Ph.D.Lab Director QLAB5 DriveCherry Hill, NJ 08003www.QLABusa.com Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 14, 2006 Report Share Posted September 14, 2006 Hi Dr. Tang, "Our kind of science" explained in plain English. I like that. Unless you can put millions of humans in cages and conduct the study, you will never know. That is well said. And that is my point. There is no minimun level of exposure to mycotoxins established. Like you say, "unless you can put millions of humans in cages and conduct the study, you will never know." Unfortunately, in the court room, you need to find out who is one of those sensitive individuals and who is one of the others that just tries to get some money, which is a difficult process. Yes, but basing anything on false data does not help to promote legitimate science within the courtroom. For one to say "It could not be" in regard to mycotoxin exposure is not a true scientific statement. (2) Can medications make you sick? Does-response relationship is for the majority of the population. It's never about the individuals. Pharmaceutical companies spend a lot of money doing animal studies, human trials. Does that guarantee that no one ever got sick from taking their medications? Comparing to pharmaceutical studies, you need to determine the biomarker, dosage, exposure, etc. in environmental toxiclogy studies. And, that's very difficult. Yes. That's true. And when you look at the population as a whole, I would think that the percentage of people who become very ill from mycotoxin exposure is a very small percentage. But that does not mean these people are not sick and should be able to receive proper medical treatment. As an example, my daughter CF. Only one in 2000 Caucasians are born with CF. Does that mean she shouldn't be able to receive treatment? (3) Multiple toxicities of one chemical Many chemicals have toxicity in higher concentrations & carcinogenicity (or a different toxic effect) in lower concentrations. Can you say that no other toxicity can exist at concentrations below no-observed- adverse-effect levels (NOAELs) of pulmonary inflammation and hemorrhage caused by Stachy spores? No, you cannot. No, I cannot. The difficulties in studying toxicity of chemicals in low concentrations is that you need a fairly large size of animals (maybe human) and long term of observation. Most of the time, it's not financially feasible. Maybe more funding will become available when the conscienceness level is raised. I don't think even with funding one could establish the minumum of mycotoxins because of that little bothersome delimma of not being able to administer them to humans. These are different that establishing dose response for chemicals because of all the varying components, varying routes of exposure simultaniously, varying time periods at varying dosing in the real world, etc. I don't think this is an area where a clear minimum dose can be established. What we do know is 1.Molds can produce mycotoxins. 2.The Russian study in humans and the Creasia in rats indicate symptoms that are consistant of "tremors, lethargy, stilted gait, and, in some animals, prostration" etc. 3.These are the same symptoms many complain of after exposure in water damaged buildings. 4. There is nothing that would indicate these illnesses are implausible from an indoor exposure besides the rats with math added in the ACOEM Mold Statement. So which makes more sense? People, who have never been liars before and are reporting symptoms known to be indicative of mycotoxin exposure, are now liars? Or, Maybe there is a little problem within the calculations of the rats and the math that the IOM says isn't legitimate science. Sharon: I think it is important for everyone to find out who is the real victim and who is not. That's what is so frustrating to me. Everyone is a victim in this scenario - whether it's physical or financial. There should not be victims at all. If physicians were aware that molds, mycotoxins, mvoc's, and water damaged buildings in general can indeed cause serious illness, then people would know to address their symptoms early before they became debilitating. There would be nothing for anyone to be a victim of. The mountain would turn into nothing more than a mold hill. Yes, I believe mold (I didn't use "mycotoxins") can make people sick, but not everyone live in a house with some (or a lot of) mold is sickened by mold even if they are actually sick. That is true. Not all the illnesses in the world are caused by molds or mycotoxins. But if someone is experiencing primarily autoimmune or respiratory symptoms and they are living and working within a moldie environment, this is an aspect of a possible cause of illness that should be investigated, and either treated or ruled out. Just like AIDs or MS, etc, physicians have to check for what is the root of the symptoms. And many times it is molds, mycotoxins (sick environment) that is completely going unrecognized by the medical community. This, is because of the mixed messages coming out of the courtrooms. The people who pretend (or ignorantly believed) to be sicken by mold is hurting the chance of the real victims to be compensated. With all due respect Dr. Tang, the number of people who would pretend they have these illnesses is virtually nil. Do you have any idea what it is like to have a mold induced illness? It impacts not just health, but finances, family relationships, work, living environment. The stigma of being perceived as pretending (lying) is one of the most insulting aspects that many mold victims face. I don't anyone "ignorantly believes" they are sick from mold. Some may attempt to make a link between cause and illness on their own, and if the doctors were trained then the link would be made or ruled out. As far as victim compensation, you are discussing the courtroom. I am not interested in the courtroom other than how it stifles and convolutes the medical understanding. All I want is for the sick to be able to receive proper medical treatment. That's it. Ok, I should stop now before I make too much health effects comments since I am just a microbiologist. (Greg, just joking.) Thank goodness, I did take some classes and almost majored in environmental toxicology at one time. Oh, I should stop now, too, before I make too much health effect comments....regarding your health effect comments - since you are just a microbiologist (Wei, just joking). I took some classes in religion and thought about becoming a Nun (in the 3rd grade). So I think I am a pretty good example, almost doesn't cut it. But, everyone has a right to voice their opinion. And it good to know what you are thinking Dr. Tang. Without communication of differing views, nothing ever gets accomplished. WR, Sharon Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 15, 2006 Report Share Posted September 15, 2006 Sharon: A. You ARE an Advocate - almost exclusively from what I can tell. B. If you think you are a scientifically-based professional then you should be able answer ONE of the following questions with substantial merit (note: these are not the only criteria, just one). 1. How many field investigations have you performed for mold and moisture? 2. How many patients have you examined and diagnosed? 3. How many laboratory analysis for bioaerosols have you completed? 4. How many epidemiology or cases studies have you completed? 5. How many iaq remediations have you specified? 6. How many iaq remediations have you completed? 7. How many toxicology studies have you completed? If you cannot, then I would say the term "scientifically-based professional" is not appropriate for you. Also "as a self professed professional" - I think his credentials speak otherwise. C. You stated "marketing of a non-scientific concept ". Remove the word "non" and I will fully agree with the idea that the science is being marketed. If they weren't marketing the science, would you still be up in arms against them? From what I see, I think not. Thus your real issue would not be the science but the marketing. The irony is that you subscribe to the same marketing techniques that they do. Tony ........................................................................... "Tony" Havics, CHMM, CIH, PEpH2, LLCPO Box 34140Indianapolis, IN 46234 cell90% of Risk Management is knowing where to place the decimal point...any consultant can give you the other 10%â„ This message is from pH2. This message and any attachments may contain legally privileged or confidential information, and are intended only for the individual or entity identified above as the addressee. If you are not the addressee, or if this message has been addressed to you in error, you are not authorized to read, copy, or distribute this message and any attachments, and we ask that you please delete this message and attachments (including all copies) and notify the sender by return e-mail or by phone at . Delivery of this message and any attachments to any person other than the intended recipient(s) is not intended in any way to waive confidentiality or a privilege. All personal messages express views only of the sender, which are not to be attributed to pH2 and may not be copied or distributed without this statement. -----Original Message-----From: iequality [mailto:iequality ] On Behalf Of snk1955@...Sent: Monday, September 11, 2006 4:51 PMTo: iequality Subject: Re: Re: Serious Breach of Ethics within the AIHA Sharon is an advocate and not a scientifically based professional. She also has issues associated with family illnesses that she associates with mould. As such she is very biased in her views. No facts will change her mind as she is a true believer. She really should not be allowed to continue using this list as her personal soundingboard. Dr. , I find this above statement to be quite insulting. Not to toot my own horn, but I have more to raise the national awareness of the legitimacy of these illnesses than most. I have moderated US Senate Staff Briefing. I have changed Conflict Interest policies within major medical associations. I have brought many physicians and researchers together to share their information in a new light. But mostly what I have done is to use my professional background to research and demonstrate how the marketing of a non-scientific concept has been carried out and used as a weapon against the ill. And I would like to state right here and now, what I am discussing is far more scienfically founded than what you are attempting to state. What YOU, as a self professed professional, are attempting to argue is that one can take a rodent study, apply some extrapolated math and deduce all human illness is not plausible from mycotoxin exposure. Read your own words, then think about how ridiculous that concept really is. And then read the Chapter on Mycotoxins within the Damp Indoor Spaces and Mold Report. Tell me from there, who between the two of us is more adeptly discussing true scientific understanding of the matter. Sharon Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 17, 2006 Report Share Posted September 17, 2006 Hey Tony, You have artfully avoided and continue to avoid the billion dollar question: "Is it accepted science to be able to take a single, high dose, acute rodent study - apply extrapolated math and deduce all human illness is not plausible (highly unlikely at best, even for the most vulnerable of subpopulations) from mycotoxin exposure within an indoor environment? Yes________ No_________ That's it's, pal. Real simple. I am not even going to bother getting down in the dirt of who is most qualified to answer what. Some would say "Ask the experienced, not the learned". So what. Irrelevant. The only scientific question of relevance, is the one stated above that I have put to you several times, and you never answer. So, Tony, that's it. One little question. What is the answer, Tony? "Is it accepted science to be able to take a single, high dose, acute rodent study - apply extrapolated math and deduce all human illness is not plausible (highly unlikely at best, even for the most vulnerable of subpopulations) from mycotoxin exposure within an indoor environment? Yes________ No_________ Sharon Sharon: A. You ARE an Advocate - almost exclusively from what I can tell. B. If you think you are a scientifically-based professional then you should be able answer ONE of the following questions with substantial merit (note: these are not the only criteria, just one). 1. How many field investigations have you performed for mold and moisture? 2. How many patients have you examined and diagnosed? 3. How many laboratory analysis for bioaerosols have you completed? 4. How many epidemiology or cases studies have you completed? 5. How many iaq remediations have you specified? 6. How many iaq remediations have you completed? 7. How many toxicology studies have you completed? If you cannot, then I would say the term "scientifically-based professional" is not appropriate for you. Also "as a self professed professional" - I think his credentials speak otherwise. C. You stated "marketing of a non-scientific concept ". Remove the word "non" and I will fully agree with the idea that the science is being marketed. If they weren't marketing the science, would you still be up in arms against them? From what I see, I think not. Thus your real issue would not be the science but the marketing. The irony is that you subscribe to the same marketing techniques that they do. Tony ........................................................................... "Tony" Havics, CHMM, CIH, PEpH2, LLCPO Box 34140Indianapolis, IN 46234 cell Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 18, 2006 Report Share Posted September 18, 2006 This reminds of the question: Have you stopped beating your wife? so Sharon - have you stopped beating your kids? (just kidding on this one) It presumes facts not in order for relevance. In your question (which has always been referenced to either ACOEM or the Robbins paper): "Is it accepted science to be able to take a single, high dose, acute rodent study - apply extrapolated math and deduce all human illness is not plausible (highly unlikely at best, even for the most vulnerable of subpopulations) from mycotoxin exposure within an indoor environment?" Presumes that only a "single, high dose, acute rodent study" was used in the underlying basis. Presumes the implied idea that only "apply extrapolated math" was used as opposed to time tried methods of risk extrapolation which the EPA uses every day and even espouses. Presumes that "deduce all human illness is not plausible" was a conclusion when the term "all" was never used and it was certainly stated that these toxic agents can and do cause adverse effects (hence an effect in a rat). Thus - the question is improperly posed with facts not in evidence for the relevant discussion (in a court I'd say you provided no foundation for the question). So give me a relevant question with facts in order. At least mine were relevant. Tony ........................................................................... "Tony" Havics, CHMM, CIH, PEpH2, LLCPO Box 34140Indianapolis, IN 46234 cell90% of Risk Management is knowing where to place the decimal point...any consultant can give you the other 10%â„ This message is from pH2. This message and any attachments may contain legally privileged or confidential information, and are intended only for the individual or entity identified above as the addressee. If you are not the addressee, or if this message has been addressed to you in error, you are not authorized to read, copy, or distribute this message and any attachments, and we ask that you please delete this message and attachments (including all copies) and notify the sender by return e-mail or by phone at . Delivery of this message and any attachments to any person other than the intended recipient(s) is not intended in any way to waive confidentiality or a privilege. All personal messages express views only of the sender, which are not to be attributed to pH2 and may not be copied or distributed without this statement. -----Original Message-----From: iequality [mailto:iequality ] On Behalf Of snk1955@...Sent: Sunday, September 17, 2006 2:05 PMTo: iequality Subject: Re: Re: Serious Breach of Ethics within the AIHA Hey Tony, You have artfully avoided and continue to avoid the billion dollar question: "Is it accepted science to be able to take a single, high dose, acute rodent study - apply extrapolated math and deduce all human illness is not plausible (highly unlikely at best, even for the most vulnerable of subpopulations) from mycotoxin exposure within an indoor environment? Yes________ No_________ That's it's, pal. Real simple. I am not even going to bother getting down in the dirt of who is most qualified to answer what. Some would say "Ask the experienced, not the learned". So what. Irrelevant. The only scientific question of relevance, is the one stated above that I have put to you several times, and you never answer. So, Tony, that's it. One little question. What is the answer, Tony? "Is it accepted science to be able to take a single, high dose, acute rodent study - apply extrapolated math and deduce all human illness is not plausible (highly unlikely at best, even for the most vulnerable of subpopulations) from mycotoxin exposure within an indoor environment? Yes________ No_________ Sharon Sharon: A. You ARE an Advocate - almost exclusively from what I can tell. B. If you think you are a scientifically-based professional then you should be able answer ONE of the following questions with substantial merit (note: these are not the only criteria, just one). 1. How many field investigations have you performed for mold and moisture? 2. How many patients have you examined and diagnosed? 3. How many laboratory analysis for bioaerosols have you completed? 4. How many epidemiology or cases studies have you completed? 5. How many iaq remediations have you specified? 6. How many iaq remediations have you completed? 7. How many toxicology studies have you completed? If you cannot, then I would say the term "scientifically-based professional" is not appropriate for you. Also "as a self professed professional" - I think his credentials speak otherwise. C. You stated "marketing of a non-scientific concept ". Remove the word "non" and I will fully agree with the idea that the science is being marketed. If they weren't marketing the science, would you still be up in arms against them? From what I see, I think not. Thus your real issue would not be the science but the marketing. The irony is that you subscribe to the same marketing techniques that they do. Tony ........................................................................... "Tony" Havics, CHMM, CIH, PEpH2, LLCPO Box 34140Indianapolis, IN 46234 cell Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 18, 2006 Report Share Posted September 18, 2006 My apologies, Tony. Sleep deprivation does funny things to names. I've been too busy lately and mistakes happen. I just happy my mistake was a name not a fact. It is my experience Dr. RE Gotts is listed in papers that tend to be of the naysaying variety in the interest of special interest. I'm waiting to hear how many patients he is currently seeing as something other than a ME. When did he or Coreen Robbins or Ed Light or any other the other ususal " defense " suspects help a little old lady trampled while suffering asthma? I'm waiting to hear if their is redemption for their ilk. I have no problems with " defense " work so long as it is " honest " . I turn down clients who are not interested in being honest. I'll bet you think the same way. Regards, Greg Weatherman > > > > Greg- > > > > > > > > Here is my response (in underline): > > Sharon is an advocate and not a scientifically based professional. She > > also has issues associated with family illnesses that she associates > > with mould. As such she is very biased in her views. No facts will > > change her mind as she is a true believer. She really should not be > > allowed to continue using this list as her personal soundingboard. > > > She raises good points even if she is not very scientific but, she is trying and learning. I see professionals make ludicrous statements all the time and nobody gives them the scarlet letter of " unscientific " like those Globaltox or Veritox folks deserve. I saw Sharon Kramer ask several questions at the Surgeon General's conference in Washington DC. > > As far as a sounding board, I think she should keep doing what she is doing so long as she is " raising the level of conscienceness " - bad pun intended. This could also be an unofficial IAQA slogan for this year's conference in Nashville. > > > > > SLIPPERY SLOPE: The two rat studies (intratracheal installation of > > > > Stachybotrys) done by Dr. Rao at Harvard with Harriet Burge as a co- > > author show that mycotoxins and nothing else are responsible for the > > > > health outcomes of the rats. Please read BOTH studies. > > > > > > > > I have read both studies. I have only one technical problem with the > > studies and that is the use of methanol extracted spores. Methanol is a > > good fixative and denatures proteins. The authors state that " Some > > glucans, extracellular polysaccharides, lipids, and allergens, which can > > also cause inflammation, may have been extracted or altered by the > > methanol. In addition, the methanol treatment sterilized the spores. > > Thus, the lack of effects associated with the methanol-extracted S. > > chartarum spores cannot be attributed solely to the absence of > > mycotoxins. " These studies are a good start. > > POINT TAKEN WITH COMMENTS: There are some animal studies cited by Dr. Ritchie Shoemaker that show rats given lethal doses of fumonisin B (mycotoxin from Fusarium). One group was given fumonisin and all died. One group was given fumonisin B and cholestyramine and lived just like the control group. Glucans, extracellular polysaccharides, lipids, and allergens had nothing to do with the results. I would give a citation but, you need to go reread Dr. Shoemaker's papers. > > His patients usually show real progress as they take cholestyramine for 2 weeks or more. I know some of his patients and the results are night and day. This medication is listed in the EPA medical handbook for removing neurotoxins like chlorpyrifos. Dr. Shoemaker was documented on the Discovery Health TV show for treating patients for pfisteria. He is used the same cholestyramine for that problems too. He was the runner-up for national MD of the year after that year. Curiously, he had a microscope but sends samples to microbiologists for their opinions. He does not claim to be a microbiologist or mycologist. > > > > > COMPLEX QUESTION: How can dose be derived from those studies since > > > > the spores were counted with a hemocytometer at 200X magnification? > > > > Most environmental labs use 400X magnification as the minimum level > > > > of microscopy for mold. How much mycelial matter and fragments of > > > > spores or conidia can you see at 200X magnification? > > > > > > > > It is easy to count S. chartarum spores at 200X magnification. > > See above for highlighed question not answered. Then go to the Texas Tech Study where they used an electron microscope for Stachybotrys particles (submicron) and showed the presence of mycotoxins. Ever wonder why qPCR is so much more reliable than spore traps? Ever wonder why there are more complaints after remediation than before? Maybe those HEPA filtered air cleaners are not doing the job all the time for all people. > > > > > > > > FALSE DILEMNA: Most of the medical community points to allergic > > > > reactions that can be as severe as RADS for the lungs. They point > > > > to common allergies like irritations of the skin, eyes, nose and > > > > throat. I am amazed everyone is still behind the curve with hormone > > > > disregulation. > > > > > > > > There are many diseases associated with hormone disregulation. > > > > > Typical response for misdirection because the statement goes nowhere just like an ancient sophist. I keep a copy of The dialogues of Plato on my bookshelf. > > Here is a medical wonder: Certain symptons can lead an MD to diagnose asthma even though there is no " allegedly " known cause of asthma. The moment a cause is known for a patient, the condition is then diagnosed as RADS. Medicine is littered with diagnoses with no known etiology or cause. MDs pump the patients full of drugs for the symptoms but fail to identify the cause and remove the source. If we claim the mantra of " source removal " for mold and IAQ, why do MDs get to " spray and go " - literally. > > A few years ago, MDs were called quacks for suggesting agent orange exposure can lead to adult onset diabetes or type 2 diabetes. Now, the tide had shifted and the VA is investigating why so many Vietnam veterans have diabetes compared to any other subpopulations. > > > > > > CASE IN POINT: A patient of Dr. Ritchie Shoemaker has the usual > > > > high leptin levels and low aMSH (alpha melanocyte stimulating > > > > hormone) levels because leptin is not being converted into aMSH. > > > > aMSH is a precursor to melatonin which is necessary for proper sleep > > > > and works in conjuction with IGF (insulin growth hormone) or HGH > > > > (human growth hormone) for the sake of argument. Melatonin is > > > > supposed to be higher at night so we can sleep and lower in the day > > > > when serotonin (carbohydrate craving) is higher all due to light > > > > exposure - alledgedly. > > > > > > > > This Shoemaker patient has a history of diabetes in the family tree > > > > like many of Shoemaker's patients, along with sleep apnea. When the > > > > Shoemaker patient takes melatonin pills, he/she can sleep like a > > > > baby. If the melatonin is not taken, sleep is difficult at best. > > > > The mold exposure came from an office building rented by the federal > > > > government. These problems did not exist before exposure. > > > > > > > > This patient verifies Dr. Ritchie Shoemaker's theories by the need > > > > for melatonin to sleep. > > > > > > > > Your very confusing point is what? > > > > > > > > Please see the following web site (http://www.chronicneurotoxins.com/) > > for an overview of Dr. Shoemaker's bio-toxin theories. He is not exactly > > practicing mainstream medicine. Please see the FDA warning letter to Dr. > > Shoemaker. ( http://www.fda.gov/foi/warning_letters/g4710d.htm > > <http://www.fda.gov/foi/warning_letters/g4710d.htm> ) > > > > I'm aware of the situation and you can hear the same story said in court and depositions: He gave a prescription for a product that is the same for dogs and people except the product literature insert is different. A mistake was made by the manufacturer not Dr. Shoemaker. > > > > > > > > I'm asking for the " so-called " professionals to think before they > > > > advertise their " alledged " understanding of environmental illnesses. > > > > > > > > I do not advertise at all. Your company is actively involved in > > promoting the notion that mould remediation is essential. You are also a > > promoter of Dr. Shoemaker's ideas. > > > > > > > > Dr. Burge knows more about environmental illness than you or Dr. > > Shoemaker will ever know. > > Dr. Burge needs to stop talking about health effects as if she is the last word on medicine. I do not hold a medical degree. Here is some easy information to support Dr. Shoemaker's theories and refute Harriet Burge's attempts to hold the floor a little longer than she should in a convention where she has little standing. > > 1. Patients must be screened for HLA genotypes before they are given " cyclosporin " to help recieve an organ like a liver or kidney. If they have an HLA genotype, they will develop type 2 diabetes or adult onset diabetes from the cylosporin medication (according to e-medicine). Cyclosporin is a naturally occuring mycotoxin produced by more than one form of mold. > > 2. A State researcher has shown an association between HLA genotypes and Gulf War syndrome. (Just interesting for thought.) > > Dr. Shoemaker had thousands of patients and tests for allergic reactions like Ig-E. His data says their is no correlation for allergies but the effects are neurotoxic - immune system and nervous system. If you know how corticosteriods work, you should be able to figure it out - really. > > On a more positive note: I have never seen Dr. Chin Yang or Dr. Steve Vespers claim to know medicine. They point to probabilities that need to be investigated. They are each peers to Harriet Burge. > > I also note that Dr. Harriet K. Amman, toxicologist, put her name on Dr. Shoemaker's paper. She wrote the chapter on mycotoxins in the ACGIH book, Bioaerosols: Assessment & Control (1999). She obviously disagrees. She is a toxicologist not a microbiologist. Call me crazy but, I will go with the toxicologist. I'm sure Harriet Burge is a wonderful microbiologist and did a lot of research for allergic responses in Florida but, that is all. I would trust a veterinarian for race horses before I trusted a microbiologist when it comes to health effects. > > Final note: Any paper that contains the name, Dr. Gots M.D., is suspect. I saw the NBC Dateline investigation where he and his firm were implicated in medical examiner services for State Farm Insurance involving medical claims from car wrecks. The paper cited by Phil Havics is dead in the water just because Dr. Gots is a co- author. I said it before today; Dr. Gots does his literature reviews at the 7-eleven comic book section. > > Please don't take my comments personally. I'm doing my part to raise the level of conscienceness. > > Regards, > > Greg Weatherman > > Arlington VA 22202 > > gw@... > > > > > > > > Cheers, > > > > > > > > > > > > > > > > > > > > F. , Ph.D., MPH, D(ABMM), CIC, HEM > > > > Microbial Epidemiologist > > > > Children's Hospital > > > > Department of Epidemiology B-276 > > > > 1056 East 19th Ave. > > > > Denver, Colorado 80218 > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 20, 2006 Report Share Posted September 20, 2006 Sharon, I'm not sure you're old enough to remember the Saccharine case maybe 40 years ago when the FDA pulled the product off the market because rodent tests showed very high doses caused tumors some of which were malignant. Had the rodent tests not shown at the extreme dosage tumors developing there most probably would never have been any question of the safety of the product. As it turned out those tests were discredited in later years as being not relavent to human conditions. To me the mycotoxin tests you are questioning are showing the dosages being used do not cause harm to humans. I see nothing unscientific with extrapolating data to predict a human effect. What I am believing is we are seeing a susceptibility problem where certain unique humans are allergic to the products of mold in a way yet unknown to science. Dr. Shoemaker is probably correct in that there is a cause and efect between mold and sickness. But also I'm suspecting Dr. Gotts may also be correct in that the mold is not directly or simply causing the effect. So the question to answer is how is mold causing illness. Let us appreciate that in most if not all the court cases have not denied the plaintiffs were sick. Where the plaintiffs lost, the courts decided mold was not a direct cause of the sickness. Where the plaintiffs won the courts decided there was a negligent contribution to the illness not necessarily a direct cause and effect. Sincerely, Ken Gibala ========================== > > > Hey Tony, > > You have artfully avoided and continue to avoid the billion dollar question: > > " Is it accepted science to be able to take a single, high dose, acute rodent > study - apply extrapolated math and deduce all human illness is not > plausible (highly unlikely at best, even for the most vulnerable of subpopulations) > from mycotoxin exposure within an indoor environment? > > Yes________ No_________ That's it's, pal. Real simple. > > I am not even going to bother getting down in the dirt of who is most > qualified to answer what. Some would say " Ask the experienced, not the learned " . > So what. Irrelevant. > > The only scientific question of relevance, is the one stated above that I > have put to you several times, and you never answer. > > So, Tony, that's it. One little question. What is the answer, Tony? > > " Is it accepted science to be able to take a single, high dose, acute rodent > study - apply extrapolated math and deduce all human illness is not > plausible (highly unlikely at best, even for the most vulnerable of subpopulations) > from mycotoxin exposure within an indoor environment? > > Yes________ No_________ > > > > > > Sharon > > Sharon: > > A. You ARE an Advocate - almost exclusively from what I can tell. > > B. If you think you are a scientifically- If you think you are a > scientifically answer ONE of the following questions with substantial merit (note: > these are not the only criteria, just one). > > 1. How many field investigations have you performed for mold and moisture? > 2. How many patients have you examined and diagnosed? > 3. How many laboratory analysis for bioaerosols have you completed? > 4. How many epidemiology or cases studies have you completed? > 5. How many iaq remediations have you specified? > > 6. How many iaq remediations have you completed? > > 7. How many toxicology studies have you completed? > > If you cannot, then I would say the term " scientifically-If you cannot, > then I would say the term " scien > > Also " as a self professed professional " - I think his credentials speak > otherwise. > > C. You stated " marketing of a non-scientific concept " . > > Remove the word " non " and I will fully agree with the idea that the science > is being marketed. If they weren't marketing the science, would you still be > up in arms against them? > > From what I see, I think not. Thus your real issue would not be the science > but the marketing. The irony is that you subscribe to the same marketing > techniques that they do. > > Tony > ................................................................... ........ > " Tony " Havics, CHMM, CIH, PE > pH2, LLC > PO Box 34140 > Indianapolis, IN 46234 > > cell > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 24, 2006 Report Share Posted September 24, 2006 " kengibs " wrote: > > Sharon, > > I'm not sure you're old enough to remember the Saccharine case maybe 40 years ago when the FDA pulled the product off the market because rodent tests showed very high doses caused tumors some of which were malignant. > Cyclamates! Grape Nehi: Favorite drink of M.A.S.H.'s " Radar " . Mine too! A real bit of nostalgia. I remember the scare they gave us. And then to find out later that they were completely wrong and bankrupted the Nehi company because of a flawed testing methodology! Glad I never gave up butter for that articial stuff now that they have reversed themselves on the health benefits of margarine. - Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 25, 2006 Report Share Posted September 25, 2006 A BRIEF HISTORY OF TIME W. Hawking Our Picture of the Universe " Any physical theory is always provisional, in the sense that it is only a hypothesis: you can never prove it. No matter how many times the results of experiments agree with some theory, you can never be sure that the next time the result will not contradict the theory. On the other hand, you can disprove a theory by finding even a single observation that disagrees with the predictions of the theory... Each time new experiments are observed to agree with the predictions the theory survives, and our confidence in it is increased; but if ever a new observation is found to disagree, we have to abandon or modify the theory. " ! " you can disprove a theory by finding even a single observation that disagrees with the predictions of the theory. " ! " ...if ever a new observation is found to disagree, we have to abandon or modify the theory. " Quote Link to comment Share on other sites More sharing options...
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