Nineteenth Annual International Symposium

on

Man and His Environment in Health and Disease







Special Focus



The Environmental Aspects of Neurotoxicity













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 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 24 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 2001 conference will focus "The Environmental Aspects of Neurotoxicity", toxic damage to the brain and nerves. 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 Neurotoxicity.
  • Use new concepts and treatments to help better diagnose and manage many patients with chemical sensitivity and Neurotoxicity.
  • Apply the concepts of this conference to your practice using nutrition and environmental manipulation for the treatment of Neurotoxicity.
  • Use the information presented to enhance the effectiveness, cost-efficiency, and competitiveness of your practice in relation to Neurotoxicity.




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 field of Environmental Aspects of Neurotoxicity.



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.)



Thursday and Saturday afternoon, we will have a case study/panel discussion. This session will consist of various faculty members discussing real cases. The audience is encouraged to participate in these discussions.



GIVEN IN COOPERATION



William J. Rea, M.D., F.A.C.S.

Symposium Chairman,

American Environmental Health Foundation,

Environmental Health Center - Dallas,

Dallas, Texas

Bertie Griffiths, Ph.D.,

Environmental Health Center - Dallas

Dallas, Texas



Satoshi Ishikawa, M.D.

Clinical Environmental Health Center, Kitasato Hospital

The Kitasato Institute

Machida-shi, Tokyo Japan



Kaye H. Kilburn, M. D.

University of Southern California Medical Center

Keck School of Medicine

Los Angeles, CA



William J. Meggs, M.D., Ph.D.

E. Carolina University School of Medicine

Dept. of Emergency Medicine

Greenville, NC



















































TABLE OF CONTENTS,

THURSDAY, JUNE 7, 2001







Thursday faculty listing ....................................................................................................................... 5



Thursday schedule ................................................................................................................................ 6



Abstracts and handouts



Seba ......................................................................................................................................... 8



Beck ......................................................................................................................................... 10



Kilburn ..................................................................................................................................... 12



Muller-Mohnssen ..................................................................................................................... 15



Furlong ..................................................................................................................................... 17



Rea ......................................................................................................................................... 20



Auger ........................................................................................................................................ 22



Baird ....................................................................................................................................... 24



THURSDAY, JUNE 7, 2001 FACULTY



Pierre Auger, M.D.

Clinique De Santé Au Travail et De Santé Environnementale

Montreal, Quebec Canada

514/849-5201



Deborah Baird, M.D.

Environmental Health Center-Dallas

Rockwall, TX

972/771-1106



C. Malcolm Beck

Garden-Ville, Inc.

San Antonio, TX

201/651-6115



Clement E. Furlong, Ph.D.

Department of Genetics

University of Washington

Seattle, WA

206/543-1193



Kaye H. Kilburn, M. D.

University of Southern California Medical Center

Keck School of Medicine

Los Angeles, CA

323/442-1830



Helmuth Muller-Mohnssen, Ph.D.

Ludwig-Maximilians Univ. Munich

Ismaning/Menich, Germany

011-49-89-969444



William J. Rea, M.D.

Environmental Health Center - Dallas

Dallas, TX

214/3684132



Doug Seba, Ph.D.

Alexandria, VA 22313

703/949-1055









NINETEENTH ANNUAL INTERNATIONAL SYMPOSIUM

ON MAN AND HIS ENVIRONMENT





SCHEDULE FOR THURSDAY, JUNE 7, 2001





11:00 a.m. REGISTRATION



12:45 p.m. WELCOME/MODERATOR: William J. Rea, M.D., George C. Miller, II, M.D., Gary R. Oberg, M.D.



1:00 Doug Seba, Ph.D. "Environmental Update 2001: A Health Odyssey"

1:20 Q & A



1:30 C. Malcolm Beck "Insects and Our Health"

1:50 Q & A

2:00 Kaye H. Kilburn, M. D. "Neurotoxicity from Chlorine and Hydrogen Sulfide"

2:20 Q & A



2:30 H. Muller-Mohnsen, Ph. D, "Health Effects Caused by Pyrethrine or Pyrethroid Exposure in Civil Aircrew Members"

2:50 Q & A



3:00 BREAK WITH EXHIBITORS



MODERATOR: Jean A. Monro, M.D.



3:30 Clement E. Furlong, Ph.D."The Human Paraoxonase (PON1) Polymorphism: Role in Detoxication of Organophosphorus Insecticides"

3:50 Q & A



4:00 William J. Rea, M.D. "Neurotoxicity-Central Nervous System"

4:20 Q & A



4:30 Pierre L. Auger M.D., "Chronic Toxic Encephalopathies Apparently Related to Exposure to Toxicogenic Fungi"

4:50 Q & A



5:00 CASE STUDIES & PANEL/MODERATOR: Allan D. Lieberman, M.D.

1.) Deborah Baird, M.D. "Seven Year Case Study of Acute Neurotoxicity"



2.) Case Study



6:00 ADJOURN

























THURSDAY, JUNE 7, 2001



ABSTRACTS



AND



HANDOUTS





























Abstract Information & Notes



Douglas B. Seba, Ph.D. Date of talk: Thursday, June 7, 1:00 p.m

Phone: 703/949-1055

P.O. Box 1417, #323 Fax: n/a

Alexandria, VA 22313 E-mail: n/a



Medical School Attended: Ph.D., University of Miami

Residency: n/a

Board Certifications: n/a

Current Faculty Appointments: None

Current Job Description: Independent Marine Scientist

Other Information: 35 Years of Experience in Toxicology and Environmental Chemicals



Disclosure Statement: None



SPEECH TITLE: "Environmental Update 2001: A Health Odyssey"



The information below has been provided by the speaker.



1.) Goals and objectives: To review major environmental phenomenon as we enter the next millennium



2.) Outline of talk/abstract: Synthetic chemicals, radionuclides, global warming, and increasing dust will be reviewed for contemporary aspects



3.) Conclusion of what is to be learned: That there are a plethora of adverse health effects at vast distances from their environmental origin



4.) References: Drawn from the most recent contemporary science news sources at the time of presentation



ENVIRONMENTAL UPDATE 2001: A HEALTH ODYSSEY



Douglas B. Seba



Objectives

This paper will review major environmental phenomenon as we enter the next thousand years. An odyssey is a long wandering or voyage usually marked by many changes in fortune and that certainly describes human health as we stand on this millennial cusp. This review should help set the perspective for this entire conference.



Abstract

Synthetic chemicals, radionuclides, electronic smog, global warming and increasing dust all vie to be the leading causes of compromised health as we enter this new era. Dust alone carries endocrine disruptors and carcinogens, heavy nuclides and large insects, organic debris and bacteria, fungi, and viruses. It is a virtually soup of assaults on our health and it is everywhere. As old forgotten plagues once again become the stuff of daily headlines we must quickly embrace the paradigm of environmental health if we are to keep the health gains of the last millennium.



In just the last 50 years or 5% of the millennium the average visibility east of the Mississippi River has decreased by one-half and an area the size of Canada over the Indian Ocean south of India has become covered in constant haze. People lost the ability to see Venus during the day early in the millennia (30%). Thus, no one alive today is breathing air even remotely as clean as our ancestors of a few dozens generations ago. This is a true challenge to our continued health progress.



Conclusion

There are a plethora of adverse health effects at vast distances from their environmental origin. Understanding their fate and transport is essential to patient environmental health.



References

References will be drawn from the most recent contemporary science news sources at the time of presentation.

















































Abstract Information & Notes



C. Malcolm Beck Date of talk: Thursday, June 7, 1:30 p.m.

Garden-Ville, Inc. Phone: 210/651-6115

7561 East Evans Rd. Fax: 210/651-9231

San Antonio, TX 78266 E-mail: n/a



Medical School Attended: n/a

Current Job Description: Full time researching and giving presentations all over U.S. on understanding nature. Average 80 talks or slide presentations a year to Universities, Colleges, Master Gardeners, Farmers, Ranchers, Home Owners Assn Etc.



Disclosure Statement: None



SPEECH TITLE: "Insects and Our Health"



The information below has been provided by the speaker.



1.) Goals and objectives: To change peoples perception of insects, to prove they were all designed for our benefit.



2.) Outline of talk/abstract: Using color slides of insects to show the different life stages of insects, and benefits of each, and how to control troublesome ones without using toxic products.



3.) Conclusion of what is to be learned: If studied from correct point of view you discover that every living creature has something to show, teach or tell us, give us or prevent us from doing stupid things.



4.) References: A life time of playing with bugs and studying insects and their relation to human, animal and plant life, reading many books and publications, mostly, a burning desire to understand why the insects exist.





INSECTS & OUR HEALTH



C. Malcolm Beck



Of all the millions of insect species known, only one percent are considered pests. If we truly understood the role of these so-called bad bugs, however, we wouldn't be so quick to condemn.



Of all the living creatures on this planet, only humans have a free will to love, hate, reason and think logically. Every other living thing is programmed too only be what it is and do what it does.



If we consider ourselves to be the highest and most intelligent creatures on Earth, should not everything else, including the pest, be here to be of service and aid to us, to give us something, does something for us, to teach us something or even prevent us from doing something? If we study from this point of view, we soon discover reasons for pests. Instead we put our money and research into designing toxic ways to destroy pests. More than two billion pounds of pesticide selling for $24 billion are used each year in this country. Discovering reasons, for the existence of pests and nontoxic ways of controlling them would cut severely into the profits of this industry.



Organic gardeners and good farmers have known for years that weak, sick plants attract and can be destroyed by the pest insects and diseases. This is Nature's law, Survival of the Fittest. The so-called bad bugs are here to cull the plants so only the best survive to produce healthy food and seed for generations to come. The lady bugs and other predators and parasitic insects are here acting as a police force to keep the plants' culling insects in check so they can't overdo the culling job. Science has proven this with discovery that lady beetles prefer to feed on pest insects that randomly get on healthy plants. My own research has proven that plants have an immune system, bu only when plants are properly grown and are healthy.



The pests are one of the ways Nature speaks to us. They tell us when our soil is becoming weaker and our environment is getting more polluted. We must set our pride aside and listen. Nature is an infallible teacher. She has the answers. But, she doesn't force us to listen. She doesn't force us to learn. We have a free will. She allows us to stupidly ignore her and destroy the environment and ourselves with our pseudo-science, while we try to dominate her.



We either learn to listen and survive, or we will deteriorate to near extinction. Then, Nature can and will renew.



Sources: A lifetime of playing with bugs and studying insects and their relation to human, animal and plant life. Many books and periodic publications. Mostly a burning desire to understand why the insects exist.





































Abstract Information & Notes



Kaye H. Kilburn, M. D. Date of talk: Thursday, June 7, 2:00 p.m.



University of Southern California Medical Center Phone: 323/442-1830

Keck School of Medicine Fax: 323/442-1833

2025 Zonal Ave., CSC-201 E-mail: kilburn@usc.edu

Los Angeles, CA 90033



Medical School Attended: University of Utah College of Medicine

Residency: University of Utah Hospitals

Board Certifications: California, Louisiana, North Carolina, Missouri, Wyoming, New York

Current Faculty Appointments: Professor of Medicine, University of Southern California Keck School of Medicine

Current Job Description: Director of Environmental Sciences Lab, Ralph Edgington Professor of Medicine, University of Southern California - Keck School of Medicine

Other Information: Editor-in-Chief, Archives of Environmental Health and President & Director, Neuro-Test, Inc.



Disclosure Statement: None





SPEECH TITLE: "Neurotoxicity from Chlorine and Hydrogen Sulfide"



The information below has been provided by the speaker.



1.) Goals and objectives: To visualize and contrast the effects of chlorine and hydrogen sulfide on human brain function from epidemiological studies using neurobehavioral measurements.



2.) Outline of talk/abstract: Abstract furnished



3.) Conclusion of what is to be learned: Chlorine has permanent effects that worsen progressively to atrophy. Inhibition of blink reflex appears reversible. Hydrogen sulfide may hit and run with great damage but low doses insidiously subtract function. A breath or two of ether at industrial concentrations damages the brain irreversible.



4.) References: Kilburn KH and Warshaw RH: Hydrogen sulfide and reduced sulfur gases adversely affect neurophysiological functions. Toxicol Ind Health 11:185-197, 1995.



Kilburn KH: Effects of a hydrochloric acid spill on neurobehavioral and pulmonary function. J Occup Environ Med 38:1018-1025,1996.



Kilburn KH: Exposure to reduced sulfur gases impairs neurobehavioral function. So Med J 90:997-1006, 1997.



Kilburn KH: Evaluating health effects from exposure to hydrogen sulfide: Central Nervous System Dysfunction. Envion Epidemio Toxicol 1:207-216, 1999.





NEUROTOXICITY FROM CHLORINE AND HYDROGEN SULFIDE



Kaye H. Kilburn, M.D.

University of Southern California

Keck School of Medicine

2025 Zonal Avenue, CSC 201

Los Angeles, CA 90033

E-mail: kilburn@usc.edu





Chlorine

We tested for effects on the central nervous system (CNS) and lung of chlorine and "spent" potassium creosol (cresylate). A train derailment in a narrow Montana canyon that exposed about 1,000 people at home when tank cars ruptured. Seven weeks after the spill 97 exposed people were evaluated and 57 were studied after 3.3 years. Twenty-six people were tested on both occasions. Balance, reaction time, color discrimination, contrast sensitivity, visual field performance, blink reflex latency, verbal recall, problem solving, and long-term memory including vocabulary were tested. Pulmonary functions were measured by spirometry. Questionnaires assessed medical histories, mood states, the frequencies of 37 symptoms, other chemical exposures and preexisting disorders. Comparisons were made to 22 unexposed people from a nearby city. Seven weeks after the exposure, five test scores were significantly different from unexposed groups including balance with eyes closed, simple reaction time, numbers of abnormal visual quadrants, vocabulary and information. Moods state scores and symptom frequencies were elevated. After 3.3 years the additional abnormalities included choice reaction time, balance with eyes open, color discrimination errors in both eyes, visual field performance on the right, Culture Fair and verbal recall, immediate and delayed. Exposure at home to chlorine and creosol produced persistent CNS impairment that increased after 3 years.



Hydrogen Sulfide

The aim was to determine whether proximity to Dakota City lagoons generating hydrogen sulfide (H2S) was associated with diminished neurobehavioral function. The 51 Dakota City exposed subjects were compared first to the Dakota City unexposed group, second to a Wickenburg, AZ unexposed (standard control) group and third with a Tennessee unexposed group. We measured color vision, visual fields, balance, reaction time, blink reflex latency, grip strength and hearing. In addition, cognitive functions, perceptual motor speed as in peg placement and trail making, verbal recall and long-term memory (cultural awareness) were tested. Comparisons were made as a group and by individual abnormalities after adjusting for age, sex, education and other factors. The 51 exposed people averaged 5.8 abnormalities, the "unexposed" group showed 4.3 abnormalities compared to 2.2 in the Wickenburg unexposed group. The local unexposed group was different from Wickenburg unexposed group. Significant differences between the exposed and Wickenburg unexposed group were found for choice reaction time, balance with the eyes open (balance with the eyes closed was close at p<.07), blink reflex latency, color vision errors, (vocabulary was close p<.057) and fingertip number writing errors, a total of 5 abnormalities. Several years of H2S exposure was associated with neurobehavioral impairment. Other impairment in local controls may be due to atrazine or famphur (a phosphorothiotic ester).

























Notes:

Abstract Information & Notes



Helmuth Muller-Mohnssen, Ph.D. Date of talk: Thursday, June 7, 2:30 p.m.



Ludwig-Maximilians Univ. Munich Phone: 011-49-89-969444

Ismaning/Menich Fax: same

Germany E-mail: n/a





Medical School Attended:

Residency:

Board Certifications:

Current Faculty Appointments:

Current Job Description:

Other Information:

Vita

1928 born in Bremen, Germany

1951 state medical examination Marburg/Lahn

1952 MD, Marburg/Lahn, Germany

1968 Habilitation for Physiology Ludwig-Maximilians-University, Munich (LMU)

Educational background:

1952-1956, Institute of Pathology, University of Münster/Westfalen, Germany (Prof. Giese),

1952-1957 1956-1960 Physiological Institute, University of the Saarland (Prof. Stämptli).

1960-1993 Head of Department of Physiology in the federal center of environmental research GSF, Neuherberg/Munich.

1963 Retired

Working Fields

1. Development of collateral circulation induced by stenosing coronary sclerosis.

2. Hydrodynamic mechanisms involved in thrombogensis and atherogenesis,

3. Intravital-microscopical studies of the Node of Ranvier of isolated single motor nerve fiber during its electrophysiological function.

4. The stationary electrophysical basis of impulse-generation by the excitable nerve fiber membrane (Textbook: "Physics of nervous excilation with an introduction to methodology of physiological research", Munich 1979).

5. Epistemological basis of research politics



SPEECH TITLE: "Health Effects Caused by Pyrethrine or Pyrethroid Exposure In Civilian Air Crew Members"



The information below has been provided by the speaker.



1.) Goals and objectives: Determination of the occupational stress factor responsible for the increase of illness in civilian air crew members observed since 1988. (20)



2.) Outline of talk/abstract: Application of the usual clinical criteria of cause and effect relationship furnished evidence that in most of these patients pyrethrin/pyrethroid exposure had triggered the onset of the disease and that the disease exhibited the clinical characteristics of pyrethroid intoxication. (39)



3.) Conclusion of what is to be learned: Insecticide exposure is an avoidable stress factor in civilian aviation. Therefore it is up to the decision of the persons responsible for insecticide application in aircraft and contract hotels to counteract the increase of illness. (35)



4.) References:

Muller-Mohnssen, H., Hahn, K. (1995): About a method of early recognition of neurotoxic diseases (Exemplified by Pyrethroid intoxication) in German, Gesundheitswesen 57, 214-222.



Muller-Mohnssen, H. (1999): Chronic sequelae and irreversible injuries following acute pyrethroid intoxication. Toxicological letters, 107, 161-175 (further references).

HEALTH EFFECTS CAUSED BY PYRETHRINE OR PYRETHROID EXPOSURE

IN CIVILIAN AIR CREW MEMBERS

H. Müller-Mohnssen

Ludwig-Maximilians-University

Munich, Germany





Since 1988 it was observed in Germany that there has been a considerable increase in reports of illness with inability to work in crew members of long distance flights. Though the clinical pictures of illness exhibit resemblance for different patients, the symptoms that lead to inability to fly are different as follows: I). Mucocutaneous alterations: Conjunctivitis, alopecia, disfiguring weeping eczema of uncovered skin which flares up after in-flight spray missions, after entering the aircraft or hotel. ii). Cerebro-organic disorders: decrease of intellectual performance, increasing loss of memory, mixup of words, word finding difficulties, narcoleptic attacks alternating enhanced arousal and agitation. Abrupt nausea is observed followed by black out with collapse from seconds up to minutes (person falls down the stairs or, while car driving, wakes up when the car has come to standstill off the road), sudden attacks of clouding of consciousness with complete loss of orientation for 30 to 60 min (persons being at a familiar place suddenly does not know where they are). iii). Movement disturbances: walking "like on cotton", problems with correct estimation of distances (walking into door frames or missing stair steps). Clumsy while serving (when pouring the coffee, missing the cup and spattering the passenger). iiii). Suspicion of autoimmune diseases: multiple sclerosis, collagenosis, thrombocytopenia. In 80% of the patients the fitness to practice another occupation was obtained one year after termination of flying activity. As a cause of the illness to the flight crew members the occupational stress was considered arising from: 1.) Enhanced psychophysical strain due to irregular way of life, lack of sleep, jet lag, temperature jump, loss of social contacts; 2). Cosmic radiation; 3). Insecticide exposure in aircraft and hotels. The diagram demonstrates the latency period, i.e. the time interval from the beginning of the employment on long distance flights till the complaints exceed the threshold of perception (n=65). Ordinate: year, Abscissa: number of person sorted according to start of flying. Each person is represented by two vertically arranged marks; circles: beginning of occupation on long distance aircraft, filled squares: onset of illness. If the unavoidable components of stress (1 and 2) would cause the illness, the latency should be almost constant, i.e., the upper dotted line should run parallel to the lower. The results show, however, that the illness begins independently from the date of employment at a fixed date around 1992. Obviously there is no causal relation of illness with the stress components 1 and 2 but with a component firstly appearing between 1960 and 1992. The time span of 4 years between the introduction of pyrethroids for aircraft disinfection (1988) and outbreak of illness in the air crew members corresponds to the latency of 4,7 (±2,5) years of chronic pyrethrine/pyrethroid intoxication after indoor disinfection. The symptoms leading to inability to work depend on which of the three clinical phenotypes of pyrethroid-intoxication is expressed in the particular patient. In the majority of air crew members the I-(immunmodulatory-) type was found.



























Notes:

Abstract Information & Notes



Clement E. Furlong, Ph.D. Date of talk: Thursday, June 7, 3:30 p.m.



Department of Genetics Phone: 206/543-1193

University of Washington Fax: 206/543-0754

Box 357360 E-mail: clem@u.washington.edu

Seattle, WA 98195-7360



Medical School Attended: Ph.D. 1968, Biochemistry, University of California, Davis

Residency: n/a

Board Certifications: n/a

Current Faculty Appointments: Departments of Genetics and Medicine, Division of Medical Genetics

Current Job Description: Research in human biochemical genetics

Other Information:



Disclosure Statement: Bager Corporation (research support)





SPEECH TITLE: "The Human Paraoxonase (PON1) Polymorphism: Role in Detoxication of Organophosphorus Insecticides"



The information below has been provided by the speaker.



1). Goals and Objectives: The goals are be to explain the effects on organophosphorus sensitivity of several polymorphisms in the coding and promoter regions of the human paraoxonase (PON1) gene on human chromosome 7. Biochemical, genetic and animal model studies will be described.



2.) Outline of talk:



Outline of Lecture



  • History of the Human PON1 Polymorphism.
  • Cloning and Characterization of the Human and Rabbit PON1 cDNA's and the Human PON1 Gene.
  • Early Animal Model Studies
  • PON1 Knockout Mouse Model System Studies
  • The effect of the PON1 Polymorphism on Sensitivity to Diazoxon, Chlorpyrifos oxon and Paraoxon
  • The Bottom Line, Catalytic Efficiency of the PON1 Q192R Isoforms Determines in vivo Efficacy for Detoxications.


3.) Conclusion of what is to be learned: The major point to be learned from lecture #1 is that both the levels of expression of PON1 as well as the isoform expressed can be important in determining risk for exposure to specific organophosphorus (OP) compounds. The second point to be stressed is that the genetic variability in PON1 determines primarily sensitivity to the oxon forms of diazinon and chlorpyrifos and not the parent insecticides themselves (organophosphorothioates). The surprising point to be made is that contrary to what the name of the enzyme would imply, high levels of the high activity PON1 probably do not provide much protection against exposure to paraoxon (or parathion). The usefulness of the mouse model system for understanding OP metabolism in humans will be discussed



4.) References:



Augustinsson KB, Barr M (1963) Age variation in plasma arylesterase activity in children. Clin. Chem. Acta 8:568-573



Brophy VH, Jarvik GP, Richter RJ, Rozek LS, Schellenberg GD, Furlong CE (2000) Analysis of paraoxonase (PON1) L55M status requires both genotype and phenotype (In Process Citation). Pharmacogenetics 10:453-60



Clendenning JB, Humbert R, Green ED, Wood C, Traver D, Furlong CE (1996) Structural organization of the human PON1 gene. Genomics 35:586-9



Costa LG, McDonald BE, Murphy SD, Omenn GS, Richter RJ, Motulsky AG, Furlong CE (1990) Serum paraoxonase and its influence on paraoxon and chlorpyrifos-oxon toxicity in rats. Toxicol Appl Pharmacol 103:66-76



Costa LG, Richter RJ, Murphy SD, Omenn GS, Motulsky AG, Furlong CE (1987) Species differences in plasma paraoxonase correlate with sensitivity to paraoxon toxicity. In: Costa LG, Galli CL, Murphy SD (eds) Toxicology of Pesticides: experimental, clinical and regulatory perspectives, Springer-Verlag, Heidelberg, pp 263-266



Davies HG, Richter RJ, Keifer M. Broomfield CA, Sowalla J. Furlong CE (1996) The effect of the human serum paraoxonase polymorphism is reversed with diazoxon, soman and sarin. Nat Genet 14:334-6



Ecobichon DJ, Stephens DS (1973) Perinatal development of human blood esterases. Clin Pharmacol Ther 14:41-7



Hassett C, Richter RJ, Humbert R, Chapline C, Crabb JW, Omiecinski CJ, Furlong CE (1991) Characterization of cDNA clones encoding rabbit and human serum paraoxonase: the mature protein retains its signal sequence. Biochemistry 30:10141-9



Li WF, Costa LG, Furlong CE (1993) Serum paraoxonase status: a major factor in determining resistance to organophosphates. J Toxicol Environ Health 40:337-46



Li WF, Costa LG, Richter RJ, Hagen T, Shih D, Tward A, Lusis AJ, et al (2000) Catalytic efficiency determines the in-vivo efficacy of PON1 for detoxifying organophosphorus compounds. Pharmacogenetics 10:767-779



Li WF, Furlong CE, Costa LG (1995) Paraoxonase protects against chlorpyrifos toxicity in mice. Toxicol Lett 76:219-26



Richter RJ, Furlong CE (1999) Determination of paraoxonase (PON1) status requires more than genotyping. Pharmacogenetics 9:745-53



Shih DM, Gu L, Xia, YR, Navab M, Li WF, Hama S, Castellani LW, et al (1998) Mice lacking serum paraoxonase are susceptible to organophosphate toxicity and atherosclerosis. Nature 394-284-7



Notes:

Abstract Information & Notes



William J. Rea, M.D. Date of talk: Thursday, June 7, 4:00 p.m



Environmental Health Center - Dallas Phone: 214/368-4132

8345 Walnut Hill Lane, Suite 220 Fax: 214/691-8432

Dallas, TX 75231 E-mail: wjr@ehcd.com



Medical School Attended: Ohio State University College of Medicine

Residency: University of Texas SW Medical School; Parkland Memorial Hospital; Baylor Medical Center, Veteran's Hospital; Children's Medical Center

Board Certifications: American Board of Surgery; American Board of Thoracic Surgery; American Board of Environmental Medicine

Current Faculty Appointments: n/a

Current Job Description: M.D./President - Environmental Health Center - Dallas



Disclosure Statement: None





SPEECH TITLE: "Neurotoxicity-Central Nervous System"



The information below has been provided by the speaker.



1.) Goals and objectives: Understand what Neurotoxicity is



2.) Outline of talk/abstract: A series of cases with this problem will be presented, diagnosis and treatment.



3.) Conclusion of what is to be learned: Neurotoxicity is common and should be diagnosed and can be treated.



4.) References: Chemical Sensitivity, Volumes I, II, III, IV



NEUROTOXICITY - CENTRAL NERVOUS SYSTEM



William J. Rea, M.D., F.A.C.S, F.A.A.E.M.

Yaqin Pan, M.D.



Abstract: One hundred patients (ages 12-75; F-61; M-39; average 45), who had chronic chemical exposure at their work place were studied. Exposure source varied but was mainly from solvents in the ambient air. The patients used no protective gear. The main complaints were neurological symptoms 49%; (headaches, migraines, short-term memory loss, inability to concentrate, loss of concentration, vertigo, light headedness), fibromyalgia, fatigue, arthritis, arthralgia, and musculoskeletal symptoms 51%. All patients were not able to stand on their toes with their eyes closed or able to walk a straight line with their eyes closed. Associated symptoms included respiratory symptoms (shortness of breath, asthma, bronchitis) 35%; ENT (hearing loss, tinnitus, hoarseness, laryngeal edema, dysphasia) 35%; GI (irritable bowel syndrome, malabsorption, diarrhea) 18%; cardiovascular (vasculitis, chest pain, hypertension, cardiomyopathy, angioedema, mitral valve disease) 30%; endocrine (ovarian imbalance, PMS, hypothyroid, thyroiditis) 94%; eye (cataract, vision loss) 2%; skin (rash) 1%. 100% had chemical sensitivity including 6 implants (chin, breast, hip) 2 mercury toxicants; food sensitivity 89%; biological inhalant sensitivity 76%; EMF sensitivity 3%; candidiasis 4%.



Outline: Toxic solvent exposure was evident in 54 patients whose blood was measured with 1,1,1 trichloroethane 45%; benzene in 24%; trimethylbenzene 19%; xylene 9 %; dichloromethane 13%; chloroform 2%; trichloroethylene 7%; tetrachloroethylene 7%; ethylbenzene 2% and dichlorobenzene 2%. Another segment of solvents measured in these patients were the aliphatic hydrocarbon patients who had 3-methylpentane 89%, 2-methylpentane 85% and n-Hexane 75%. One (1) had n-pentane and 7% cyclopentane; 28 patients were measured for chlorinated pesticides. 100% had DDE, 46% trans nonachlor, 25% oxychlorodane, 14% heptachlor epoxide, 31% had hexachlorobenzene, 18% B-BHC, 14% Dieldrin, 98% of the patients were sensitive to food and 93% sensitive to mold, 74% to trees and grasses. 76 patients had intradermal skin tests for chemicals with ethanol 55%; formaldehyde 47%; cologne 96%; cigarette smoke 64%; metal testing performed on 16 patients show at 81% sensitivity to nickel and 69% to zinc sulfate. Double blind inhaled challenge revealed sensitivity to 1,1,1,trichloroethane 20%; formaldehyde 16.7%; toluene 16.9%; 16 organophosphate pesticide 16.7%; phenol 12.5%; chlorine 11.1%, ethanol 6.2%. T-lymphocytes 58% low, T4 3.5% low and 21% high; T8 lymphocytes 59% low and 15% high; B-lymphocytes 3% low, 4% high; CMI 3/7 33%; 4/7 27%; 5/7 20%; 6-7 9%; 2/7 13%.



Triple camera brain SPECT scan had 81 patients measured and 81 were positive for Neurotoxicity. Posturography was performed in 78 patients with 79% having abnormal sensory organization and 44 abnormal motor organization. Pupillography showed 84% abnormalities. Heart rate variability was performed on nine patients. All were abnormal. Specific utaneous thermography was performed in 20 patients with 95% rigid (low) response and 5 % hypersensitive response.



Conclusion: Treatment consisted of a massive avoidance of pollutants in air, food and water. Injection therapy, oral and intravenous nutrition, sauna therapy and autogenous lymphocytic factor. There was a significant 82% improvement rate.



Goals:

1. To understand the signs and symptoms of central neuropathy.

2. To be able to diagnose central neuropathy.

3. To be able to treat central neuropathy.















Abstract Information & Notes



Pierre Auger, M.D. Date of talk: Thursday, June 7, 4:30 p.m.



Clinique De Santé Au Travail et De Santé Environnementale Phone: 514/849-5201

3666 St-Urbain Fax: 514/731-0668

Montreal, Quebec H2X 2P4 Canada E-mail: pierrelauger@qc.aira.com



Medical School Attended: Laval University

Residency: Toronto-Quebec, Paris-London

Board Certifications: Occupational Medicine (Royal College)

Current Faculty Appointments: Adjoint Proffessor McGill

Current Job Description: Occupational Environmental Medicine Practice - Clinical Practice and Preventive Medicine.



Disclosure Statement: None



SPEECH TITLE: "Chronic Toxic Encephalopathies Apparently Related to Exposure to Toxicogenic Fungi"



The information below has been provided by the speaker.



Authors: Pierre L. Auger, MD, Pierrot Pépin IH, J. David Miller PhD., Manfreid Gareis D.V.M., PhD., Julien Doyon PhD., Rémi Bouchard MD, Marie-France Pinard PhD., Claude Mainville Ing.



1.) Goals and objectives: Description of four cases of toxic encephalopathies possibly caused by a prolonged exposure to toxin producing filamentous fungi in the workplace. We will also demonstrate that complete fungal evaluation with species identification and complementary cytotoxicity testing can be useful to identify possible causes of health effects of mold exposure.



2.) Outline of talk/abstract: Fungal toxins have irritant, immunosuppressive, neurotoxicological and carcinogenetic effects (Henry 1993). Recent report have suggested neurotoxic effects (Croft 1986, Johanning 1996). We report four cases who were diagnosed type 2b solvent type syndrome concurrent with a sensitive neuropathy in one occupant and novel asthma in a second.



First building is a harbour station built over a crawl space with the presence of Aspergillus Fumigatus, A. Versicolor, Penicillium aurantiogriseum. In this building a 42-year old director along with his 32-year old secretary have commenced to suffer from neuropsychological and systemic symptoms and novel asthma in the secretary. Improvement is noticed after 3 - 4 months after removal from exposure. Irreversible sequelae are described 15 months later: slight attention deficit in the director and asthma in the secretary.



Second building is a medical office in which severe flooding occurred during the Winter. In Spring, an environmental evaluation yielded the presence of Penicillium crustosum, P, brevicompactum, Fusarium incarnatum. Important neuropsychological deficits more or less similar in both are found. Improvement is noted upon removal from exposure. The pediatrician died of renal failure because of light chains disease. The female was left with irreversible brain damage.



3.) Conclusion of what is to be learned: The four workers presented with findings similar to solvent encephalopathies (Lindsberg 1995). In an occupational setting, an acute CNS disease with tremor was related to exposure to high levels of Aspergillus (Gordon 1993). The presence of toxicogenic molds in an environment suggests that when two or more occupants of dwelling suffer from neuropsychological symptoms, a detailed exposure analysis should be done with a neuropsychological evaluation on these same occupants.



4.) References:

Croft WA, Jarvis BJ, Yatawara CS. 1986 Airborne outbreak of trichothecene toxicosis Atmosph. Environm. 20: 549-558



Gordon KE, Masotiti RE, Waddell WR 1993 Tremorgenic encephalopthy: a role of mycotoxins in the production of CNS disease in human? Can. J. Neurol. Science 20: 237-37



Henry KM, Cole EC, 1993. A review of mycotoxicosis in indoor air J. Tooxicol Environm. Health 38: 183-93



Johanning E., Biagini R., Hull D. Morey P, Jarvis B. Landsbergis P 1996 Health and Immunology Study Following Exposure to Toxicogenic (Stachybotrys chartarum) in a water-damaged office Int. Arch. Occup. Environm. Health 68: 207-218



Lundberg I, Hogstedt C, Liden C, Nise CJ 1995. Organic Solvents and Related Compounds In Rosenstock I, Cullen MR editors Textbook of Clinical Occupational and Environmental Medicine Philadelphia Saunders WB 31: 766-84





































































Abstract Information & Notes



Deborah Baird, M.D. Date of talk: Thursday, June 7, 5:00 p.m.



5915 Volunteer Place Phone: 972/771-1106

Rockwall, TX 75037 Fax: n/a

E-mail: drbaird@msn.com



Medical School Attended: Handemann University of Medicine - Philadelphia

Residency: Psychiatry, Pediatrics, Fellowship in Developmental Disabilities

Board Certifications: American Board of Pediatrics

Current Faculty Appointments: None

Current Job Description: Retired from Private Pediatrics - Doing Locum Tenens - - - and having fun!

Other Information: Currently working on Implant Syndrome book with Dr. Rea.



Disclosure Statement: None



CASE STUDY: "Seven Year Case Study of Acute Neurotoxicity"





Notes:











TABLE OF CONTENTS,

FRIDAY, JUNE 10, 2001







Friday faculty listing ....................................................................................................................... 5



Friday schedule ................................................................................................................................ 6



Abstracts and handouts



Bell ....................................................................................................................................... 8



Beck ...................................................................................................................................... 9



Laibow ................................................................................................................................. 11



Muller-Mohnssen ................................................................................................................. 12



Millqvist ............................................................................................................................... 16



Bounias ................................................................................................................................. 17



Wright .................................................................................................................................. 21



Meggs ................................................................................................................................... 22



Jaeckle .................................................................................................................................. 23



Shinn .................................................................................................................................... 26



Croley ................................................................................................................................... 28



Garrett .................................................................................................................................. 32

Notes:











FRIDAY, JUNE 9, 2001 FACULTY





C. Malcolm Beck

Garden-Ville, Inc

San Antonio, TX

210/651-6115



Iris R. Bell, M.D.

Program in Integrative Medicine

University of Arizona

College of Medicine

Tucson, AZ

520/626-3512



Professor Michel Bounias

University of Avignon, France

BioMathematic's and Toxicology Unit,

Chemin du Petit Bosquet

Saint-Christol D'Albion F-84390, France

011 33 490 750 888



Thomas E. Croley, Ph.D.

Ideal Health Clinic of Allen

Allen, TX

972/727-2800



J. Howard Garrett

The Natural Way/WBAP Radio

Dallas, TX



Richard Jaeckle, M.D.

Dallas, TX

214-696-0964



Rima E. Laibow, M.D.

Alexandria Institute of Natural and Integrative Medicine

Croton on Hudson, NY

914/827-9557



William J. Meggs, M.D., Ph.D.

E. Carolina University School of Medicine

Dept. of Emergency Medicine

Greenville, NC

252/816-2954



Eva Millqvist, M.D.

Allergy Centre, Department of Respiratory Medicine

Sahlgrenska University Hospital

Gothenburg, Sweden

011/46-31-3423635



Helmuth Muller-Mohnssen, Ph.D.

Ludwig-Maximilians Univ. Munich

Ismaning/Menich

Germany

011-49-89-969444



Eugene A. Shinn

U.S. Geological Survey

St. Petersburg, FL

727/803-8747 ext.3030



Jonathan V. Wright, M.D.

Tahoma Clinic

Kent, WA

206/631-8920

NINETEENTH ANNUAL INTERNATIONAL SYMPOSIUM

ON MAN AND HIS ENVIRONMENT



SCHEDULE FOR FRIDAY, JUNE 8, 2001



8:15 ANNOUNCEMENTS/MODERATOR: William J. Meggs, M.D.



8:30 Iris R. Bell, M.D. "Neural Sensitization Model for Environmental Illness"

8:50 Q & A



9:00 C. Malcolm Beck "Re-mineralizing the Earth"

9:20 Q & A



9:30 Rima E. Laibow, M.D. "Neurotoxicity of Heavy Metals: The Ubiquitous Menace"

9:50 Q & A



10:00 BREAK WITH EXHIBITORS/MODERATOR: Bertie Griffiths, Ph.D.



10:30 Helmuth Muller-Mohnssen, Ph.D. "Pyrethroid Intoxication Showing Three Types of Clinical Expression"

10:50 Q & A

11:00 Eva Millqvist, M.D. "Sensitivity to Chemicals-A Theoretical Background to a Possible Explanation"

11:20 Q & A



11:30 Professor Michel Bounias, Ph.D. "Anticipatory Mental Imaging and 'NeuroBioFeedFarther' in Neurotoxicology"

11:50 Q & A



12:00n BUFFET LUNCH WITH EXHIBITORS



MODERATOR: Charlie Hinshaw Jr., M.D.

1:30 Jonathan V. Wright, M.D. "Modification of Steroid Metabolism with Foods, Minerals, Phytochemicals, and A Vitamin"

2:20 Q & A



2:30 William J. Meggs, M.D. "Controversies in Solvent Neurotoxicity"

2:50 Q & A



3:00 BREAK WITH EXHIBITORS



3:30 Richard Jaeckle, M.D."Neurotoxicity of Molds & Mycotoxins"

3:50 Q & A



4:00 Eugene Shinn, Ph.D."Transoceanic Soil Dust Transport and Medical Implications"

4:20 Q & A



4:30 Thomas E. Croley, Ph.D. "Balancing the Energy Flow of the Autonomic Nervous System"

4:50 Q & A



5:00 Howard Garrett, "BOP, the Basic Organic Program"

5:20 Q & A



5:30 ADJOURN



6:30-8:30 p.m. Tour of Environmental Health Center, American Environmental Health Foundation, and visit with William J. Rea M.D.









FRIDAY, JUNE 8, 2001



ABSTRACTS



AND



HANDOUTS



Abstract Information & Notes



Iris R. Bell, M.D. Date of talk: Friday, June 8, 8:30 a.m.



Program in Integrative Medicine Phone: 520/626-3512

University of Arizona Fax: 520/626-3518

College of Medicine E-mail: ibell@u.arizona.edu

P.O. Box 245153

Tucson, AZ 85724



Medical School Attended: Stanford

Residency: U. of California - San Francisco

Board Certifications: Psychiatry with added qualification in Geriatric Psychiatry

Current Faculty Appointments: Associate Professor of Psychiatry

Current Job Description: Director of Research, Program in Integrative Medicine, University of Arizona College of Medicine



Disclosure Statement: None



SPEECH TITLE: "Neural Sensitization Model for Environmental Illness"



The information below has been provided by the speaker.



1.) Goals and objectives: To review rationale for the neural sensitization model for environmental illness and laboratory evidence relevant to the model



2.) Outline of talk/abstract: Sensitization is a neurobiological process in which repeated intermittent responses to an exogenous substance or stressor initiate progressive increases in the size of the last response. This talk will review features of sensitization, its release to EI, and physiological data consistent with model.



3.) Conclusion of what is to be learned: Sensitization is a visible hypotheses for CNS/ANS dysfunction in EI for which there is accumulating supportive data.



4.) References:

Bell, IR et al. Neural sensitization model for multiple chemical sensitivity: overview of theory and empirical evidence. Toxicol Indust Health 1999; 15:295-304.



Fernandez M. et al EKG sensitization during chemical exposure in women with and without chemical sensitivity of unknown etiology. Toxicol Indust Health 1999; 15:305-312.



Abstract Information & Notes



C. Malcolm Beck Date of talk: Friday, June 8, 9 a.m.



Garden-Ville, Inc. Phone: 210/651-6115

7561 East Evans Rd. Fax: 210/651-9231

San Antonio, TX 78266 E-mail: n/a



Medical School Attended: n/a

Current Job Description: Full time researching and giving presentations all over U.S. on understanding nature. Average 80 talks or slide presentations a year to Universities, Colleges, Master Gardeners, Farmers, Ranchers, Home Owners Assn Etc.



Disclosure Statement: None





SPEECH TITLE: "Re-mineralizing the Earth"



The information below has been provided by the speaker.



1.) Goals and objectives: To show the needs of minerals to create fertile soil, to grow healthy plants.



2.) Outline of talk/abstract: To show with color slides the many test I did with plants in containers grown with and without rock minerals, and field test with & without minerals.



3.) Conclusion of what is to be learned: Using rock sand and dust can grow healthy plants with excellent flavor & nutrition and have immunity to pest and disease, even cold, heat - drought & flood.



4.) References: A life time of growing plants, vegetable, fruit, nuts. In the field and containers, using soil to soilless mixes to study the effects of with & without minerals and a constant study in field of agriculture, biology, botany & geology.



Re-Mineralizing the Earth



C. Malcolm Beck



All life on earth is given birth and sustained by a thin layer of soil that covers the dry lands of this planet. The quality of that thin soil layer determines the quantity and quality of the AIR we breathe, the WATER we drink and the FOOD we eat. If we let the quality of our topsoil degrade to any degree, the life it supports degrades along with it.



Fertile topsoil is made from life forms - living and decaying - in the presence of mineral rocks. The first life on earth was simple and small. Bacteria and fungi could live on rock surfaces, etch away at the rock, exude on it, and die and decompose rocks. These microscopic creatures created the first organic matter which filtered into the cracks and crevices of the rocks to form organic acids that dissolved more rock. The organic matter and rock minerals together became our first soil. The soil building process went on and on until larger, more complex plants could get a foothold. The death and decay of these higher plants built soil even faster.



Green plants collect the sun's energy and combine it with elements from the air and earth to make energy and food for still other forms of life. The living, dying and decaying of all life forms build with added interest to the soil's bank account. Once modern man intervenes, however, the balance changes. Overexposing the soil with bad tillage practices, plus the forced production of conventional agriculture using high analysis fertilizers and pesticides, seriously strain the health of the soil and the quality of the food it produces.



Modern chemical fertilizers contain no energy. The microbial life needed to process the chemicals into proper plant foods have to draw their energy from the soil organic matter and humus reserves. When the soil organic content runs low, the soluble fertilizer is not properly processed. The plants pick up the food in unbalanced ratios, causing them to become stressed, which in turn, invites pest insects and diseases to attack the plants, then toxic pesticides are used.



Meanwhile, some of the soluble fertilizer and pesticides are leaching away to pollute surface and ground water, which sickens more life. As humus runs low and soil life dies, the soil loses vital crumb structure and proper ability to absorb water. Normal rains quickly run off carrying humus and mineral-rich topsoil with it. Exposed subsoil is quickly dried by the sun. During dry spells wind erosion takes place.



As the soil loses mineral and humus, its strength, integrity and ability to produce life with strength and integrity are also lost. But if we have the will, soil can be rebuilt. Humans have intervened to hasten the loss of topsoil. We can intervene to create new topsoil. Nature has supplied us with plenty of mineral rock through deposits such as limestone and greensand and through tectonic exposures of basalt, lava and granite. By spreading the dust and sands of these rocks where needed and by recycling and rebuilding organic matter, we can rebuild the integrity and strength of the soil. Then the health and well-being of life on Mother Earth can be sustained.



Sources: A lifetime of growing plants, vegetables, fruit and nuts, in the field and containers. Using soil and soilless mixes to study the effects of with and without minerals. And a constant study in the fields of agriculture, biology, botany and geology.

Abstract Information & Notes



Rima E. Laibow, M.D. Date of talk: Friday, June 8, 9:30 a.m.



Alexandria Institute of Natural and Integrative Medicine Phone: 914/827-9557

10 Old Post Road South Fax: 914/827-3995

Croton on Hudson, NY 10520-2350 E-mail: laibow@juno.com



Medical School Attended: Albert Einstein College of Medicine

Residency: Lincoln Hospital and St. Luke's Hospital

Board Certifications: 1) Diplomate American Board of Forensic Examiners,

2) Diplomate American Board of Traumatic Stress Studies,

3) Diplomate Neurotherapy Certification Board.

Current Faculty Appointments: N/A

Current Job Description: Medical Director of the Alexandria Institute of Natural and Integrative Medicine

Other Information: 1) Senior Medical Editor Alternative Medicine: The Definitive Guide

2) Author: The Medical Applicatiions of NeuroBioFeedBack in Evans and Aberbanel, Introduction to Quantitatve EEG and NeuroBioFeedBack, Academic Press, 1999

3) President: NeuroTherapy Certification Board

4) Past President: Quantitative EEG Technicians Certification Board

5) Editorial Board, Journal of Neurotherapy.



Disclosure Statement: None





SPEECH TITLE: "Neurotoxicity of Heavy Metals: The Ubiquitous Menace"



The information below has been provided by the speaker.



1.) Goals and objectives: To identify common neurotoxins and their effects on the CNS and its regulation of organism wide functions.



2.) Outline of talk/abstract: Neurotoxic metals assault the organism from a variety of sources. Their effects are pervasive and their presence is ubiquitous. Pathogenic effects go well beyond neuropsychiatric dysfunction of mood and cognition, poisoning enzyme systems in the CNS while clinging tightly to their heavy metals represents one of the most significant challenges to robust health in our environment.



3.) Conclusion of what is to be learned: Practitioners will have an increased index of suspicion which will allow them to identify heavy metal neurotoxicity with great precision.



4.) References: (1) "Rea, WM J. Chemical Sensitivity Vol 1, Lewis Publishers, Boca Raton, 1992, Passim."

(2) "Rea, Wm J. Chemical Sensitivity Vol 3, Lewis Publishers, Boca Raton, 1995 Passim."

(3) "Rea, Wm J. Chemical Sensitivity Vol 4, Lewis Publishers, Boca Raton, 1995 Passim."

(4) "Bounais, Michel, Traite'de Toxicologie General: Du Nivgau Moleculaire A\L'echelle Planetaire, Springer, New York, 1999."





Abstract Information & Notes



Helmuth Muller-Mohnssen, Ph.D. Date of talk: Friday, June 8, 10:30 a.m.



Ludwig-Maximilians Univ. Munich Phone: 011-49-89-969444

Ismaning/Menich Fax: same

Germany E-mail: n/a



Medical School Attended:

Residency:

Board Certifications:

Current Faculty Appointments:

Current Job Description:

Other Information:

Vita

1928 born in Bremen, Germany

1951 state medical examination Marburg/Lahn

1952 MD, Marburg/Lahn, Germany

1968 Habilitation for Physiology Ludwig-Maximilians-University, Munich (LMU)

Educational background:

1952-1956, Institute of Pathology, University of Münster/Westfalen, Germany (Prof. Giese),

1952-1957 1956-1960 Physiological Institute, University of the Saarland (Prof. Stämptli).

1960-1993 Head of Department of Physiology in the federal center of environmental research GSF, Neuherberg/Munich.

1963 Retired

Working Fields

1. Development of collateral circulation induced by stenosing coronary sclerosis.

2. Hydrodynamic mechanisms involved in thrombogensis and atherogenesis,

3. Intravital-microscopical studies of the Node of Ranvier of isolated single motor nerve fiber during its electrophysiological function.

4. The stationary electrophysical basis of impulse-generation by the excitable nerve fiber membrane (Textbook: "Physics of nervous excilation with an introduction to methodology of physiological research", Munich 1979).

5. Epistemological basis of research politics



Disclosure Statement: None



SPEECH TITLE: "Pyrethroid Intoxication Showing Three Types of Clinical Expression"



The information below has been provided by the speaker.



1.) Goals and objectives: Early detection of new anthropogen diseases with the aid of quantitative analysis of the patients complaints and of exchange of the quantified subjective data between the medical practitioners concerned with the patient (32).



2.) Outline of talk/abstract: In order to collect the minimum number of patients necessary to establish the diagnosis of a new anthropogen disease (35), cooperation of physicians is necessary. Physicians will base their tentative diagnosis mainly on information about complaints and their history obtained by the patient-doctor-dialogue. They will then be able to minimize the diagnostic expenditure by appropriate selection of technical diagnostic procedures to exclude/verify the tentative diagnosis. Because the oral doctor-patient-dialogue is lost for an exchange of data, it was modeled and recorded by a computer-program which can be installed on a PC and allow to mail and recheck the results by round robins like results of laboratory tests (108).

3.) Conclusion of what is to be learned: The patients' affirmations about their complaints represent data which are reproducible like the results of sensory-physiological tests and referring reliably to the underlying organic disorders (25).



4.) References:

Muller-Mohnssen, H., Hahn, K. (1995): About a method of early recognition of neurotoxic diseases (Exemplified by Pyrethroid intoxication) in German, Gesundheitswesen 57, 214-222.



Muller-Mohnssen, H. (1999): Chronic sequelae and irreversible injuries following acute pyrethroid intoxication. Toxicological letters, 107, 161-175 (further references).

Pyrethroid Intoxication Showing Three Types of Clinical Expression



H. Müller-Mohnssen

Ludwig-Maximilians-University

Munich, Germany



This study investigates whether chronic pyrethroid intoxication including residues after acute pyrethroid intoxication can be diagnosed by showing a characteristic clinical pattern. Pyrethroid exposure was documented by anamnesis, laboratory findings, and a standardized 97 item complaint questionnaire in which a five point scale allowed each patient to rate his or her complaints. Zero denoted the preexposure state. Two pooled collectives comprising patients with clinical evidence of pyrethroid intoxication according to the clinical criterial of causal-relationship between exposure and complaints (table) were included into the study: a): the pyrethroid-collective (n = 145), whose members have been exposed in the interior of houses and b), the air-hostess-collective (n = 57) having been exposed in passenger planes. A control-collective sampled at random and being representative of the average German population completed the same questionnaire (n = 414, including n = 356 persons declaring themselves healthy). Average values of the collective complaint intensities MBM were for a) MBM = 1,53 and for b) MBM = 1,63 against MBM = 0,3 obtained for the control group of healthy persons (MBM = 4,0 is the maximum possible value). The average pyrethroid load expressed in mg/kg house dust or cabin dust was a) 587 and b) 690 respectively versus 0,22 found in the average German household. Complaints referring to psychometrically measurable organic mental disorders (decrement of intellectual performance, emotional condition and affectivity) show nearly the same intensities in all patients of collectives a) and b). Opposed to this the intensities of complaints concerning clinical disorders of the peripheral and autonomic nervous system and disorders of other organs differed in different patients, showing three types of clinical expression:



E-(encephalitis-) type. The disease starts abruptly after a symptomless interval of 4-7 days with pain and other perception disorders on account of an often electrophysiologically verifiable sensible polyneuropathy (PNP), combined with movement disturbances reminiscent to cerebellar ataxia. Depending on the severity of disease the symptoms, which are comparable to those of inflammatory neurological diseases, ascend from peripheral nerves-predominantly lower legs- to central regions of CNS and demand exclusion, for instance, of Polyneuritis, polyradiculitis, Guillain-Barré, multiple sclerosis.



P-(pseudo-dopaminodeficiency) type. This type is observed after long term low dose exposure but also after high dose exposure in persons producing no acute reaction because of higher resistency. The symptoms start imperceptible slow with hypermyotonia and movement disorders, reminiscent to M. Parkinson, correlated with pain syndrome of the locomotor-system as well as with disorders of gastrointestinal, urogenital and cardiovascular regulation which are stronger than in the other clinical types.



I- (Immunomodulatory) type. This type impresses as worsening of preexistent allergical diathesis and lead to respiratory obstruction, mucocutaneous alterations and immune suppression with deficient defense against acute infection diseases, mainly of respiratory and urinary tract as well as against chronic opportunistic infection (Candida). More rarely are seen autoimmune diseases (thrombocytopenic purpura, hemolytic anemia, sclerodermia, multiple sclerosis). In most cases health condition improves after stopping of exposure.



Table (Pyrethroid Intoxication showing three types of clinical expression)



A causal relationship between pyrethroid exposure and the exposed subject's complaints was assumed if the following criteria were met by the patient:



1. Concomitant diseases were excluded by the physicians in charge and the influence of insecticides other than pyrethroids is negligible.



2. Other persons simultaneously exposed within the same environment fall ill exhibiting similar symptoms



3. Complaints, which firstly appeared after begin of exposure mitigate after interruption of exposure and aggravate after re-exposure.



4. In case of acute intoxication: a high-concentration exposure due to self-application of insecticides (spraying or brushing) can be documented - in case of chronic intoxication: Pyrethroids are detected in the patient's environment and his or her body fluids or tissues: more than 10 mg Pyrethroid/kg house dust, more than 1.5 g pyrethroid metabolite/ 1 urine and more than 0,1 g Pyrethroid/kg hair (values for permethrine). Detection of a specific antigen-antibody reaction by means of Epicutan- and intracutantest. Detection of specific sensibilization by lymphocyte transformation test in the sense of a type-IV-immune response against pyrethroids or pyrethrins.



5. Duration of latency period and severity of the health effects of the person in question correspond to those of a multitude of patients who have been exposed to a similar dose. In case of acute intoxication the latency period between the begin of a documented exposure and the onset of illness was measured, in case of chronic intoxication the time interval between the end of a permanent exposure and the decrease of complaints.



6. The clinical picture resembles that of a multitude of patients who have been exposed to the same chemical substance.





Abstract Information & Notes



Eva Millqvist, M.D. Date of talk: Friday, June 8, 11:00 a. m.



Allergy Centre, Department of Respiratory Medicine Phone: 011/46-31-3423635

Sahlgrenska University Hospital Fax: 011/46-31-417824

Gothenburg, S-413 45, Sweden E-mail: eva.millqvist@medfak.gu.se



Medical School Attended: Karolinska Institute, Stockholm, Sweden

Residency: Gothenburg

Board Certifications: M.D., Ph.D.

Current Faculty Appointments:

Current Job Description: Research in Asthma and Asthma like Conditions. Working with patients sensitive to strong scents and chemicals.

Other Information: Working with developing a new method to test chemical sensitivity.



Disclosure Statement: None





SPEECH TITLE: "Sensitivity to Chemicals. A Theoretical Background to a Possible Explanation"



The information below has been provided by the speaker.



1.) Goals and objectives: To present a theoretical background to what may happen in patients with airway sensitivity to chemical irritants like strong scents, smoke and car exhausts.



2.) Outline of talk/abstract: The pathophysiology of airway chemical sensitivity, i.e. asthma-and allergy-like symptoms induced by chemical irritants, may be related to increased sensitivity of free, overreactive nerve endings in the respiratory mucosa because such patients cough more after capsaicin provocation than do healthy subjects and patients with asthma.



3.) Conclusion of what is to be learned: In patients who experience airway symptoms induced by very low levels of chemical irritants, it seems likely that it is not the smell that causes problems but a sensory hyperreactivity of the common chemical sense induced via the trigeminal nerve.



4.) References:

  • Milliqvist E, Bende M, Löwhagen O. Sensory hyperreactivity - a possible mechanism underlying cough and asthma-like symptom. Allergy 1998;53:1208-12.
  • Milliqvist E, Bende M, Löwhagen O. Quality of life and capsaicin sensitivity in patients with sensory airway hyperreactivity. Allergy 2000;55:540-545.
  • Millqvist E. Cough provocation with capsaicin is an objective way to test sensory hyperreactivity in patients with asthma-like symptoms. Allergy 2000;55:546-550.


Abstract Information & Notes



Professor Michel Bounias Date of Talk: Friday, June 8, 11:30 a.m.



University of Avignon, France Phone: 011 33 490 750 888

BioMathematic's and Toxicology Unit, Fax: same

Chemin du Petit Bosquet E-mail: n/a

Saint-Christol D'Albion F-84390, France



Medical School Attended: University of Lyon: INSA School of Engineers; Faculty of Sciences 3rd cycle

Residency: Same as above

Board Certifications: Docteur d'Etates Sciences/DEA (3rd cycle) in Biometrics/Engineer in Biochemistry

Current Faculty Appointments: Professor, Director of Research (Nat'l. Officer), Ministerial Expert

Current Job Description: 1.) Theoretical research: Mathematical foundations of existence of physical universe and biological systems, up to brain and conscious perception functions.

2.) Toxicology (from molecular to Planetary levels): Applications of Mathematical theory.



Other Information: About 400 scientific papers published, 10 books authored

1.) Elaboration of a new deontology for the management of Planet Earth, foundations of a chart of objective rights of all living organisms.

2.) Editorial Activity (CoEditor and chief advisor of Scientific Journals)

3.) Musicologist and Composer

4.) Symphonies, lieders for soprano, etc.)



Disclosure Statement: None





SPEECH TITLE: "Anticipatory Mental Imaging and ' NeuroBioFeedFarther' in Neurotoxicology"



The information below has been provided by the speaker.



1.) Goals and objectives: Identification of theoretical foundations of NeuroBioFeedback and neurotoxicological implications, from the mathematics of conscious perceptions.



2.) Outline of talk/abstract: Conditions for existence of a physical space also involve the foundations of conscious perception, up to mental imaging, which exhibits anticipatory properties. Mental images are arguably constructed from both outer and inner information and anticipatory processes underly homeostatic control. Health can thus be restored from altered states by directed feeding of the brain with corrected mental images standing for farther targets of improved status.



3.) Conclusion of what is to be learned: The mechanisms and importance of developmental neurotoxicology and of chemical hypersensitivity, via mental imaging of the unconscious type are emphasized.



4.) References: Bounias, M., Bonaly, A., 1997. BioSystems, 42, 191-205. Dube, M., et al., 2000.Peptides (NY), 21(6), 793-801. Osterberg, K., et al., 2000 Scand. J. Work, Environ. Health, 26(3), 219-226. Bounias, M., 2000. Amer. Inst. Phys. CP 517, 233. Bounias M., Bonaly A., 2001, Amer Ins. Phys. CP in press. Andersen, H., et al., 2000. Toxicology, 144(1-3), 121-127.etc. (23 ref.).

Anticipatory Mental Imaging and "NeuroBioFeedFarther" in Neurotoxicology



M. Bounias

Research Director and Professor, University of Avignon and INRA-DSPE,

BioMathematics & Toxicology Unit

Chemin du Petit Bosquet, F-84390

Saint-Christol d' Albion, France



A. Stubblebine and R.E. Laibow

The Alexandria Institute of Natural and Integrative Medicine

Croton-on-Hudson, New York



Summary: A mathematical proof of existence of a physical universe justifies existence of conscious perception, up to mental imaging which exhibits anticipatory properties. Thus directed restoration of correct relationships between homeostasy-related mental images and the control of the organism is possible: this founds NeuroBioFeedback. A set of neurotoxicological targets is derived from the model.



  1. Introduction and preliminaries. Brain is a structure produced by Universe and released in our observable spacetime. Thus neurotoxicity is not independent from the foundations of the existence of Universe, which has been proved to be justified by mappings of topologically closed abstract mathematical subspaces(6-7). A necessary and sufficient condition for existence of the latter is the existence of the empty set, as a primary axiom(8). The same conditions also provide justifications for existence of conscious perception(6-9): neuronal chaining Cauchy-like sequences lead to sets of fixed points of the Banach type, associated with input of information from outside, via perceptive signals representing mathematical paths (Jordan-Veblen's theorem). These sets of fixed points are stable parts standing for mental images. Then the need for self-reference associated with outside perception is fulfilled by the Brouwer's theorem stating that in a closed space all continued functions own a fixed point. Proofs were further given that the mathematical space underlying the functionally of the brain system fulfills the required conditions(10-12) and that the mental imaging also owns fractal properties, and even more importantly that it is an anticipatory process(13).


  2. Brain and anticipatory mental imaging. In anticipatory processes the state of a system at time (t) depends on states at (t+i)i1 (i.e. mathematical incursivity or hyperincursivity) (22).Since the brain is able to construct mental images of future situations, it can adjust a succession of decisions and actions to the best possible fitting of the living organism to a given goal. The intersection of the respective sets of Brouwers' type and Banach type fixed points predicts that a kind of mental images is produced by molecular information from inside the organism through neuronal configurations likely to be unconscious at least from the autonomous nervous system. Mental images reflect bursts of outside perceptions, abstracts thoughts, subjective images, but also the state of functioning and metabolic control of homeostasy of the organism through molecular feedback loops from inside the body to brain receptors.


  3. Neuronal foundations of NeuroBioFeedback. Experimental data support the above Proposition. EEG changes reflecting neuronal configurations in the cortex are associated with the stimulation of receptors involved in autonomous metabolic feedback and control(1,2,3,15,16,19,20,23,25,26,29,31,32,34) besides EEG responses elicited by conscious feelings(21,24,30,33) and HPA responses to stress(18). Sensory perception has thus logically found critical in developmental neurotoxicity(3,4) while developmental toxicity imprints delayed responses(28). Mentally induced brain changes(5) must not be confused with true chemical sensitivity(27). Neurotoxicity must thus have to be detected and treated at many target sites of the brain-body reciprocal interactions.


  4. Discussion and conclusions. A disease may fix mental images of altered states; then homeostatic processes turn to wrong control operations. Corrected mental images with anticipatory characteristics must thus be constructed and substituted for the wrong ones in order to turn back the brain functioning progressively to anticipatively corrected goals. This can be farther achieved through feedback loops based on the EEG activity records targeted on improvement of frequencies spectra associated with rehabilitation of patients(14). Thus: the clinical effects of NeuroBioFeedback treatments find their justification through a NeuroBioFeedFarther' system of anticipatory mental imaging.




References

(1)Akhmetova, E. et al., 2000. Eksp. Klin Farmakol. 63, 7. (2)Andersen, H. et al., 2000 Toxicology, 144, 121. (3)Agar, A. et al., 2000 J. Basic Clin. Physiol. Pharmacol., 11, 17. (4)Benesova, O. et al., 1999. Gen. Physiol. Biophys., 18, 21. (5)Biegon, A., et al., 1990. Psychopharmacology, 100, 165. (6)Bounias, M. et al., 1994 J. Ultra Scientist of Physical Sciences, 6,251. (7)Bonaly, A., Bounias, M., 1995. Physics Essays, 8,236. (8)Bounias, M. et al., 1997. Physics Essays, 10, 633, (9)Bounias M. et al., 1997. BioSystems, 42, 191. (10)Bounias, M. et al., 1996. Indian J. Theoretical Phys., 44, 303. (11)Bounias, M., 1997, J. Ultra Scientist of Physical Sciences 9,139. (12) Bounias, M., 2000 Amer. Inst. Phys. CP517, 233. (13) Bounias, M., et al., 2001 Amer. Inst. Phys. CP (in press). (14)Bounias, M., et al, (2001). J. Neurotherapy (in press) (15)Chapman, C. et al., 1998, Neuroscience, Oxford 86, 1307. (16)Cobb, S. et al., 2000. Neuropharmacology 39, 1933. (17)Cordero, I. Et al., 1998. Behavioral Neurosci., 112, 885. (18)Cox, C. et al., 2000 P.N.A.S., 97, 9724. (19)Czarnecka, E. et al., 1996. Alcohol 13, 221. (20)Dafters, R., et al., 1999. Psychopharmacology (Ber), 145, 82. (21)Dube, M. et al., 2000. Peptides (NY), 21, 793. (22)Dubois, M.P., 1998. Int. J. General Systems, 27, 141. (23)Gronfier, C. et al., 1998 Am J. Physiol., 175, E94 (24)Izumi, T., 1998. Hokkaido Igaku Zasshi, 73, 463. (25)Kim, C. et al, 1996, Korean J. Pharmacol. 32,293. (26) Kovalev, G. et al., 2000. Eksp. Klin. Farmakol. 63, 3 (27)Osterberg, K., et al., 2000 Scand. J. Work Environ. Health 26, 219. (28)Metcalfe, T., et al., 2000 Environ. Toxicol. Chem. 19, 1893. (29)Rodriguez de Lores Arnaiz, G. et al., 2000 Regul. Pept. 88, 21. (30)Shin, H. et al., 1999 Korean J. Physiol. Pharmacol., 3, 237. (31)Sinor, A. et al., 2000 Neurosci. Lett., 290, 213. (32)Tan, X. et al., 1998. Life Sci. 63, 675. (33)Wang, Y-Q. et al., 2000. Neurosci. Lett. 290, 193. (34)Yun, J. et al., 1999 Korean J. Physiol. Pharmacol., 3, 245. (35)Yun, J. et al., 1999. Korean J. Physiol. Pharmacol. 3, 245.

Abstract Information & Notes



Jonathan V. Wright, M.D. Date of talk: Friday, June 8, 1:30 p.m.



Tahoma Clinic Phone: 206/631-8920

515 W. Harrison St., Ste 200 Fax: 253/850-5639

Kent, WA 98032 E-mail: drjvwright@yahoo.com



Medical School Attended: University of Michigan

Residency: Group Health Hospital Family Practice 1969-71

Board Certifications: N/A

Current Faculty Appointments: N/A

Current Job Description: Medical Director Tahoma Clinic



Disclosure Statement: Meridian Valley Laboratories





SPEECH TITLE: Modification of Steroid Metabolism with Foods, Minerals, Phytochemicals, and A Vitamin



The information below has been provided by the speaker.



1.) Goals and objectives:



2.) Outline of talk/abstract: Talk will review results of use of foods, cobalt, iodine, Di-Indolylethane & Indole-3-Carbinol, Chrysin, & Vitamin A in modulation of steroid metabolism



3.) Conclusion of what is to be learned: Minerals, botanicals, & vitamins can be used to modify steroid metabolism



4.) References:



"Modification of Steroid Metabolism with Foods,

Minerals, Phytochemicals and A Vitamin"



Jonathan V. Wright, M.D.





ABSTRACT
 

Options available to practitioners for safe, effective modulation of steroid metabolism are increasing. Brassica vegetables, soy, and flaxseed have all been shown to favorably influence the 2/16a hydroxyestrogen ratio (a "risk factor" for estrogen related cancers. Supplemental indole-3-carbinol and di-indolylmethane do the same. Vitamin A increases low levels of 17-B estradiol. Black cohosh can also stimulate increased estrogen production, while Vitex may favorably increase progesterone levels. Chrysin in many cases inhibits "abnormal" aromatization of androgens to estrogens. Boron raises circulating levels of estrogens and progesterone in postmenopausal women, and testosterone levels in men in their 50s and upwards. respectively.

Examples of the little-known observation that iodine increases the complete metabolization of estrogens to estriol will be shown.

The novel observation of estrogen hypermetabolization and hyperexcretion, clinical manifestations of this problem, and correction of both symptomatic and laboratory manifestations by cobalt will be described, with examples.















Abstract Information & Notes



William J. Meggs, M.D., Ph.D. Date of talk: Friday, June 8, 2:30 p. m.