23rd Annual International Symposium
on
Man and His Environment in Health and Disease
Special Focus
The Autonomic Nervous System and Its
Relationship to Environmental Pollutants Including the Cardiovascular System
and Electromagnetic Sensitivity
Sponsored by
American Environmental Health Foundation
and
University of
Physician
Accreditation/Credit:
This activity has been planned and implemented in
accordance with the Essential Areas and policies of the Accreditation Council
for Continuing Medical Education through the joint sponsorship of the
University of North Texas Health Science Center at
Fort Worth Office of Professional & Continuing Education and the American
Environmental Health Foundation. The University of
North Texas Health Science Center at Fort Worth Office of Professional &
Continuing Education is accredited by the ACCME to provide continuing medical
education for physicians.
The University of North Texas
Health Science Center at
The University of North Texas
Health Science Center at
The University of North Texas
Health Science Center anticipates this program for 24 hours in Category 2A CME
credit hours, pending approval from the American Osteopathic Association.
Nursing
Accreditation/Credit:
To receive a certificate of successful completion,
participants must attend the activity in its entirety and complete and return
the activity evaluation credit request form.
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.
FINANCIAL CONSIDERATION
AEHF is a nonprofit organization that was founded in 1975 to provide education and research into Environmental Medicine. This year’s Symposium is our 23rd Annual International Symposium and is our major vehicle for educating the medical professional.
Funding for the symposium is provided by registration fees from physicians and exhibitors. Proceeds from the AEHF store cover the shortfall between registration fees and expenses for the conference. AEHF does not receive grants or any outside financial support for our education. Donations are accepted and used toward research into environmental medicine.
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 2005 conference will focus on “The Autonomic
Nervous System and Its Relationship to Environmental Pollutants Including the
Cardiovascular System and Electromagnetic Sensitivity”. 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
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To provide new insights in The
Autonomic Nervous System and Its Relationship to Environmental Pollutants
and the environmental causes behind many problems you see.
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To present new diagnostic and treatment modalities to help you improve
the quality of care for your complex patients.
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To provide concepts, tools that will enhance your practice.
OBJECTIVES OF THE MEETING
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Improve the outcome of treating patients with sensitivities to The Autonomic Nervous System and Its Relationship
to Environmental Pollutants.
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Use new concepts and treatments to help better diagnose and manage many
patients with environmentally triggered problems and sensitivities to The Autonomic Nervous System and Its
Relationship to Environmental Pollutants.
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Apply the concepts of this conference to your practice by using
nutrition and environmental manipulation for the treatment of sensitivities to The Autonomic Nervous System and Its
Relationship to Environmental Pollutants.
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Use the information presented to enhance the effectiveness,
cost-efficiency, and competitiveness of the physician in relation to The Autonomic Nervous System and Its
Relationship to Environmental Pollutants.
INTENDED AUDIENCE
M.D.=s, D.O.=s, medical students, nurses,
nutritionists and other health professionals interested in the concepts and
practice of Environmental Medicine, Occupational Medicine and Toxicology.
EDUCATIONAL FORMATS
#
Plenary
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Panels Discussions
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Case Studies
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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
William J. Rea, M.D.,
F.A.C.S.
Symposium
Chairman,
American
Environmental Health Foundation,
Environmental
Bertie B. Griffiths, Ph.D.,
Environmental
Kaye H. Kilburn, M. D.
University
of Southern
William J. Meggs, M.D., Ph.D.
Brody
Department of Emergency Medicine
23rd Annual International
Symposium
on Man and His Environment
Schedule
Colin
Little M.D.
William J.
Meggs, M.D., Ph.D.
ABSTRACTS
AND
HANDOUTS
Objectives & Notes
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Colin
Little, M.D. |
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The Environmental Unit |
Phone: 011/61-0398881345 |
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Fax: 011/61-398881369 |
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Email: [email protected] |
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Training: |
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Current Job Description: |
Physician and Allergist, Research participant in CSIRO project on cow’s milk intolerance in adults. |
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Medical School/University Attended: |
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MB,
BS, MRCP ( |
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Other Information: |
Current trends in Immunology Vol3 (2000) pgs131-144; Proceedings Soc Exp Biol Med Vol 224 (2000) pgs 264-272; Exp Biol Med (Mini review) Vol227 (2002) pages 438-444; Infect Immun Vol 68 (2000) pgs 3840-47 |
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SPEECH TITLE: “Interactions Between Immune and Autonomic Systems in Patients Sensitive to Foods and Chemicals” At the end of this Presentation, the participant should be able to: 1. Understand connections between immunity and sensory nerves. 2. Interactions between sensory nerves and brain centers (incl. ANS) 3. Application of this knowledge to examples of food intolerance and chemical sensitivity. The above information was provided by the
Speaker. |
INTERACTIONS BETWEEN
IMMUNE AND AUTONOMIC SYSTEMS IN PATIENTS SENSITIVE TO FOODS AND CHEMICALS.
There is limited knowledge of the interaction between the immune and autonomic nervous systems. This discussion focuses on sources of afferent stimuli in patients with sensitivity disorders and discusses the current data on autonomic function in clinical conditions where food or chemical sensitivity may be important.
Studies over the past decade have demonstrated that immune stimuli signal the central nervous system not only by the humoral route but via sensory fibres, particularly c fibres relaying pain sensation. The vagus nerve is the principal conveyor of these neural stimuli but the glossophayrngal and trigeminal nerves almost certainly have a similar function. This sensory information is relayed to the brain stem, particularly the Nucleus Tractus Solitarus, amygdala and hypothalamus. Complex interactions occur with autonomic centers with (potentially) variable autonomic responses. Such responses may influence the function of the gut, respiratory tract and other sites such as the heart and skin. Other concurrent influences on the central nervous system will further modulate these responses.
There is increasing evidence for activation of the sensory nerves in patients with food intolerance associated with symptoms of an Irritable Bowel Syndrome. Patients with this disorder have a heightened responsiveness of the gut sensory nerves, increased mast cell numbers in the gut wall, evidence for local mast cell degranulation and close apposition between sensory nerve endings and mast cells. In children with cow’s milk intolerance, studies have shown increased levels of the cytokine TNFα in the gut wall and in fecal fluid. This cytokine is a potent activator of c fibres.
There is also evidence that patients with chemical sensitivity show a heightened responsiveness of sensory nerves of the respiratory tract. One recent study demonstrated the release of neuropeptides from sensory nerves following chemical exposure. Such changes were not seen on a control group. Studies by Millqvist have demonstrated that chemically sensitive subjects have a lower threshold of the cough response to capsaicin. Increased levels of the cytokine TNFα have been detected in the sputum of patients with idiopathic cough and such patients also show increased levels of substance P in nasal lavage specimens. Finally, chemically sensitive patients have increased NGF in nasal secretions after capsaicin inhalation.
A study by a Dutch group may provide insight as to how chemicals may cause a heightened responsiveness of sensory nerves. They sensitized mice with dintrofluoro benzene. A subsequent challenge with dintrobenzene sulphonic acid released TNFα into the tracheal fluid within fifteen minutes. This TNFα increased the susceptibility of sensory neurones to both the chemical (dintrobenzene sulphonic acid) and also capsaicin. Antibodies to TNFα and TNFα receptor inhibited these effects. The process was shown to be mast cell dependent. Subsequent communication indicates that the immune response to the chemical is mediated by TH1 cells and that kappa light chains may be involved.
As mentioned, there are complex interactions between nuclei in the brain stem and centers mediating sympathetic and parasympathetic responses. For this reason stereotyped responses by the autonomic nervous system are unlikely to occur and will be contingent on other influences – stress, sleep-waking cycles, hormonal fluctuations etc. Data on the effects of cytokines released in peripheral tissues on local autonomic function is limited and also probably influenced by multiple parameters.
In general the peripheral release of cytokines such as IL-1 and TNFα activate the sympathetic nervous system with the release of moradrenaline, particularly in lymphoid organs. Immunological stimuli affecting the gut induces the release of acetylcholine from efferent parasympathetic fibres. This mediator inhibits cytokine release by macrophages and is thought to be protective against shock. In some tissues, for example the jejunum and atria, IL-1 and TNFα inhibit not adrenaline release. The general view to date is that the response of organisms innervated by the autonomic nervous system varies in response to the type of immune activation.
Although no firm conclusions can be drawn, it is useful to list the findings on autonomic function in a number of clinical conditions where there may be underlying sensitivity to foods and chemicals. They include vasomotor rhinitis, irritable bowel syndrome, migraine and chronic fatigue syndrome.
The data on autonomic function in vasomotor rhinitis is of considerable interest. Studies show a hypoactive sympathetic response. The situation is less clear cut in the irritable bowel syndrome. There are reports of increased parasympathetic and reduced sympathetic activity in patients with increased intestinal motility. The converse may apply in patients with decreased motility. There may be “dysregulation” of autonomic function but no clear cut pattern. In migraine sympathetic activity appears to be reduced with depletion of noradrenaline stores, at leas tin the pupil. In the chronic fatigue syndrome there is again evidence of abnormal autonomic function without a consistent pattern. The tentative view is that the autonomic system is dysregulated.
In these conditions there may be efferent signaling, derived from immune responses, at least in some cases. The subsequent effects on autonomic function may depend on not only this signaling but on other concurrent influences on brain centers affecting autonomic function.
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Objectives & Notes
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Lynn
Clarkson |
Date
of talk: |
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Clarkson Soy Products, LLC P.O. Box 80 Cerro Gordo, IL
61818-0080 |
Phone: 800/252-1638 |
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Fax: 217/763-2111 |
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Email: [email protected] |
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Training: |
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Current Job Description: |
President of Clarkson Grain Company |
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SPEECH TITLE: “Organic Markets – from Grains and Oilseeds to Fibers” At the end of this Presentation, the participant should be able to: 1. Understand the scope of organic agriculture. 2. Understand the organic market price structure. 3. Have a perspective on the trends in organic food and fiber. The above information was provided by the
Speaker. |
Abstract:
Title: Organic Markets – from grains and oilseeds to fibers
Presentation to the American Environmental Health Foundation’s 23rd Annual Int’l Symposium
By: Lynn Clarkson
Organic
farming is the brightest spot in
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Objectives & Notes
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William J.
Meggs, M.D., Ph.D. |
Date
of talk: |
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Brody PCMH, 3ED-311, Department of Emergency Medicine |
Phone: 252/744-2954 |
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Fax: 252/744-3589 |
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Email: [email protected] |
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Training: |
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Current Job Description: |
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Current Faculty Appointments: |
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Medical School/University Attended: |
University
of |
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Internship: |
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Residency: |
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Board Certifications: |
Medical Toxicology, Internal Medicine, Emergency Medicine |
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Other Information: |
Co-author
of “The Inflammation Cure”, Scientific Progress in |
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SPEECH TITLE: “Environmental Hydrogen Sulfide: Rethinking Acceptable Exposure Levels” At the end of this Presentation, the participant should be able to: 1. To know the toxicity of acute & chronic exposures to hydrogen sulfide 2. To know the toxicity experienced in communities living near industrial facilities releasing hydrogen sulfide. 3. To know changes in regulatory status of hydrogen sulfide. The above information was provided by the
Speaker. |
Environmental Hydrogen Sulfide:
Rethinking Acceptable Exposure Levels
William Joel Meggs, MD, PhD
Hydrogen sulfide is a colorless gas that is heavier than air. It is extremely toxic as an irritant gas, cellular toxin, and has a noxious odor. Communities are exposed to hydrogen sulfide from pulp plants, refineries, decay of organ matter and composting of manure, slaughter houses and tanneries, and from volcanic activity. Community levels can range from tens to hundreds of parts per billion. Textbook authors and regulating bodies have considered toxic levels to be above a part per million. Several studies of communities have shown a high level of disease in persons exposed to hydrogen sulfide in levels traditionally considered safe. The experience with hydrogen sulfide points out the fallacies associated with setting safe limits for toxic substances.
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Objectives & Notes
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Cyril
Smith, Ph.D. |
Date
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Eccles, |
Phone: 011/44-161-789-4768 |
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Fax: |
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Email: [email protected] |
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Training: |
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Current Job Description: |
Retired |
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Other Information: |
Smith
C.W. (2002) Effects of Electromagnetic
Fields in the Living Environment. Proc. Intl. Conf. Electromagnetic
Environments and Health in Buildings, Royal College of Physicians, London,
16-17 May, 2002. In: Clements-Croome D (Ed.). Electromagnetic Environments and Health in
Buildings. Smith CW. (2003) Guest Editorial – Straws in the Wind. Journal Alternative and Complementary Medicine 9(1): 1-6. Smith CW. (2003) Guest Editorial – Energy Medicine United. Complementary Therapies in Nursing and Midwifery 9(4):169-175 (Nov 2003). Smith CW. (2004) Quanta and Coherence Effects in Water and Living Systems. J Altern Complement Med. 10(1);69-78. |
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SPEECH TITLE: “ANS Involvement in Chemical and Electromagnetic Sensitivities” At the end of this Presentation, the participant should be able to: 1. Appreciate the duality between frequency and chemical structure 2. Understand the ANS interactions and ANS stability 3. Appreciate the effects of chemicals and electromagnetic fields, acupuncture, and homoeopathy on the ANS. The above information was provided by the
Speaker. |
23rd ANNUAL INTERNATIONAL SYMPOSIUM
ON MAN & HIS ENVIRONMENT
Abstract
“Electromagnetic
Sensitivity and the ANS”
and
“ANS
Involvement in Chemical and Electromagnetic Sensitivities”
Cyril Smith, Ph.D.
The first part of these two presentations is intended to enable the participant to recognize Electromagnetic Sensitivities in patients, to appreciate the importance of endogenous and exogenous frequencies and the relationship between these frequencies and the autonomic nervous system.
The second part is intended to explain the duality between frequencies and chemical structure and their relation to autonomic nervous system stability criteria and interactions in living systems. The effects of interactions between chemical in the body and environmental electromagnetic fields is explained in terms of the endogenous frequencies on acupuncture meridians and linkages between specific acupuncture points and points in the autonomic nervous system.
The
conclusions are that Voll’s
link between these specific acupuncture points and the ANS gives an insight
into how environmental frequencies can interact with the ANS.
The Multiple Frequency Effect in
coherent systems shows how the frequency signatures of chemicals can behave
like environmental frequencies and vice versa.
References to the writer’s publications on “Electrical Hypersensitivity and Water Phenomena”, and previous presentations at these International Annual Symposia on “Man and His Environment in Health and Disease” held in Dallas, Texas, from 1986- 2000 are listed in the Handout which also includes some definitions of electromagnetic quantities.
A
set of “Notes for Patients on Electrical Sensitivities” written for the
Breakspear hospital,
(They
are listed in the Friday section of your syllabus at
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Objectives & Notes
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Mohamed B.
Abou-Donia, Ph.D. |
Date
of talk: |
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Laboratory of Neurotoxicology Dept. of Pharmacology and Cancer Biology, Box 3813 |
Phone: 919/684-2221 |
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Fax: 919/681-8224 |
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Email: [email protected] |
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Training: |
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Current Job Description: |
Professor of Pharmacology and Cancer Biology |
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Current Faculty Appointments: |
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Medical School/University Attended: |
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N/A |
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N/A |
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Board Certifications: |
American Board of Toxicology (ABT), and Academy of Toxicological Sciences (ATS) |
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Other Information: |
Book Editor, Neurotoxicology, CRC; Publications: more than 300. |
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SPEECH TITLE: “Stress Augments Chemical – Induced Neurotoxicity” At the end of this Presentation, the participant should be able to: 1. Know that exposure to stress alone results in neuronal cell damage. 2. Realize that stress increases chemical-induced neurotoxicity. 3. Both chemicals and stress induce neuronal injury via oxidative stress by increasing neuronal reactive oxygen species. The above information was provided by the
Speaker. |
Stress Augments Neurological Deficits
Induced by Combined Exposure to Pyridostigmine
Bromide, DEET, and Permethrin. Mohamed B. Abou-Donia, Ashok
Shetty, and Ali A. Abdel-Rahman,
Department of Pharmacology and Cancer Biology, Duke University Medical center,
Durham,
Exposure to a combination of stress and low doses of chemicals pyridostigmine bromide (PB), DEET and permethrin in adult rats, a model of Gulf War exposure, produces blood-brain-barrier (BBB) disruption and neuronal cell death in the cingulate cortex, dentate gyrus, thalamus and the hypothalamus. In this study, neuropathological alterations in other areas of the brain where no apparent BBB disruption was observed was studies following the above exposure. Animals exposed to both stress and chemicals exhibited decreased brain AChE activity in the midbrain, brainstem and the cerebellum and a decreased m2 muscarinic ACh receptor ligand binding in the midbrain and the cerebellum. These alterations were associated with significant neuronal cell death, reduced MAP-2 expression, and increased GFAP expression in the cerebral cortex and the hippocampal subfields CA1 and CA3. In the cerebellum, the neurochemical alterations were associated with Purkinje cell loss and increased GFAP immunoreactivity in the white matter. However, animals subjected to either stress or chemicals alone did not show any of the above changes in comparison to vehicle treated controls. Collectively, the above results suggest that prolonged exposure to a combination of stress and the chemicals PB, DEET and permethrin can produce significant damage to the cerebral cortex, hippocampus and the cerebellum, even in the absence of apparent BBB damage. As these areas of the brain are respectively important for the maintenance of motor and sensory functions, learning and memory, and gait and coordination of movements, the above alterations could lead to many physiological, pharmacological, and behavioral abnormalities, particularly motor deficits and learning and memory dysfunction. (Supported in part by the U.S. Army Medical Research and Materiel Command under contract project order DAMD 17-99-1-9020).