Guest guest Posted May 31, 2007 Report Share Posted May 31, 2007 I've found an interesting article about the symposium on " Man and His Environment in Health and Disease. Special Focus: Innovative Aspects and Treatment of Molds, Mycotoxins and Chemical Sensitivity " The whole text can be found at the following URL: http://www.aehf.com/articles/2003Symp.htm Here are some of the interesting excerpts from the text. --------------------------------------- 21st Annual International Symposium on Man and His Environment in Health and Disease Special Focus Innovative Aspects and Treatment of Molds, Mycotoxins and Chemical Sensitivity Sponsored by American Environmental Health Foundation and American Academy of Environmental Medicine This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Environmental Medicine (AAEM) and the American Environmental Health Foundation. The American Academy of Environmental Medicine is accredited by the ACCME to provide continuing medical education for physicians. The American Academy of Environmental Medicine designates this educational activity for a maximum of 21.5 hours in Category 1 credit toward the AMA Physician=s Recognition Award. Each physician should claim only those hours of credit that he/she actually spent in the activity. Reprints are available from American Environmental Health Foundation. This volume is not to be reproduced, all or in part, without the written permission of American Environmental Health Foundation. INTRODUCTION SYMPOSIUM PURPOSE Since 1981, the International Symposium has been recognized as one of the most advanced medical forums in the world addressing the research and treatment of environmental effects on health and disease. The 2003 conference will focus on " Innovative Aspects and Treatment of Molds, Mycotoxins and Chemical Sensitivity " . For this year=s conference, we have assembled a faculty of top international experts for you. This Conference presents the most current information available while providing guidelines to identify, diagnose, treat and to prevent environmentally triggered responses in the body. GOALS OF THE MEETING ! To provide new insights into the mechanisms and the environmental causes behind many problems you see. ! To present new diagnostic and treatment modalities to help you improve the quality of care for your complex patients. ! To provide concepts, tools that will enhance your practice. OBJECTIVES OF THE MEETING ! Improve the outcome of treating patients with chronic disease, nutritional problems and chemical sensitivity. ! Use new concepts and treatments to help better diagnose and manage many patients with chronic disease, nutritional problems and chemical sensitivity. ! Apply the concepts of this conference to your practice by using nutrition and environmental manipulation for the treatment of chronic disease, nutritional problems and chemical sensitivity. ! Use the information presented to enhance the effectiveness, cost-efficiency, and competitiveness of your practice in relation to chronic disease, nutritional problems and chemical sensitivity. INTENDED AUDIENCE M.D.=s, D.O.=s, D.D.S.=s, medical students, nurses, nutritionist, and all other health professionals interested in the concepts and practice of Environmental Medicine, Occupational Medicine and Toxicology. EDUCATIONAL FORMATS # Plenary # Panels Discussions # Case Studies # Question & Answer Sessions. CONFERENCE FORMAT The AEHF Committee has selected some of the leading experts in the fields of chronic disease, nutrition and chemical sensitivity. Each speaker=s presentation will last approximately 20 minutes and will be followed by a 10 minute question and answer session. All speakers are encouraged to use any and all appropriate audio/visual aids. (A brief outline of the speech is included in this booklet.) GIVEN IN COOPERATION J. Rea, M.D., F.A.C.S. Symposium Chairman, American Environmental Health Foundation, Environmental Health Center - Dallas, Dallas, Texas Bertie B. Griffiths, Ph.D., Environmental Health Center - Dallas Dallas, Texas Kaye H. Kilburn, M. D. University of Southern California Medical Center Keck School of Medicine Los Angeles, CA J. Meggs, M.D. Dept. of Emergency Medicine E. Carolina Univ. School of Medicine Greenville, NC Allan D. Lieberman, M.D. Center for Occupational Environmental Medicine North ton, SC Mycotoxins in Indoor Climates Tapani Tuomi As of present, analyzing for mycotoxins in indoor environments is difficult, if the goal is to assess the health consequences of extensive water damage on the occupants of a particular building. There is accumulating evidence on the presence of mycotoxins in crude building materials1-7 as well as a body of indirect evidence linking the presence of mycotoxins in indoor environments to health problems5, 8-15. It is frequently maintained that mycotoxins present in bulk materials infested with toxigenic fungi are carried to indoor air by fungal propagules. It follows that the route of exposure to mycotoxins in indoor environments is inhaling dust particles containing toxigenic fungal propagules2. Dose-responses of humans to airborne mycotoxins are not known and it seems that mycotoxin concentrations in inhalable dust would have to be some 100-fold higher than what is frequently encountered in indoor environments for air sampling to be feasible on a general level. If air sampling is not attempted, deposited dust constitutes one step closer to the composition of indoor air with respect to mycotoxins. There are numerous studies from agricultural environments establishing that mycotoxins present in bulk material are - given the right circumstances - carried into dust. For instance, trichothecene concentrations of 0,1-1 µg/g dust, aflatoxin concentrations of 0,02-5 µg/g dust, ochratoxin A concentrations of 0,2-70 ng/g dust, and zearalenone concentrations of 20-100 ng/g dust have been reported during grain handling and from other agricultural settings16-21. In laboratory settings, Sorensen et al.22 found satratoxin concentrations in the 10 µg/g dust-range, whereas Smoragiewicz et al.6 detected trichothecenes in deposited dust from a moisture problem building in amounts exceeding 0.4-4 µg/g and Engelhart et al.23 found sterigmatocystin (2-4 ng/g) in carpet dust from a damp indoor environment. It follows that samples of deposited dust should be considered alongside with bulk samples when assessing the presence of mycotoxins in indoor environments. In agricultural settings, aflatoxin concentrations of 0,01 - 1000 ng/m3 and eoxynivalenol (DON) concentrations of 3-20 ng/m3 have been reported in air17-18, 20-21, 24-25. In indoor environments, satratoxin in concentrations of 0,1-0,5 ng/m3 and unidentified trichothecenes in concentrations of 1-35 ng/m3 have been found22-23. It seems therefore, that irrespectively of the environmental setting, whether agricultural or indoor environments, measurement of airborne mycotoxins generally require use of high-volume samplers in combination with sensitive chemical or immunological methods of analysis. Risk-assessment on the inhalation of mycotoxins cannot be made based on the analysis of bulk samples of construction materials. Neither can mycotoxin contents of deposited dust serve as basis of risk-assessment. Therefore, with the development of more efficient methods of sampling and analysis, air sampling will help us better understand the health consequences of exposure to mycotoxins in indoor climates and perhaps will at some point enable estimation of dose-responses of humans to airborne mycotoxins. In conclusion, a wide range of mycotoxins are potentially present in indoor climates harboring moldy surfaces. It has proven difficult, however, to establish the presence of mycotoxins in indoor air. This does not take away from the fact, however, that mycotoxins may contribute to the variety of symptoms experienced by patients exposed to moldy propagules in indoor climates. REFERENCES: 1Andersson et al., Appl Environ Microbiol, 1997, 63: 387-393; 2Croft et al., Mycopathologia, 1986, 151:93-98; 3Flappan et al., Environ Health Perspect, 1999, 107: 927-930; 4Gravesen et al., Environ Health Perspect, 1999, 107: 505-508; 5Johanning et al., Int Arch Occup Environ Health, 1996, 68: 207-218; 6Smoragiewicz et al., Int Arch Occup Environ Health, 1993, 65: 113-7; 7Tuomi et al., Appl Environ Microbiol, 2000, 66, 1899-1904; 8 Auger et al., Am J Ind Med, 1994, 25: 41-2; 9Hodgson et al., J Occup Environ Med, 1998, 40: 241-9; 10, Atm Environ, 1992, 26A: 2163-2172; 11Morb Mortal Wkly Rep, 1994, 43: 881-883; 12Morb Mortal Wkly Rep, 1995, 44: 67-74; 13Morb Mortal Wkly Rep, 1997, 46: 33-35; 14Rautiala et al., Am Ind Hyg Assoc J, 1996, 57: 279-84; 15 et al., Fems Microbiol Lett, 1992, 79:337-43; 16 Lappalainen et al., Atmosph Environ, 1996, 30, 3059-3065; 17Burg et al., Am Ind Hyg Assoc J, 1981, 42:1-11; 18Burg et al., Am Ind Hyg Assoc J, 1982, 43:580-587; 19Silas et al., Am Ind Hyg Assoc J, 1987, 48:198-201; 20Selim et al., Am Ind Hyg Assoc J, 1998, 42:252-256; 21Palmgren et al., Am Ind Hyg Assoc J, 1983, 44:485-488; 22Sorenson et al., Appl Environ Microbiol, 1987, 53: 1370-5; 23Engelhart et al., Appl Environ Microbiol, 2002, 68:3886-3890; 24Ghosh et al., Am Ind Hyg Assoc J, 1997, 58:583-586; 25Kussak, Ph.D. Thesis, Umeå University, Umeå, Sweden, 1995. 22Johanning et al., Unpublished data pertaining to filter no. 1 in Johanning et al., Proceedings: Indoor air 2002; 23Yike et al., Appl Environ Microbiol, 1999, 65: 88-94. Immunological and Neurophysiological Abnormalities in Adults with Exposure to Molds W. , M.D. High, M.D., Ph.D. Ebere Anyanwu, M.S., Ph.D. Medical Center for Immune and Toxic Disorders Houston, Texas Objective: The objective of this study was to evaluate the immunological and neurophysiological effects in patients (378) who presented to our medical center with various adverse health problems due to documented exposure to indoor toxigenic molds. Exposure to indoor toxigenic molds and the subsequent effects on humans is ranked high among environmentally related disorders. Recently, occupational exposures in nonagricultural settings have been investigated using modern immunological laboratory tests. Few studies exist that take into account the combined immunological and neurophysiologic effects in humans. Methods: We studied retrospectively patients with documented toxigenic mold exposure at measured levels in their residence using previous medical records, questionnaires, serum testing for antibodies to molds, serum immune function testing and neurophysiological testing including electroencephalogram (E.E.G.), brainstem auditory evoked response (B.A.E.R.), visual evoked potentials (VEP), and nerve conduction velocity (NCV). Results: Findings from indoor environmental studies on the patients' residence (exposure site) were positive for specific levels of exposure to toxigenic molds including Penicillium, Aspergillus, Fusarium, Chaetomium, and Stachybotrys species. There was a positive correlation between findings from the neurophysiological and immunological studies and the exposure to indoor molds found in the residence. The objective immunological and neurophysiological findings were significantly abnormal, indicating both immunotoxic and neurotoxic effects. Conclusions: A statistically significant number of patients with known chronic exposure to toxigenic molds developed immunologic and neurophysiologic abnormalities. Our findings revealed the extent to which toxigenic molds can affect the immunological and neurological systems of environmentally exposed individuals. Further work is encouraged in this regard. -----The Pathology of Trichothecene Mycotoxicosis In Humans------- 1. The Fingerprint of the Agent Causing the Disease is Displayed Within the Cells or Tissue of The Body. 2. Degeneration and Necrosis of The Entire Central Nervous System, Cardiovascular, lung, Digestive Tract, Spleen, Liver, Kidney, Pancreas, Immune, Skin, Reproductive, Eye, Urinary Bladder and Prostate. 3. The Signs and Symptoms Described For Trichothecene Mycotoxicosis Match the Pathology Observed. 4. Every Cell in The Body is Affected or Susceptible to Trichothecene Mycotoxins When Exposed. 5. The Exposed Cells Are Not Allowed to Grow and Make Cellular Products in The Rough Endoplasm Reticulum Represents of First Mechanism of Action on The Cells. 6. The Burning or Denaturation of Tissue From the Epoxide Molecule is Another Mechanism of Action on The Cells of The Body Causing Intense Scarring of Organs. (Like Phenol) 7. The Rapidly Turnover Organs Systems Are Affected The Most Severe, G.I. Tract, Immune System and Reproductive, (like radiation damage) 8. The Central Nervous System is Severely Affected and is A Primary Target Organ. The Neurons in the Cerebral Hemispheres, White and Grey Matter, Brain Stem and even the Ependymal Cells. The Purkinje Cells of The Cerebellum Are Severely Affected That Affect Motion and Balance. The Dorsal and Ventral Motor Neurons Are Destroyed Causing Amyotrophic Lateral Sclerosis. Peroxidation of Peripheral Nerves is Also Observed. The Central Nervous System is The Organ Most Affected as Reported By People Exposed to Toxic Mold. 9. Lack of Cellular Production, Epoxide- Peroxidation of Lipid Membranes, Loss of Vessels, Loss of Oxygen From Severe Lung Scarring, and Loss of Proper Nutrients Due Loss of Functional Absorption of Intestine Affect the Brain and All Organs of The Body. 10. The Trichothecene Mycotoxins are Cumulative in Their Health Effects on Organ Systems. 11. Trichothecene Mycotoxins are " Hit and Run " Poisons and are not Stored in The Body. 12. Inhalation of Trichothecene Mycotoxins Are More Poisonous As Observed by The Intense Scarring of The Alveolar Tissue Than Consumption Due To The Neutralization of Mycotoxin by Bacteria. 13. Depression of the Immune System Allows for Increase Infections by Bacteria, Viral, Fungal and Cancer to Form. 14. Yeasts are allowed to Colonize the Intestine Tract Because They Are Resistant to Trichothecene Mycotoxins. 15. Yeast Can Cause Diabetes Mellitus, Gout and Prevent Proper Liver Function to Detoxify Xenobiotics. 16. Trichothecene Mycotoxins are Released Within the Urine and Feces as Evidenced by The Pathology Observed Within Those Tissues. 17. Children Exposed to Trichothecene Mycotoxins are 100 to 1000 X more susceptible because stems are killed not allowing for additional growth within the individual. 18. There is No Safe Level of Exposure to Trichothecene Mycotoxins. 19. The third Mechanism For Trichothecene Mycotoxicosis is To Develop Anaphylaxis to Mold Allergens When Mycotoxin Leaves The Body. Dr. Croft, (Medical Pathologist) Stages of Mycotoxicosis: For Inhalation of Mycotoxin The three Stages (1-3) ranging from lower to higher severity of poisoning were modified according to exposure via the air as opposed to ingestion already established (Forgacs et al., 1962; Joffe, 1971). A separate Stage of convalescence occurs when a patient is completely removed from the contaminated premises and the source of mycotoxin or mold spores. Stage 1: The primary changes are in the brain, respiratory and immune systems, mucus membranes and gastrointestinal tract. Signs and symptoms may include burning sensation in the mouth, tongue, throat, palate, esophagus, and stomach, which is a result of the action of the toxin on the mucous membranes and skin in the exposed areas. Moist areas of the body armpits, under breasts, belt line and groin are more sensitive or first affected. Patients may report burning within the eyes, ears and nose. Patients also reported that their tongues felt swollen and stiff. Mucosa of the oral cavity may be hyperemic. Mild gingivitis, stomatitis, glositis, and esophagitis developed. Inflammation, in addition to gastric and (small and large) intestinal mucosal, resulted in vomiting, diarrhea and abdominal pain. Excessive salivation, headache, dizziness, weakness, fatigue and tachycardia were also present. There may be fever and sweating. The respiratory system develops burning sensations and congestion. Severe exposure to mycotoxin within the lungs may lead to congestion, edema and failure, due to caustic action. Body temperature remains normal and controllable by the patient. The poisoning appears and disappears relatively quickly in this Stage with the exception of, lungs and central nervous system. Initially (Stage 1), the patient's symptoms are very uncomfortable or painful. As the poisoning continues and the patient progress toward Stage 2, he or she becomes accustomed to the presence of the mycotoxin and a quiescent period follows due to lack of nerve sensation. Depending on exposure levels, the first Stage may last from 3 - 9 days. In scoring the 50 signs and symptoms listed in Tables-1 and 2, an average score range of 20-45 represents Stage 1. Stage 2 : This Stage is often called the latent Stage or incubation period because the patient feels apprehensive, but is capable of normal activity in the beginning of this Stage. Every organ of the body is affected by degeneration and necrosis with continued exposure. The primary target organs for an individual become evident over time, due to biological variation. These are disturbances in the central and autonomic nervous systems resulting in headaches, mental depression, loss of short-term memory, loss of problem-solving ability, various neuropsychiatric manifestations, meningism, severe malaise and fatigue, narcolepsy, loss of temperature control, hyperesthesia or numbness of body areas, and cerebellar dysfunction including hypotonia, attitude and gait, dysmetria, asthenia, vertigo, disturbances of speech, and loss of balance (Best, 1961). Spinal cord degeneration may also be observed in gait and reflex abnormalities, such as the ability to drive vehicles, ride bicycles or pass sobriety tests (inability to tolerate ethyl alcohol). Attention deficient disorder may be observed in children. Various systems may include: Eyes: visual disturbances, floating objects, light sensitive, lack of tears, burning and itching. Ears: burning, itching, and loss of hearing. Immune and hematopoietic: progressive loss of white and red cells including a decrease of platelets and hemoglobin, and high susceptibility to bacterial, mycotic and viral infections, debilitating chemical and allergies. Gastrointestinal: metallic taste in mouth, tooth loss, gum problems, stomatitis, sores in gums and throat, nausea, vomiting, diarrhea or constipation, excessive flatulence, abdominal distention, hepatitis, pancreatitis, and diabetes mellitus. Respiratory : burning and bleeding from nasal membranes, respiratory difficulty, asthma, extreme susceptibility to cold, flu and pneumonia. Skin: thinning of hair on head, burning on face, rashes, irritation, and edema. Renal: proteinuria, possible hematuria. Reproductive: irregular ovarian cycles, increased menstrual flow, fibroid growths in uterus, cystic development in mammary glands, and tumors of mammary and prostate glands. Musculoskeletal : somatitis, muscle weakness, spasms, cramps, joint pain, enlargement of joints in hand, and clubbing of fingers. Cardiovascular: chest pain, palpitations, ruptures of atrial walls, myocardial infection and aneurysm of arteries. The skin and mucous membranes may be icteric, pupils dilated, the pulse soft and labile, and blood pressure may decrease or increase. The body temperature does not exceed 38 degree C and the patient may be afebrile, or chilled. Visible hemorrhagic spots may appear on the skin. Thoughts of suicide may be prominent in the person's mind at this time or anytime in Stage 2. Human bonding is very important for survival. Degeneration and hemorrhages of the vessels marks the transition from the second to the third Stage of the disease and may not be consistently observed. The degeneration of the vital organs including serious respiratory insufficiency or asthma and CNS degeneration will take the patient into Stage three along with development of necrotic angina. If exposure continues, depending on exposure levels, Stage 2 may continue from weeks to months or even years until the symptoms of the third Stage develop. Evaluating the 50 signs and symptoms (Table-1 and 2) by assigning a score (0-least intense to 5-most intense or severe) to each symptom, we have determined that an average score range of 45-180 represents Stage 2. Stage 3: Severe degeneration of the vital organs. The transition from the second to the third Stage is sudden. In this Stage, the patient's resistance is already low, and violent severe symptoms are present, especially under the influence of stress, or associated with physical exertion and fatigue. The first visible sign of this Stage may be lung, brain or heart failure (heart attack), with or without the appearance of petechial hemorrhage on the skin of the trunk, the axillary and inguinal areas, the lateral surfaces of the arms and thighs, the face and head, and in serious Cases, the chest. The petechial hemorrhages vary from a few millimeters to a few centimeters in diameter. There is increased capillary fragility and any slight trauma may cause the hemorrhages to increase in size. Aneurysms of the brain or aorta may be observed by angiography. Hemorrhages may also be found on the mucous membranes of the mouth and tongue, and on the soft palate and tonsils. There may be severe interstitial thickening or scarring of the lungs, or respiratory failure. Nasal, gastric and intestinal hemorrhages and hemorrhagic diathesis may occur. Necrotic angina begins in the form of catarrhal symptoms and necrotic changes soon appear in the mouth, throat, and esophagus with difficulty and pain on swallowing. Severe degeneration of the skin on the face, eyelids, and loss of lashes is also often present. Necrotic lesions may extend to the uvula, gums, buccal mucosa, larynx, vocal cords, lungs, stomach, and intestines and other internal organs such as the liver and kidneys and are usually contaminated with a variety of avirulent bacteria. Bacteria infection causes an unpleasant odor from the mouth due to the enzymatic activity of bacteria on proteins. Areas of necrosis may also appear on the lips and on the skin of the fingers, nose, jaws, and eyes. Regional lymph nodes are frequently enlarged. Esophageal lesions may occur and involvement of the epiglottis may cause laryngeal edema and aphonia (loss of voice). Death may occur by strangulation. Patients may suffer an acute parenchymatous hepatitis accompanied by jaundice. Bronchopneumonia, pulmonary hemorrhages, and lung abscesses are frequent complications. Tumors may develop of various organs, including skin, urinary bladder, brain, mammary gland, bone, immune, liver, prostate, possibly resulting in death. The most common cause of death is brain failure due to both direct effects of the mycotoxin on the central nervous system and indirect effects due to respiratory failure or lack of oxygen to the brain caused by the severe caustic inflammation (fibrinous exudation) reaction with the lung tissue, rendering it non-functional. Again, using the scoring system represented in Tables-1 and 2, an average score of greater or equal 180 represents Stage 3. Stage of Convalescence: The course and duration of this Stage 3 depends on the intensity of the poisoning and complete removal of the patient from the premises or source of mycotoxin. Therefore, the duration of the recovery period is variable. There is considerable cellular necrosis and scarring to all major organs of the body in which cells will not regenerate, including the brain, spinal cord, eyes, lung, heart, liver, pancreas, kidney, adrenal, and blood vessels. If the disease is diagnosed during the first Stage, hospitalization is usually unnecessary, but allergies and asthma should be monitored closely. If the disease is diagnosed during the second Stage and even at the transition from the second to third Stages, early hospitalization may preserve the patient's life. If however, the disease is only detected during the third Stage, death cannot be prevented in most Cases. 1. Croft, W. A., Jastromski, B. M., Croft, A. L., and s, H. A., " Clinical Confirmation of Trichothecene Mycotoxicosis in Patients Urine " , In: Journal of Environmental Biology 23(3), 301-320 (2002) 2. .Forgacs, J., and W. T. Carll : Mycotoxicoses. In : Advances in Veterinary Science. Academic Press, New York and London, pp 273-372 (1962). How Molds and Mycotoxins Affect Human Brains Kaye H. Kilburn, M.D. University of Southern California, Keck School of Medicine Background: Mold spores and mycotoxins produce airway irritation, asthma and bleeding. Neurobehavioral and respiratory symptoms suggested testing. Methods: Neurobehavioral functions as means of percent predicted were compared in 65 consecutive mold exposed adults and 202 community controls. Measurements included balance, choice reaction time, color discrimination, blink reflex, visual fields, grip, hearing, problem solving, verbal recall, perceptual motor speed, and memory. Check lists surveyed histories, mood states and symptom frequencies (Kilburn 2002a and 2002b). Findings: Exposed persons had abnormal balance, reaction time, blink reflex latency, color discrimination, visual fields, and grip. Also digit symbol substitution, peg-placement, trail making, verbal recall, and picture completion scores were reduced. Twenty-one of 26 tested functions were abnormal. Airways were obstructed and vital capacities reduced. Mood scores and symptom frequencies were elevated. Interpretation: Mold exposures indoors were associated with neurobehavioral impairment probably from mycotoxins, such as trichothecenes. Correlation of human impairment with measured mycotoxins is the next step (Johanning et all 1999 and 2002, Nielsen and Thrane 2001). REFERENCES 1. Kilburn KH. Janus Revisted, Molds Again. Arch Environ Health 2002a;57(1):7-8. 2. Kilburn KH. Inhalation of Moulds and Mycotoxins. Eur J Oncol 2002b;7(3):____. 3. Johanning E et al. Clinical Experience and Results of a Sentinel Health Investigation Related to Indoor Fungal Exposure. Environ Health Perspect 1999;107(3):489-494. 4. Johanning et al. Airborne Mycotoxin Sampling and Screening of Trichothecenes in Fungal Cultures - Using Gas Chromatography - Tandem Mass Spectrometry. J Chromatography A 2002;929(1):75-87. Quote Link to comment Share on other sites More sharing options...
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