21st
Annual International Symposium
on
Man and His Environment in Health and
Disease
Special Focus
Innovative Aspects and
Treatment of Molds, Mycotoxins and Chemical
Sensitivity
Sponsored by
American Environmental
Health Foundation and
American Academy of
Environmental Medicine
This activity has been
planned and implemented in accordance with the Essential Areas and policies of
the Accreditation Council for Continuing Medical Education (ACCME) through the
joint sponsorship of the American Academy of Environmental Medicine (AAEM) and
the American Environmental Health Foundation. The American Academy of Environmental
Medicine is accredited by the ACCME to provide continuing medical education for
physicians.
The American Academy of
Environmental Medicine designates this educational activity for a maximum of
21.5 hours in Category 1 credit toward the AMA Physician=s Recognition Award. Each physician should claim only those
hours of credit that he/she actually spent in the
activity.
Reprints are available from American Environmental Health
Foundation. This volume is not to
be reproduced, all or in part, without the written permission of American
Environmental Health Foundation.
INTRODUCTION
SYMPOSIUM
PURPOSE
Since 1981, the
International Symposium has been recognized as one of the most advanced medical
forums in the world addressing the research and treatment of environmental
effects on health and disease. The
2003 conference will focus on “Innovative Aspects and
Treatment of Molds, Mycotoxins and Chemical Sensitivity”. For this year=s conference, we have
assembled a faculty of top international experts for you. This Conference presents the most
current information available while providing guidelines to identify, diagnose,
treat and to prevent environmentally triggered responses in the
body.
GOALS OF THE
MEETING
!
To provide new insights into
the mechanisms and the environmental causes behind many problems you
see.
!
To present new diagnostic
and treatment modalities to help you improve the quality of care for your
complex patients.
!
To provide concepts, tools
that will enhance your practice.
OBJECTIVES OF THE
MEETING
!
Improve the outcome of
treating patients with chronic disease, nutritional problems and chemical
sensitivity.
!
Use new concepts and
treatments to help better diagnose and manage many patients with chronic
disease, nutritional problems and chemical sensitivity.
!
Apply the concepts of this
conference to your practice by using nutrition and environmental manipulation
for the treatment of chronic disease, nutritional problems and chemical
sensitivity.
!
Use the information
presented to enhance the effectiveness, cost-efficiency, and competitiveness of
your practice in relation to chronic disease, nutritional problems and chemical
sensitivity.
INTENDED AUDIENCE
M.D.=s, D.O.=s, D.D.S.=s, medical students, nurses,
nutritionist, and all other health professionals interested in the concepts and
practice of Environmental Medicine, Occupational Medicine and
Toxicology.
EDUCATIONAL
FORMATS
#
Plenary
#
Panels
Discussions
#
Case
Studies
#
Question & Answer
Sessions.
CONFERENCE
FORMAT
The AEHF Committee has
selected some of the leading experts in the fields of chronic disease, nutrition
and chemical sensitivity.
Each speaker=s presentation will last
approximately 20 minutes and will be followed by a 10 minute question and answer
session. All speakers are
encouraged to use any and all appropriate audio/visual aids. (A brief outline of the speech is
included in this booklet.)
GIVEN IN COOPERATION
William J. Rea, M.D.,
F.A.C.S.
Symposium
Chairman,
American Environmental
Health Foundation,
Environmental Health Center
- Dallas,
Dallas,
Texas
Bertie B. Griffiths,
Ph.D.,
Environmental Health Center
- Dallas
Dallas,
Texas
Kaye H. Kilburn, M.
D.
University of Southern
California Medical Center
Keck School of
Medicine
William J. Meggs, M.D.
Dept. of Emergency
Medicine
E. Carolina Univ. School of
Medicine
Greenville,
NC
Allan D. Lieberman, M.D.
Center for Occupational Environmental Medicine
North Charleston, SC
21st ANNUAL INTERNATIONAL
SYMPOSIUM
SCHEDULE
Thursday, June 19,
2003
7:00 a.m.
REGISTRATION
8:50
WELCOME/MODERATOR: William J.
Rea, M.D.
9:00
Douglas B. Seba, Ph.D., Independent Marine Scientist, Alexandria,
VA: “Environmental Update 2003:
Molds, Dust, Global Warming”
9:20
Q&A
9:30
Tapani Tuomi, Laboratory Chief, Finnish Institute of Occupational
Health, Helsinki, Finland: “Mycotoxins in Indoor
Climates”
9:50
Q & A
10:00
BREAK
10:30
William J. Meggs, M.D., Professor of Toxicology, Dept. of
Emergency Medicine, E. Carolina Univ. School of Medicine, Greenville, NC: “Systemic Anaphylactic Reactions to
Molds and Other Aeroallergens”
10:50
Q & A
11:00
William J. Rea, M.D., Director, Environmental Health Center
B Dallas, Dallas, TX: “Diagnosis of Mold & Mycotoxin
Sensitivity”
11:20
Q & A
11:30
Andrew W. Campbell, M.D., Clinical Immunotoxicologist, Center for
Immune, Environment and Toxic Disorders, Spring, TX: “Immunological and Neurophysiological
Abnormalities in Adults with Exposure to Molds”
11:50
Q & A
12:00 p.m. Lunch
in the Primebird Restaurant
MODERATOR: Wallace Rubin,
M.D.
1:30
Professor Tang G. Lee, AAA, Professor, Faculty of
Environmental Design, University of Calgary, Calgary, Alberta, Canada: “Molds in Native Housing and SIDS
Potential”
1:50
Q & A
2:00
William A. Croft, D.V.M., Ph.D., Private Practice, Mycotoxins,
Environmental Diagnostic Group Inc., Madison, WI: “Pathology of Trichothecene
Mycotoxins in Man”
2:20
Q & A
2:30
Kaye H. Kilburn, M.D., Director of Environmental Sciences Lab,
Ralph Edgington Professor of Medicine, University of S. California Medical
Center, Keck School of Medicine, Los Angeles, CA: “How Molds and Mycotoxins Affect
Human Brains”
2:50
Q & A
3:00
BREAK
3:30
Kalpana D. Patel, M.D., Director of Environmental Health Center
Buffalo, Northwest Center for Allergy & Environmental Medicine, Buffalo, NY:
“What is New and Different in the Diagnosis and Management of Different Skin
Disorders B Itching Eczema and
Urticaria”
3:50
Q & A
4:00
Katherine Warsco, Ph.D., Department of Interior Design, East
Carolina University, Greenville, NC:
“Teaching Design for Good Indoor Air
Quality”
4:20
Q & A
4:30
Michael R. Gray, M.D., M.P.H., Internal Occupational Medicine
Certified Independent Medical Examiner, Progressive Health Care Group, Benson,
AZ: “Molds, Mycotoxins & Public Health: a Clinicians
Perspective”
4:50
Q & A
5:00
Panel Discussion: How to evaluate moldy house? Chris Rea,
William J. Rea, M.D., Geoffrey Hutton, William Croft, D.V.M., Ph.D., and Larry
Foster
6:00
AJOURN
Douglas Seba, Ph.D.
Date of talk:
Thursday, June 19, 2003, 9:00am
P.O. Box 1417, #323
Phone:
703/949-1055
Alexandria, VA 22313
Fax:
N/A
E-mail:
N/A
Major and date of Graduation:
Environmental Oceanography - 1970
Current Job Description:
Independent Marine Scientist
Other Information:
Forty years experience in Ecology and Chemicals
Disclosure Statement:
None
SPEECH TITLE:
“Environmental Update 2003: Molds, Dust, Global
Warming”
The speaker has provided the information
below.
1.) Goals and objectives: To review selected environmental phenomena that
contributes to patient exposure to biochemicals and molds
2.) Outline of talk/abstract: Molds, xenobiotics, genetics, dust, global warming,
fate and transport mechanisms, and wildlife anomalies will all be reviewed for
contemporary aspects.
3.) Conclusion of what is to be learned: That adverse health effects can occur at vast distances
from their environmental origins and put physicians and patients in a constant
state of exposure and challenge.
4.) References:
Taken from a broad spectrum of media, websites and scientific publications
relevant to the moment.
Environmental Update 2003: Molds,
Dust Global Warming
Douglas B. Seba
The world is both a moldy and dusty place. Both may be increasing in the natural
environment perhaps aided by global warming. There also appears to be an increase in
these moieties in indoor environments as we spend increasing amounts of time in
air conditioning. Certainly
structural mold insurance claims have increased greatly in states, like Texas
and Florida, where climate change has increased warmth. Florida is also first among all large
states in both total cancer and increase in pediatric cancers being over double
that of California, for example. Dust from Africa, containing numerous molds,
has also increased in Florida over the last few decades, as well as throughout
the Caribbean and the entire United States as far west as New Mexico and north
to Canada. Additionally, relative
humidity has increase about 10% over the fifty years in the Caribbean and
extending into the southeast U.S.
All of these factors combine to make more nutrients and moisture
available for mold growth. Asthma
cases are also increasing nationally, but the increase in the Southeast is
outpacing the rest of the country and there is a connection between molds/dust
and asthma.
African dust is a quantitative source of hormonally
active environmental agents. Global
assessment of endocrine disrupters show pervasive distribution throughout the
environment including the human body.
Recent work with bisphenyl A at very low levels inducing highly
significant increases in chromosomal aberrations in mouse eggs, frog deformities
caused by interaction between parasites and atrazine, or degradated fluorinated
telomers found in human blood are contemporary examples of these environmental
agents.
These agents profoundly affect the state of your health
as they trigger genes that would not otherwise be expressed. Thus, the nascent field of
toxicogenomics will rapidly expanded as the role of endocrine disruptors as
biomarkers is investigated. These
continuing and emerging sciences will also change the focus of environmental
regulation.
Examples of the items will be personally applied by the
author to ongoing research in wildlife anomalies in the Bitterroot Mountains of
Montana.
Abstract Information & Notes
Tapani Tuomi
Date of talk:
Thursday, June 19, 2003, 9:30am
Finnish Institute of Occupational Health (FIOH)
Phone:
358-9-47472926
Arinatie 3 A
Fax:
358-9-5061087
Helsinki, Finland FIN-00370
E-mail:
[email protected]
School Attended: Helsinki University of
Technology
Major and date of Graduation:
DR, Chemical Engineering (Applied Microbiology),
1995
Current Faculty Appointments:
Docent in Environmental Chemistry and Microbiology, Helsinki Univ. of
Technology
Current Job Description:
Laboratory Chief, Laboratory of Chemistry and Microbiology, Finnish
Inst. Of Occupational Health,
Helsinki, Finland
Disclosure Statement:
None
SPEECH TITLE: “Mycotoxins in Indoor
Climates”
The speaker has provided the information
below.
1.) Goals and objectives: To present current literature on the presence of
mycotoxins in indoor climates and to discuss the possibility for carry-over of
mycotoxins from contaminated indoor surfaces to air.
2.) Outline of talk/abstract: It has been recognized that mycotoxin-producing fungi
can proliferate and produce mycotoxins in damp building materials in
water-damaged building. Mycotoxins
are also frequently found in deposited dust from indoor environments. There is very little evidence, however,
on the presence of mycotoxins in indoor air. This suggests that the air-concentration
of mycotoxins even in buildings hampered by long-standing water-damage and
following mold-damage is below the limit of detection of contemporary methods of
analysis. The talk will examine the
spectra of mycotoxins found on building materials naturally contaminated by
fungi, as well as the evidence on the presence of mycotoxins in inhalable air in
damp buildings.
3.) Conclusion of what is to be learned: A wide range of mycotoxins are potentially present in
indoor climates harboring moldy surfaces.
It has proven difficult, however, that mycotoxins may contribute to the
variety of symptoms experienced by patients exposed to moldy propagules in
indoor climates.
4.) References:
Skaug et al., 2001, Mycopathologia, 151:93-8, Page and Trout, 2001, AIHAJ 2001
Sep-Oct; 62(5):644-8, Peltola et al, 2001, Appl Environ Microbiol. 2001, 67:3269-74, Tuomi et al., 2000,
appl. Environ. Microbiol,
66:1899-1904
Mycotoxins in Indoor
Climates
Tapani
Tuomi
As of present, analyzing for
mycotoxins in indoor environments is difficult, if the goal is to assess the
health consequences of extensive water damage on the occupants of a particular
building. There is accumulating evidence on the presence of mycotoxins in crude
building materials1-7 as well as a body of indirect evidence linking
the presence of mycotoxins in indoor environments to health problems5,
8-15. It is frequently maintained that mycotoxins present in bulk
materials infested with toxigenic fungi are carried to indoor air by fungal
propagules. It follows that the route of exposure to mycotoxins in indoor
environments is inhaling dust particles containing toxigenic fungal
propagules2.
Dose-responses of humans to
airborne mycotoxins are not known and it seems that mycotoxin concentrations in
inhalable dust would have to be some 100-fold higher than what is frequently
encountered in indoor environments for air sampling to be feasible on a general
level. If air sampling is not attempted, deposited dust constitutes one step
closer to the composition of indoor air with respect to mycotoxins. There are
numerous studies from agricultural environments establishing that mycotoxins
present in bulk material are - given the right circumstances - carried into
dust. For instance, trichothecene concentrations of 0,1-1 µg/g dust, aflatoxin
concentrations of 0,02-5 µg/g dust, ochratoxin A concentrations of 0,2-70 ng/g
dust, and zearalenone concentrations of 20-100 ng/g dust have been reported
during grain handling and from other agricultural settings16-21. In
laboratory settings, Sorensen et al.22 found satratoxin
concentrations in the 10 µg/g dust-range, whereas Smoragiewicz et
al.6 detected trichothecenes in deposited dust from a moisture
problem building in amounts exceeding 0.4-4 µg/g and Engelhart et
al.23 found sterigmatocystin (2-4 ng/g) in carpet dust from a damp
indoor environment. It follows that samples of deposited dust should be
considered alongside with bulk samples when assessing the presence of mycotoxins
in indoor environments.
In agricultural settings,
aflatoxin concentrations of 0,01 - 1000 ng/m3 and eoxynivalenol (DON)
concentrations of 3-20 ng/m3 have been reported in air17-18,
20-21, 24-25. In indoor environments, satratoxin in concentrations of
0,1-0,5 ng/m3 and unidentified trichothecenes in concentrations of 1-35
ng/m3 have been found22-23. It seems therefore, that
irrespectively of the environmental setting, whether agricultural or indoor
environments, measurement of airborne mycotoxins generally require use of
high-volume samplers in combination with sensitive chemical or immunological
methods of analysis. Risk-assessment on the inhalation of mycotoxins cannot be
made based on the analysis of bulk samples of construction materials. Neither can mycotoxin contents of
deposited dust serve as basis of risk-assessment. Therefore, with the
development of more efficient methods of sampling and analysis, air sampling
will help us better understand the health consequences of exposure to mycotoxins
in indoor climates and perhaps will at some point enable estimation of
dose-responses of humans to airborne mycotoxins.
In conclusion, a wide range
of mycotoxins are potentially present in indoor climates harboring moldy
surfaces. It has proven difficult, however, to establish the presence of
mycotoxins in indoor air. This does not take away from the fact, however, that
mycotoxins may contribute to the variety of symptoms experienced by patients
exposed to moldy propagules in indoor climates.
REFERENCES:
1Andersson et al., Appl
Environ Microbiol, 1997, 63: 387-393; 2Croft et al., Mycopathologia,
1986, 151:93-98; 3Flappan et al., Environ Health Perspect, 1999, 107:
927-930; 4Gravesen et al., Environ Health Perspect, 1999, 107:
505-508; 5Johanning et al., Int Arch Occup Environ Health, 1996, 68:
207-218; 6Smoragiewicz et al., Int Arch Occup Environ Health, 1993,
65: 113-7; 7Tuomi et al., Appl Environ Microbiol, 2000, 66,
1899-1904; 8 Auger et al., Am J Ind Med, 1994, 25: 41-2;
9Hodgson et al., J
Occup Environ Med, 1998, 40:
241-9; 10Miller, Atm Environ, 1992, 26A: 2163-2172; 11Morb
Mortal Wkly Rep, 1994, 43: 881-883; 12Morb Mortal Wkly Rep, 1995, 44:
67-74; 13Morb Mortal Wkly Rep, 1997, 46: 33-35; 14Rautiala
et al., Am Ind Hyg Assoc J, 1996, 57: 279-84; 15Smith et al., Fems
Microbiol Lett, 1992, 79:337-43; 16 Lappalainen et al., Atmosph
Environ, 1996, 30, 3059-3065; 17Burg et al., Am Ind Hyg Assoc J,
1981, 42:1-11; 18Burg et al., Am Ind Hyg Assoc J, 1982, 43:580-587;
19Silas et al., Am Ind Hyg Assoc J, 1987, 48:198-201;
20Selim et al., Am Ind Hyg Assoc J, 1998, 42:252-256;
21Palmgren et al., Am Ind Hyg Assoc J, 1983, 44:485-488;
22Sorenson et al., Appl Environ Microbiol, 1987, 53: 1370-5;
23Engelhart et al., Appl Environ Microbiol, 2002, 68:3886-3890;
24Ghosh et al., Am Ind Hyg Assoc J, 1997, 58:583-586;
25Kussak, Ph.D. Thesis, Umeå University, Umeå, Sweden, 1995.
22Johanning et al., Unpublished data pertaining to filter no. 1 in
Johanning et al., Proceedings: Indoor air 2002; 23Yike et al., Appl
Environ Microbiol, 1999, 65: 88-94.
Abstract Information &
Notes
William J. Meggs, M.D., Ph.D.
Date of talk:
Thursday, June 19, 2003, 10:30am
Brody School of Medicine
East Carolina University
Phone:
252/744-2954
600 Moye Blvd., Room 4W54
Fax:
252/744-3589
Greenville, NC 27858
E-mail:
[email protected]
Medical School Attended:
University of Miami
Major and date of Graduation:
M.D., 1979
Residency:
University of Rochester
Board Certifications:
Medical Toxicology, Allergy & Immunology, Internal Medicine,
Emergency Medicine
Current Faculty Appointments:
Professor & Chief of Toxicology
Current Job Description:
Physician
Other Information:
Author of “The Inflammation Cure” to be published in Sept. 2003. Editor of “Health & Safety in
Agriculture, Forestry, & Fisheries.”
Author of numerous research articles and textbook
chapters.
Disclosure Statement:
None
SPEECH TITLE:
“Systemic Anaphylactic Reactions to Molds and Other
Aeroallergens”
The speaker has provided the information
below.
1.) Goals and objectives:
$
To present the signs, symptoms, treatment, epidemiology, and prognosis of
systemic anaphylaxis
$
To discuss the clinical situations in which systemic anaphylaxis can
occur to aeroallergens
$
To discuss the mechanisms of systemic anaphylaxis
2.) Outline of talk/abstract:
Aeroallergens are proteins found in the air on mold spores, pollen
grains, and from animals. Humans become sensitized by the production of IgE
antibodies to these antigens. Most commonly aeroallergen exposures are by
inhalation, and the most common symptoms are rhino sinusitis, conjunctivitis,
and asthma. Less commonly, reactions such as urticaria, dermatitis, and systemic
anaphylaxis can occur from inhalation exposures to aeroallergens. The clinical
presentation, diagnosis, treatment, and mechanism of systemic anaphylaxis will
be discussed, and situations in which systemic anaphylaxis can occur from
aeroallergen exposures will be presented. These include inhalation induced
systemic anaphylaxis, dermal exposures, the alpine slide syndrome, and ingestion
of honeybee pollen containing aeroallergens.
3.) Conclusion of what is to be learned:
Aeroallergens can lead to systemic anaphylaxis from inhalation,
ingestion, and dermal exposures.
4.) References:
Chivato T, Juan F, Montoro A, Laguna R. Anaphylaxis
induced by ingestion of a pollen compound. J Investig Allergol Clin Immunol 1996
May-Jun; 6(3): 208-9.
Eriksson NE, Formgren H, Svenonius E. Food
hypersensitivity in patients with pollen allergy. Allergy 1982 Aug; 37(6):
437-43
Mansfield LE, Goldstein GB. Anaphylactic reaction after
ingestion of local bee pollen. Ann Allergy 1981 Sep; 47(3):
154-6
McGrath KG. Anaphylaxis. In Grammar LC, Greenberger PA,
eds., Patterson=s Allergic Diseases. 6th
Edition. Lippncott Williams &
Wilkins. Philadelphia, 2002. Chapter 20, pp 415-436.
Patterson R, Harris KE. Idiopathic Anaphylaxis. In
Grammar LC, Greenberger PA, eds,
Patterson=s Allergic Diseases. 6th
Edition. Lippncott Williams &
Wilkins. Philadelphia, 2002. Chapter 20, pp 415-436.
Spitalny KC, Farnham JE, Witherell LE, Vogt RL, Fox RC,
Kaliner M, Casale TB. Alpine slide anaphylaxis. N Engl J Med 1984 Apr
19;310(16):1034-7
Abstract Information & Notes
William J. Rea, M.D.
Date of talk:
Thursday, June 19, 2003, 11:00am
Environmental Health Center - Dallas
Phone:
214/368-4132
8345 Walnut Hill Lane, Ste. 220
Fax:
214/691-8432
Dallas, TX 75231
E-mail:
[email protected]
Medical School Attended:
Ohio State University College of Medicine
Major and date of Graduation:
M.D., 1962
Residency:
UTSWS
Board Certifications:
American Board of Surgery, American Board of Thoracic Surgery, American
Board of Environmental Medicine
Current Faculty Appointments:
Professor of Medicine, Capital University of Integrative Medicine,
Washington, DC
Current Job Description:
President, Environmental Health Center - Dallas
Disclosure Statement:
None
SPEECH TITLE: “Diagnosis of Mold and Mycotoxin
Sensitivity”
The speaker has provided the information
below.
1.) Goals and objectives: 1.) To understand the cause. 2.)Understand the diagnostic tests. 3.) To understand their value in pulmonary
function.
2.) Outline of talk/abstract: Mold Tests
used in diagnosing - building inspection and mold plates, SPECT-Brain Scan,
autonomic nervous system, evaluation through pupillography and HRV, balance
test, psychological - neuro-evaluation, blood tests, skin tests, and urine test
for mycotoxins.
3.) Conclusion of what is to be learned: How to
diagnose and individual with mold exposure
4.) References: Chemical
Sensitivity, Volume 2, 3
Abstract Information & Notes
Andrew W. Campbell, M.D.
Date of talk:
Thursday, June 19, 2003, 11:30am
Medical Center for Immune & Toxic Disorders
Phone:
281/981-8989
25010 Oakhurst, Ste. 200
Fax:
281/681-8787
Spring, TX 77386
E-mail:
[email protected]
Medical School Attended:
Universidad Autonoma de Guadalajara, Mexico, School of
Medicine
Major and date of Graduation:
M.D., June 1974
Residency:
1974-1975 - Guadalajara, Mexico, Pediatrics, Obstetrics & Gynecology;
1977 - Resident, General Surgery Orlando Regional Medical Center, Orlando,
Florida; 1978 - Resident, Family Medicine, Department of Family Practice,
Medical College of Georgia, Augusta, Georgia
Board Certifications:
American Board of Family Practice, American Board of Forensic Examiners,
and American Board of Forensic Medicine
Current Job Description:
Private Solo Practice
Other Information:
Published several articles; Recent awards include Marquis Who=s Who in America and Marquis Who=s Who in Medicine and Healthcare
Disclosure Statement:
None
SPEECH TITLE:
“Immunological and Neurophysiological Abnormalities in Adults with
Exposure to Molds”
The speaker has provided the information
below.
1.) Goals and objectives: Understanding the effects of toxigenic fungi and
mycotoxins as they affect humans, especially
neurotoxicity.
2.) Outline of talk/abstract:
3.) Conclusion of what is to be learned:
4.) References:
Will provide list
Immunological
and Neurophysiological Abnormalities in Adults with Exposure to
Molds
Andrew W. Campbell, M.D.
William High, M.D., Ph.D.
Ebere Anyanwu, M.S., Ph.D.
Medical Center for Immune and Toxic
Disorders
Houston, Texas
Objective: The objective of this study was to
evaluate the immunological and neurophysiological effects in patients (378) who
presented to our medical center with various adverse health problems due to
documented exposure to indoor toxigenic molds. Exposure to indoor toxigenic molds and
the subsequent effects on humans is ranked high among environmentally related
disorders. Recently, occupational
exposures in nonagricultural settings have been investigated using modern
immunological laboratory tests. Few
studies exist that take into account the combined immunological and
neurophysiologic effects in humans.
Methods: We studied retrospectively patients with
documented toxigenic mold exposure at measured levels in their residence using
previous medical records, questionnaires, serum testing for antibodies to molds,
serum immune function testing and neurophysiological testing including
electroencephalogram (E.E.G.), brainstem auditory evoked response (B.A.E.R.),
visual evoked potentials (VEP), and nerve conduction velocity (NCV).
Results: Findings from indoor environmental
studies on the patients’ residence (exposure site) were positive for specific
levels of exposure to toxigenic molds including Penicillium, Aspergillus,
Fusarium, Chaetomium, and Stachybotrys species. There was a positive correlation between
findings from the neurophysiological and immunological studies and the exposure
to indoor molds found in the residence.
The objective immunological and neurophysiological findings were
significantly abnormal, indicating both immunotoxic and neurotoxic
effects.
Conclusions: A
statistically significant number of patients with known chronic exposure to
toxigenic molds developed immunologic and neurophysiologic abnormalities. Our findings revealed the extent to
which toxigenic molds can affect the immunological and neurological systems of
environmentally exposed individuals.
Further work is encouraged in this regard.
Abstract Information & Notes
Professor Tang G. Lee, AAA
Date of talk:
Thursday, June 19, 2003, 1:30pm
Faculty of Environmental Design
The University of Calgary
Phone:
403/220-6608
2500 University Dr. NW
Fax:
403/284-4399
Calgary, Alberta T2N 1N4
E-mail:
[email protected]
Canada
Major and date of Graduation:
Site planning and architecture, 1975
Current Faculty Appointments:
Professor of Architecture (Building Science and Environmental
Health). Also Adjunct Professor at
the University of Manitoba, and visiting scholar at the Lyle center for
Regenerative Studies, California State Polytechnic University,
Pomona
Current Job Description:
Conducting research investigations and teaching environmental health,
particularly indoor air quality, building science and
sustainability.
Other Information:
Conducts comprehensive indoor air quality investigations in an
interdisciplinary team for those cases that could not be solved by other indoor
air quality consultants. Also
designs buildings such as medical clinics, institutions and residences that
feature low toxicity.
Disclosure Statement:
None
SPEECH TITLE: “Molds in Native Housing and SIDS
Potential”
The speaker has provided the information
below.
1.) Goals and objectives: To
understand the environmental conditions of native housing and its impact on
occupant health. To develop appropriate housing design, construction and
maintenance of native housing to minimize building deterioration and resulting
health impacts.
2.) Outline of talk/abstract: Many
native houses are built without regards to climate and cultural needs. Premature
deterioration of these houses created conditions for microbial amplification.
The resulting occupant symptoms reduced their potential for achieving a quality
of life and may even aggravate SIDS. Recommendations for proper site planning,
design and maintenance is presented.
3.) Conclusion of what is to be learned: Building
deterioration will impact occupant health and well-being. Better quality
buildings are needed to ensure occupant health.
4.) References:
Wilson, C.E. Sudden infant death syndrome and
Canadian Aboriginals: bacteria and infections. FEMS Immunology and
Medical Microbiology 25 (1999) 221-226. Federation of European Microbiological
Societies, Elsevier Science.
Lee, T.G. and Stooke, T. Mould propagation
resulting from air pressure differences across the building envelope.
Proceedings of the 9th International Conference on Indoor Air
Quality and Climate (Indoor Air 2002), Monterey, California, June 30
B July 5.
Abstract Information & Notes
William A. Croft, D.V.M., Ph.D.
Date of talk:
Thursday, June 19, 2003, 2:00pm
Environmental Diagnostic Group Inc.
Phone:
715/757-3756
521 Hilltop Dr.
Fax:
715/757-9302
Madison, WI 53711
E-mail:
[email protected]
Veterinary School Attended:
University of Minnesota
Medical School Attended:
University of Wisconsin, Madison, Wisconsin
Major and date of Graduation:
Ph.D. in Medical Pathology from the University of Wisconsin, Madison,
Wisconsin.
Current Job Description:
Study Human diseases within the environment from outbreak of human
disease as a Medical Pathologist.
Other Information:
Was on Faculty of the University of Wisconsin as Medical Pathologist, was
accepted by the National Institute of Health as a Medical Pathologist, qualified
to research human diseases. Obtain
over $900,000 of highly competitive research grants from the national Institute
of Health while at the University of Wisconsin.
Disclosure Statement:
None
SPEECH TITLE:
“Pathology of Trichothecene Mycotoxins in
Man”
The speaker has provided the information
below.
1.) Goals and objectives: To demonstrate the pathologic changes in the primary
target organs after inhalation verses ingestion exposure to Trichothecene
Mycotoxins in man.
2.) Outline of talk/abstract: A. History
of Mycotoxicosis, B. Detection of
"Sick Buildings” ingestion verses inhalation exposure. Signs and Symptoms expressed by over
6,000 patients exposed to Trichothecene Mycotoxins, attempting to establish
diagnosis. C. The pathologic changes associated with
inhalation exposure to trichothecene mycotoxins. D.
The primary organs involved with inhalation
Mycotoxicosis.
3.) Conclusion of what is to be learned: The primary target organs of this disease and how this
mycotoxin affects every cell in the body.
4.) References:
a. Croft,
W.A., Jarvis, B.B., and Yatawara, C.S.,: Airborne Outbreak of Trichothecene
Toxicosis, In: Atmospheric Environ, 20(3), 549-552 (1986).
b. Croft,
W.A., Jastromski, B.M., Croft, A.L., and Peters, H.A., "Clinical Confirmation of
Trichothecene Mycotoxicosis In Patient Urine," In: Journal of Environmental
Biology 23(3), 301-320 (2002).
The
Pathology of Trichothecene Mycotoxicosis In Humans
1.
The
Fingerprint of the Agent Causing the Disease is Displayed Within the Cells or
Tissue of The Body.
2.
Degeneration
and Necrosis of The Entire Central Nervous System, Cardiovascular, lung,
Digestive Tract, Spleen, Liver, Kidney, Pancreas, Immune, Skin, Reproductive,
Eye, Urinary Bladder and Prostate.
3.
The Signs and Symptoms Described For
Trichothecene Mycotoxicosis Match the Pathology Observed.
4.
Every
Cell in The Body is Affected or Susceptible to Trichothecene Mycotoxins When
Exposed.
5.
The
Exposed Cells Are Not Allowed to Grow and Make Cellular Products in The Rough
Endoplasm Reticulum Represents of First Mechanism of Action on The
Cells.
6.
The
Burning or Denaturation of Tissue From the Epoxide Molecule is Another Mechanism
of Action on The Cells of The Body Causing Intense Scarring of Organs. (Like
Phenol)
7.
The
Rapidly Turnover Organs Systems Are Affected The Most Severe, G.I. Tract, Immune
System and Reproductive, (like radiation damage)
8.
The
Central Nervous System is Severely Affected and is A Primary Target Organ. The Neurons in the Cerebral Hemispheres,
White and Grey Matter, Brain Stem and even the Ependymal Cells. The Purkinje Cells of The Cerebellum Are
Severely Affected That Affect Motion and Balance. The Dorsal and Ventral Motor
Neurons Are Destroyed Causing Amyotrophic Lateral Sclerosis. Peroxidation of Peripheral Nerves is
Also Observed. The Central Nervous
System is The Organ Most Affected as Reported By People Exposed to Toxic
Mold.
9.
Lack
of Cellular Production, Epoxide- Peroxidation of Lipid Membranes, Loss of
Vessels, Loss of Oxygen From Severe Lung Scarring, and Loss of Proper Nutrients
Due Loss of Functional Absorption of Intestine Affect the Brain and All Organs
of The Body.
10.
The
Trichothecene Mycotoxins are Cumulative in Their Health Effects on Organ
Systems.
11.
Trichothecene Mycotoxins are “Hit and
Run” Poisons and are not Stored in The Body.
12.
Inhalation
of Trichothecene Mycotoxins Are More Poisonous As Observed by The Intense
Scarring of The Alveolar Tissue Than Consumption Due To The Neutralization of
Mycotoxin by Bacteria.
13.
Depression of the Immune System Allows
for Increase Infections by Bacteria, Viral, Fungal and Cancer to
Form.
14.
Yeasts
are allowed to Colonize the Intestine Tract Because They Are Resistant to
Trichothecene Mycotoxins.
15.
Yeast Can Cause Diabetes Mellitus, Gout
and Prevent Proper Liver Function to Detoxify Xenobiotics.
16.
Trichothecene Mycotoxins are Released
Within the Urine and Feces as Evidenced by The Pathology Observed Within Those
Tissues.
17.
Children Exposed to Trichothecene
Mycotoxins are 100 to 1000 X more susceptible because stems are killed not
allowing for additional growth within the individual.
18.
There
is No Safe Level of Exposure to Trichothecene Mycotoxins.
19.
The
third Mechanism For Trichothecene Mycotoxicosis is To Develop Anaphylaxis to
Mold Allergens When Mycotoxin Leaves The Body.
Dr.
William Croft, (Medical Pathologist)
Stages of Mycotoxicosis: For Inhalation of
Mycotoxin
The three Stages (1-3) ranging from lower to higher
severity of poisoning were modified according to exposure via the air as opposed
to ingestion already established (Forgacs et al., 1962; Joffe, 1971). A separate Stage
of convalescence occurs when a patient is completely removed from the
contaminated premises and the source of mycotoxin or mold spores.
Stage
1: The primary changes are in the
brain, respiratory and immune systems, mucus membranes and gastrointestinal
tract. Signs and symptoms may include burning sensation in the mouth, tongue,
throat, palate, esophagus, and stomach, which is a result of the action of the
toxin on the mucous membranes and skin in the exposed areas. Moist areas of the
body armpits, under breasts, belt line and groin are more sensitive or first
affected. Patients may report burning within the eyes, ears and nose. Patients
also reported that their tongues felt swollen and stiff. Mucosa of the oral
cavity may be hyperemic. Mild gingivitis, stomatitis, glositis, and esophagitis
developed. Inflammation, in addition to gastric and (small and large) intestinal
mucosal, resulted in vomiting, diarrhea and abdominal pain. Excessive
salivation, headache, dizziness, weakness, fatigue and tachycardia were also
present.
There may be fever and sweating. The respiratory system
develops burning sensations and congestion. Severe exposure to mycotoxin within
the lungs may lead to congestion, edema and failure, due to caustic action. Body
temperature remains normal and controllable by the patient. The poisoning
appears and disappears relatively quickly in this Stage with the exception of,
lungs and central nervous system. Initially (Stage 1), the patient’s symptoms
are very uncomfortable or painful. As the poisoning continues and the patient
progress toward Stage 2, he or she becomes accustomed to the presence of the
mycotoxin and a quiescent period follows due to lack of nerve sensation.
Depending on exposure levels, the first Stage may last from 3 - 9 days. In
scoring the 50 signs and symptoms listed in Tables-1 and 2, an average score
range of 20-45 represents Stage 1.
Stage 2 :
This Stage is often called the latent
Stage or incubation period because the patient feels apprehensive, but is
capable of normal activity in the beginning of this Stage. Every organ of the
body is affected by degeneration and necrosis with continued exposure. The
primary target organs for an individual become evident over time, due to
biological variation. These are disturbances in the central and autonomic
nervous systems resulting in headaches, mental depression, loss of short-term
memory, loss of problem-solving ability, various neuropsychiatric
manifestations, meningism, severe malaise and fatigue, narcolepsy, loss of
temperature control, hyperesthesia or numbness of body areas, and cerebellar
dysfunction including hypotonia, attitude and gait, dysmetria, asthenia,
vertigo, disturbances of speech, and loss of balance (Best, 1961). Spinal cord
degeneration may also be observed in gait and reflex abnormalities, such as the
ability to drive vehicles, ride bicycles or pass sobriety tests (inability to
tolerate ethyl alcohol). Attention deficient disorder may be observed in
children. Various systems may include: Eyes: visual disturbances, floating objects,
light sensitive, lack of tears, burning and itching. Ears: burning,
itching, and loss of hearing. Immune and hematopoietic: progressive loss
of white and red cells including a decrease of platelets and hemoglobin, and
high susceptibility to bacterial, mycotic and viral infections, debilitating
chemical and allergies. Gastrointestinal: metallic taste in mouth, tooth
loss, gum problems, stomatitis, sores in gums and throat, nausea, vomiting,
diarrhea or constipation, excessive flatulence, abdominal distention, hepatitis,
pancreatitis, and diabetes mellitus. Respiratory : burning and bleeding
from nasal membranes, respiratory difficulty, asthma, extreme susceptibility to
cold, flu and pneumonia. Skin: thinning of hair on head, burning on face,
rashes, irritation, and edema. Renal: proteinuria, possible hematuria.
Reproductive: irregular ovarian cycles, increased menstrual flow, fibroid
growths in uterus, cystic development in mammary glands, and tumors of mammary
and prostate glands. Musculoskeletal : somatitis, muscle weakness,
spasms, cramps, joint pain, enlargement of joints in hand, and clubbing of
fingers. Cardiovascular: chest pain, palpitations, ruptures of atrial
walls, myocardial infection and aneurysm of arteries.
The skin and mucous membranes may be icteric, pupils
dilated, the pulse soft and labile, and blood pressure may decrease or increase.
The body temperature does not exceed 38 degree C and the patient may be
afebrile, or chilled. Visible hemorrhagic spots may appear on the skin. Thoughts
of suicide may be prominent in the person’s mind at this time or anytime in
Stage 2. Human bonding is very important for survival.
Degeneration and hemorrhages of the vessels marks the
transition from the second to the third Stage of the disease and may not be
consistently observed. The degeneration of the vital organs including serious
respiratory insufficiency or asthma and CNS degeneration will take the patient
into Stage three along with development of necrotic angina. If exposure
continues, depending on exposure levels, Stage 2 may continue from weeks to
months or even years until the symptoms of the third Stage develop. Evaluating
the 50 signs and symptoms (Table-1 and 2) by assigning a score (0-least intense
to 5-most intense or severe) to each symptom, we have determined that an average
score range of 45-180 represents Stage 2.
Stage 3:
Severe degeneration of the vital organs. The
transition from the second to the third Stage is sudden. In this Stage, the
patient’s resistance is already low, and violent severe symptoms are present,
especially under the influence of stress, or associated with physical exertion
and fatigue. The first visible sign
of this Stage may be lung, brain or heart failure (heart attack), with or
without the appearance of petechial hemorrhage on the skin of the trunk, the
axillary and inguinal areas, the lateral surfaces of the arms and thighs, the
face and head, and in serious Cases, the chest. The petechial hemorrhages vary
from a few millimeters to a few centimeters in diameter. There is increased
capillary fragility and any slight trauma may cause the hemorrhages to increase
in size.
Aneurysms of the brain or aorta may be observed by
angiography. Hemorrhages may also be found on the mucous membranes of the mouth
and tongue, and on the soft palate and tonsils. There may be severe interstitial
thickening or scarring of the lungs, or respiratory failure. Nasal, gastric and
intestinal hemorrhages and hemorrhagic diathesis may occur. Necrotic angina
begins in the form of catarrhal symptoms and necrotic changes soon appear in the
mouth, throat, and esophagus with difficulty and pain on swallowing. Severe
degeneration of the skin on the face, eyelids, and loss of lashes is also often
present.
Necrotic lesions may extend to the uvula, gums, buccal
mucosa, larynx, vocal cords, lungs, stomach, and intestines and other internal
organs such as the liver and kidneys and are usually contaminated with a variety
of avirulent bacteria. Bacteria infection causes an unpleasant odor from the
mouth due to the enzymatic activity of bacteria on proteins. Areas of necrosis
may also appear on the lips and on the skin of the fingers, nose, jaws, and
eyes. Regional lymph nodes are frequently enlarged. Esophageal lesions may occur
and involvement of the epiglottis may cause laryngeal edema and aphonia (loss of
voice). Death may occur by strangulation.
Patients may suffer an acute parenchymatous hepatitis
accompanied by jaundice. Bronchopneumonia, pulmonary hemorrhages, and lung
abscesses are frequent complications. Tumors may develop of various organs,
including skin, urinary bladder, brain, mammary gland, bone, immune, liver,
prostate, possibly resulting in death. The most common cause of death is brain
failure due to both direct effects of the mycotoxin on the central nervous
system and indirect effects due to respiratory failure or lack of oxygen to the
brain caused by the severe caustic inflammation (fibrinous exudation) reaction
with the lung tissue, rendering it non-functional. Again, using the scoring
system represented in Tables-1 and 2, an average score of greater or equal 180
represents Stage 3.
Stage of
Convalescence: The course and duration
of this Stage 3 depends on the intensity of the poisoning and complete removal
of the patient from the premises or source of mycotoxin. Therefore, the duration
of the recovery period is variable. There is considerable cellular necrosis and
scarring to all major organs of the body in which cells will not regenerate,
including the brain, spinal cord, eyes, lung, heart, liver, pancreas, kidney,
adrenal, and blood vessels. If the disease is diagnosed during the first Stage,
hospitalization is usually unnecessary, but allergies and asthma should be
monitored closely. If the disease is diagnosed during the second Stage and even
at the transition from the second to third Stages, early hospitalization may
preserve the patient’s life. If however, the disease is only detected during the
third Stage, death cannot be prevented in most Cases.
1.
Croft, W. A., Jastromski, B. M., Croft, A. L., and Peters, H. A.,
“Clinical
Confirmation of
Trichothecene Mycotoxicosis in Patients Urine”, In: Journal of
Environmental
Biology 23(3), 301-320 (2002)
2.
.Forgacs, J., and W. T. Carll : Mycotoxicoses. In : Advances in
Veterinary
Science.
Academic Press, New York and London, pp 273-372 (1962).
Abstract Information & Notes
Kaye H. Kilburn, M.D.
Date of talk:
Thursday, June 19, 2003, 2:30pm
University of Southern California
Keck School of Medicine
Phone:
323/442-1830
2025 Zonal Ave., CSC-201
Fax:
323/442-1833
Los Angeles, CA 90033
E-mail:
[email protected]
Medical School Attended:
University of Utah College of Medicine
Major and date of Graduation:
1954
Board Certifications:
American Board of Internal Medicine, American Board of Preventive
Medicine
Current Faculty Appointments:
Professor of Medicine University of Southern California Keck
School
Current Job Description:
Ralph Edgington Professor - Academic Medicine Teaching, Research on
Neurotoxicology, Pulmonary Disease
Other Information:
Author
240 peer reviewed papers; Book: Chemical Brain Injury, NY, John Wiley and
Sons, 1998; President Neurotest Inc.; Develop test and use of Neurobehavioral
methods in evaluated brain damage from chemicals; hydrogen sulfide, PCBs,
pesticides, chlorine, ammonia, molds and mycotoxins
Disclosure Statement:
Neuro-test Inc.
SPEECH TITLE: “How Molds and Mycotoxins Affect Human
Brains”
The speaker has provided the information
below.
1.) Goals and objectives: Review the evidence from patients studied that show
neurophysiological impairments: balance, vision, reaction time and on problem
solving and memory.
2.) Outline of talk/abstract: Sixty-five adults were studied using 26 neurobehavioral
tests, pulmonary function measurements and serum and saliva antibody
titers
3.) Conclusion of what is to be learned: The human brain is the major target and premature aging
is produced. Temporally parallel
effects on pulmonary airways cause small airways obstruction and other organs
may be involved.
4.) References:
see abstract
How Molds and Mycotoxins Affect
Human Brains
Kaye H. Kilburn, M.D.
University of Southern California,
Keck School of Medicine
Background:
Mold spores and mycotoxins produce airway irritation, asthma and bleeding. Neurobehavioral and respiratory symptoms
suggested testing.
Methods:
Neurobehavioral functions as means of percent predicted were compared in 65
consecutive mold exposed adults and 202 community controls. Measurements included balance, choice
reaction time, color discrimination, blink reflex, visual fields, grip, hearing,
problem solving, verbal recall, perceptual motor speed, and memory. Check lists surveyed histories, mood
states and symptom frequencies (Kilburn 2002a and 2002b).
Findings:
Exposed persons had abnormal balance, reaction time, blink reflex latency, color
discrimination, visual fields, and grip.
Also digit symbol substitution, peg-placement, trail making, verbal
recall, and picture completion scores were reduced. Twenty-one of 26 tested functions were
abnormal. Airways were obstructed
and vital capacities reduced. Mood
scores and symptom frequencies were elevated.
Interpretation:
Mold exposures indoors were associated with neurobehavioral impairment probably
from mycotoxins, such as trichothecenes.
Correlation of human impairment with measured mycotoxins is the next step
(Johanning et all 1999 and 2002, Nielsen and Thrane 2001).
REFERENCES
1.
Kilburn KH. Janus Revisted,
Molds Again. Arch Environ Health
2002a;57(1):7-8.
2.
Kilburn KH. Inhalation of
Moulds and Mycotoxins. Eur J
Oncol 2002b;7(3):____.
3.
Johanning E et al. Clinical
Experience and Results of a Sentinel Health Investigation Related to Indoor
Fungal Exposure. Environ Health
Perspect 1999;107(3):489-494.
4.
Johanning et al. Airborne
Mycotoxin Sampling and Screening of Trichothecenes in Fungal Cultures - Using
Gas Chromatography - Tandem Mass Spectrometry. J Chromatography A
2002;929(1):75-87.
Abstract Information & Notes
Kalpanna D. Patel, M.D.
Date of talk:
Thursday, June 19, 2003, 3:30pm
65 Wehrle Dr.
Phone:
716/833-2213
Buffalo, NY 14225
Fax:
716/833-2244
E-mail:
[email protected]
Medical School Attended:
BJ Medical College, India
Residency:
University of Texas Health Science Medical School at San
Antonio
Board Certifications:
American Board of Pediatrics, American Board of Environmental
Medicine
Current Faculty Appointments:
Associate Professor of Pediatrics, Suny, Buffalo
Current Job Description:
President/Director AEHC-Buffalo
Other Information:
Elected Appointments: President of American Board of Environmental
Medicine, President of International Board of Environmental
Medicine
Disclosure Statement:
None
SPEECH TITLE: “What Is New And Different in The
Diagnosis And Management of Different Skin Disorders - Itching Eczema And
Urticaria”
The speaker has provided the information
below.
1.) Goals and objectives:
1) To
demonstrate importance of good environmental and dietary history of mold and
mycotoxin exposure for the diagnosis and management of different skin disorders.
2) To demonstrate importance of Intradermal mold antigen
testing and the efficacy of maximum tolerated end point, dose of mold antigen to
obtain optimal response to relieve different skin
conditions.
2.) Outline of talk/abstract:
$
Presentation of different
cases having different symptomatology that failed to respond to traditional
management.
$
To demonstrate
effectiveness of Environmental Medicine approach in treatment of these
cases.
$
Discussion of newer
methods for the diagnosis and treatment of mold related skin
disorders.
3.) Conclusion of what is to be learned:
1) Exposure to mold has become an enigma in homes as
well as newer and older sick buildings.
2) Mold plays a major role in the immune dysfunction and
development of inhalant sensitivity.
3) Chronic health problems like intense itching, eczema
urticaria fatigue and many others can be effectively treated without drug
therapy if the source of the problem is detected and treated
effectively.
4.) References:
Abstract Information & Notes
Katherine Warsco, Ph.D.
Date of talk:
Thursday, June19, 2003, 4:00pm
East Carolina University
Phone:
252/328-6929
152 Rivers Building, ECU
Fax:
252/328-4276
Greenville, NC 27834
E-mail:
[email protected]
Medical School Attended:
NA (Ph.D. College of Human
Ecology, Michigan State University)
Major and date of Graduation:
Family and Child Ecology, 1988
Residency:
NA (Doctoral Internship B Energy Information Administration, US Department of
Energy, Washington D.C.)
Board Certifications:
NA
Current Faculty Appointments:
Interior Design Program, School of Human Environmental Sciences, East
Carolina University, Greenville, NC
Current Job Description:
Chair, Department of Apparel Merchandising and Interior Design, School of
Human Environmental Sciences, East Carolina University, Greenville,
NC
Other Information:
Founder of Environmental Quality in Interiors Network, Interior Design
Educators Council
Disclosure Statement:
None
SPEECH TITLE: “Teaching Design for Good Indoor Air
Quality”
The speaker has provided the information
below.
1.) Goals and objectives: The
purpose of this speech is to report on the development of an environmental
education curriculum that bridges fields of medicine, building science, and
design to address indoor air pollution, environmental illness, and interior
design. As a result of
participation in this curriculum, students of interior design will be able to
apply design criteria to address the following issues:
a)
Application of non-toxic and radon-resistant construction
practices;
b)
Removal, isolation, and/or dilution of chemicals released into indoor air
by appliances, cleaning solvents, pesticides, and the off gassing of synthetic
materials, adhesives, and finishes;
c)
Selection and layout of HVAC and lighting systems to avoid the buildup of
moisture and the collection of dust;
d)
Selection of furniture, cabinetry, and surface finishes that provide
inhospitable conditions for microbial growth; and
e)
Accessible design of living quarters to facilitate movement by a
chemically sensitized client suffering from episodes of reduced stamina and
mobility.
2.) Outline of talk/abstract: An
environmental education curriculum was developed to assist students in exploring
linkages between micro-climate, architectural shell, interior space plan,
building systems, materials specification, indoor air quality, and environmental
illness. In the context of a
national design competition, students applied a series of programming exercises
to develop solutions for a hypothetical residential design problem. Exercise 1 required students to identify
effects of chemical and biological contaminants on building occupants based on
patient profiles published in Volume III of William Rea’s series on chemical
sensitivity. Exercise 2 required
students to identify sources, paths of entry and design solutions for chemical
and biological irritants. Exercise
3 required students to identify the effects of Multiple Chemical Sensitivity on
physical dexterity as applied to an anthropometric model developed by Ralph
Faste. Exercise 4 required students
to outline design solutions for controlling indoor air quality. Students applied a series of schematic
diagramming exercises to a hypothetical building and residential site located in
a hot, humid climate to explore the following:
a)
Orienting the building and fenestration for day lighting and ultraviolet
light, passive solar and winter heat movement, and passive cooling and
prevailing winds;
b)
Radon resistant construction practices;
c)
Interior spatial arrangement to facilitate movement of building occupants
with low stamina and exhaustion of pollutants in a depressurized building;
d)
Interior spatial arrangement to isolate sleeping quarters to provide a
pollutant-free sanctuary; and
e)
Specification of building materials, and interior finishes, fabrics, and
equipment to remove contaminants from the interior-breathing zone.
3.) Conclusion of what is to be learned: This
environmental education project represents a first attempt to partner with the
Environmental Protection Agency to employ student design competitions as a
vehicle for disseminating scientific environmental information to post-secondary
schools of interior design in the U.S.
Fulfilling sponsor expectations for developing a curriculum inclusive of
the major threats to human health by indoor air was complicated by conflicting
assumptions within the scientific community as to what constitutes environmental
disease. Although this curricular
tool was successful in providing a thorough overview of indoor air quality
design considerations, deliberately retaining the complexity of issues within a
multi disciplinary framework challenged the definition of acceptable boundaries
for a problem addressed by interior designers. Future efforts to integrate
environmental health issues in interior design curricula must balance the need
to avoid unidimensional problem solving with limitations to the scope of
training for interior design students.
Increasing collaboration among schools of design and health sciences to
provide opportunities for multi disciplinary problem solving would ensure design
solutions are grounded in current knowledge of the effects to health of
biological and chemical indoor contaminants.
4.) References: See
attached
Katherine Warsco
East Carolina University
Goals and
objectives
The
purpose of this speech is to report on the development of an environmental
education curriculum that bridges fields of medicine, building science, and
design to address indoor air pollution, environmental illness, and interior
design. As a result of
participation in this curriculum, students of interior design will be able to
apply design criteria to address the following issues:
a.
Application of non-toxic
and radon-resistant construction practices;
b.
Removal, isolation, and/or
dilution of chemicals released into indoor air by appliances, cleaning solvents,
pesticides, and the off gassing of synthetic materials, adhesives, and
finishes;
c.
Selection and layout of
HVAC and lighting systems to avoid the buildup of moisture and the collection of
dust;
d.
Selection of furniture,
cabinetry, and surface finishes that provide inhospitable conditions for
microbial growth; and
e.
Accessible design of
living quarters to facilitate movement by a chemically sensitized client
suffering from episodes of reduced stamina and mobility.
A
curriculum was proposed for improving the quality of interior design instruction
for addressing indoor air pollution and environmental illness through
residential interior design. The
purpose of the project was:
a.
To develop, disseminate,
and implement materials and methods for assisting post-secondary instructors and
students of design to increase their knowledge of indoor air quality
issues;
b.
To promote the application
of this knowledge to develop innovative solutions for radon-resistant,
non-toxic, and allergy-free interiors; and
c.
To provide opportunities
for interdisciplinary problem solving, drawing from the fields of medicine,
architecture and engineering to address residential design solutions for
medically at-risk populations such as the elderly and the
infirm.
This project targeted 460 faculty and their students in
two- and four-year university interior design programs in the US. The coastal southeast region was the
focus of this environmental illness project because the following factors make
indoor air quality concerns critical components of the building design
process:
a.
The population exceeds the
national average for age 65 years and older and percent of elderly both in
poverty and in poor health;
b.
For coastal states such as
Florida, housing stock exists with radon levels exceeding EPA limits; and
c.
Hot and humid climate
conditions increase microbial growth and the release of chemicals that incite
toxic and allergic reactions among the hypersensitive.
The
vehicle used to improve the quality of interior design instruction was a
national student design competition and teacher’s supplement. A competition was developed
incorporating requirements for the design of a residential setting for a retired
couple who suffered from environmental illness. Included in the competition were the
following components linked to principles of environmental
design:
a.
Site profile. Students were asked to design a
retirement residence in Northern Florida in a county where radon gas is
prevalent in levels that exceed the EPA limit. The hot, humid micro-climate posed
medical problems concerning microbial growth. Lots were selected from a housing
development that adheres to tenets of sustainable design in order to integrate
principles of enviroscaping (i.e., environmentally safe & energy conscious
landscaping practices) and sustainable construction with the residential design
problem. Sustainable construction
building codes released by the John D. and Catherine T MacArthur Foundation and
information from a market survey conducted by the University of Florida Center
for Construction and the Environment were made available for use in this
competition.
b.
Building profile. Students were asked to modify a design
given of a Florida Cracker House, a vernacular archetype suitable for hot, humid
climates predating mechanized air conditioning and development of synthetic
building materials. Focusing on a
process of archetypal ideation developed by Ronald Haase, students explored
traditional principles of passive cooling to address good indoor air
quality.
c.
Client profile. Students were given information
concerning the needs and characteristics of a hypothetical client family. The medical case histories were based on
actual patient case reports from the Environmental Health Center-Dallas,
Texas. Students were introduced to
medical profiles as a source of information regarding client responses to toxin
and allergen exposures within building interiors.
d.
Drawings. Site plans, building elevations,
foundation plan, roof plan and floorplan were included in hard copy and made
available in electronic format.
Information was provided to assure compliance with the Southern Building
Code regarding foundation design and break-away construction to address the
velocity of hurricane-force winds and coastal flooding of the
foundation.
e.
Resources. Order forms were included for literature
and electronic media pertaining to designing for indoor air quality, hot humid
climates, and environmental illness.
A
supplement to the competition provided a suggested teaching plan for integrating
the competition in university instruction.
The teaching plan included learning objectives, suggested readings,
discussion questions, and examples of student outcomes. In the context of the national design
competition, students applied a series of programming exercises to develop
solutions for a hypothetical residential problem:
a.
Patient Profile. In Table 1, students were required to
identify effects of chemical and biological contaminants on building occupants
based on patient profiles published in Volume III of William Rea’s Series on
chemical sensitivity (Rea, W., 1996).
In Table 2, students were required to identify sources, paths of entry
and design solutions for chemical and biological irritants based on information
provided in the suggested textbook, Your Home, Your Health and Well-Being
(Rousseau, Rea, and Enwright, 1990).
The purpose of these exercises was to gain understanding of the linkages
between pollutant sources in the built environment and medical symptom behaviors
of building occupants. Students
explored translating medical data into design parameters for use in the process
of design ideation for a hypothetical client family.
b.
Disability
Compensation. In Table 3, students
were required to identify the effects of chemical sensitivity on physical
dexterity as applied to “The Enabler,” an anthropometric model developed by
Ralph Faste (Rashko, B., 1991).
The purpose of this exercise was to identify design requirements
associated with selective physical disabilities for use in the process of design
ideation for a hypothetical client family.
c.
IAQ Solutions. In Table 4, students were required to
outline design solutions for controlling indoor air quality in the “sanctuary;”
the primary sleeping quarters for their hypothetical client couple. In Table 5, students provide a material
assessment for client health and well-being. Building materials, finishes and
furnishing materials, and building systems (i.e., plumbing, electrical, heating
and appliances) were chosen according to a rating-for-safety system developed by
Rousseau and Rea (Rousseau, et. al., 1990). Students intertwined issues of materials
science with aesthetic considerations in their development of a residential
prototype for benign design.
Students applied a series of schematic diagramming
exercises to a hypothetical building and residential site located in a hot,
humid climate as a means to explore principles from the following areas of
design:
a.
Micro-Climate Design. Students explored orientation of
openings in the architectural shell for daylighting, passive solar and winter
heat movement, and passive cooling and prevailing winds to address building
occupant thermal comfort, reduce consumption of fossil fuels for heating and
cooling, and dilute airborne contaminants in the near environment.
b.
Enviroscaping and
Sustainable Development. In
the manner of case studies of the Kanapaha Botanical Gardens and the Florida
House Learning Center, students were required to develop conceptual plot
plans. Specification of drought
tolerant plants indigenous to the climate minimized irrigation as a habitat for
mold and use of chemical fertilizers that were a source of toxins for their
chemically sensitive clients.
c.
Radon-Resistant
Construction Practices. Students
explored radon mitigation techniques for homes with above-grade foundations in
terrain prone to coastal flooding.
d.
Accessible Design. Students considered human activity
patterns influenced by loss of stamina, general muscle weakness, and chronic
fatigue characteristic of medical conditions of the age and chemical sensitivity
of their clients. Structural and
nonstructural design solutions were explored to support daily routines of the
non-ambulatory and infirm.
e.
Non-Toxic, Allergy-Free
Design of the “Sanctuary.”
Students explored the design of sleeping quarters free of environmental
irritants that might interfere with healing and revitalization. Strategies for removing and
isolating indoor contaminants were explored with regards to design of mechanical
systems, space planning, and specification of furnishings, finishes, equipment,
and accessories for residential interiors.
Of
the 460 competition packets mailed to US members of the Interior Design
Educators Council, thirteen universities participated with thirty-nine
submissions. Although every
region except the Northwest was represented in the competition, three-fourths of
the submissions were from universities in hot, humid climates. A three-member jury independently ranked
student entries. Criteria used to
evaluate submissions included the following:
a.
The design solution is
appropriate for sustainable development considerations of the climate, terrain,
and vernacular archetype (15%)
b.
The design solution
reflects an accurate and sensitive application of principles of radon-resistant,
non-toxic, allergy-free, and accessible design (40%)
c.
The solution represents
innovative design for the “sanctuary,” addressing specific medical conditions of
the clients as explained in the patient profiles of the design program
(10%)
These criteria constituted 65% of the overall evaluation
score. Winning submissions were
selected from top scores, ranging from 81-90/100 points. Jurors provided numerical and open-ended
responses to student submissions.
Faculty and students participating in the competition received written
feedback as to the strengths and weaknesses of each submission according to
disciplinary perspectives represented by the jury.
Student outcomes
presented as illustration for exercises in the teacher’s supplement received
national attention. Conceptual
designs prepared by an undergraduate research assistant, Michelle Puckett
Jenkins were awarded first place in two national student competitions: a) a call
for student design entries sponsored by Affordable Comfort Inc., an
interdisciplinary organization that promotes environmentally friendly,
energy-efficient, healthy building practices; and b) a national lighting
competition sponsored by Cooper/Halo Metalux, Inc. These projects received external
validation from juries comprised of educators and practitioners in the fields of
building construction, architecture, and mechanical
engineering.
This environmental
education project demonstrated viable linkages between the arts and sciences in
addressing indoor air quality and environmental illness. Employing a student design competition
as a vehicle for disseminating scientific environmental information provided a
thorough overview of indoor air quality design considerations. Increasing collaboration among schools
of design and health sciences to provide opportunities for multidisciplinary
problem solving would ensure design solutions would be grounded in current
knowledge of the effects to health of biological and chemical indoor
contaminants.
American Lung Association. (1992). Indoor Air Pollution
Fact Sheet: Radon. Atlanta, GA:
American Lung Association.
American Lung Association, Environmental Protection
Agency, Consumer Products Safety Commission, & American Medical Association.
(1994). Indoor Air Pollution: An Introduction for Health
Professionals (Government document 1994-523-217/81322). Washington, D.C.:
American Lung Association
Environmental Protection Agency, Consumer Product Safety
Commission, & American Medical Association. (1998). Trends in Cigarette
Smoking. Morbidity & Mortality Weekly
Report, 47(43).
Axelrad, B. (1993). Improving IAQ: EPA's program. EPA Journal, 4(October-December),
14-17.
Beecher, M. A., & Davies, B. (2002, March 19-24). Shades of Green: The Philosophical
Challenges of Ecological Responsibility in Interior Design Education and
Practice. Paper presented at the Mesas and the Mysteries: On the Edge of Imagination/Green Design,
Santa Fe, NM.
Bode, M., & Munson, D. (1995). Controlling Mold Growth in the Home,
[Guidance Document]. Kansas State University Agricultural Experiment Station and
Cooperative Extension Service. Available:
http://www.oznet.ksu.edu/library/hous2/mf2141.pdf [2002, November
11].
Browner, C.M. (1993). Environmental Tobacco Smoke: EPA's report. EPA Journal, 4(October-December),
18-22.
Canada Mortgage and Housing Corporation. (1993). The Clean Air Guide: How to Identify and Correct
Indoor Air
Problems in Your Home (NHA 6695;
NH15-8311993E). Eobicode, ON: Canada Mortgage and Housing
Corporation.
Coleman, C. (1999). Life-cycle design: Leaving future generations a legacy. Perspective (Spring/Summer), 27-28,
30.
Danko, S., Eshelman, P., & Hedge, A. (1990). A
taxonomy of health, safety, and welfare implications of interior design
decisions. Journal of Interior Design
Education and Research, 16(2), 19-30.
Fernández-Caldas, E., Trudeau, W. L., & Ledford, D.
K. (1994). Environmental control of indoor biologic agents. Journal of Allergy & Clinical
Immunology, 94(2), 404-412.
Guerin, D. A. (1992). Issues facing interior design
education in the twenty-first century. Journal of Interior Design Education and
Research, 17(2), 9-16.
Haase, R. W. (1992). Classic Cracker: Florida's Wood-Frame Vernacular
Architecture. Sarasota: Pineapple Press.
Hasell, M. J., & Scott, S. C. (1996). Interior
Design Visionaries' Explorations of Emerging Trends. Journal of Interior Design, 22(2),
1-14.
Human Ecology Action League. (1992). Chemicals Can
Effect Your Health . Atlanta, GA: Human Ecology Action
League.
Inman, M., & Shea, J. (1993, October, 1993). Housing problems for older adult households
in the southeast. Paper presented at the Paper presented at the 1993 annual
meeting of the American Association of Housing Educators, Columbus,
OH.
Kibert, C. J. E. (1995). Sustainability Rationale: Analysis of Sustainable Construction
Aspects of the Abacoa Development (Unpublished Manuscript ). Gainesville:
University of Florida Center for Construction and
Environment.
Kibert, C. J. E. (1996). Sustainable Construction
Code--Residential: For the Abacoa
Development (Unpublished Manuscript ). Gainesville: University of Florida
Center for Construction and Environment.
Kloeppel, J. E. (1993, April, 1993). Beware the fungus
among us: Emissions from mold &
fungus may be culprits in indoor air problems. Georgia Tech News,
1-4.
Lechner, N. (1991). Heating, Cooling, Lighting: Design Methods for Architects. New
York: John Wiley & Sons.
Marcinowski, F., Lucas, R. M., & Yeager, W. M.
(1994). National and regional distributions of airborne radon concentrations in
U.S. homes. Health Physics, 66(6),
699-706.
Mendler, S. (2002). LEED: A Roadmap for Added Value. Perspective: Journal of the International
Interior Design Association(Winter 2002), 42-49.
Miller, B. R., Miller, P. B., & Bateman, M. S.
(2002, March 19-24). Two's Company,
Three's a Good Team: Multidisciplinary Teams are a 21st Century Necessity.
Paper presented at the Mesas and the Mysteries: On the Edge of Imagination/Green
Design, Santa Fe, NM.
Miller, J. W. (2002). Green Home Building. Perspective: Journal of the International
Interior Design Association(Fall 2003), 22-27.
Moussatche, H., King, J., & Rogers, T. S. (2002,
March 19-24, 2002). Material Selection in
Interior Design Practice. Paper presented at the Mesas and the Mysteries: On
the Edge of Imagination/Green Design, Santa Fe, NM.
Odom, J. D.,& DuBose, G. (1996). Preventing Indoor Air Quality Problems in
Hot, Humid Climates: Design and
Construction Guidelines (Unpublished manuscript). Orlando: CH2M Hill, Inc.,
Disney Development Co.,.
Peart, V. (1993). Indoor air quality in Florida: Formaldehyde (Fact Sheet He 3205).
Gainesville: University of Florida Cooperative Extension
Service.
Raschko, B. (1991). Housing Interiors for the Disabled &
Elderly. New York: Van Nostrand Reinhold.
Rea, W. J. (1996). Chemical Sensitivity (Vol. 3). Boca
Raton: CRC Press.
Rousseau, D., Rea, W. J., & Enwright, J. (1990). Your Home, Your Health, &
Well-Being. Berkeley: Ten Speed Press.
Science Advisory Board. (1990). Reducing risk: Setting priorities and strategies for
environmental protection (Government Report SAB-EC-90-021). Washington,
D.C.: The Science Advisory Board.
Seltzer, J. M. (1995). Creating healthy indoor environments: A road map for the future (Vol. 10).
Philadelphia: Hanley & Belfus.
Sexton, K. (1993). An inside look at air pollution. EPA Journal, 19(4),
9-12.
US Environmental Protection Agency. (1993). Targeting Indoor Air Pollution: EPA's Approach and Progress
(Bulletin EPA 400-R-92-012). Washington D.C.: U.S. Environmental Protection
Agency, Air and Radiation.
US Environmental Protection Agency. (2001a, May 28,
2002). Healthy Buildings, Healthy People:
A Vision for the 21st Century, [Guidance Document]. US Environmental
Protection Agency. Available: http://www.epa.gov/iaq/hbhp/index.html [2002,
November 11].
US Environmental Protection Agency. (2001b, December 31,
2001). Mold Remediation in Schools and
Commercial Buildings, [Guidance Document]. US Environmental Protection
Agency. Available: http://www.epa.gov.iaq/pubs [2002, November
11].
Warsco, K. (1997a). Designing for Good Indoor Air
Quality in a Hot, Humid Climate:
Student Design Competition . Unpublished competition materials prepared
for US EPA Environmental Education Grants Program, Washington,
D.C.
Warsco, K. (1997b). Teaching Supplement to the Student
Design Competition: Designing for
Good Indoor Air Quality in a Hot, Humid Climate: Unpublished supplement to
competition materials prepared for US EPA Environmental Education Grants
Program, Washington, DC.
Waxman, H. A. (1993). The view from congress. EPA Journal, 19(4),
38-39.
Wilson, K. P. (2002). The Case for Green Design. Perspective: Journal of the International
Interior Design Association(Winter 2002), 21-26.
Zummos, S. M., & Karol, M. H. (1996). Indoor air
pollution: Acute adverse health
effects and host susceptibility. Environmental Health, January-February,
25-29.
Abstract Information & Notes
Michael R. Gray, M.D., M.P.H.
Date of talk:
Thursday, June 19, 2003, 4:30pm
300 S.
Ocotillo
Phone:
520/586-9111
Benson, AZ 85602
Fax:
520/586-9091
E-mail:
[email protected]
Medical School Attended:
University of Cincinnati, College of Medicine; University of Illinois
School of Public Health
Major and date of Graduation:
M.D., 1974; M.P.H., 1978
Residency:
1975-77 Internal Medicine, Cook County Hospital, Chicago, IL; 1977-78
Chief Resident, Internal Medicine, Cook County Hospital, Chicago,
IL
Current Job Description:
Medical Director, Progressive Healthcare Group, Benson, AZ, 1988-present;
Medical Director and Board Chairman, Benson Ambulance Service, Benson, AZ,
1990-present
Other Information:
Published several articles
Disclosure Statement:
Cholestyramine
SPEECH TITLE:
“Mold, Mycotoxins & Public Health: a Clinicians
Perspective”
The speaker has provided the information
below.
1.) Goals and objectives: To help
clinical practitioners recognize and treat systemic illnesses associated with
mixed molds and mycotoxins
2.) Outline of talk/abstract: A
descriptive epidemiologic survey of the results of clinical evaluations of 250
patients exposed to mixed, toxigenic, structural molds and mycotoxins will be
presented
3.) Conclusion of what is to be learned: How to
evaluate and manage mycotoxicosis
4.) References:
Bibliography provided with handouts.
Mold, Mycotoxins, and Public
Health
Michael R. Gray, M.D., Robert C.
Crago, Ph.D., Kaye Kilburn, M.D.
Clinical evaluations of 250 patients compiled from
1994-2003, are presented in a clinically based descriptive epidemiologic study
with results compared to unexposed controls, general reference ranges, and
national databases for multiple parameters measured. Abnormalities of immune function,
pulmonary function, and neurocognitive function and impairment, are presented
confirming that exposure to mixed toxigenic structural filamentous, terrestrial
molds (e.g., Stachybotrys sp., asperigillius/Penicillium sps., Fusarium,
etc), and their associated mixed mycotoxins (eg., aflatoxin, rubrotoxin,
sterigmatocystin, vomitoxin, tremulotoxin, zearalanone, trycothecenes, T-2
toxin, etc.) collectively induce mycotoxicosis, a clinical syndrome
resulting from infectious and toxic neuroimmunopathophysiologic effects. Key features include: immune toxicity
with hyper activation and simultaneous suppression, small airways obstruction
and reactivity, and neurological toxicity involving multiple neurophysiologic
processes (e.g., balance, visual perception, peripheral vision, simple and
choice reaction time, blink reflex, etc.).
21st ANNUAL INTERNATIONAL
SYMPOSIUM
ON MAN & HIS
ENVIRONMENT
Friday, June 20, 2003
7:00 a.m.
Breakfast with Drucker Labs, Michelangelo Room
8:00 a.m.
ANNOUNCEMENTS/MODERATOR: Sherry A. Rogers,
M.D.
8:05
Eugene A. Shinn, U.S. Research Geologist, Geological Survey, St.
Petersburg, FL: “Update:
Transoceanic Soil Dust Transport and Medical
Implications”
8:25
Q & A
8:35
Lester Friedlander, B.A., D.V.M., Wyalusing, PA: “Molds and Mycotoxins in the Food
Chain”
8:55
Q& A
9:05
Katherine Warsco, Ph.D., Department of Interior Design, East
Carolina University, Greenville, NC:
“Interior Design for a Mold-Free
Environment”
9:25
Q & A
9:35
Aristo Vojdani, Ph.D., M.T., Director, Immunosciences
Laboratories, Inc., Beverly Hills, CA:
“Immunotoxicology of Molds and Mycotoxins”
9:55
Q & A
10:05
BREAK WITH EXHIBITORS
10:30
Bruce Small, Director of Envirodesic Certification Program,
Georgetown, Ontario, Canada: “Prescription for Preventing Mold and for Mold
Remediation”
10:50
Q & A
11:00
Martha Stark, M.D., Department of Psychiatry, Harvard Medical
School, Boston, MA:
“Mysterious Mental Illnesses, Pernicious
Poisons”
11:20
Q & A
11:30
John H. Boyles, Jr., M.D., Dayton Ear, Nose & Throat Surgeons
Inc., Centerville, OH: “Diagnosis & Treatment of Inhalant and Mold
Allergy”
11:50
Q & A
12:00n
OPEN LUNCH
MODERATOR: Kaye H. Kilburn, M.D.
1:00 p.m.
David C. Straus, Ph.D., Department of Microbiology, Texas Tech
University Health Science Center, Lubbock, TX: “The Role of Fungi in Sick Building
Syndrome”
1:20
Q & A
1:30
Tapani Tuomi, Laboratory Chief, Finnish Institute of Occupational
Health, Helsinki, Finland:
“Mycotoxins in Cigarettes and in Tobacco
Smoke”
1:50
Q & A
2:00
Mohamed B. Abou-Donia, Ph.D., Duke University Medical Center,
Durham, NC: “Acute Exposure to Sarin Increases Blood Brain Barrier
Permeability & Induces Neuropathological Changes in the Rat Brain: Dose
Response Relationship”
2:20
Q & A
2:30
Sherry A. Rogers, M.D., Medical Director, Northeast Center for
Environmental Medicine, Author, Syracuse, N.Y.: “Rescuing the Heart as Toxic Target
Organ”
2:50
Q & A
3:00
BREAK WITH EXHIBITORS
3:30
Bruce Jarvis, Ph.D., Department of Chemistry & Biochemistry,
University of Maryland, College Park, MD: “History and Toxicology of
Mycotoxicoses”
3:50
Q & A
4:00
David C. Straus, Ph.D., Department of Microbiology, Texas Tech
University Health Science Center, Lubbock, TX: “Recent Research in Sick Building
Syndrome”
4:20
Q & A
4:30
William J. Rea, M.D., Director, Environmental Health Center
B Dallas, Dallas, TX: “Treatment of Mold & Mycotoxin
Exposure”
4:50
Q & A
5:00
Panel Discussion: “How and when to remodel a moldy
building” Donald P. Dennis,
M.D., Larry Foster, Professor Tang G. Lee, AAA, David C. Straus, Ph.D., Bruce
Small, and Tapani Tuomi
6:00
RECEPTION WITH THE EXHIBITORS
FRIDAY, JUNE 20,
2003
ABSTRACTS
AND
HANDOUTS
Abstract Information & Notes
Eugene A. Shinn
Date of talk:
Friday, June 20, 2003, 8:05am
U.S. Geological Survey
Phone:
727/803-8747 ext.3030
600 4th Street South
Fax:
727/803-2032
St. Petersburg, FL 33701
E-mail:
[email protected]
Medical School Attended:
University of Miami, Florida - honorary Ph.D., University of South
Florida, 1998
Current Faculty Appointments:
Adjunct professor University of South Florida and University of
Miami
Current Job Description:
Research Geologist
Other Information:
Through geology/earth surface processes, I developed a theory that
pathogens transported in African dust to the Caribbean caused the ongoing demise
of coral reefs - this led to human health effects, especially asthma in the
Caribbean.
Disclosure Statement:
SPEECH TITLE:
“Update: Transoceanic Soil Dust Transport and Medical
Implications”
The speaker has provided the information
below.
1.) Goals and objectives:
2.) Outline of talk/abstract:
3.) Conclusion of what is to be learned:
4.) References:
Update: Transoceanic Soil Dust
Transport and Medical Implications
E.A. Shinn, Christina A. Kellogg, Dale W. Griffin, Carles W. Holmes, Virginia H. Garrison, Douglas B.
Seba
Increasing transoceanic dust flux may affect public
health, especially among chemically sensitive and medically compromised
individuals. Indigenous dust in the
western U.S. is known to transport the valley fever pathogen Coccidioides
immitis, but the effects of African dust, which transports bacteria,
viruses, and spores of fungi, including numerous species of Aspergillus
have not been investigated until recently.
Estimates of annual African dust flux to the Amazon
basin, Caribbean, and southeast U.S. range into the hundreds of millions of
tons. Flux of African dust to the
Caribbean and U.S. has increased dramatically since 1970 because of the ongoing
drought in North Africa. The
drought is a result of fluctuations in the North Atlantic Oscillation (NAO), and
long-term dust monitoring in Barbados and Miami shows a direct correlation with
the NAO. The incidence of asthma on
Barbados and Trinidad, documented by the Caribbean Allergy and Respiratory
Association (CARA), is among the highest in the world and has increased 17- fold
since 1973. Recent studies in
Trinidad indicate a correlation between dust events and pediatric admissions for
respiratory distress.
Of the over 250 microbial isolates identified from
African dust, roughly 30% were pathogenic; capable of infecting plants, animals,
or humans with compromised immune systems.
In addition to viable bacteria, fungi and viruses dust contains organic
debris, insects, and various toxic metals including naturally occurring
radioactive isotopes Be-7 and Pb-210.
Recent studies indicate that iron in African dust triggers red tides that
in turn aerosolize toxins that have pronounced effects on humans living near
marine shorelines.
Abstract Information & Notes
Lester C. Friedlander, B.A., D.V.M.
Date of talk:
Friday, June 20, 2003, 8:35am
P.O. Box 534 Phone: 570/746-3072
Wyalusing, PA 18853 Fax: 570/746-1386
E-mail:
[email protected]
Undergraduate School Attended:
Northland College, Ashland, WI
Araneta University Foundation, College of Veterinary Medicine, Metro
Manila, Philippines
Major and date of Graduation:
BA, 1971: DVM,1979
Board Certifications:
None
Current Faculty Appointments:
None
Current Job Description:
Independent Researcher, Consultant
Other Information:
Chronic Wasting Disease Workshop – Veterinary Professional C.E. UNIV. of Minnesota, College of
Veterinary Medicine. Co-Authored: Accumulation 0f 2.8 Dihydroxyadenine in Bovine
Liver, Kidneys, and Lymph Nodes.
Journal of Veterinary Pathology
28:99-109(1991)
Disclosure Statement:
None
SPEECH TITLE: “Molds and Mycotoxins in the Food
Chain”
The speaker has provided the information
below.
1.) Goals and objectives: To
inform and educate health professionals that there are molds and mycotoxins in
the foods we eat. Furthermore to explain and list the symptoms of mycotoxins in
both humans and animals
2.) Outline of talk/abstract: Please
refer to page 2
3.) Conclusion of what is to be
learned: There are many mycotoxins in our
environments with similar symptoms in humans
4.) References:
1. Black, Kevin. “Aflatoxins in Corn” (Dec.
1996): 2 pag. Online. Internet. 20, Feb. 1997
2. Cheeke, Peter R., Lee R. Shull. ed.
Natural Toxicants in Feeds and Poisonous Plants. Westport: AVI Publishing
1985.
3. Hascheck, Wanda M. “Selected Mycotoxins Affecting
Animal and Human Health”: Academic Press 2002
4.
GIPSA, Technical Services Division: “ Grain Fungal Diseases &
Mycotoxin Reference” USDA 2003
5. http://vm.cfsan.fda.gov/~frf/iupac.html
http://www.btny.purdue.edu/NC129/
http://pasture.ecn.purdue.edu/~grainlab/
http://www.ces.ncsu.edu/drought/dro-29.html
http://www.aces.edu/department/grain/ANR767.htm
http://www.ianr.unl.edu/pubs/pesticides/g790.htm
http://www.ipm.iastate.edu/ipm/icm/1998/1-19-1998/btdiscon.html
http://www.scisoc.org/feature/Btcorn/Top.html
Lester Friedlander, B.A.,
D.V.M.
1.)
Goals and
objectives:
To inform
and educate health professionals that there are molds and mycotoxins in the
foods we eat. Furthermore, to explain and list the symptoms of mycotoxins in
both humans and animals.
2.)
Outline of
talk/abstract:
I.
Introduction
A.
Condensed History of Mycotoxicology (Early 1960’s to
Present)
II.
Classification of
Mycotoxins
A.
Aflatoxins
B.
Trichothecenes
C.
Fumonisins
D. Zearalenone
E.
Ochratoxin
A
F.
Ergot
Alkaloids
III.
How We Consume
Mycotoxins
A.
How mycotoxins get into
your Food
1.
Growth
2.
Storage
3.
Transportation
B.
Mycotoxins Carried by
Animals
1.
General
Carriers
2.
Species
Specific
3.
Rarities
IV.
Conclusion
A.
Current Mycotoxin
Standards
B.
High risk
areas
Abstract Information & Notes
Katherine Warsco, Ph.D.
Date of talk:
Friday, June 20, 2003, 9:05am
East Carolina University
Phone:
252/328-6929
152 Rivers Building, ECU
Fax:
252/328-4276
Greenville, NC 27834
E-mail:
[email protected]
Medical School Attended:
NA (Ph.D. College of Human
Ecology, Michigan State University)
Major and date of Graduation:
Family and Child Ecology, 1988
Residency:
NA (Doctoral Internship – Energy Information Administration, US
Department of Energy, Washington D.C.)
Current Faculty Appointments:
Interior Design Program, School of Human Environmental Sciences, East
Carolina University, Greenville, NC
Current Job Description:
Chair, Department of Apparel Merchandising and Interior Design, School of
Human Environmental Sciences, East Carolina University, Greenville,
NC
Other Information:
Founder of Environmental Quality in Interiors Network, Interior Design
Educators Council
Disclosure Statement:
None
SPEECH TITLE: “Interior Design For A Mold-Free
Environment”
The speaker has provided the information
below.
1.) Goals and objectives: This
speech will provide an overview of current thinking within the professional
community of interior design with regards to methods of proactive environmental
design. Objectives include
identifying current >best practices= advice of a general and conceptual nature for the types
of mold problems experienced in many homes, schools and office facilities. Current thinking is based on a
comparison of philosophical positions of the interior design community evident
among practitioners and educators of interior design and agricultural experiment
station cooperative extension specialists.
2.) Outline of talk/abstract: Presented
here are proactive approaches to achieving mold-free building interiors along
with strategies for mold remediation in building interiors resulting from water
leakage, condensation, or flooding.
Interior design decisions impact prevalence of moisture and nutrient
matter through space planning and specification of interior finishes, fabrics,
furnishings, and equipment. Also,
covered are current efforts in the development of certification programs to rate
building materials and interior products.
This speech concludes with trade-offs between >best practices= advice and other considerations regarding up-front
building costs, building maintenance and operation, and building occupant
comfort, health and well-being.
3.) Conclusion of what is to be learned: Interior
design practice and education contribute to the prevention and remediation of
mold growth in indoor environments.
The literature points to a need for interior designers to be educated
from a perspective of eco-materialism that links indoor material choices to
building occupant health.
4.) References: See
attached
Interior
Design For A Mold-Free Environment
Katherine
Warsco, Ph.D.
East
Carolina University
Goals and
objectives
This
speech will provide an overview of current thinking within the professional
community of interior design with regards to methods of proactive environmental
design. Objectives include
identifying current ‘best practices’ advice of a general and conceptual nature
for the types of mold problems experienced in many homes, schools and office
facilities. Current thinking is
based on a comparison of philosophical positions of the interior design
community evident among practitioners and educators of interior design and
agricultural experiment station cooperative extension
specialists.
Presented
here are proactive approaches to achieving mold-free building interiors along
with strategies for mold remediation for moisture intrusion due to water
leakage, condensation, and flooding.
The US Environmental Protection Agency and East Carolina University
supported the development of an environmental education curriculum. A design competition and teacher’s
supplement were developed to assist educators and students of interior design to
explore linkages between microclimate, architectural shell, interior space plan,
mechanical systems, materials specification, indoor air quality, and
environmental illness. Excerpts
from student submissions to this competition, shown in this presentation serve
to illustrate interior design for a mold-free environment.
Proactive
Approach
Interior
design decisions impact prevalence of moisture and nutrient matter that support
microbial growth through space planning of the building interior and
specification of interior finishes, furnishings, fabrics, and equipment. Strategies for removing, isolating, and
diluting moisture and nutrient matter in the building interior follow two
schools of thought; they typically either focus on the natural environment
(i.e., healthy planet), or they focus on the interaction of the building and the
building occupant (i.e., healthy people).
Architectural and engineering ventilation strategies illustrate these
approaches. A ‘healthy planet’
design approach might use a negative pressurized architectural shell that
maximizes airflow through interior breathing zones. Benefits to the planet include reduced
fossil fuel consumption for heating, ventilating and air conditioning. A ‘healthy people’ design approach might
use a positive pressurized architectural shell that balances and filters airflow
within interior breathing zones.
Although ventilation strategies are largely within the domains of
architecture and engineering, Interior design decisions intertwine with those of
allied building fields to impact the ultimate success of these approaches to
address mold-free design.
Ventilation
(dilution) strategies are addressed through space planning and design of
mechanical systems.
a.
Arranging
fenestration and interior partitions to facilitate natural ventilation will dry
moisture-laden areas and exhaust indoor contaminants.
b.
Arranging
air inlets and air outlets to facilitate cross-ventilation will dry
moisture-laden stored items and exhaust indoor
contaminants.
c.
Specifying
fans will exhaust moisture-laden air prevalent in rooms such as kitchens,
bathrooms, hobby rooms, and utility rooms.
d.
Specifying
air-to-air exchanger units can be used to filter incoming air for interior
living spaces and to exhaust contaminants at their source.
Reactive Approach
Strategies
to minimize exposure to contaminants in indoor air as a result of moisture
intrusion focus on their removal, isolation, and dilution. These strategies are
a response to flooding and damage control for water leakage and
condensation.
Caveats to ‘best practices’
advice
Important trade-offs
should be factored into design decisions between ‘best practices’ advice and
other considerations regarding upfront building costs, building maintenance and
operation, and building occupant comfort, health and well-being. These considerations are relevant to
ventilation strategies and specification of interior products.
Procedures
for operating mechanical systems, designing passive convection systems, and
tightening the architectural shell to address reductions in energy consumption
can be counterproductive to occupant health.
Certification Programs
& Consultancies
Certification
programs and consultancies have emerged in the fields of building sciences and
industrial hygiene. Current
efforts in the development of certification programs to rate building materials
and interior products include the following:
a.
Leadership
in Energy and Environmental Design (LEED) program is a voluntary certification
program that analyzes content of building materials in new facilities (US Green
Building Council, 2002; Mendler, 2002).
Beginning with exterior materials, the program is currently focusing on
interior materials for commercial buildings and eventually will develop a
materials rating system for remodeling of old buildings. Criteria of this program include
recycled content, energy efficiency, and VOC emissions.
b.
Air
Quality Sciences, Inc. has a Greenguard certification program that rates
building materials according to biologicals and toxins (Air Quality Sciences,
Inc., 2002).
c.
Industrial
Hygiene association regulates a mold remediation certification program that has
been developed along the lines of asbestos removal and radon mitigation
(American Industrial Hygiene Association’s EMLAP Program).
d.
McDonough
Braungart Design Chemistry (MBDC) and Environmental Protection Encouragement
Agency (EPEA) provide consulting services on chemical composition of interior
products from the perspective of ‘cradle-to-cradle’ impact on the natural
environment and wellness of building occupants (McDonough, 2003).
The Interior Design
Community
Interior design practice
and education contribute to the prevention and remediation of mold growth in
indoor environments. The literature
points to three prevailing philosophical perspectives with regards to interior
design practice that influences approaches to achieving a mold-free
environment.
A
traditional materialist philosophy, Indicative of mainstream interior design
practice values materials for their appearance, durability, and availability
(Nielson & Taylor, 2002).
Designers subscribing to this philosophy have focused on client
considerations to the exclusion of ecological considerations of protecting and
preserving the natural environment.
If economy is a consideration, the expectation is that designing with
ecologically sensitive products will increase the cost for completion of the
project (Beecher and Davies, 2002).
Historically, knowledge underlying interior design decisions has been
held by an elite group and applied on behalf of an elite clientele.
An
eco-materialism philosophy, indicative of a growing interest in the green design
movement and sustainable design movement values materials for their
environmental sensitivity over availability, convenience, or appearance (Beecher
and Davies, 2002). This philosophy
embraces an ecology-centered approach that expands traditional measures of
building performance (e.g., cost per square feet, minimum standards for air
quality) to include issues of building occupant comfort, satisfaction, and
overall well-being. Health factors
affecting material selections would include VOC emissions and susceptibility to
allergens and toxins. Long-term
environmental impact would be considered in tandem with upfront building costs
(Moussatche, King, and Rogers, 2002).
Knowledge based on the science of product quality can effect changes to
the way interior products are manufactured, the composition of interior
products, and the specification of products by the interior designer (McDonough,
2003).
A
Human ecology (Home Economics) philosophy, indicative of a cooperative extension
approach to design values materials for their durability and for wise use of
natural resources within a tradition of supporting health and wellness in the
family. This philosophy embraces a
holistic approach to design decisions that includes considerations of the
environment and human needs (e.g., University of Florida, University of
Minnesota, Kansas State University).
Knowledge based on science and best practices developed by federal and
state government (e.g., programs addressing disaster relief for flooding) is
translated to a layman’s language to empower the consumer.
Conclusions - Toward a
Hybrid Model of Benign Design
The
professional community of design education and practice could benefit from the
development of a design model that reflects a merger of values indicative of an
aesthetic tradition (beautiful design), a science of product quality evolving
from the environmental movement (contaminant-free design), and the cooperative
extension tradition of empowering individuals and families (user-driven
design). Needed to support
this model is a more comprehensive metrics to evaluate building performance
inclusive of measures of improved occupant health and well-being and life-cycle
analyses of interior products that provide measures of long-term impact to the
natural environment.
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Abstract Information & Notes
Aristo Vojdani, P.H.D., M.T.
Date of talk:
Friday, June 20, 2003, 9:35am
Immunosciences Lab., Inc.
Phone:
301/657-1077
8693 Wilshire Blvd., Suite 200
Fax:
310/657-1053
Beverly Hills, CA 90211
E-mail:
[email protected]
Medical School Attended:
Bar-Ilan University Ramat-Gan Israel
Major and date of Graduation:
Immunology 1976
Residency:
University of California Los Angeles 1979-2001
Board Certifications: Laboratory Medicine
Current Faculty Appointments: A Clinical Professor UCLA Dept. Neurobiology
Current Job Description:
Research in the field of Neuroimmunology at Immunosciences Lab. And at UCLA School of
Medicine
Disclosure Statement:
Part owner of Immunosciences Lab.
Inc., and have financial interest in the company.
SPEECH TITLE:
“Immunotoxicology of Molds and Mycotoxins”
The speaker has provided the information
below.
1.) Goals and objectives: To understand the impacts of molds and mycotoxins on
the human immune system
2.) Outline of talk/abstract: 1. Sign
and symptoms of patients exposed to toxigenic molds in water-damaged
building. 2. Detection of mucosal immune response to
molds. 3. Detection of cellular and humoral immune
responses to molds and mycotoxins.
4. Neurotoxicity induction
by molds and mycotoxins.
3.) Conclusion of what is to be learned: A.
Exposure to toxigenic molds and mycotoxins can induce type 1 to type 4
allergic reactions. B. Allergy evaluation by skin test or in
vitro tests for detection of IgE mediated allergies are not enough for detection
of molds induced toxicity. C. Prolonged and intense exposure to molds
and mycotoxins is associated with disorders of mucosal, cellular and humoral
immune system.
4.) References:
1. Vojdani
et al., Antibodies Against Molds and Mycotoxins after Exposure to Toxigenic
Fungi in a Water Damaged Building (submitted)
2. Mahfoud
R., et al., The Mycotoxin Patulin Alters the Barrier Function of the Intestinal
Epithelium: Mechanism of Action of the Toxin and Protective Effect of
Glutathione. Toxicology and Applied
Pharmacology 181:209, 2002
Abstract Information & Notes
Bruce Small
Date of talk:
Friday, June 20, 2003, 10:30am
Small & Rubin Ltd.
Phone:
905/702-8615
100 Rexway Drive
Fax:
905/873-6260
Georgetown, Ontario L7G 1R5
E-mail:
[email protected]
Canada
Medical School Attended:
University of Toronto, Engineering Science, B.A.Sc., Southern Illinois
University, Physics and Design, M.S. 1975
Current Job Description:
Director of the Enviorodesic Certification Program, a private sector
initiative to identify and foster the development of building materials and
other products that will lead to healthier indoor
environments.
Other Information:
Executive Director of Technology and Health Foundation, a Canadian
charity focused on environmental health.
Disclosure Statement:
Icynene Inc. and Cogent Environmental Solutions
SPEECH TITLE:
“Prescription for Preventing Mold and for Mold
Remediation”
The speaker has provided the information
below.
1.) Goals and objectives: To outline
common causes of mold growth and regrowth in buildings. To outline primary means of preventing
mold growth and regrowth in buildings.
2.) Outline of talk/abstract: Existing
building and maintenance practices predispose many buildings to mold
growth. Current mold remediation
methods and building reconstruction practices may also lead to mold
regrowth. Environmental physicians
are in a unique position to specify effective building science principles to
promote mold-free buildings and more effective remediation. When designed, built and maintained with
sufficient thought and care, there is no reason for buildings to go
moldy.
3.) Conclusion of what is to be learned: Proper use
of rain screens, air barriers, and vapor barriers can alleviate some of the
primary causes of building envelope moisture penetration and mold growth. Timely maintenance is also
paramount. Homeowners, school
boards and building managers armed with this knowledge are in a better position
to avoid occupant mold exposures.
Physicians can play a role by advocating the use of good building science
to prevent mold growth.
4.) References: To be
included in presentation notes.
Useful web sites on building science for avoiding mold
growth:
http://www.aiha.org/GovernmentAffairs-PR/html/prmoldsources.htm
http://www.cdc.gov/nceh/airpollution/mold/moldfacts.htm
http://www.epa.gov/iaq/molds/
http://www.buildingscience.com/housesthatwork/default.htm
http://www.buildingscience.com/resources/mold/default.htm
http://www.envirodesic.com/sfl/HomeEnergyArticle.pdf
Abstract Information & Notes
Martha Stark, M.D.
Date of talk:
Friday, June 20, 2003, 11:00am
3 Ripley St.
Phone:
617/244-7188
Newton Centre, MA 02459-2209
E-mail:
[email protected]
Medical School Attended:
Harvard Medical School
Major and date of Graduation:
M.D., 1974
Residency:
Adult Psychiatry Residency - The Cambridge Hospital/Cambridge,
MA
Child Psychiatry Fellowship - Massachusetts Mental Health Center/Boston,
MA
Board Certifications:
None (Board-Eligible in Adult and Child/Adolescent
Psychiatry)
Current Faculty Appointments:
Faculty: Harvard Medical School; Boston Psychoanalytic Institute;
Massachusetts Institute for Psychoanalysis; Center for Psychoanalytic Studies,
Massachusetts General Hospital; Department of Continuing Education,
Massachusetts Mental Health Center; Continuing Education Program, Massachusetts
School of Professional Psychology; and Program of Continuing Education, Smith
College School for Social Work.
Current Job Description:
Private practice of psychiatry/psychoanalysis; various faculty
appointments and teaching responsibilities; teaching/supervising analyst at
several local psychoanalytic institutes; speaking engagements at training
institutes around the country; completing fourth book and at work on fifth
book
Other Information:
Author of four books
Disclosure Statement:
none
SPEECH TITLE:
“Mysterious Mental Illnesses, Pernicious
Poisons”
The speaker has provided the information
below.
1.) Goals and
objectives:
a.
To understand that
mycotoxins have the power both to intoxicate and to poison
b.
To appreciate all the
mysterious ways in which mycotoxins can affect the mind (and the
brain)
2.) Outline of
talk/abstract: Mycotoxins have figured
more prominently in human affairs than most would have suspected B in both good ways and
bad. They have been used since
earliest times as mind-altering hallucinogens and, as such, have promoted
psychedelic/mystical experiences.
Furthermore, evidence suggests that these poisons have also been
responsible for “bewitching” people (as Happened, for example, in Salem,
Massachusetts, during the 17th century). Particularly virulent strains have been
known to cause bizarre physical ailments, mystifying mental disorders, and, in
some instances, a slow steady decline into deathBwhich is why some
mycologically savvy mystery writers have recognized that some mycotoxins are
perfect murder weapons! Finally,
mycotoxins are now understood to have been responsible for wiping out whole
groups of people who had the misfortune of consuming foods contaminated with
mold (as happened, for example, during the Irish potato
famine).
3.) Conclusion of what is
to be learned:
a. To develop a healthy respect for
mycotoxins and their potency
b. To recognize that patients with certain
mysterious mental illnesses (patients once described as simply "mad" or
"deranged") are actually suffering from poisoning by
mycotoxins
4.)
References:
Hudler, G.W. (2000). Magical Mushrooms, Mischievous
Molds. Princeton, NJ: Princeton
University Press. Princeton and
Oxford: Princeton University Press
Matossian, M.K.
(1989). Poisons of the Past:
Molds, Epidemics, and History.
New Haven and London: Yale University Press.
Schaechter, E. (1998). In the Company of Mushrooms: A
Biologist=s Tale. Cambridge, MA: Harvard University
Press.
MYSTERIOUS MENTAL ILLNESSES, PERNICIOUS POISONS
Martha Stark. M.D. -- Harvard Medical School
Harvard Health Letter (January
2003) – “The
Truth About Mold”
“Most experts say there's more fear than fact to 'toxic
mold.’”
neither mental illness nor
mental health can be meaningfully understood without reference to the brain and
the nervous system
our minds do not exist in a vacuum, they are linked to the chemistry of
the brain
molds can have a negative
effect on human health in three ways:
1. as pathogens (whereby they take
up residence either in or on the body of those whose immune systems are
compromised)
result: infectious
symptoms
2. as allergens (whereby they
provoke either immediate or delayed hypersensitivity reactions in those who are
sensitized to molds)
result: allergic
symptoms
3. as toxins (whereby they poison
otherwise healthy individuals)
result: toxic symptoms
neurotoxic symptoms when the brain is
involved
moisture + warmth --->
germination of the spore
balloon-like protuberances (hyphae) that exude powerfully toxic
digestive enzymes, which systematically break down whatever they can find to
feed upon
the hyphae then take back in what's left of the ravaged substrate, where
it is further degraded in order to nourish the mold's relentless
growth
what happens when mycotoxins
come into contact with the brain?
although we have yet to understand the exact mechanism of action whereby
mold toxins affect how we feel, think, and act, there is much that we can
learn about both mental illness and mental health by studying the impact of
various mycotoxins on the brain and, more particularly, on brain
neurotransmitters and their receptors
in fact, mycotoxins have been found to bear a striking resemblance to
specific neurotransmitters in the brain--especially
serotonin
in other words, mycotoxins are in a prime position to compete with
serotonin for (re-)uptake at various postsynaptic 5-HT (5-hydroxytryptamine)
receptor sites
in essence, mycotoxins appear to affect the central nervous system at
the level of the synapse
Claviceps
purpurea - a
perniciously poisonous mold that produces a variety of mycotoxins known as
ergot alkaloids
ingestion of products made from ergot-infected rye (like bread)
--->
ergot poisoning, a disease that is thought to
have affected the physical and mental health of people throughout much of the
Middle Ages
gangrenous
ergotism
involves an ergot alkaloid that can be such a powerful vasoconstrictor that it
can restrict entirely the flow of blood to body parts, particularly the
extremities
convulsive, hallucinogenic
ergotism
involves an ergot alkaloid that has a more direct effect on the
brain
symptoms range from (1) vomiting, diarrhea, and general lethargy; to (2)
a sensation of ants crawling on the skin (formication), twitching, and grotesque
distortion of limbs; to (3) vivid hallucinations and seizures similar to those
associated with epilepsy
the mental effects of ergot poisoning are said to be unremittingly
unpleasant: fright, outright panic,
and an inability to maintain a sense of distance in the face of such strange
experiences
the historian Mary
Matossian (in her book Poisons of the Past) has hypothesized that
“bewitched” people in central Europe between the 16th and 19th centuries were
actually exhibiting symptoms of ergot poisoning (both gangrenous and
convulsive)
furthermore, the women (and men) in Salem, Massachusetts, accused in
1692 of being witches (and wizards) either were themselves afflicted with
ergotism or, interestingly, were wrongly accused by others who had become
paranoid and delusional because they were afflicted with
ergotism
from earliest times,
mycotoxins have been implicated as the cause of several major human
epidemics
but, from earliest times, mycotoxins have also been found to produce
mind-altering, consciousness-enhancing, mind-expanding, bewitching,
intoxicating, inebriating, psychedelic, hallucinogenic experiences that have
afforded the user much pleasure
many of the most respected
Greek philosophers--like Plato and Socrates--were inspired to formulate
some of their greatest thoughts when they were under the influence of certain
“magical mushrooms” (and their mycotoxins)
hallucinogenic mushrooms (also known as 'shrooms) are still in use today as
recreational drugs
chemical analyses of 'shrooms
have determined that they contain psilocybin and psilocin, psychoactive
substances that closely resemble serotonin (the "feel good" hormone)--which
lends further credence to the hypothesis that all the major plant hallucinogens
contain substances similar in chemical composition to psychoactive chemicals
within the brain
1938 - birth of the psychedelic age
a young German chemist, Dr. Albert Hofmann, began experimenting
with lysergic acid, the chemical backbone of the ergot
alkaloids
five years later, he was able to synthesize lysergic acid
diethylamide--LSD
Dr. Hofmann described his first
unintentional use of LSD as a "not unpleasant intoxicated-like condition"
involving “interesting imagery” that lasted for several
hours
“...all objects appeared in unpleasant, constantly changing colors, the
predominant shades being sickly green and blue. When I closed my eyes, an unending
series of colorful, very realistic, and fantastic images surged in upon me. A remarkable feature was the manner in
which all acoustic perceptions (e.g., the noise of a passing car) were
transformed into optical effects, every sound invoking a corresponding colored
hallucination constantly changing in shape and color like pictures in a
kaleidoscope. At about one o'clock
I fell asleep and awoke the next morning feeling perfectly well.”
Hofmann noted that some of the
more bizarre symptoms he endured on subsequent “trips” were remarkably similar
to those accompany schizophrenia
amongst other things, schizophrenics frequently speak of having
out-of-body experiences and “interpret” sights and sounds in distinctly
idiosyncratic ways--much as he had when he was
“tripping”
Hofmann's experience certainly lent support to the hypothesis that
certain mental illnesses, initially presumed to be purely psychic in nature,
might actually have a biochemical cause
but actually long before Dr.
Hofmann's discovery of LSD, Indians in southern Mexico had discovered
these same mushrooms growing in the wild--intoxicating mushrooms that proved to
be hallucinogenic when ingested
the visions so produced were thought to be divinely inspired and
capable of leading to spiritual enlightenment
in the 1950s, Gordon
Wasson spent time in Mexico studying the effects of these inebriating
mushrooms
“The sacred mushrooms of Mexico
seize hold of you with irresistible power.
They lead to a temporary schizophrenia in which your body lies heavy as
lead on the mat ... while your soul flies off to the ends of the world and
indeed to other planes of existence.”
“I experienced
hallucinations...visions of palaces, gardens, seascapes, and mountains... With the speed of thought, you are
translated wherever you desire to be, and you are there, a disembodied eye,
poised in space, seeing but not seen, invisible, incorporeal. ...All of <your> senses are
equally affected, and the human organism as a whole is lifted to a place of
intense experience. A drink of
water ... is transformed, leaving you breathless with wonder and delight. The emotions and intellect are similarly
stepped up. Your whole being is
aquiver with life.”
“What is happening to you seems
freighted with significance, beside which the humdrum events of every day are
trivial. All these things you see
with an immediacy of vision that leads you to say to yourself: 'Now I am seeing for the first time,
seeing direct without the intervention of mortal eyes.’”
and in 1960, at the
Center for Research in Personality at Harvard University, Dr. Timothy
Leary (with his colleague Dr. Richard Alpert) was doing his own
experimenting with magical mushrooms
“I was whirled through an
experience which could be described ... as above all and without question the
deepest religious experience of my life.”
more generally, it would seem
that magical mushrooms (and their mycotoxins) are appealing in large part
because they transport the user into other realms where knowledge is
intuitive, non-linear, dynamic, rather than reasoned, linear,
ordered
intense experiences of vivid colors and abstract patterns alternate with
visions of mystical union, cosmic connectedness, and transcendence of the usual
boundaries of time and place
later still, none other than the
CIA began its own experimentation with the hallucinogenic drugs produced
by magical mushrooms
they were searching for a mind-control agent that would allow them
more effectively to interrogate suspected spies, preferably without the spy's
knowledge of this interrogation
but the magical mushrooms were
found to have many untoward and some potentially lethal side
effects
so by the late 1960s, early
1970s, all scientific experimentation (whether in the laboratories of academic
institutions or governmental agencies) had ground to a halt
the psychoactive ingredients in
magical mushrooms appear to alter a person's state of consciousness, affecting
how she feels, thinks, and acts
overall, her senses are heightened, her feelings are exaggerated, and
her perceptions are intensified
emotional changes may occur suddenly,
dramatically, unpredictably
the distinction between past, present, and future may become
blurred
cognitive impairment may take the form of fluctuating attention, a short
attention span, memory loss, word finding difficulties
there is often a profusion of vague ideas and a preoccupation with
philosophical and existential issues--but because of impaired judgment and
illogical thought processes, the person may imagine that she has “discovered”
new truths when, in fact, she is creating “word salads” (akin to those produced
by schizophrenics) that usually do not stand up to the light of
day
as noted earlier, although the
exact mode of action of mycotoxins in the brain has not yet been established,
presumably both LSD and psilocybin are psychoactive chemicals that alter how
we feel, think, and act by disrupting the action of the neurotransmitter
serotonin--a monoamine chemical messenger known to play a major role in the
regulation of mood, energy, appetite, libido, sleep, and cognitive
functioning
many of the effects of LSD are through serotonin-mediated pathways
(particularly those involving the dorsal raphe nucleus, which lies along the
midline of the brainstem and projects to most parts of the brain, including the
cerebral cortex and the limbic system)
the hallucinogenic effects of
LSD have mainly been attributed to the interaction of this drug with the
serotonergic system, but it seems more likely that there are complex
interactions of LSD with dopaminergic and noradrenergic target sites as
well
studies suggest that LSD
not only penetrates the blood-brain barrier but slips slyly into the
transmission site inside the nerve cells themselves
it can mimic serotonin to the point where the brain thinks it is
serotonin and consequently shoots it across the synaptic
cleft
when LSD reaches the other side, it is accepted by the serotonin receptor
sites (particularly the 5-HT2A receptor sites)--but now the jig is up, because
the LSD cannot carry the message any further
in essence, the LSD blocks or "antagonizes" the normal activity of the
serotonergic relay system
instead, the electrical impulse
(the action potential) generated by the LSD at the receptor site is redirected
more or less randomly down either new or less familiar pathways--pathways that
may not have been highly conditioned, pathways that may not have been frequently
traveled
it could be said that consciousness is “redirected” to unimprinted
areas of the cortex, thus the variety of "interpretations" of sensations,
emotions, and perceptions that accompany hallucinogenic
experiences
in fact, sensory perceptions
may blend in a phenomenon known as synesthesia, a cross-circuiting of brain
information in which a person sees sound, smells color, or hears
motion--evidence that there is a problem with sensory
integration
in sum, the work of Hofmann
and other researchers who have devoted their lives to studying mycotoxins
points not to a separation but to an association between the brain and the
mind
more specifically, biochemical events that take place in the brain with
respect to neurotransmitters and their receptors are the physical correlates of
psychic experiences that take place in the mind with respect to how a person
feels, thinks, and acts
indeed, the mind does not exist
in a vacuum; it is linked to the biochemistry of the brain
References:
Cook, Robin (1994). Acceptable Risk. New York: Berkley Books.
Grafton, Sue (1992). “I” is for Innocent. New York: Fawcett Crest.
Greene, Graham (1978). The Human Factor. New York: Simon and
Schuster.
Harvard Health Letter - Volume
28 - Number 3 - January 2003.
Hudler, George W. (1998). Magical Mushrooms, Mischievous
Molds. Princeton,
NJ: Princeton University
Press.
Kavaler, Lucy (1965). Mushrooms, Molds, and
Miracles. New York: A Signet Book.
Masters, Robert, & Houston,
Jean (2000). The Varieties of
Psychedelic Experience. Rochester, VT: Park Street Press.
Matossian, Mary K. (1989). Poisons of the Past. New Haven: Yale University
Press.
Ramachandran, Vilayanur, &
Hubbard, Edward. Hearing Colors,
Tasting Shapes.
In Scientific American, May 2003.
Restak, Richard M. (1994). Receptors. New York: Bantam.
Schaechter, Elio (1997). In the Company of Mushrooms. Cambridge, MA:
Harvard University Press.
Stahl, Stephen M. (2000). Essential Psychopharmacology, 2nd
edition. London: Cambridge University
Press.
Abstract Information & Notes
John H. Boyles, M.D.
Date of talk:
Friday, June 20, 2003, 11:30am
Dayton Ear, Nose & Throat Surgeons Inc.
Phone:
937/434-0555
7076 Corporate Way
Fax:
937/434-7413
Centerville, OH 45459
E-mail:
N/A
Medical School Attended:
Northwestern University Medical School, Chicago,
Illinois
Major and date of Graduation:
M.D., 1960
Internship:
Latter-Day Saints Hospital, Salt Lake City, Utah; Northwestern University
Medical School, Chicago, Illinois (1964-1967)
Board Certifications:
American Board of Otolaryngology and American Board of Environmental
Medicine
Current Faculty Appointments:
Assistant Clinical Professor, Wright State Medical
School
Current Job Description:
Private Practice - Dayton Ear, Nose and Throat Surgeons,
Inc.
Other Information:
Published several articles
Disclosure Statement:
None
SPEECH TITLE:
“Diagnosis & Treatment of Inhalant and Mold
Allergy”
The speaker has provided the information
below.
1.) Goals and objectives: How to properly diagnose and treat mold sensitivities
through allergic desensitization using SET and traditional build-up
therapy.
2.) Outline of talk/abstract: Practitioners must know the prevalent molds in their
geographic location, and be able to test the individual sensitivity for each
mold. In addition, they should be
able to test and properly treat TOE sensitivity.
3.) Conclusion of what is to be learned: Treatment of mold sensitivity is extremely important in
an allergic patient, and must be controlled before one goes on to testing of
food and chemical sensitivity.
4.) References:
Diagnosis & Treatment of
Inhalant and Mold Allergy
John H. Boyles, Jr.,
M.D.
For centuries, we have known that mold exposure and
infestation is injurious to human health.
In this presentation, we want to emphasize the importance of recognizing
fungus infections, and treating them effectively. This includes the controversial concept
of Candidiasis. We also seek to
explain the importance of fungus allergy, and how to diagnose and treat
it.
We will also show the importance of fungal contamination
of buildings, how it relates to human health, and how it may be
eradicated.
Abstract Information & Notes
David C. Straus, Ph.D.
Date of talk:
Friday, June 20, 2003, 1:00pm
Texas Tech University
Phone:
806/743-2523
Department of Microbiology
Fax:
806/743-2334
Texas Tech University Health Sciences Center
E-mail:
[email protected]
Lubbock, TX 79430
Graduate School Attended:
Loyola University of Chicago
Major and date of Graduation:
Microbiology - May 1974
Current Faculty Appointments:
Professor of Microbiology & Immunology
Current Job Description:
Teaching and Research
Other Information:
Member Sigma Xi, American Society for Microbiology, American Academy of
Microbiology
Disclosure Statement:
Assured IAQ7 of Dallas, TX
SPEECH TITLE:
“The Role of Fungi in Sick Building
Syndrome”
The speaker has provided the information
below.
1.) Goals and objectives: To educate the audience on how fungi produce the
phenomenon known as sick building syndrome
2.) Outline of talk/abstract: I will describe what organisms are important in sick
building syndrome and how they produce the associated
symptoms.
3.) Conclusion of what is to be learned: Fungi cause health problems inside buildings by the
production of spores and mycotoxins
4.) References:
Cooley et al. 1998. Correlation between the prevalence of
certain fungi and sick building syndrome.
Occup. Environ. Med 55:579-584. McGrath et al. 1999. Continually measured fungal profiles in
Sick Building Syndrome. Curr. Microbiol. 38:33-36.
The
Role of Fungi in Sick Building Syndrome
By David C. Straus,
Ph.D.
Texas Tech
University
Health Sciences
Center
Lubbock, Texas
79430
Man has known about the consequences of having mold (a form of fungi)
grow inside his buildings for over 3,300 years. Verses in the Old Testament of
the Bible (Leviticus 14:33-45) describe how mold infested houses should
not be occupied, and could potentially lead to the destruction of the house.
Therefore, it should not be surprising that mold-infestation of our buildings
still remains a problem. What is different now than in the time of Leviticus, is
we now know what the problematic fungi are and we know what products they
produce that we should be concerned with.
Sick Building Syndrome (SBS) is a lay term, which is characterized by a
constellation of symptoms. These symptoms include itchy eyes, congestion,
scratchy throat, nausea, headaches, fatigue, and decreased attention span. This
phenomenon was first described in 1982 and published in 1984 (1). It literally
means that there is something inside a particular building that can make people
sick. It does not usually refer to a bacterial pneumonia like Legionairre’s
Disease that can be a consequence of being in a building with a certain
bacterium in the air conditioning system. Legionairre’s Disease is caused by the
bacterium Legionella pneumophila and is an actual infection. In this
case, when the person leaves the building, the organism leaves with him. In the
case of SBS, the fungi (for the most part) stay inside the building. However, we
do know that fungal spores travel with us on and in our clothing
(2).
We are constantly breathing microorganisms, both inside
and outside, and the immune system of a healthy individual normally has no
problem clearing the lungs of these living particles. However, immunocompromised
individuals (like those with Acquired Immunodeficiency Syndrome or AIDS) are at
an increased risk of a fungal pneumonia due to the inhalation of living fungal
spores. Fungi can cause human disease by at least four different mechanisms.
They are 1) allergic rhinitis (hay fever), 2) hypersensitivity pneumonitis
(which is due to the sensitization and recurrent exposure to inhaled fungal
spores), 3) toxicity (certain fungi produce toxic substances called mycotoxins),
and 4) infection. The latter is not usually an important part of SBS, but the
possibility exists for it to occur.
We get into trouble with fungi or mold when we allow
them to grow inside our homes, schools, or commercial buildings. Fungi
essentially need four things to grow: food, water, oxygen, and the appropriate
temperature. If water enters a building where it should not be and cellulose
containing building structures becomes wet, mold can use the building material
as a food source. Fungi particularly like the paper on sheetrock, ceiling tiles
and pressed particleboard. They use these materials as a food source because
they are made of cellulose, which is the most abundant organic material on the
planet. It is the job of fungi to break down organic material. So we should not
be surprised when they begin to grow in our wet buildings. In fact, we should be
surprised if it did not happen.
We recently published several studies where we examined
the role of mold on building materials, in animals, and in SBS. The first study
was a two-year investigation of 48 U.S. public schools (3). In that study we
showed that spores of Penicillium species and the presence of
Stachybotrys species inside schools correlated with the prevalence of
SBS, and when these organisms were removed, and the conditions that allowed them
to grow in the first place were remediated, the SBS-associated symptoms were
significantly reduced.
In another study (4), examining a contaminated hotel in the Southwestern
United States, we showed that even though the outside fungal profile is
continually changing, the indoor fungal profile in a “sick building” tends to
remain unchanged. Because it appeared from the above studies that the inhalation
of Penicillium chrysogenum spores played a role in SBS, we undertook
studies to determine the consequences of long-term intranasal instillation of
Penicillium chrysogenum spores in a mouse model. We discovered that when
mice inhale Penicillium chrysogenum
spores, the spores remain viable for up to 36 hours in the lungs of these
animals (5). We later found that the
long-term inhalation of viable (but not nonviable) Penicillium
chrysogenum spores induced type 2 T-helper cell mediated (Th2) inflammatory
responses such as an increase in total and spore specific serum IgE and
IgG1, together with bronchial alveolar lavage fluid levels of
interleukins 4 and 5 and peripheral and airway eosinophilia, which are mediators
of allergic reactions (6). Finally, in an effort to elucidate ways to prevent
fungal mediated SBS, we evaluated fungal growth on cellulose-containing and
inorganic ceiling tile (7). We showed that inorganic ceiling tile did not
support the growth of Cladosporium, Penicillium and Stachybotrys
while the cellulose-containing ceiling tile did. These results demonstrate that
it will be possible to develop mold-resistant building materials and possibly
decrease the occurrence of SBS.
What then are the health effects of exposure to mold inside our
buildings? We believe that Penicillium and Stachybotrys are two of
the most important genera in SBS and we believe that these two organisms affect
people in different ways. Other workers have shown that Penicillium
species spores were good potentiators of asthma (8). As stated above, we have
shown that the long-term inhalation of viable Penicillium chrysogenum
spores by mice results in an inflammatory reaction in their lungs (6). As
regards Stachybotrys exposures, we believe that the reported health
effects are due to the mycotoxins and its role in SBS is probably due to the
production of these compounds. However, much more work needs to be done in this
area before this can be conclusively shown. Some of the most potent mycotoxins
produced by Stachybotrys chartarum are called trichothecenes. They are
potent inhibitors of protein synthesis (9). The symptoms most commonly reported
by individuals who have been exposed to S. chartarum include loss of
balance, hair loss, hearing loss, mucosal bleeding, rashes, and vomiting
(personal communications). The above symptoms are consistent with those observed
when trichothecene mycotoxins were injected intravenously (0.077 mg/kg) daily
for 5 days in patients with hepatic metastases. The well-known effect of the
trichothecene mycotoxins on rapidly dividing cells was the impetus for their
evaluation as antitumor drugs in the late 1970’s. The trichothecene examined in
these studies was 4,15-Diacetoxyscripenol or DAS (anquidine) (10). DAS in these
patients demonstrated no antitumor activity and was so toxic its use was
discontinued. The signs and symptoms of toxicity reported by these patients were
hair loss, vomiting, burning erythema, diarrhea, confusion, ataxia, fever,
chills, and hypotension.
In conclusion it appears that fungi are important in SBS but the exact
roles of their spores and mycotoxins remains to be elucidated. However, it
appears quite clear that the inhalation of high concentrations of fungal spores
is responsible for the respiratory complications (allergies, hypersensitivity
pneumonitis and asthma) associated with SBS. A high number of peer-reviewed
scientific publications are available to support this hypothesis (8, 11, 12, 13,
14, 15, 16, 17, 18). Although the data seem to indicate the importance of
Penicillium and Stachybotrys species in this phenomenon, we
believe that other fungi such as Chaetomium species (19),
Alternaria species (8), Memnoniella species (9), and
Aspergillus species (20) also play a role.
REFERENCE
1. Finnigan, M.S., Pickering, C.A.C., and Burge, P.S.
(1984). The sick building syndrome: prevalence studies. British Medical
Journal, 289,1573-1575.
2. Dart,
B.L., and Obendorf, S.K. (2000) Retention of Aspergillus Niger spores on textiles. In Nelson, C.N. and N.W. Henry
(ed). Performance of Protective
Clothing: Issues and Priorities for
the 21st Century: Seventh Volume, ASTM STP 1386. American Society for Testing and
Materials, West Conshohocken, PA, pg 251-268.
3. Cooley, J.D., Wong, W.C., Jumper, C.A., and Straus,
D.C. (1998). Correlation between the prevalence of certain fungi and sick
building syndrome. Occupational and Environmental Medicine, 55,
579-584.
4. McGrath, J.J., Wong, W.C., Cooley, J.D., and Straus,
D.C. (1999). Continually measured fungal profiles in sick building syndrome.
Current Microbiology, 38, 33-36.
5. Cooley,
J.D., W.C. Wong, C.A. Jumper, and D.C. Straus. (1999). Cellular and humoral response in an
animal model inhaling Penicillium
chrysogenum spores. Proceedings
of the Third International Conference on Bioaerosols, Fungi and Mycotoxins, pp
403-410.
6. Cooley, J.D., Wong, W.C., Jumper, C.A., Huston, J.C.,
Williams, H.J., Schwab, C.J., and Straus, D.C. (2000). An animal model for
allergic penicilliosis induced by the intranasal instillation of viable
Penicillium chrysogenum conidia. Thorax, 55,
489-496.
7. Karunasena, E., Markham, N., Brasel, T., Cooley,
J.D., and Straus, D.C., (2000). Evaluation of fungal growth on
cellulose-containing and inorganic ceiling tile. Mycopathologica 150:
91-95.
8. Licorish, K., Novey, H.S., Kozak, P., Firshter, R.D.,
and Wilson, A.F., (1985). Role of Alternaria and Penicillium
spores in the pathogenesis of asthma. Journal of Allergy and Clinical
Immunology, 76, 819-825.
9. Jarvis, B.B., Sorenson, W.G., Hintikka, E.L.,
Nikulin, M., Zhou, Y., Jiang, J., Wang, S., Hinkley, S., Etzel, R.A., and
Dearborn, D. (1998), Study of toxin production by isolates of Stachybotrys
chartarum and Memnoniella echinata isolated during a study of
pulmonary hemosiderosis in infants. Applied and Environmental
Microbiology, 64, 3620-3625.
10. Wannemacker, R.W., and Wiener, S.L. (1997).
Trichothecene Mycotoxins. In Textbook
of Military Medicine, Part I. Warfare, Weaponry, and the Casualty, Medical
Aspects of Chemical and Biological Warfare, (eds). Zajtchuk, R, and Bellamy,
R.F. Published by the Office of the Surgeon General, Chapter 34, pp
655-676.
11.
Apostolakos, M.J., Rossmore, H., and Beckett, W.S. (2001). Hypersensitivity pneumonitis from
ordinary residential exposures. Environmental Health Perspectives, 109,
979-981.
12.
Jaakkola, M.S., Nordman, H., Piipari, R., Uitti, J., Laitinen, J.,
Karjalainen, A., Hahtola, P., and Jaakkola, J. (2002). Indoor dampness and molds and
development of adult-onset asthma: A population-based incident case-control
study. Environmental Health Perspectives, 110,
543-547.
13. Jacob,
B., Ritz, B., Gehring, U., Koch, A., Bischof, W., Wichman, H.E., and Heinrich,
J. (2002) Indoor exposure to molds and allergic sensitization. Environmental Health Perspectives, 110,
647-653.
14. Dales,
R.E., Burnett, R., and Zwanenburg, H. (1991). Adverse health effects among adults
exposed to home dampness and molds.
American Review of Respiratory
Disease, 143, 505-509.
15.
Dhasmage, S., Bailey, M., Roven, J., Abeyawickrama, K., Cao, D., Guest,
D., Rolland, J., Forbes, A., Thien, F., Abramsch, M., and Walters, E.H.
(2002). Mouldy houses influence
symptoms of asthma among atopic individuals. Clinical and Experimental Allergy, 32,
714-720.
16. Downs, S.H., Mitakakis, T.L., Marks, G.B., Car,
N.G., Belousova, E.G., Leuppi, J.D., Xuah, W., Downie, J.R., Tobias, A., and
Peat, J.K. (2001). Clinical
importance of Alternaria exposure in
children. Respiratory and Critical Care Medicine,
164, 455-459.
17. Fung, F., Tappen, D., and Wood, G. 2000. Alternaria-associated asthma. Applied Occupational and Environmental
Hygiene, 150, 924-927.
18. Fergusson, R.J., Milne, L.J.R., and Crompton, G.K.
(1984.) Penicillium allergic
alveolitis: faculty installation of central heating. Thorax, 39,
294-298.
19. Abbott, S.P., Sigler, L., McAleer, R., McGough,
D.A., Rinaldi, M.G., and Mizell, G. (1995). Fatal cerebral mycoses cause by the
ascomycete Chaetomium strumarium. Journal of Clinical
Microbiology, 33, 2692-2698.
20. Hodgson, M.J., Morey, P., Leung, W.Y., Morrow, L.,
Miller, D., Jarvis, B.B., Robbins, H., Halsey, J.F., and Storey, E. (1998).
Building-associated pulmonary disease from exposure to Stachybotrys
chartarum and Aspergillus versicolor. Journal for Environmental
Medicine, 40, 241-249.
Abstract Information &
Notes
Tapani Tuomi
Date of talk:
Friday, June 20, 2003, 1:30pm
Finnish Institute of Occupational Health (FIOH)
Phone:
358-9-47472926
Arinatie 3 A
Fax:
358-9-5061087
Helsinki, Finland FIN-00370
E-mail:
[email protected]
School Attended:
Helsinki University of Technology
Major and date of Graduation:
DR, Chemical Engineering (Applied Microbiology),
1995
Current Faculty Appointments:
Docent in Environmental Chemistry and Microbiology, Helsinki Univ. of
Technology
Current Job Description:
Laboratory Chief, Laboratory of Chemistry and Microbiology, Finnish
Inst. Of Occupational Health,
Helsinki, Finland
Disclosure Statement:
None
SPEECH TITLE:
“Mycotoxins in Cigarettes and in Tobacco
Smoke”
The speaker has provided the information
below.
1.) Goals and objectives: To present current literature on the mycotoxin content
of tobacco products as well as research data on the carry-over of mycotoxins to
mainstream and side stream tobacco smoke
2.) Outline of talk/abstract: The harvesting and production of tobacco products is
vulnerable to contamination by mycotoxin producing fungi. There is evidence that tobacco products
may contain aflatoxins and aflatoxins have been suggested to contribute to the
cancer outcome of smokers. The talk
will review current literature on the mycotoxin content of tobacco
products. Potential exposure routes
are discussed and research data presented on the mycotoxin content of cigarettes
as well as data of an attempt to estimate the carry-over of mycotoxins to
mainstream and side stream tobacco smoke.
3.) Conclusion of what is to be learned: Tobacco products are potential sources of mycotoxins -
as are many other agricultural products.
Tobacco stored in curing barns may become contaminated with aflatoxin and
it is becoming recognized that aflatoxins should be monitored during the
production of tobacco products.
Recently, techniques have been developed to inhibit mycotoxin production
in refined agricultural products, including tobacco. The talk examines the evidence for the
carry-over of mycotoxins to mainstream and side stream
smoke.
4.) References:
Tuomi et al., 2001, Analyst, 126:1545-1550, El-Maghraby and Abdel_Sater,
Zentralbl Mikrobiol, 1993, 148:253-64; Subbiah V., USPO, 1997, U.S. Patent
5,698,599; Georggiett et al., Rev Fac Cien Med Univ Nac Cordoba 2000, 57:95-107,
Welty and Lucas, Appl Microbiol, 1969: 17:360-365
Mycotoxins in Cigarettes and in
Tobacco Smoke
Tapani Tuomi
Cigarettes are natural products produced from the leaves
of Nicotina tabacum. Before or after harvesting, tobacco leaves may
become infected by common sapphrophytic and/or pathogenic fungi. Particularly
fungi belonging to the following genus or genera, that have been established in
different studies, on a variety of tobacco products, raise concern that tobacco
products including cigarettes may contain mycotoxins: Aspergillus flavus,
Aspergillus fumigatus, Fusarium spp. (F. solani, F. moniliforme
and F oxysporum), Stachybotrys chartarum, Trichoderma
viride1,2,3. As of present, the aflatoxins B1-2 and
G1-2, T-2 toxin and zearalenone have been found in cigarettes or in
chewing tobacco1,2,4. Mycotoxins have not, however, been detected in
either side-stream or mainstream tobacco smoke. In one study, aflatoxins
artificially added to cigarettes were upon smoking detected in the cigarette
filter but not in tobacco smoke1.
During the smoking of cigarettes, gas-phase temperatures
reach 850°C at the core of the firecone5. Solid phase temperatures
reach 800°C at the core and 900 or greater at the char line5. Core
temperatures are high enough to carbonize the tobacco and produce an oxygen
deficient region where smoke constituents are formed through reductive
processes. Temperatures behind the char line drop rapidly to the range 200-400
°C within 2 mm of the char line, enabling steam distillation of tobacco
components5. Some 1200 chemical components, including nicotine,
n-parafines and terpenes are distilled into mainstream smoke in the region
behind the char line5. Side stream smoke is produced mainly between
puffs when the firecone temperatures are 200-300°C lower than during puffs, and
the smoke is convectively driven in the reverse direction of airflow
accompanying a puff5. This results in quantitative and qualitative
differences of individual components between mainstream and side stream smoke.
Side stream smoke is richer than mainstream smoke in cancerogenous nitrosamines
and in tar, as well as in nicotine5. Environmental tobacco smoke is
composed mainly of diluted side stream smoke, which as a result of emission and
distribution into ambient air differs from side stream smoke in particle size
and mass -distribution, as well as in the distribution of compounds between
particle and gas -phases5.
As
a result of these dynamic processes, resulting in the production of mainstream
smoke inhaled by the smoker and environmental tobacco smoke inhaled both by the
smoker and passive smokers, it is impossible to define the faith of mycotoxins
potentially present in cigarettes without performing chemical analysis of side
stream and mainstream smoke from native cigarettes and from cigarettes spiked
with mycotoxins already present in native cigarettes. Such tests cannot, as of
yet, be found in the literature. It is possible that aflatoxins or other toxins
originally present in raw or stored tobacco are neutralized by
ammoniation6. Different
curing processes might also affect the distribution of mycotoxins potentially
present in tobacco.
In
conclusion, tobacco products are potential sources of mycotoxins - as are many
other agricultural products. Tobacco stored in curing barns may become
contaminated with aflatoxin produced by Aspergillus flavus as well as
other mycotoxins, including fumitremorgins, produced by Aspergillus
fumigatus. It is becoming recognized that mycotoxins should be monitored
during the production of tobacco products.
Recently, techniques have been developed to inhibit mycotoxin production
in refined agricultural products, including tobacco. It has not been established
as of yet, however, that mycotoxins are carried-over to mainstream and side
stream smoke.
REFERENCES: 1El-Maghraby
and Abdel-Sater, Zentralbl Mikrobiol, 1993, 148: 253-64; 2Warke et
al., J. Food Prot., 1999, 62: 678-686; 3Verweij et al., JAMA, 2000, 284: 2875;
3Welty and Lucas, App Micro, 1969, 17: 360-365; 4Georgiett
et al., Rev Fac Cien Med Univ Nac Cordoba, 2000, 57: 95-107; 5Jenkins
et al., Mainstream and side stream tobacco smoke, In The chemistry of
environmental tobacco smoke: composition and measurement, M. Eisenberg, Ed,
Lewis Publishers, Boca Raton, Florida, 2000, p. 49-75; 6Subbiah V.,
USPO, 1997, U.S. Patent 5,698,599.
Abstract Information & Notes
Mohamed B. Abou-Donia, Ph.D.
Date of talk:
Friday, June 20, 2003, 2:00pm
Duke University Medical Center
Laboratory of Neurotoxicology
Phone:
919/684-2221
Dept. of
Pharmacology and Cancer Biology
Fax:
919/681-8224
Box 3813
E-mail:
[email protected]
Durham, NC 27710
Medical School Attended:
University of California, Berkeley, CA
Major and date of Graduation:
Agricultural Chemistry, 1967
Residency:
North Carolina
Board Certifications:
American Board of Toxicology: Academy of Toxicological
Sciences
Current Faculty Appointments:
Professor of Pharmacology and Cancer biology
Current Job Description:
Teaching Toxicology to medical and graduate students carrying out
research.
Disclosure Statement:
SPEECH TITLE: “Acute Exposure to Sarin Increases
Blood Brain Barrier Permeability and Induces Neuropathological Changes in the
Rat Brain: Dose Response Relationship”
The speaker has provided the information
below.
1.) Goals and objectives:
2.) Outline of talk/abstract:
3.) Conclusion of what is to be learned:
4.) References:
ACUTE EXPOSURE TO SARIN INCREASES
BLOOD BRAIN BARRIER PERMEABILITY AND INDUCES NEUROPATHOLOGICAL CHANGES IN THE
RAT BRAIN: DOSE RESPONSE RELATIONSHIP. MB
Abou-Donia1, AA Abdel-Rahman1, and AK
Shetty2,3.
Departments of1Pharmacology and Cancer Biology,
2Neurobiology, and 3Surgery (Neurosurgery), Duke
University Medical Center, Durham NC 27710
In this study, we evaluated the early changes in the
adult rat brain after a single exposure to different doses of sarin. Adult male
rats were exposed to sarin by a single intramuscular injection at a doses of 1,
0.5, 0.1, and 0.01 x LD50 corresponding to 100, 50, 10 and 1 mg sarin /kg body weight of animals. Twenty-four hours after this treatment,
both sarin-treated and vehicle-treated (controls) animals were processed for:
(i) plasma butyrylcholinesterase (BChE) activity; (ii) brain
acetylcholinesterase (AChE) and m2 muscarinic acetylcholine receptor (m2 mAChR)
ligand binding assays; (iii) analysis of blood brain barrier (BBB) permeability
using [H3] hexamethonium iodide uptake assay and immunohistochemistry
for BBB protein; and (iv) histopathological analyses of the brain using H&E
staining, and microtubule-associated protein (MAP-2) and glial fibrillary acidic
protein (GFAP) immunohistochemistry.
Animals treated with 1 and 0.5 x LD50 sarin exhibited a significant
decrease in plasma BChE (58-70% of control). Animals treated with 1 x LD50 also
exhibited a significant inhibition of AChE in the cerebrum, brainstem, midbrain,
and the cerebellum (54-69% of control) associated with a decrease in m2 mAchR
ligand binding in the cerebrum (39% of control). m2 mAChR ligand binding however, showed
a significant increase in the brainstem (250-300% of control) following exposure
to all doses of sarin. Analysis of [H3] hexamethonium iodide uptake
demonstrated a significant increase in BBB permeability in animals treated with
1xLD50 sarin. Where as, animals treated with 0.5XLD50 exhibited significant
increased in BBB permeability only in brainstem and midbrain. Quantitative
histopathological analysis in the latter group of animals also revealed a
significant decrease in the expression of BBB protein, a diffuse neuronal cell
death and a decrease in MAP-2 positive elements within the cerebral cortex and
the hippocampus, and degeneration of Purkinje cells in the cerebellum. While animals treated with 0.5 and 0.1 x
LD50 did not exhibit the above changes, animals treated with 0.5 x LD50 showed
Purkinje neuron loss in the cerebellum. Results of this study indicate that, the
early brain damage after acute exposure to sarin is dose-dependent, and that
exposure to 1 x LD50 sarin induces significant damage in many regions of the
adult rat brain by 24 hours after exposure. The early neuropathological changes
observed after a single dose of 1 x LD50 sarin could lead to a profound
long-term neuronal degeneration in many regions of the brain, and resulting
behavioral abnormalities. Supported, in part, by the U.S. Army Medical Research
and Materiel Command Contract: DAMD 17-98-C-8027.
Abstract Information & Notes
Sherry A. Rogers, M.D.
Date of talk:
Friday, June 20, 2003, 2:30pm
Northeast Center for Environmental Medicine
Phone:
315/488-2856
2800 W.
Genesee St.
Fax:
315/488-7518
Syracuse, NY 13219
E-mail:
N/A
Medical School Attended:
S.U.N.Y Health Sciences Center at Syracuse formerly Upstate Medical
Center, State University of New York
Major and date of Graduation:
1969
Board Certifications:
(1) Family Practice, (2) Environmental Medicine
Fellowship American College Nutrition, Fellowship American College
Asthma, Allergy & Immunology
Current Job Description:
Clinician 33 years, lecturer, author 14 books monthly referenced
newsletter 15 years
Other Information:
Latest book: Detoxify or Die, with over 700 references showing
reversibility of nearly all disease (Prestigepublishing.com or
detoxifyordie.com)
Disclosure Statement:
None
SPEECH TITLE:
“Rescuing the Heart as Toxic Target Organ”
The speaker has provided the information
below.
1.) Goals and objectives: Learn of the evidence that environmental chemicals are
unavoidably ubiquitous, bioaccumulate, and cause disease which can be
reversed.
2.) Outline of talk/abstract: The heart slowly bioaccumulate ubiquitous environmental
toxins and nutrient deficiencies which cause all symptoms. Reversing even the most severe heart
disease is possible when molecular biochemical principles are appreciated,
versus masking symptoms with drugs.
3.) Conclusion of what is to be learned: No cardiovascular problem is hopeless until the true
causes have been found.
4.) References:
Rea, WJ, Chemical Sensitivity, Vol.
I-IV, 1992-97, CRC Press, Boca Raton
Bralla, JA, Lord RS, Laboratory Evaluations, Molecular
Medicine, Meta Metrix, Norcross, GA, 2002
Beasley, VR, Trichothecane Mycotoxicosis, CRC Press,
Boca Raton, 1989
Rescuing the heart as toxic
organ:
Reversing the damage from
mycotoxins, Solanaceae, heavy metals,
pesticides, phthalates, styrene,
PCBs, hydrocarbons and other
xenobiotics
Sherry A. Rogers M.D., ABFP, ABEM, FACAAI,
FACN
prestigepublishing.com
Objectives: to
appreciate the enormous amount of evidence showing that environmental toxins are
C
ubiquitous and
unavoidable
C
bioaccumulate
C
cause nearly every
symptom and disease
imaginable
C
Using the heart as an
example of one target organ, we will show how medical science has now proven
that removal of toxins from the body allows healing, leaving the
prognostic value of the diagnosis or medical label
meaningless
Abstract:
The heart and cardiovascular system have a finite number
of recognizable symptoms to express imbalance and disease. Cardiac arrhythmias, angina, infarct,
congestive heart failure, mycarditis, hypertension, hypercoagulability,
hypercholesterolemia and vasculitis are among the most common. Scientists agree 95% of cancer is caused
by only two things: diet and environment.
And the same formula turns out to be true for a multitude of diseases
especially those of the cardiovascular system.
With this in mind, a logical first step would be to
identify nutrient deficiencies as well as toxic accumulations, and then proceed
to correct these. As an example,
multiple nutrient deficiencies are commonly observed to by the underlying
defects causing cardiac arrhythmia.
Instead it is treated as a deficiency of calcium channel blockers. This robs the patient of the opportunity
to identify the extremely common fatty acid and mineral deficiencies that lead
to damaged calcium channels. Added
to the nutritional deficiencies are commonly PCBs and mercury, as simple
examples of ubiqutously unavoidable xenobiotics, that also damage proper
function of calcium channels.
Clearly the patient has only one course to follow with medications, and
that is to slowly get worse, because no one has identified and fixed what is
broken. Meanwhile calcium channel
blockers cause MRI-proven shrinking and deterioration of the brain and
cognition.
On the other hand, damaged calcium channels have been
repaired, improving drug-dependent/resistant cardiac symptoms while reducing
medications. Clearly we are
proceeding in the wrong direction by seeing all heart disease as a deficiency of
multiple drugs, and scientific evidence will be presented for the rationale for
exchanging this approach for that of evidence-based molecular
medicine.
Conclusions:
regardless of the medical label applied to any malfunction in the heart, there
are usually identifiable nutrient deficiencies and toxic overloads which when
corrected, allow for reversal of disease with reduction of symptoms and
medications.
References:
Rea, WJ, Chemical Sensitivity, Volumes I-IV, CRC
Press, Boca Raton FL, or www.aehf.com, 1992-97
Bralley JA, Lord RS, Laboratory Evaluations in
Molecular Medicine, Institute for Advanced Molecular Medicine,
1-800-221-4640, Norcross GA, 2002
Beasley VR, Trichothecene Mycotoxicosis:
Pathophysiologic Effects, Volume II, CRC Press, Boca Raton FL,
1989
AACME rules prohibit listing a source of over 700
references for this presentation
Abstract Information & Notes
Bruce Jarvis, Ph.D.
Date of talk:
Friday, June 20, 2003, 3:30pm
Department of Chemistry & Biochemistry
Phone:
301/405-1843
University of Maryland
Fax:
301/314-9121
College Park, MD 20742
E-mail:
[email protected]
Education:
B.A., Ohio Wesleyan University, Delaware, Ohio, 1963; Ph.D. University of
Colorado, Boulder, Colorado, 1966; Postdoctoral Research Associate, Northwester
University, Evanston, Illinois, 1966-67
Other:
Instructor of Chemistry (Part-time), Northwestern University, Evanston,
Illinois, 1966; Assistant Professor, University of Maryland, 1967-71; Associate
Professor, University of Maryland, 1971-79; Visiting Scholar in Residence,
University of Virginia, 1975-76; Professor of Chemistry, University of Maryland,
1979-Present; Program Officer, Organic Synthesis, NSF 1987-88; Associate Chair
1988-89, 1992-1993, 1998-1999; Acting Chair 1989-90; Chair, Department of
Chemistry and Biochemistry, 1993-1998; Visiting Professor, Dept. of Biotechnology, Danish Technical
Univ., 1999-2000.
Disclosure Statement:
None
SPEECH TITLE:
“History and Toxicology of Mycotoxicoses”
The speaker has provided the information
below.
1.) Goals and objectives: Present
history and overview of animal and human toxicoses associated with exposure to
fungal toxins
2.) Outline of talk/abstract: Animals
and humans have a long history of exposure, mainly through ingestion, to toxins
produced by filamentous fungi, e. g. Aspergillus, Fusarium, Penicillium,
Alternaria, etc. The mode of exposure is most commonly through contamination
of food and feed, and symptoms range from mild discomfort to death. Many fungal
toxins (mycotoxins) are immunosuppressants; some are among the most potent
carcinogens known.
Although most of our experience with exposure to
mycotoxins has been gained in an agricultural setting, recent concern has been
centered on inhalation exposure to mold spores generated in damp buildings and
homes. The problems associated with extrapolating data from the agricultural
settings to those found in buildings will be discussed.
3.) Conclusion of what is to be learned: Exposure
to mycotoxins is not a new problem, but it has many, many variables that often
make it difficult to relate symptoms in individuals to exposure to specific
toxigenic fungi. There are certainly many notorious cases of mycotoxicoses
(mainly in animals, but some in humans) where this linkage between exposure to
mycotoxins and adverse health outcome (e. g. death) is clear. However, such
cases in indoor environments, where exposure is through relatively low levels of
toxigenic fungi, are very often problematic, and the case for cause and effect
much more difficult to establish.
4.) References: 1. B. B.
Jarvis, “Chemistry and Toxicology of Molds Isolated from Water-damaged
Buildings,” in Mycotoxins and Food Safety:
Adv. Exp. Med. Biol. Vol 504: 42-53. J. W. DeVries, M. Trucksess,
and L. Jackson, eds., Kluwer Academic/Plenum (2002).
Abstract Information & Notes
David C. Straus, Ph.D.
Date of talk:
Friday, June 20, 2003, 4:00pm
Texas Tech University
Department of Microbiology
Phone:
806/743-2523
Texas Tech University Health Sciences Center
Fax:
806/743-2334
Lubbock, TX 79430
E-mail:
[email protected]
Graduate School Attended:
Loyola University of Chicago
Major and date of Graduation:
Microbiology - May 1974
Current Faculty Appointments:
Professor of Microbiology & Immunology
Current Job Description:
Teaching and Research
Other Information:
Member Sigma Xi, American Society for Microbiology, American Academy of
Microbiology
Disclosure Statement:
Assured IAQ7 of Dallas, TX
SPEECH TITLE:
“Recent Research in Sick Building Syndrome”
The speaker has provided the information
below.
1.) Goals and objectives: To acquaint the audience in recent research examining
the role of fungi in sick building syndrome
2.) Outline of talk/abstract: Recent research on this topic will be
presented.
3.) Conclusion of what is to be learned: That fungi growing inside building is what is primarily
responsible for the phenomenon known as sick building
syndrome.
4.) References:
Cooley et al. 1998. Occupat. Environ. Med. 55:579-584. McGrath et al. 1999. Curr. Microbiol. 38:33-36. Cooley et al. 2000. Thorax 55:489-496. Karunasena et al. 3001. Mycopathologica
150:91-95.
Abstract Information & Notes
William J. Rea, M.D.
Date of talk:
Friday, June 20, 2003, 4:30pm
Environmental Health Center - Dallas
Phone:
214/368-4132
8345 Walnut Hill Lane, Ste. 220
Fax:
214/691-8432
Dallas, TX 75231
E-mail:
[email protected]
Medical School Attended:
Ohio State University College of Medicine
Major and date of Graduation:
M.D., 1962
Residency:
UTSWS
Board Certifications:
American Board of Surgery, American Board of Thoracic Surgery, American
Board of Environmental Medicine
Current Faculty Appointments:
Professor of Medicine, Capital University of Integrative Medicine,
Washington, DC
Current Job Description:
President, Environmental Health Center - Dallas
Disclosure Statement:
None
SPEECH TITLE: “Treatment of Mold and Mycotoxin
Exposure”
The speaker has provided the information
below.
1.) Goals and objectives: To tech the clinician how to treat mold and mycotxin
exposure.
2.) Outline of talk/abstract: Avoidance of molds and toxic chemicals; injection
therapy; nutrition; heat therapy; and massage; immune
modalities
3.) Conclusion of what is to be learned: How to treat mycotoxins and mold
exposure.
4.) References:
Chemical Sensitivity, Volume IV
21st
ANNUAL INTERNATIONAL SYMPOSIUM
ON MAN
& HIS ENVIRONMENT
SCHEDULE
Saturday, June 21, 2003
7:45 a.m.
ANNOUNCEMENTS/MODERATOR: Kalpana Patel,
M.D.
8:00
Chris Rea, Environmental Consultant, R.H. of Texas, Dallas,
TX: “The Identification and Remediation of Mold
and Mycotoxin Problems in a House”
8:20
Q & A
8:30
Wallace Rubin, M.D., Private Practice, Metaire, LA: “Mold and
Chemical Sensitivity Related Inner Ear Disease”
8:50
Q& A
9:00
Donald P. Dennis, M.D., F.A.C.S., Atlanta, GA, “Treatment of
Allergic Fungal Sinusitis by Decreasing the Environmental Air Fungal Load and
Anti-Microbial Nasal Sprays Based on 14 Years Clinical Observation in 639
Patients”
9:20
Q & A
9:30
Geoffrey Hutton, Architect, Hutton & Rostron Environmental
Investigations, Guildford, Surrey, England: “The Way We Build
Now”
9:50
Q & A
10:00
BREAK WITH EXHIBITORS
10:30
William J. Meggs, M.D., Professor of Toxicology, Department of
Emergency Medicine, E. Carolina University School of Medicine, Greenville,
NC: “The Need for a National
Environmental Medical Unit”
10:50
Q & A
11:00
Allan D. Lieberman, M.D., Medical Director, Center for
Occupational Environmental Medicine, North Charleston, SC: “Explosion of Mold Cases in Homes,
Work Places and in Occupational Medical Practices”
11:20
Q & A
11:30
Nancy A. Didriksen, Ph.D., Environmental Health Psychologists,
Richardson, TX: “Neurocognitive
Deficits in Individuals Exposed to Toxigenic Molds”
11:50
Q & A
12:00n
BUFFET LUNCH WITH THE EXHIBITORS
MODERATOR: William J. Meggs,
M.D.
1:30
Jean A. Monro, M.D., Medical Director, Breakspear Hospital,
Hertsfordshire, England: “Treatment of Cancer with Mushroom
Products”
1:50
Q & A
2:00
Larry Foster, Environmental Consultant, Enviro-Cure, Atlanta,
GA: “General Reasons and Causes
of Sick Buildings that are a Result of Airborne
Biohazards”
2:20
Q & A
2:30
Theodore R. Simon, M.D., Private Nuclear Medicine Practice,
Nuclear Medicine, Dallas, TX:
“Neurotoxicity: Mold Exposure Versus All
Causes”
2:50
Q & A
3:00
BREAK WITH EXHIBITORS
3:30
Donald P. Dennis, M.D., F.A.C.S., Atlanta, GA: “Guidelines and
Theory for Treatment of Chronic Fungal Sinusitis with Reduction of Environmental
Air Mold Loan and Anti-microbial Nasal Sprays based on 14 Years Clinical
Observation in 639 Patients”
3:50
Q & A
4:00
Larry Foster, Environmental Consultant, Enviro-Cure, Atlanta,
GA: “Toxic Molds: The XXI
Century Mold Rush”
4:20
Q & A
4:30
CASE STUDIES: Richard
Jaeckle, Ph.D., Andrew Campbell, M.D., Donald P. Dennis, M.D., William J. Rea,
M.D., John H. Boyles, Jr., M.D., Kaye H. Kilburn, M.D.
6:00
AJOURN
SATURDAY, JUNE 21,
2003
ABSTRACTS
AND
HANDOUTS
Abstract Information & Notes
Chris Rea
Date of talk:
Saturday, June 21, 2003, 8:00am
P.O. Box 780392
Phone:
214/351-6681
Dallas, TX 75378
Fax:
214/358-2177
E-mail:
N/A
Other Information:
In business for 18 years. Examined over 1,000 houses and buildings for
problems that relate to or cause environmental illness. This includes construction and
renovations flaws, mold and bacteria problems, and chemical and pesticide
problems. Completed several hundred
renovation and construction projects, all done to environmentally safe
standards. Worked on projects all
over the United States, Mexico, Canada and Germany.
Disclosure Statement:
SPEECH TITLE: “The
Identification and Remediation of Mold and Mycotoxin Problems in a
House”
The speaker has provided the information
below.
1.) Goals and objectives:
2.) Outline of talk/abstract:
3.) Conclusion of what is to be learned:
4.) References:
The
Identification and Remediation of Mold and Mycotoxin Problems in a
House
The
problem of mold and fungus growth in homes and buildings has received a great
amount of press over the last 3 years. The majority of stories have centered
around lawsuits against insurance companies, builders, landlords and sometimes
municipal authorities. Less often, but probably more significant for the health
care professional, are the sensationalized stories about the health effects that
some individuals have suffered as a result of living in a moldy home. However,
there have been relatively few stories about the best way to determine if a
house is moldy, why it is moldy, and if it does have a problem with mold growth,
how this should be corrected.
Fungal
growth and the resulting mycotoxins contamination that goes along with it can
cause many different types of health problems. This is well documented and will
be discussed by other speakers in this conference. Further, the specific problem
of fungal contamination in a home is a very old problem that has probably
existed since humans began dwelling indoors.
When
people started living indoors, and in particular began to construct closed in
homes they inevitably set up the conditions for fungal growth. The factors that
cause a home to be moldy are varied and they can change drastically depending on
the climate in the area where a home is constructed, they type of construction,
materials used, building techniques employed, etc. Knowledge of these variables
is crucial in diagnosing why a house has developed a mold problem. This answer
to this question is THE MOST IMPORTANT piece of information necessary in
determining how to clean up a moldy house.
This
talk will present a basic overview, with a case study, in the techniques used to
diagnose fungal problems in a house. The factors and variables that cause fungal
growth in homes will also be discussed. Finally, some of the techniques used to
solve the problems and clean up the house will also be used.
Abstract Information & Notes
Wallace Rubin, M.D. Date of talk: Saturday, June 21, 2003, 8:30am
3434 Houma Boulevard, Suite 201
Phone:
504/888-8800
Metairie, LA 70006
Fax:
504/455-6796
E-mail:
[email protected]
Medical School Attended:
University of Illinois College of Medicine
Major and date of Graduation:
1946
Residency:
Tulane University, Department of Otolaryngology
1949-1951
Board Certifications:
American Board of Otolaryngology 1953
Current Faculty Appointments:
Clinical Professor of Otolaryngology - LSU
Current Job Description:
Solo Practitioner
Disclosure Statement:
None
SPEECH TITLE:
“Mold, Chemical Sensitivity Related Inner Ear
Disease”
The speaker has provided the information
below.
1.) Goals and objectives: The mold and chemical sensitivity immunologic
mechanisms as they relate to inner ear disease.
2.) Outline of talk/abstract: Patient presentations that will objectively document
these causative mechanisms as they relate to the diagnosis and treatment of
inner ear disease.
3.) Conclusion of what is to be learned: The methodologies for diagnostic documentation of the
causative mechanisms and the approaches to etiologic treatment will be
specifically presented.
4.) References:
1.
Rubin, W: How do we use
state of the art vestibular testing to diagnose and treat the dizzy
patient? An overview of vestibular
testing and balance system integration.
Neurol Clin 1990; 8:225-234.
2.
Rubin, W: Site of lesion
vestibular function testing.
Laryngoscope 1985; 95:386-390
3.
Rubin, w: Biochemical
evaluation of the patient with dizziness.
Semin Heal 1989; 10:151-159.
Mold and Chemical Sensitivity
Related Inner Ear Disease
Wallace Rubin,
M.D.
The biochemical, metabolic, hormonal, and neurotransmitter influences as
they relate to hearing and balance problems have just begun to be explored. The inner ear is, in fact, an internal
body organ. The diagnostic and
therapeutic direction for the evaluation of the neurotological patient should be
oriented to confirm an etiological mechanism. This can be accomplished only if our
testing modalities are used in a way that is topographically diagnostic. This approach would than logically
culminate in a systematic etiological investigation. I will present a patient example of this
type of difficulty with mold and chemical sensitivity and show how the proper
evaluation and treatment are significant.
The Questions to be answered by the neurotological evaluation
are:
1.
What neurotological tests
can be used for site of lesion confirmation?
2.
Which biochemical,
immunologic, metabolic, and hormonal tests are indicated?
3.
What modalities of therapy
can then be efficacious?
Brookes GB. Circulating immune complexes in Meniere’s
disease.
Arch Otolaryngol 1986; 112:536-40.
Clemis JD. Allergy of the inner
ear.
Ann Allergy 1967; 25:370-6.
Clemis JD. Allergic cochleovestibular
disturbances.
Tans AM Acad Opthalmol Otol 1972; 76:59-65
Clemis JD. Cochleovestibular disorders and
allergy.
Otol Clin North AM 1974; 7:757-80.
Criep HL. Allergic vertigo.
Penn Med J 1939; 43:258-282
Derebery MJ, Rao V, Siglock TH, et al. Meniere’s
disease. An immune complex mediated illness?
Laryngoscope 1991; 101:225-229
Derebery MJ, Valenzuela S. Meniere’s Syndrome and
Allergy.
Otolaryngologic Clinics of North America 1992;Vol
25#1:213-23.
Duke WW. Meniere’s syndrome caused by
allergy.
JAMA 1923; 81:2179-81
Endicott JN, Stucker FJ. Allergy in Meniere’s disease
related fluctuating hearing loss primarily findings in a double blind cross over
clinical study.
Laryngoscope 1971; 87:1650.
Futaki T, Yamane M, Shirahata A. Immunologic analysis of
IgG and other protein fractions in endolymph obtained from endolymphatic sac of
Meniere patients and a control.
Acta Otolaryngol 1985; 4191:71-8.
Harris JP. Immunology of the inner ear: response of the
inner ear to antigen challenge.
Otolaryngol Head Neck Sug 1983; 91:18-23
Powers WH. Allergic factors in Meniere’s
disease.
Trans Am Acad Ophtalmol Otol 1973; 77:22-9.
Stahle J, Deuschl H, Johansson SG. Meniere’s disease and
allergy, with special reference to immunoglobulin E and IgE (regain) antibody in
serum.
Int J.Equil Res 1974; 4:22-27.
Williams HL. Allergy of the inner ear – Meniere’s
disease.
Arch Otol 1952; 16:24-44.
Abstract Information &
Notes
Donald P.
Dennis, M.D., F.A.C.S.
Date of talk:
Saturday, June 21, 2003, 9:00am
ENT & Facial Plastic Surgery, L.L.C.
Phone:
404/355-1312
3193 Howell Mill Rd., Suite 215
Fax:
404/352-2798
Atlanta, GA 30327
E-mail:
[email protected]
Major and date of Graduation:
MD, 1974
Residency:
Otolaryngology - Head & Neck Surgery, John’s Hopkins
Hospital
Board Certifications:
American Board of Otolaryngology & Head & Neck
Surgery
Current Faculty Appointments:
ENT Department, Northside Hospital
Current Job Description:
Private Practice, Atlanta
Disclosure Statement:
None
SPEECH TITLE: “Treatment of Allergic Fungal Sinusitis
by Decreasing the Environmental Air Fungal Load and Anti-Microbial Nasal Sprays
Based on 14 Years Clinical Observation in 639Patients”
The speaker has provided the information
below.
1.) Goals and objectives:
2.) Outline of talk/abstract:
3.) Conclusion of what is to be learned:
4.) References:
Treatment of Allergic Fungal
Sinusitis by Decreasing the Environmental Air Fungal Load and Anti-Microbial
Nasal Sprays Based on 14 Years Clinical Observation in 639
Patients
By
Donald P. Dennis, M.D.,
F.A.C.S.
Atlanta, Georgia
Treatment Strategy:
In September 1999 Mayo Clinic published an article that
pegs 93% of all chronic sinusitis as being caused by mold. The most likely mechanism of formation
of sinusitis is, a Type 2 Gell Coombs reaction. As mold is breathed into the nasal
mucosa intact eosinophylls migrate through the mucosa and bind to IgG antibodies
in the nasal mucus. The mold
antibody complex binds to the mold and the eosinophyll lyses, releasing major
basic protein, which pits the mucosa.
These pits trap mucous so that the mucous cannot drain. The stagnant mucous gets infected which
causes nasal polyps and thickening of the lining, which obstructs the outflow of
mucous. The polyps cause more
infection and the infection causes more polyps and then there is a viscous
cycle, which perpetuates itself.
This reaction is most likely a type 2 hypersensitivity reaction. All type 2-hypersensitivity reactions
stop when the antigen (mold in this case) is removed. We knew from 20 years of clinical
experience that when patients cleaned their environmental air their sinusitis
improved. The air mold level
required for health was discovered by testing the one hour gravity plate
exposure inside each chronic sinusitis patient=s home and following them by endoscopic photographs as
remediation of mold was done. Over
600 patients homes were tested for mold before and after mold remediation. It was discovered that a mold count of
0-4 colonies with a one-hour gravity plate exposure was required for the sinus
mucosa to clear by endoscopic photography.
Normal saline nasal irrigation with a combination of
antifungal-antibacterial-anti-inflammatory nasal sprays were found to markedly
improve mucosal recovery. A
ASystemic Fungal Syndrome@ was observed in some patients consisting of memory
loss, hearing loss, dizziness, arthritis, fibromyalgia, dermatitis, ataxia,
muscle weakness, disorientation, and GI disturbance. These patients likely hypersensitivity
mechanism was a Gell-Coombs Type 3 and 4 reactions. Many different ways of mold remediation
and nasal sprays were tested and a protocol was developed that was easy for the
patient to implement and cost effective.
An effective environmental and nasal treatment protocol was
developed. The environmental
treatment consists of a HEPA air filter combined either with either botanical
oil evaporation, or non-ozone ionization, with vent covers sprayed with
botanical extract. Whole house
fogging was also developed to bring the colony counts down to zero in 1
hour.
Attached are 3 photos.
Fig. 1 is an endoscopic photo showing the mold count in
the patient=s room air before and after room air mold remediation
with the endoscopic photographs showing the purulent infection clearing after
the mold count drops to 4 colonies.
Fig. 2
shows the colony count dropping from TNTC to 0 in six days using the Wein 2500
room unit.
Fig. 3
shows the mold colony count going from TNTC to 0 in 1 hr. and 1 colony in 2
hrs.
Note
EPA "Introduction to Indoor air Quality: A Reference
Manual" uses 50 CFU/m3 as a beginning concern and 10,000 as a problem amount
using an Anderson sampler. The
equivalents of Gravity feed to Anderson Sampler for 3 minutes @ 28.3 L/min
are:
CFU Comparison
|
Gravity Fed |
Anderson Sampler
Range |
Anderson avg. |
|
1 |
40-400 |
345 |
|
2 |
1100-1200 |
1198 |
|
3 |
2100-2500 |
2401 |
|
4 |
3400-3500 |
3496 |
|
5 |
4800-5000 |
4913 |
|
6 |
6200-6300 |
6263 |
|
7 |
7500-7600 |
7531 |
|
8 |
8700-8900 |
8745 |
|
9 |
9900-10,100 |
9978 |
|
10 |
11,000-11,300 |
11,254 |
|
11 |
12,500-12,600 |
12,513 |
|
12 |
13,700-14,000 |
13,749 |
|
|
|
|
Therefore in reality the value for mold safe air using
an Anderson sampler is 3400-3500 cfu (colony forming units).
Abstract Information & Notes
Geoffrey Hutton
Date of talk:
Saturday, June 21, 2003, 9:30am
Hutton & Rostron Environmental Investigations
Phone:
011/44-1483-203221
Gomshall, Guildford
Fax:
011/44-1483-202911
Surrey, UK GU5-9QA
E-mail:
[email protected]
Current Job Description:
Partner in private, specialist architectural practice and Chairman of a
firm of environmental; investigators
Other Information:
Hutton & Rostron (H&R) is a firm of architects, health and legal
professionals with scientific support specializing in building pathology. Investigation of building defects and
loss prevention is an important part of its activities. Although maintenance is often reactive,
a proactive policy is preferred and for this reason reliable and time-related
data is acquired for diagnosis and warning
Disclosure Statement:
None
SPEECH TITLE: “The Way We Build
Now”
The speaker has provided the information
below.
1.) Goals and objectives: To introduce the delegates to the nature of building
construction, the materials and the consequences for the environment and
health.
2.) Outline of talk/abstract: The background of construction as a fundamental
activity to fill the many needs for shelter and working facilities, and the
impact these have on the environment, disease and perceptions of health, fashion
and the technology involved.
3.) Conclusion of what is to be learned: Intricacy of construction and engineering services may
no necessarily be beneficial and the increasing use of products depending on
volatile components for manufacturer or maintenance is a
hazard.
4.) References:
None
THE WAY WE BUILD NOW
Geoffrey H Hutton, ARIBA, DipArch
(Dist)
Building design is a multi-factorial equation of
thousands of unknowns and few knowns with interactions with health at every
level, this has been resolved in the evolution of vernacular building, but not
so successfully in conceptually based design
Birds are great builders. They exploit local resources in
competition with others while optimizing the loads and traveling distance. They have to get the location and
structure right; too high in the tree and the wind will destroy the nest and too
low and a predator will get your eggs.
Too strong or elaborate construction will take longer and waste otherwise
valuable breeding or feeding time.
The nest must be defensible, inconspicuous, protect the eggs from
breakage, not harbor pests or support fungal growth, must retain sufficient heat
for insulation, be well drained and ventilated. The initial owner may decide to clear
out after a year and build a new hygienic model next season or invest in a
family home to be refurbished each year or even to be a squatter. Every climate and context has residents
and tourists who have solved their accommodation problems sufficiently well to
have survived and prospered over many generations with no insurance. We have much to learn from the blind
watchmaker
Man
too has solved the problems of climate and context in the building methods and
materials available to him either as a nomad or in a settled community with as
much convenience and defense that could be afforded. The possible solutions, if not the
result of self-help, were understood by the users and the technology was within
the grasp of the individuals concerned and shared within the community. Differentiation between building
functions was slight, the essentials of shelter and enclosure could be met by
common methods for providing spanning, load bearing and enclosing structures
relying on the inherent properties of the materials for weather resistance, load
bearing and insulation or thermal capacity. The interior was modified by the
combustion of the limited fuel available, which was of primary importance for
cooking. Such buildings continued
to serve satisfactorily for millennia and can still be found throughout the
world providing the ultimate barrier to the environment after the primary
barrier provided by clothing for the climate and season. The technology evolved incorporates the
accumulated experience acquired for practical survival and prosperity in the
conditions experienced over many generations. Such empirical knowledge includes such
issues as ventilation, temperature and evaporation from surfaces with an
elegance, which may not be perceived, and thus overlooked in
analysis
Building from the earliest times has, of course, also
served symbolic purposes demonstrating power, identity or spiritual values. These monumental characteristics are
usually achieved either at some otherwise unjustified expense and inconvenience
to the practical performance of the building, or they are ignored
altogether
Unfortunately, the empirical has been overlaid by the
monumental which is further complicated by the introduction of codes and
standards which try to capture the multi-factorial performance of buildings by
setting out criteria for aspects of structural strength, fire resistance,
thermal characteristics, ventilation, lighting etc further defined by methods of
test limited by the laboratory methods available. Such aspects of performance are inherent
in the overall construction by evolutionary optimization. Important to both birds and man is the
health of the occupants as fundamental to survival, whereas this is not of great
significance in monumental buildings (which may well be
tombs)
The
gradual incorporation of imagery and construction from monumental building into
the mainstream of the vernacular has led to the dominance of conceptual design
over the utilitarian product of evolution and the local environment. Professions developed to match, each
with a visual or engineering idea to promote, but without an overarching
experience of the interactions between the diverse needs and performance
required. In turn, they served
building owners and users with less personal appreciation of the
issues
Much of the performance required is now specific to
particular components, which, in turn, are used in assemblies and bought as a
catalogue items to achieve theoretically defined objectives. The performance of items may be known
from tests, but the consequences for the whole assembly, and particularly at the
interfaces, may not be fully understood, defined or even measurable. Further, the overall design may not be
repeated or the result of experience acquired over many projects. Consequently, failures occur due to
unanticipated effects or events, at changes of material or section, or in voids
concealed from inspection
Historically, buildings were either heavyweight, usually
masonry, or assembled from frames and infilling panels normally of timber. Each has advantages for particular
climates and occupancies. The
masonry building will have a smaller exposed surface area and a higher thermal
capacity than the frame building, which will also contain more cavities. Current building is generally of frame
and fill construction, even if faced with masonry, as modern construction tries
to limit the activities on site.
Typically, such buildings have suspended ceilings, raised floors and
paneled or cavity wall constructions creating voids which are not easily
accessible and can be contaminated and difficult to clean. Builders’ dirt and votive offerings are
frequently found in such places, which also provide the accommodation for
engineering plant and distribution services, pipes and
ductwork
Since the early 19th century, the exploitation of fossil
fuels has been the cheap and, for the time being, pervasive source of thermal
process energy in the manufacture of products such as glass, metals, cement and
bricks; and power for cutting, forming, handling and distribution of
products. Fossil fuels now provide
raw materials for plastics, fibers, dyes, paints and adhesives used in
construction, building services, furniture, soft furnishing, household utensils
and clothing, and a host of treatments in the form of cleaning agents, polishes,
insecticides, and life-style support generally. The processes involved generate
persistent wastes, and the products can have undesirable emissions and result in
toxic waste. Most of all, fossil
fuel has been used to power environmental services in buildings for heating,
ventilation and air-conditioning without which (and lifts and escalators) much
of the world would be virtually uninhabitable at the present densities. The management of such services is not
precise and the fuel is still cheap and generally available. Consequently, there is little incentive
to economize, thus environmental services consume some 60 per cent of all
fuel. In historic terms, this
relatively short-term cost-free resource has changed lifestyles to reduce the
thermal importance of clothing, increase the size of individual spaces, reduce
the need for natural light or ventilation, and medicated our surroundings. The availability of hot water, for the
dispersal of activities, such as bathing, laundry and cooking results in higher
levels of humidity. The engineering
required to provide for such conditions, over that possible by the passive
qualities of the building enclosure, becomes increasingly complex while
occupying a large proportion of the available space and requires regular and
diligent maintenance to achieve its theoretical
performance
The
environmental standards achievable by the use of engineering services inside
buildings, particularly if sealed, subjects the external envelope to greater
stresses in providing what has come to be regarded as the primary barrier to
external conditions. It must now
accommodate greater thermal movement, vapor pressure and rates of heat transfer,
as well as continuing to offer weather resistance, and in some conditions
condensation will occur within the structure
The
nature of frame and fill buildings favors the use of space heating, rather than
structural heating and high thermal capacity which results in slow adjustment to
ambient conditions and can normally be expected to give comfort with lower air
temperatures and thus less likely to suffer from condensation. Space heating (or cooling) depends on
the processing of large volumes of air, much of which is re-circulated to
economize in fuel. Such air carries
the waste products of respiration and activities in the space, which must be
processed, filtered and mixed with 'fresh' air for re-use. Such a system is liable to contamination
and condensation at a number of points even if the filters are routinely changed
and well maintained. Biological
material will form part of the contaminants and with the appropriate humidity
fungal growth can be anticipated
Depending on building use and standards of housekeeping,
the various unobserved voids may become home to insects and other pests, which
may be encouraged by the ambient conditions. They may be sustained by human litter
and food droppings, and initiate further contamination and damage to structure
and furnishings. Particular
activities such as sleeping and cooking bring particular infestations such as
house mites and cockroaches with consequences for health. Major destruction can result from fungi
such as the wet and dry rots, and wood-boring insects all of which are
indicators of poor environments and housekeeping
Very heavily serviced buildings such as hospitals could
become hygienic liabilities; the continuing cost of maintenance and the
difficulty of decontamination may make simpler disposable accommodation
viable. Ultimately, the properties
will be removed for reasons of fashion or return on investment and it seems
reasonable that this should be foreseen as part of the brief. Contamination and hazards to health
should be factors in this decision
Buildings of historic, technical, literary or national
interest should be preserved. This
helps understanding of how people lived and adapted to the climate and context
in which they lived in the thousands of years before the profligate use of
energy and how we may have to live again.
These buildings often suffer from fungal decay and insect attack due to
neglect, misuse, the introduction of modern heating, new materials and
lifestyles; but rarely due to the work of the original builders. The fungal and insect infestations can
almost invariably be dealt with by reversing the conditions causing decay and
ensuring ventilation in future
Health must become of central concern in the
equation
END
Hutton + Rostron Environmental
Investigations Limited
Netley
House, Gomshall, Surrey GU5
9QA
Tel 01483 203221 Fax 01483 202911
Email [email protected] Web: www.handr.co.uk
Abstract Information & Notes
William J. Meggs, M.D., Ph.D.
Date of talk:
Saturday, June 21, 2003, 10:30am
Brody School of Medicine
East Carolina University
Phone:
252/744-2954
600 Moye Blvd., Room 4W54
Fax:
252/744-3589
Greenville, NC 27858
E-mail:
[email protected]
Medical School Attended:
University of Miami
Major and date of Graduation:
M.D., 1979
Residency:
University of Rochester
Board Certifications:
Medical Toxicology, Allergy & Immunology, Internal Medicine,
Emergency Medicine
Current Faculty Appointments:
Professor & Chief of Toxicology
Current Job Description:
Physician
Other Information:
Author of "The Inflammation Cure" to be published in Sept. 2003. Editor of "Health & Safety in
Agriculture, Forestry, & Fisheries."
Author of numerous research articles and textbook
chapters.
Disclosure Statement:
None
SPEECH TITLE: “The Need for a National Environmental
Medical Unit”
The speaker has provided the information
below.
1.) Goals and objectives:
$
To know what an environmental control unit [environmental medical unit]
is.
$
To know the history of Environmental Medical Units in this country and
abroad.
$
To know the clinical and research uses of Environmental Medical
Units.
$
To know the need for a National Environmental Medical Units for research
studies.
2.) Outline of talk/abstract: The
concept of an Environmental Control Unit [Environmental Medical Unit] was
developed by Dr. Theron Randolph as a clinical tool to evaluate environmental
factors such as air pollutants, natural and additive dietary elements, and water
contaminants on specific disease processes. From 1966 to 1974,a number of EMUs
were opened in this country and for the evaluation of environmental factors
contributing to specific disease processes in individual patients. Though tens
of thousands of patients were treated in these units with a high degree of
patient and physician satisfaction, these units were abandoned due to economic
and political factors, the changing healthcare environment, and the refusal of
third party carriers to pay for this service. Environmental Medical Units are an
important research tool to evaluation environmental factors in a number of
syndromes and diseases. The Japanese have taken a leadership role in
establishing EMUs for medical research, in particular in evaluating effects of
sick building gases and volatile organic chemicals on cerebral function. The
case for a national EMU in the United States is presented, and the use of such a
unit to study environmental factors in specific diseases is
discussed.
3.) Conclusion of what is to be learned:
Environmental Medical Units have been very valuable as a clinical tool
and will play a prominent role in environmental medicine research in the future.
The United States should build a National Environmental Control Unit devoted to
research in environmental medicine.
4.) References:
Proceedings of the 2003 International Symposium on Indoor Air Pollution
and Health Hazards. Tokyo, Japan. January 8 to 11, 2003.
Abstract Information & Notes
Allan D. Lieberman, M.D.
Date of talk:
Saturday, June 21, 2003, 11:00am
Center for Occupational & Environmental
Medicine, PA
Phone:
843/572-1600
7510 Northforest Dr.
Fax:
843/572-1795
North Charleston, SC 29420-4297
E-mail:
[email protected]
Medical School Attended:
Chicago Medical School
Major and date of Graduation:
1960
Residency:
Children=s Memorial Hospital - Chicago
Board Certifications:
Fellowship - American Academy of Environmental
Medicine
American Board Environmental Medicine
Current Job Description:
Medical Director of Center for Occupational & Environmental
Medicine
Disclosure Statement:
None
SPEECH TITLE:
“Explosion of Mold Cases in Homes, Work Places and in Occupational
Medical Practices”
The speaker has provided the information
below.
1.) Goals and objectives: To explore the different questions of toxic mold
exposures.
2.) Outline of talk/abstract: A clinical presentation of the effects and sequelae of
3 separate sick building exposures to mold.
3.) Conclusion of what is to be learned: Patterns of Reactivity to mold, their similarities,
differences and their chronicity.
4.) References:
Explosion of Mold Cases in Homes,
Workplaces and in Occupational Medical Practices
Allan D.
Lieberman, M.D.
In practices all over the country, there has been an
explosion of patients seeking help from alleged exposure to molds both in their
homes and workplaces. The severity
of their symptoms and the multi-system spectrum of their complaints demands that
physicians seeing these patients become more knowledgeable about the serious
health effects of mold exposure.
Yet, we are told in a position paper1
published by the American College of Occupational and Environmental Medicine and
peer reviewed by the Council on Scientific Affairs, that “mold growth indoors is
undesirable but does not warrant the fear that is too often associated with
it. A careful review of the science
suggests that irrational fear of indoor mold threatens responsible public policy
more than indoor mold threatens public
health.”2
On what clinical
evidence is this opinion based?
Objective analysis requires you to believe in what you see and not see
what you believe.
The case report is the gold standard in identifying the
adverse effects of environmental exposures and it is the obligation of
physicians to report these cases.
This presentation will do just that, summarizing the findings in 48 cases
of mold exposure.
The case reports presented derive from workers in a
bank, industrial plants, teachers in schools, and people in their homes. All were knowingly exposed to molds that
were professionally evaluated, identified, and quantified. Most exposures were long-term lasting
weeks to months. Moisture was the
universal cause precipitating the growth of the indoor mold. The mold species identified varied but
the most common were:
Aspergillus
Penicillium
Cladosporium
Stachybotrys
Multiple
systems were affected confirming the multi-system injury that mold exposure can
produce. The spectrum of signs and
symptoms in descending order of frequency included:
Muscle and/or joint pain
71%
Fatigue/weakness
70%
Neurocognitive dysfunction
67%
Sinusitis
65%
Headache
65%
Gastrointestinal problems
58%
Shortness of breath
54%
Anxiety/depression/irritability
54%
Vision problems
42%
Chest tightness
42%
Insomnia
40%
Dizziness
38%
Numbness and tingling
35%
Laryngitis/hoarseness
35%
Nausea
33%
Rashes
27%
Tremors
25%
Heart palpitations
21%
Bronchitis/pneumonia
21%
Nose bleeds
13%
Nasal Septal Perforation
2%
Mold and
mycotoxin antibody titers:
23 out of 29 or 80% of patients tested showed positive
antibodies to molds and mycotoxins.
Trichothecene
38%
Aspergillus
34%
Cladosporium
31%
Penicillium
28%
Stachybotrys
28%
Conclusions:
The findings of 48 cases of serious health effects from
mold exposure suggests that mold is a significant cause of illness, impairment
and disability.
References:
1.
Hardin, B.D., Kelman,
B.J., Saxon, A., ACOEM’s evidence based statement on the Adverse Health Effects
Associated With Molds In The Indoor Environment. ACOEM’s report. Oct/Nov/Dec
2002.
2.
Brunekreff, B., 1992. Damp
Housing And Adult Respiratory Symptoms.
Allergy 47:498-502.
3.
Brunkreff, B., D.W.
Dockery, F.E. Speizer, J.H. Ware, J.D. Spengler, and B.G. Ferris. 1989. Home
Dampness And Respiratory Morbidity In Children. Am. Rev. Respir. Dis. 140:
1363-1367.
4.
Dales, R.E., H. Zwanenburg, R. Burnett,
and C.A. Franklin. 1991. Respiratory Health Effects Of Home Dampness And Molds
Among Canadian Children. Am. J. Epidemiol. 134:196-203.
5.
Packer, C.N.,
Stewart-Brown, and S.E. Fowle. 1994. Damp Housing And Adult Health: Results From
A Lifestyle Study In Worcester, England. J. Epidemiol. Community Health
48:555-559.
6.
Firhonen, I., A.
Nevalainen, T. Husman, and J. Pekkanen. 1996. Home Dampness, Molds And Their
Influence On Respiratory Infections And Symptoms In Adults In Finland. Eur.
Respir. J. 9:2618-2622.
7.
Platt, S.D., C.J. Martin,
S.M. Hunt, and C.W. Lewis. 1989. Damp Housing, Mold Growth, And Symptomatic
Health State. Br. Med. J. 298:1673-1678.
8.
Engelhart, S. et al,
Applied and Environmental Microbiology, August 2002, P.
3886-3890.
9.
Bornchag, CG. et al. Indoor Air, 2001 June 1 (2):
71.
10.
Beebe, Glenn. Toxic Carpet
Three. 1971.
11.
Andreissen, J.W., B.
Brunekreff, and W. Roemer. 1998.
Home Dampness And Respiratory Health Status In European Children. Clin. Exp. Allergy
28:1991-1200.
Abstract Information & Notes
Nancy A. Didriksen, Ph.D.
Date of talk:
Saturday, June 21, 2003, 11:30am
100 North Cottonwood Drive
Phone:
972/889-9933
Ste.
106
Fax:
972/889-9935
Richardson, TX 75080
E-mail:
N/A
Medical School Attended:
University of North Texas
Major and date of Graduation:
1986 - Health Psychology/Behavioral Medicine
Residency:
N/A
Current Faculty Appointments:
Adjunct Professor of Psychology - University of North
Texas
Current Job Description:
Private Practice, primarily evaluating and treating patients with
chemical/environmental sensitivity, Chronic Fatigue Immune Deficiency Syndrome,
and Fibromyalgia.
Other Information:
Internship - Environmental Control Unit, Northeast Community Hospital,
Bedford, TX
Disclosure Statement:
None
SPEECH TITLE: “Neurocognitive Deficits in Individuals
Exposed to Toxigenic Molds”
The speaker has provided the information
below.
1.) Goals and objectives: Describe the neurocognitive profiles of mold-exposed
patients and implications of findings as to the neurotoxic properties of
toxigenic fungi.
2.) Outline of talk/abstract: 1. General
effects of neurotoxic exposure.
2. Description of the
neurocognitive deficits observed in mold-exposed patients. 3.
Caveats of data interpretation.
4. Implications of data for
litigation and/or disability issues.
5. Implications for future
research.
3.) Conclusion of what is to be learned: Extent and kind of neurocognitive dysfunction observed
in patients exposed to toxigenic molds, implications for litigation and
disability issues, and caveats regarding data
interpretation.
4.) References:
Auger, P.L. (1994). Mycotoxins and Neurotoxicity. In Johanning, E. and Yang, C.S. (Eds.), Fungi and
bacteria in indoor air environments (Proceedings of the International
Conference, Saratoga Springs, New York).
Eastern New York Occupational Health Program.
Mandell, M.
(1976). Mold allergy as a
major cause of bio-ecologic mental illness. In L. Dickey (Ed.), Clinical
ecology (pp.
259-261). Springfield, Il:
Charles C.
Thomas.
Johanning, E.
(Ed.). (2001). Bioaerosols, fungi and mycotoxins:
Health effects, assessment, prevention and
control. Albany, NY:
Fungal Research Group (FRG), Inc.
Boyd Printing Company, Inc.
Nancy A.
Didriksen, Ph.D.
Goals and
Objectives:
1.
Describe the
neuropsychological test results of patients reporting primary exposures to
toxigenic molds.
2.
Describe the types of
neurocognitive deficits found most frequently in mold-exposed
individuals.
3.
Discuss the physical,
psychological, and neurocognitive symptoms endorsed most frequently on the
checklists and whether the reported neurocognitive symptoms are consistent with
neuropsychological findings.
4.
Discuss confounding
variables in data analysis and their importance in disability and litigation
issues.
5.
Implications for future
research.
Relatively few studies are available regarding the
neurocognitive deficits resulting from exposure to toxigenic molds. Dr. Marshall
Mandell (1976) reported cerebral reactions including inability to concentrate
and confusion during provocative testing with various mold extracts and reviewed
the biological sources of antibiotics with proven neurotoxic properties. More
recently, cognitive impairment associated with exposure to toxigenic fungi has
been reported by Gordon, Johanning, and Haddad (2001). Auger, Pépin, Miller,
Gareis, et. al. (2001) have reported chronic toxic encephalopathies apparently
related to exposure to toxigenic fungi. Baldo, Ahmad, and Ruff (2002) have
described the neuropsychological performance of patients following mold exposure
with impairment observed in visuospatial learning and memory, verbal learning
and psychomotor speed.
The neurocognitive data of 41 patients (mean age 47.95,
mean educational level 15.32) reporting primary mold exposures were examined in
the present study. Neuropsychological test batteries of varying
comprehensiveness (including the Halstead-Reitan Neuropsychological Test
Battery) were administered. Test results were compared with normative data.
Deficits were found primarily on measures of executive functions, psychomotor
problem-solving, and incidental memory. Scores on the Wechsler Memory Scale-III
fell within normal limits, overall, with greatest impairment on measures of
visual memory. Fifty-seven percent of patients demonstrated mild to moderate
impairment, overall, on the Halstead-Reitan Battery. Forty-two percent
demonstrated mild to severe impairment on the Comprehensive Neuropsychological
Screen with an additional 17 percent scoring in a low-normal range. Scores on
measures of specific neuropsychological abilities showed some impairment of
sensory and motor functions. IQ scores fell generally within expected ranges,
overall.
Physical Symptoms reported most frequently on the
Physical Symptom Checklist included fatigue, low energy, headaches, difficulty
remaining asleep, weakness, sinus discomfort, skin problems, decreased balance
and coordination, mucus, difficulty falling asleep, and “sick all over.”
Psychological symptoms most frequently reported on the Psychological Symptom
Checklist included present performance inferior to prior performance or level of
functioning, overwhelming
exhaustion, fatigue, or weariness, “cloudy, foggy, spacey,” “This is not
me,” difficulty getting started in the morning, worry about bodily dysfunction,
tense, difficulty setting and reaching goals, inability to cope well with daily
or other stressors, irritability, decreased libido, and feels like “insides are
racing.” Frequently endorsed neurocognitive symptoms on the Neurocognitive
Symptom Checklist included decreased immediate and short-term memory, decreased
concentration, decreased attention, difficulty remembering the names of things
or people, intellectual inefficiency, word-finding problems, decreased
comprehension, decreased long-term memory, easily distracted, loses train of
thought, and poorly organized.
Age, sex, and educational norms were utilized in
addition to the standardization group norms to determine whether a decrement in
functioning had occurred. Additionally, prior levels of educational and
occupational performance were considered in the interpretation of test results,
particularly important for disability determination. All patients to whom a
malingering test had been administered scored within normal limits.
Many factors, including time elapsed from exposure to
evaluation (0-67 months), duration of exposure (less than 1 month to 12 years),
other environmental exposures/sensitivities, motivation of the individual,
reactions to environmental incitants at the time of evaluation, head trauma
and/or other neurological conditions, medications, metabolic disorders, and past
or present drug and alcohol abuse were considered in the interpretation of
individual test data and to determine whether the observed deficits were due
primarily to mold exposure. These factors are particularly important for
litigation issues.
Conclusions:
The neuropsychological
test data of mold-exposed individuals present a pattern of deficits quite
similar to those found in patients exposed to other neurotoxins including
solvents, pesticides, and metals. Results suggest that the molds to which these
patients were exposed have neurotoxic properties. Deficits do not appear as
severe as those observed with other types of neurotoxic exposures. Possible
explanations include (1) a greater awareness of physical discomfort alerting the
individual to the toxic environment and decreasing the duration of exposure, (2)
neurotoxic effects of molds are less severe, (3) small sample size, (4)
sensitivity of tests administered, (5) individual
susceptibility.
Further research is necessary to
determine the neurotoxic effects of specific molds, types of individuals with
greater susceptibility to neurotoxic effects, factors which appear to enhance
susceptibility to adverse effects, and interventions, which promote healing
after exposure. A larger database and collaboration among various healthcare
providers are necessary.
References:
American Psychiatric Association (1990). Diagnostic and statistical manual of
mental disorders (4th Ed.) (pp. 733-34). Washington, D.C: American Psychiatric
Association.
Auger, P. L. (1994). Mycotoxins and neurotoxicity. In Johanning, E. and Yang, C. S. (Eds.),
Fungi and bacteria in indoor air environments (Proceedings of the
International Conference, Saratoga Springs, New York). Eastern New York Occupational Health
Program.
Baldo, J.V., Ahmad, L. & Ruff, R. (2002).
Neuropsychological performance of patients following mold exposure.
Applied Neuropsychology, 9(4), 193-202.
Harrell, E.H., Butler, J.R., & Didriksen, N.A.
(1986). Comprehensive
neuropsychological screen.
Unpublished assessment instrument.
Health Psychology/Behavioral Medicine Associates, 100 N. Cottonwood Dr.,
Suite 106, Richardson, TX 75080.
Heaton, R. K., Grant, I. & Matthews, C. G. (1991).
Comprehensive norms for an expanded Halstead-Reitan battery. Odessa, FL:
Psychological Assessment Resources, Inc.
Jarvis, P.E. & Barth, J.T. (1994). The Halstead-Reitan
neuropsychological battery: a guide
to interpretation and clinical applications.
Odessa, FL: Psychological
Assessment Resources, Inc.
Johanning, E. (Ed.). (2001). Bioaerosols, fungi and
mycotoxins: Health effects, assessment, prevention and control. Albany, NY: Fungal Research Group (FRG),
Inc. Boyd Printing Company, Inc.
Lezak, M.D. (1995). Neuropsychological assessment
(3rd Ed.) New York: Oxford.
Mandell, M. (1976). Mold allergy as a major cause of
bio-ecologic mental illness. In L.
Dickey (Ed.), Clinical ecology (pp. 259-261). Springfield, Il: Charles C.
Thomas.
Reitan, R.M. & Wolfson, D. (1993, 2nd Ed.). The Halstead-Reitan
neuropsychological test battery:
theory and clinical interpretation. Tucson, AZ: Neuropsychology
Press.
The Psychological Corporation. (1997). WAIS-III WMS-III technical
manual. San Antonio: The Psychological Corporation.
Wechsler, D. (1981). Wechsler adult intelligence scale -
revised. New York: Psychological Corporation.
Abstract Information & Notes
Jean A.
Monro, M.D.
Date of talk:
Saturday, June 21, 2003, 1:30pm
Breakspear Hospital
Phone:
011442261333
Hertfordshire House
Fax:
011442266388
Wood Lane, Paradise Estate
E-mail:
[email protected]
Hemel Hempstead, Herts, HP2 4FD
U.K.
Medical School Attended:
London Hospital Medical College
Major and date of Graduation:
Medicine MB, BS 1960
Current Job Description:
Medical Director of Breakspear Hospital, Hemel Hempstead,
UK
Disclosure Statement:
None
SPEECH TITLE: “Treatment of Cancer with Mushroom
Products”
The speaker has provided the information
below.
1.) Goals and objectives: To provide
information on the use of natural resources in the treatment of cancer. To highlight that these can be a
protective measure through life.
2.) Outline of talk/abstract:
3.) Conclusion of what is to be learned: Prevention
of disease and treatment can overlap.
Mushroom products can be therapeutically beneficial in prevention. There are toxic mushroom products which
have been used in chemotherapy.
4.) References:
4.
Ikekawa T. Beneficial
effects of edible and medicinal mushrooms on health care. Int J Med Mushrooms
2000;3:291-8.
5.
Monro JA. Coriolus: the
use of the medicinal mushroom Coriolus MRL as an immunotherapeutic agent in the
treatment of patients with chronic fatigue syndrome. To be published
2003.
6.
Smith JE, Rowan NJ,
Sullivan R. Medicinal mushrooms; their therapeutic properties and current
medical usage with special emphasis on cancer treatments. London: Cancer Research UK;
2002.
Dr. Jean A.
Monro,
Breakspear
Hospital,
Hemel Hempstead,
U.K.
ABSTRACT
In the treatment of
cancer, most treatments currently used are designed to be cytotoxic to the
neoplastic cells. One of the most
promising methods to be considered is an immunological method of control. No agent other than mushrooms can be
used both for prevention and treatment.
In both, mushroom species have the properties for immune modulation and
prevention of disease, which certainly is not the case with those forms of
treatment, which are cytotoxic.
Some mushroom products have other medicinal purposes; for example
antibiotics and ergot alkaloids, Penicillin, Griseofulvin and also of course
some cytotoxic agents such as Cyclosporin which are fungus-derived.
However, mushroom-derived
polysaccharides can modulate animal and human responses and inhibit tumour
growth. They influence cells
through cytotoxic macrophage activity, monocytes, neutrophils, natural killer
cells, dendritic cells, and alter chemical messengers, cytokines, which trigger
complement and acute phase responses such as the interleukins, interferons and
colony-stimulating factors.
Multi-cytokine inducers can induce gene expression of immunomodulatory
cytokines and cytokine receptors.
They can stimulate
T-cells with cell mediated
cytotoxicity and B-cells with antibody production.
In Japan, Korea and China
Phase I, II and III clinical trials have been performed and mushrooms are now
used as adjuncts to chemotherapy.
Some of the main important polysaccharide compounds that have undergone
clinical trials include :
Letinan and Schizophyllum
are T-cell oriented immuno-potentiators and require a functional T-cell
component for biological activity by way of increasing helper T-cell production,
increased macrophage production leading to a stimulation of acute phase proteins
and colony stimulating factors, which in turn affect proliferation of
macrophages, neutrophils and lymphocytes and activation of the complement
system.
PSK Krestin and PSP are
potent immuno-stimulators with specific activity for T-cells and for antigen
presenting cells such as monocytes and macrophages. Their biological activity is
characterised by their ability to increase white blood cell counts, interferon
gamma, interleukin 2 production and delayed hypersensitivity
reactions.
Epidemiologically there
have been large-scale studies of the effects of mushrooms. The anti-tumour activities of
Basidiomycetes have been studied by the National Cancer Centre Research
Institute of Japan since 1966. This
has included an epidemiological investigation over 15 years from 1972 to
1986. 174,505 people were
studied. A group of people in the
Nagano Prefecture in Japan was examined and those farmers who were producing
mushroom species Flammulina velutipes were compared with the rest of the
population. The average cancer
death rate of farmers was hugely different from those in the rest of the
population. The cancer death rate
in general was 160.1 per 100,000 and of the farmers 97.1 per 100,000. This edible mushroom is now popularly
consumed as a functional food, particularly in the Nagano
Prefecture.
In our own work we have
shown that natural killer cell numbers can be doubled within two months of
taking therapeutic doses of Coriolus which contains Krestin PSk and
PSP. We have embarked on
programs of assessment of treatment of patients with cancer with
immune-modulating mushroom products.
Why do mushroom
polysaccharides have such an amazing array of biopharmacological activities?
Polysaccharides, unlike proteins and nucleic acids, contain repetitive
structural features that are polymers of monosaccharide residues joined to each
other by glycosidic linkage. These
polysaccharides offer a high capacity for carrying biological information
because of their increased potential for structural variability. The amino acids in proteins and the
nucleotides in nucleic acids can only interconnect in one way, while the
monosaccharide units in the polysaccharides can interconnect at several points
to provide a wide range of branched molecules. The number of possible
permutations from four different sugar monosaccharides could be up to 35,560,
whereas four amino acids can only form 24 different permutations. This allows an enormous flexibility for
regulatory mechanisms of cell interactions. The responses that changes in this
highly branched structure can allow information transmission. Most of the matrix between cells is
constructed of glycoproteins in a similar way and it is the matrix, which allows
the transfer of information through the organism at an incredibly rapid rate, it
is said at the speed of sound. The
incorporation of biological
structures which are proteoglycans throughout the matrix of the body can be
likened to the equivalent of fungal structures. Biologically this can be said to be
equivalent to the incorporation within cells of mitochondria which we know of
from plant species. It could be
that this biological role that we have for proteoglycans in our structures is
being augmented and mimicked by the
polysaccharide and proteoglycans from mushroom species.
Natural killer cells are
increased in numbers by mushroom treatment. In my paper on Coriolus I quoted the work of Roitt who showed
that “NK cells are thought to
recognise structures on high molecular weight glycoproteins which appear on the
surface of virally infected cells and which allow them to be differentiated from
normal cells. This recognition
probably occurs through lectin-like [i.e. carbohydrate binding] receptors on the
NK cell surface which bring killer and target into close opposition.
Activation of the NK cell
ensues and leads to polarisation of granules between nucleus and target within
minutes and extra-cellular release of their contents into the space between the
two cells, often utilising the cytolysin perforin.
NK cells kill by
activating apoptosis.
In addition to perforin,
the granules contain tumour necrosis factor β and a family of serine proteases
termed granzymes, one of which, granzyme B, can function as an NK
cytotoxic factor. Also fully
ionised ATP which can cause apoptosis in many different cell types; the
effectors themselves are resistant probably due to a lack of ATP receptors on
their surface. These factors
sequentially induce NK-mediated lysis.
A current view is that
granzyme B kills by directly activating an endogenous family of ICE [IL-1β
converting enzyme] proteases which subsequently degrade other molecules
including the repair enzyme poly [ADP-ribose] polymerase. Chondroitin sulphate A, a
protease-resistant highly negatively charged proteo-glycan, is present in the
granules and may protect the NK cell from autolysis.
The various interferons
augment NK cytotoxicity and since interferons are produced by virally infected
cells, there is an integrated feedback defence system.
Virally infected cells can
be killed by cytotoxic T-cells and ADCC
Viral antibodies can bring
the NK cell very close to the target virally infected cell by forming a bridge
and the NK cell being activated by the complexed antibody molecules is able to
kill the virally infected cell by its extra-cellular mechanisms. This system, termed
antibody-dependent cell-mediated cytotoxicity [ADCC], has been
demonstrated in vitro.”
Natural killer cells scavenge cancer cells
similarly.
Conclusion
Of the 10 million new
cancers diagnosed worldwide annually, 1.5 million are said to have been
associated with infections, especially viruses, 3 million due to toxic exposure
and 3 million due to dietary causes.
The remainder have an unknown aetiology.
Mushrooms may be able to
address virally induced cancers as well as those due to dietary and lifestyle
causes.
References
:
1.
Ikekawa T. Beneficial effects of edible and medicinal mushrooms on health
care. Int J Med Mushrooms
2000;3:291-8.
2.
Monro JA. Coriolus: the use of the medicinal mushroom Coriolus MRL as an
immunotherapeutic agent in the treatment of patients with chronic fatigue
syndrome. To be published
2003.
3.
Smith JE, Rowan NJ, Sullivan R. Medicinal mushrooms; their therapeutic
properties and current medical usage with special emphasis on cancer
treatments. London: Cancer Research
UK; 2002.
Abstract Information & Notes
Larry Foster
Date of talk:
Saturday, June 21, 2003, 2:00pm
Enviro Cure
Phone:
404/876-3680
1280 West Peachtree Street, Suite 1606
Fax:
404/685-0971
Atlanta, GA 30309
E-mail:
N/A
Current Job Description:
Senior Environmental Consultant
Other Information:
Discovered that species of mold in the environment (indoors) were
causative factors in human sickness including allergies, arthritis, asthma,
headaches, learning disabilities, sinus infections, sleep apnea and
more.
Disclosure Statement:
None
SPEECH TITLE: “General Reasons and Causes of Sick
Buildings that are a Result of Airborne Biohazards”
The speaker has provided the information
below.
1.) Goals and objectives: To provide
information to the Physician that is a necessity for an optimum
diagnosis.
2.) Outline of talk/abstract:
I.
How a Source of Disease Begins
II.
How it Grows and Spreads
III.
How it Enters the Human System and Causes Disease
3.) Conclusion of what is to be learned: A
“New@ Broader view to Health Care (Treatment), viewing a
“womb to the tomb@ approach.
4.) References:
E.P.A. Manual on Schools and Commercial
Buildings
The Fungus Link by Doug Kaufmann
General Reasons and Causes of Sick
Buildings that are a result of airborne biohazards.
Larry
Foster
Do not buy a house (or building) that is in a gully, a
food plain, or is downhill from the path of rainwater.
Do not by a house (or building) that has had water leaks
that have not been corrected.
Do not by a house that has a flooded crawlspace, a sump
pump (a great indications of previous water problems). (See
A)
Do not buy a house that has had watermarked walls or
ceilings. In just a short time the
house can be overrun by visible colonies.
(See A1)
Things to inspect (concerns) before you buy: Attic Area – Be sure that this area is
not infested by birds, insects, rodents or varmints.
Check for visible signs of water intrusion. (See
B)
If there is blown-in fibrous insulation, it will
disintegrate and particulate. The
minute fibers become airborne and can be visually observed on the topside of
ductwork and beams and on the A.C. system.
(See C) These
particles are able to infiltrate (See D) into the living areas as
they are sucked into the A.C. and circulated through the air ducts and into the
living areas. (See
E)
In many instances the attic openings that the ceiling
(below) lights and ducting pass through in many cases are not properly
caulked. (See
F)
This can be a source of airborne fibers, molds,
bacteria, animal and insect by products that will infiltrate into the bedrooms
(below the attic) and appear to the homeowner as just acceptable “house
dust.” (See G) It
does not long before belongings are covered with mold and must be
discarded. This “house dust” causes
allergies, asthma, sleep apnea, snoring, rashes, congestion, infections and a
long list of health complaints.
(See H)
To avoid these problems when building a new home, use
insulation wrapped in plastic to prevent long-term degradation or aerolization
of any fibrous particulate. These
products are readily available at Lowe’s and Home Depot Stores.
Attic A.C. systems are a source of contamination that
not only sucks in fibers but minute mold and bacterial and insect fragments
(feces) that locate in this dark rarely used area. (See
I)
HVAC Systems (In General)
For some reason the architects and builders have not
come up with the concept that people live in the houses they design and build.
They have taken no time at all to consider that the
houses that they have completed are in fact contaminated boxes that ultimately
will cause sickness and death.
Picture a tightly insulated building that has had water
leaks or rain or high humidity during the building process. When that house (or building) is “boxed”
in, the A.C. units are being used by the contractor, which are sucking in
debris, mold, bacteria, etc.
(See J)
The air is contaminated with sheetrock dust, fibers,
cigarette smoke, chemicals and even food remnants left by laborers. The cabinets and carpets are off-gassing
formaldehyde. (See
K) All this is being
circulated by a contaminated A.C. system.
You look out a window and it is raining. The roof begins to leak and the
rainwater soaks the blown-in insulation.
Insects and rodents find wet insulation ideal nesting areas. (See
L)
The small fragments of fibers are settling through holes
around the lighting fixtures and down between two-by-fours, down the light
sockets, in the walls. (See
M)
The rain subsides and a foul odor emanates from under
the house. You walk around the
house and find a small door that enters into a two or three-foot high dirt
crawlspace (See N) that you can just about crawl around in and
find it is muddy, foul smelling and there are no drains to alleviate any
standing water (See O), which will infest the under floor beams
and flooring.
And to make things worse the one air conditioner is
located in this mud and the other one is in the damp attic along side the wet
fiberglass insulation.
It is a wonder why the A.C. systems, which are designed
fro our comfort and health, are always installed in the dirtiest, foulest, most
contaminated locations in our homes.
It is as if the homes were designed by the pharmaceutical companies. After living in a home of this
description for less than one year, your children will be diagnosed as
asthmatic. Someone will experience
respiratory ailments, sleep apnea, and chronic illness and even worse your
children’s life is being programmed with anti-biotic. Isn’t there something criminally wrong
with this picture?
Humidifiers are helpful at times. They are a source of diseases at other
times. When they are installed in
the plenum of a furnace they are designed to spray water into the ducts. This will add moisture into the house
and mold and bacteria into your lungs.
(See P) The
biohazards are spread by the air ducts (See P1) and eventually
appear coming out of the air supply.
(See P2)
Humidity (over 50%) is necessary for the growth and
habitat for dust mites. If you can
control your humidity levels to below 40%, dust mites cannot live in your
environment. If you don’t the dust
mites and their feces become airborne and can cause allergies and respiratory
complaints and aid in the spread of diseases. They are one of the top allergens of
note.
HEPA Vacuums (Not a Brand Name), a rating of 99.997 @
0.3 microns, are very effective in reducing airborne particulates and germs that
are causes of many allergies and diseases.
An average vacuum cleaner produces more dust into the air than it picks
up, it’s just that you can’t see it.
Many times the large particles of dust are just pulverized by the vacuum
and become minute microscopic airborne contaminants that may remain airborne for
months.
People with allergies and those who are hypersensitive
to dust and mold are safer in their homes if a HEPA or retrofitted HEPA is
attached to your current vacuum cleaner.
Abstract Information & Notes
Theodore R. Simon, M.D.
Date of talk:
Saturday, June 21, 2003, 2:30pm
Functional Imaging of Texas, PA
Phone:
214/528-2482
4429 Southern Avenue
Fax:
972/566-4762
Dallas, TX 75202
E-mail:
[email protected]
Medical School Attended:
Yale University
Major and date of Graduation:
M.D., 1975
Residency:
Nuclear Medicine
Board Certifications:
Nuclear Medicine
Current Job Description:
Private Practice
Disclosure Statement:
None
SPEECH TITLE:
“Neurotoxicity: Mold Exposure versus All
Causes”
The speaker has provided the information
below.
1.) Goals and objectives: Demonstrate the utility of scintigraphy in diagnosing
frequently encountered environmental illnesses.
2.) Outline of talk/abstract: Available nuclear medicine techniques will be shown as
they relate to specific illnesses with particular emphasis on the
brain.
3.) Conclusion of what is to be learned: Appropriate, cost-effective use of nuclear medicine
procedures in environmental illnesses can be achieved using a systematic
approach.
4.) References:
Neurotoxicity: Mold Exposure
versus All Causes
Theodore R. Simon,
M.D.
Goals and Objectives: We have developed an interest in neurotoxicity as
demonstrated by single photon emission computed tomography using a tracer for
glutathione function. Recently, we have attempted to focus this interest on
patients with putative neurotoxicity from mold exposure. That focus will be
explored and used as a basis for explaining the clinical utility of scintigraphy
of the brain as a clinical tool for addressing the care of environmentally
challenged patients.
The audience will learn how to determine whether this
technique is appropriate in individual patients that may require management for
environmental disease exposure.
Outline: We
have performed single photon emission computed tomography (SPECT) with
[technetium-99m]HMPaO on 30 patients taken from a sample of 153 consecutive
patients who presented with neurotoxicity and a history of mold exposure. These
data will be presented and compared with our normal sample and with previous
patients who have been examined for neurotoxicity from all
causes.
Our usual technique of early and late single photon
emission computed tomography using a triple head SPECT gamma camera and an
intravenous injection, under microprocessor control, of [technetium-99m]HMPaO
showed at least one of the findings that we expect in neurotoxicity was present
in every patient. These findings are: mismatch between the early and late
phases, shunting of the tracer to the soft tissues, temporal lobe asymmetry, and
a “salt and pepper pattern". The salt and pepper pattern is defined as multiple
hot and cold foci distributed throughout the cortex without regard to lobar
distribution.
The sample of thirty subjects to be presented was
acquired between November 22, 2000 and December 5, 2002. It consisted of 20
(67%) females and 10 (33%) males aged 5 to 67 years (average±sem= 43.3±2.18).
Overall, the population showed no severe cases with the neurotoxic pattern;
11(37%), moderate; 15(50%), mild; and 4(13%), without the pattern. This overall
distribution differs from the usual population of clinically neurotoxic
patients. Mold exposure was associated with an absence of the pattern to a
severe degree and by a higher incidence of moderate disease. Other, more subtle,
differences will be explained in the presentation.
Conclusions: Triple head single photon emission computed tomography
of the brain could be a useful adjunct to the clinical management of patients
with putative neurotoxic exposure from mold.
Abstract Information & Notes
Donald P.
Dennis, M.D., F.A.C.S.
Date of talk:
Saturday, June 21, 2003, 3:30pm
ENT & Facial Plastic Surgery, L.L.C.
Phone:
404/355-1312
3193 Howell Mill Rd., Suite 215
Fax:
404/352-2798
Atlanta, GA 30327
E-mail:
[email protected]
Major and date of Graduation:
MD, 1974
Residency:
Otolaryngology - Head & Neck Surgery, John’s Hopkins
Hospital
Board Certifications:
American Board of Otolaryngology & Head & Neck
Surgery
Current Faculty Appointments:
ENT Department, Northside Hospital
Current Job Description:
Private Practice, Atlanta
Disclosure Statement:
None
SPEECH TITLE: “Guidelines and Theory for Treatment of
Chronic Fungal Sinusitis with Reduction of Environmental Air Mold Load and
Anti-microbial Nasal Sprays Based on 14 Years Clinical Observation in 639
Patients”
The speaker has provided the information
below.
1.) Goals and objectives:
2.) Outline of talk/abstract:
3.) Conclusion of what is to be learned:
4.) References:
Title:
Guidelines and Theory
for Treatment of Chronic Fungal Sinusitis with Reduction of Environmental Air
Mold Load and Anti-microbial Nasal Sprays Based on14 Years Clinical Observation
in 639 Patients
Introduction:
Mayo Clinic study of
9-99 found 93% of all chronic rhinosinusitis (CRS) was due to Allergic fungal
sinusitis (AFS). AFS is caused by an immune response to the fungal antigen on
the nasal mucosa. The purpose of the study was to determine if antigen
(fungus) removal in the air and nasal mucosa would reverse the disease and
normalize the mucosa.
Methods
639 patients with AFS were studied. One-hour gravity SDA
agar plate exposures and Endoscopic nasal photographs were accomplished in the
patient’s environment before and after environmental remediation. Nasal fungal
cultures were accomplished initially with nasal swabs directly on SDA agar. A
protocol was developed to reduce mold in the environmental air and to reduce
mold in the nasal mucosa. Environmental air mold reductions was accomplished
with a combination of room HEPA air filtration, evaporation of Grapefruit seed
extract (GSE), vent covers with GSE spray, or non-ozone ionization in each room
the patients frequent. Nasal fungal reduction was accomplished by normal saline
nasal irrigations, and antimicrobial nasal sprays using a combination of
antibiotics- antifungals-steroids.
Results
639 patients were studied. 365 of 639 were able to
achieve a mold count of less than 4 per one-hour plate exposure. 343 of 365 or
94% showed normal nasal mucosa without infection. Of the 22 who failed to
normalize the nasal mucosa, 3 had lymphoma and 19 had positive nasal fungal
cultures. 219 did not reduce the mold count below 4 colonies and had various
degrees of mucosal disease remaining.
Conclusion
AFS is caused by an immune response to fungal antigen.
When the antigen is removed from the nose and air, the immune reaction stops and
the mucosa normalizes. Exceptions to this are other underlying diseases or
failure to find the location of mold exposure.
1.
Schubert, M.S. asuperantigen hypothesis for the pathogenesis of chronic
hypertrophic rhinosonusitris, allergic fungal sinusitis, and related disorders.
Ann Allergy, Asthsma, Immun.20014; 87:181.
2.
Ponikau JU, Sherris, Kern EB, et al. The diagnosis and incidence of
allergic fungal sinusitis. Mayo Clin Proc 1999;
74:877-884.
3.
Shin SH, Kita H. Abnormal immunologic responses to fungal antigens in
patients with chronic rhinosinusitis. J Allergy Clin Immunol 2001;
107:S163.
4.
Schubert MS, Goetz DW. Evaluation and treatment of allergic fungal
sinusitis. I. Demographics and diagnosis. J Allergy Clin Immunol 1998;
102:387-394.
Abstract Information & Notes
Larry Foster
Date of talk:
Saturday, June 21, 2003, 4:00pm
Enviro Cure
Phone:
404/876-3680
1280 West Peachtree Street, Suite 1606 Fax: &nbs l;