Re: MCS brought on by toxid mold

More | Report Post

Hi all. I don't know who Sharon is. I am Angie and new to the
board. All I meant by "get a piece of the pie," is that you should be
willing to educate yourself about toxic mold and its effects for the
sake of understanding victims and also for prevention. If you are
hard hearted enough to not do it for those reasons, and are willing
to learn more in order to take on more cases (for business purposes,)
then do it. I don't care why you educate yourself, just do it. I
say this with confidence because I believe that regardless to your
motives for learning more about toxic mold, you will learn more and
become more sensitive to victims and their needs. I believe that as
public awareness and proof grows, you'll finally resign yourself to
believing that toxic mold causes illness.

Mary, I'm not trying to sound harsh or irrational. I'm speaking from
my experience. After all, isn't that all we truly know? I know
you're not here to make friends, but your tone and responses have
been very insensitive to those who know first hand what this mold can
do. If I sound overly sensitive, I am. It's because I've had to try
to convince people for the last few years that I'm not crazy. That
my symptoms aren't psychosymatic. I never wanted to believe that my
house could be making me sick. I didn't make this stuff up. You
think I want to look crazy to people? I'm not a hypochondriac. I
believe that my family will get better. I believe that someday there
will be a treatment for the conditions we all now have.
Hypochondriacs don't wish to get better. I do. If you were to poll
hundreds of mold victims from around the country that have never met,
you'd find that we all share similar symptoms and diseases. While
some symptoms vary, there is a very common list of symptoms that we
share. If we have never met or talked to one another, but the one
trauma we all share is exposure to toxic mold, and we all share a
common list of symptoms, how can we all be making it up?

I am sharing this information in hopes to educate people. My wish is
to not insult anyone. Everyone is entitled to their opinion,
including you Mary. I just want to squelch the lack of compassion
and insensitive comments that so many victims have to continually
hear from "so called" professional people that know nothing, nor take
the time to learn anything about their situation. So please take
what I share and learn about it.

I truly pray that none of you ever have to experience what my family
has experienced. We were a family full of dreams and aspirations for
one another. My 2 children are very artistically talented and were
accepted into a prestigous art school. Their education has now been
greatly hindered due to their health problems and everyday has become
a constant struggle to keep them motivated and encouraged. They have
given up. So understand that this isn't about me. It's about
thousands of innocent children out there. School children that are
being exposed to moldy schools, teachers being made ill, and adults
that are great contributors to society that are suddently taken from
our work force and disabled. It's not as small as my family, it's a
grave injustice to our entire nation and our nation's future.

Here are some scientific studies that you may find helpful. There
are a lot of good books out there, but there are a lot of quacks
also. The only book I truly recommend for good evidence is "Mold &
Mycotoxins," by Dr. Kaye H. Kilburn, M.D.

She worked very closely with Dr. Dorr Dearborn (Case Western
University/Children's Hospital, Cleveland, Ohio)who is famous for
finding a link between pulmonary hemorrage in infants and mold
exposure. Both are reknowned for their work in the area of mold
treatment and studies.

I have a copy of the testimony Dr. Stephen C. Redd, from the CDC and
The Department of Health and Human Services gave before Congress
saying that mold can cause health problems. I would be happy to send
it to anyone that is interested. These studies may be difficult to
read and very lengthy. I would love to pass them on to anyone that
would like to have copies. Anyone that wants to contact me can email
me at moldvictimsunited@yahoo.com. Thank you for taking the time to
read this.

Angie

A FEW STUDIES:

Indoor mold exposure associated with neurobehavioral and
pulmonary impairment: a preliminary report
by PubMed
Kilburn KH.
University of Southern California, Keck School of Medicine,
Environmental Sciences
Laboratory, Alhambra, California 91803, USA. Kilburn@usc.edu
Recently, patients who have been exposed indoors to mixed molds,
spores, and
mycotoxins have reported asthma, airway irritation and bleeding,
dizziness, and
impaired memory and concentration, all of which suggest the presence
of pulmonary
and neurobehavioral problems. The author evaluated whether such
patients had
measurable pulmonary and neurobehavioral impairments by comparing
consecutive
cases in a series vs. a referent group. Sixty-five consecutive
outpatients exposed to
mold in their respective homes in Arizona, California, and Texas were
compared with
202 community subjects who had no known mold or chemical exposures.
Balance,
choice reaction time, color discrimination, blink reflex, visual
fields, grip, hearing,
problem-solving, verbal recall, perceptual motor speed, and memory
were
measured. Medical histories, mood states, and symptom frequencies
were recorded
with checklists, and spirometry was used to measure various pulmonary
volumes
and flows. Neurobehavioral comparisons were made after individual
measurements
were adjusted for age, educational attainment, and sex. Significant
differences
between groups were assessed by analysis of variance; a p value of
less than 0.05
was used for all statistical tests. The mold-exposed group exhibited
decreased
function for balance, reaction time, blink-reflex latency, color
discrimination, visual
fields, and grip, compared with referents. The exposed group's scores
were reduced
for the following tests: digit-symbol substitution, peg placement,
trail making, verbal
recall, and picture completion. Twenty-one of 26 functions tested
were abnormal.
Airway obstructions were found, and vital capacities were reduced.
Mood state scores
and symptom frequencies were elevated. The author concluded that
indoor mold
exposures were associated with neurobehavioral and pulmonary
impairments that
likely resulted from the presence of mycotoxins, such as
trichothecenes.
Publication Types:
• Clinical Trial
• Controlled Clinical Trial
• Randomized Controlled Trial
PMID: 15143851 [PubMed - indexed for MEDLINE]

*********************************************************

1: Arch Environ Health. 2003 Aug;58(8):464-74. Related Articles,
Links

Neural autoantibodies and neurophysiologic abnormalities in patients
exposed to molds in water-damaged buildings.

Campbell AW, Thrasher JD, Madison RA, Vojdani A, Gray MR, Johnson A.

Medical Center for Immune and Toxic Disorders, Spring, Texas 77386,
USA. md@immunotoxicology.com

Adverse health effects of fungal bioaerosols on occupants of water-
damaged homes and other buildings have been reported. Recently, it
has been suggested that mold exposure causes neurological injury. The
authors investigated neurological antibodies and neurophysiological
abnormalities in patients exposed to molds at home who developed
symptoms of peripheral neuropathy (i.e., numbness, tingling, tremors,
and muscle weakness in the extremities). Serum samples were collected
and analyzed with the enzyme-linked immunosorbent assay (ELISA)
technique for antibodies to myelin basic protein, myelin-associated
glycoprotein, ganglioside GM1, sulfatide, myelin oligodendrocyte
glycoprotein, alpha-B-crystallin, chondroitin sulfate, tubulin, and
neurofilament. Antibodies to molds and mycotoxins were also
determined with ELISA, as reported previously. Neurophysiologic
evaluations for latency, amplitude, and velocity were performed on 4
motor nerves (median, ulnar, peroneal, and tibial), and for latency
and amplitude on 3 sensory nerves (median, ulnar, and sural).
Patients with documented, measured exposure to molds had elevated
titers of antibodies (immunoglobulin [Ig]A, IgM, and IgG) to neural-
specific antigens. Nerve conduction studies revealed 4 patient
groupings: (1) mixed sensory-motor polyneuropathy (n = 55, abnormal),
(2) motor neuropathy (n = 17, abnormal), (3) sensory neuropathy (n =
27, abnormal), and (4) those with symptoms but no neurophysiological
abnormalities (n = 20, normal controls). All groups showed
significantly increased autoantibody titers for all isotypes (IgA,
IgM, and IgG) of antibodies to neural antigens when compared with 500
healthy controls. Groups 1 through 3 also exhibited abnormal
neurophysiologic findings. The authors concluded that exposure to
molds in water-damaged buildings increased the risk for development
of neural autoantibodies, peripheral neuropathy, and neurophysiologic
abnormalities in exposed individuals.

PMID: 15259425 [PubMed - indexed for MEDLINE]

********************************************************

Show:

1: Arch Environ Health. 2003 Aug;58(8):452-63. Related Articles,
Links

Psychological, neuropsychological, and electrocortical effects of
mixed mold exposure.

Crago BR, Gray MR, Nelson LA, Davis M, Arnold L, Thrasher JD.

Neurobehavioral Health Services, Tucson, Arizona 85712, USA.
bcbrain1@msn.com

The authors assessed the psychological, neuropsychological, and
electrocortical effects of human exposure to mixed colonies of
toxigenic molds. Patients (N = 182) with confirmed mold-exposure
history completed clinical interviews, a symptom checklist (SCL-90-
R), limited neuropsychological testing, quantitative
electroencephalogram (QEEG) with neurometric analysis, and measures
of mold exposure. Patients reported high levels of physical,
cognitive, and emotional symptoms. Ratings on the SCL-90-R
were "moderate" to "severe," with a factor reflecting situational
depression accounting for most of the variance. Most of the patients
were found to suffer from acute stress, adjustment disorder, or post-
traumatic stress. Differential diagnosis confirmed an etiology of a
combination of external stressors, along with organic metabolically
based dysregulation of emotions and decreased cognitive functioning
as a result of toxic or metabolic encephalopathy. Measures of toxic
mold exposure predicted QEEG measures and neuropsychological test
performance. QEEG results included narrowed frequency bands and
increased power in the alpha and theta bands in the frontal areas of
the cortex. These findings indicated a hypoactivation of the frontal
cortex, possibly due to brainstem involvement and insufficient
excitatory input from the reticular activating system.
Neuropsychological testing revealed impairments similar to mild
traumatic brain injury. In comparison with premorbid estimates of
intelligence, findings of impaired functioning on multiple cognitive
tasks predominated. A dose-response relationship between measures of
mold exposure and abnormal neuropsychological test results and QEEG
measures suggested that toxic mold causes significant problems in
exposed individuals. Study limitations included lack of a comparison
group, patient selection bias, and incomplete data sets that did not
allow for comparisons among variables.

PMID: 15259424 [PubMed - indexed for MEDLINE]

****************************************************

1: ScientificWorldJournal. 2003 Nov 3;3:1058-64. Print 2003 Nov 3.
Related Articles, Links

Biochemical changes in the serum of patients with chronic toxigenic
mold exposures: a risk factor for multiple renal dysfunctions.

Anyanwu E, Campbell AW, Vojdani A, Ehiri JE, Akpan AI.

Neurosciences Research, Cahers Inc., Conroe, TX, USA.
ebereanyanwu@msn.com

This paper analyzes and presents the biochemical abnormalities in the
sera of patients presenting with chronic mycosis in order to
investigate the relationship with the risks of multiple renal
disorders. The study population (n = 10) consisted of six females and
four males (mean age 36.3 years) exposed by toxic molds in their
homes and offices for an average of 2.8 years. The control group
comprised ten people, five males and five females (mean age 35.9
years) without any known exposures to toxic molds. Blood samples were
obtained from both the patients and the controls and were processed
using specific biochemical methods that included enzyme-linked
immunoabsorbent assay (ELISA). There were biochemical abnormal
concentrations in creatinine, uric acid, phosphorus, alkaline
phosphotase, cholesterol, HDH, SGOT/AST, segmented neutrophils,
lymphocytes, total T3, IgG and IgA immunoglobulins with significant
differences between patients and controls. These abnormalities were
consistent with multiple renal disorders. The major complaints of the
mycosis patients were headaches, pulmonary symptoms, allergic
reactions, memory loss, skin rashes, blurred vision symptoms,
fatigue, and runny nose. These findings were depictive of a strong
association of chronic mycosis with abnormal renal indicators. It was
concluded that, although this research was a pilot investigation,
based on the overall results, people exposed to chronic indoor
environmental toxic molds were at risk of multiple renal
complications.

PMID: 14612611 [PubMed - indexed for MEDLINE]

*****************************************************

1: Arch Environ Health. 2003 Jul;58(7):442-6. Related Articles,
Links

Health symptoms caused by molds in a courthouse.

Lee TG.

Faculty of Environmental Design, The University of Calgary, Calgary,
Alberta, Canada. lee@ucalgary.ca

A majority of occupants of a newly renovated historic courthouse in
Calgary, Alberta, Canada, reported multiple (3 or more) health-
related symptoms, and several reported more than 10 persistent
symptoms. Most required at least 1 day outside of the building to
recover from their symptoms. Molds that produce mycotoxins, such as
Stachybotrys chartarum and Emericella nidulans, were identified in
the building, along with fungal organisms of the genera Aspergillus,
Penicillium, Streptomyces, Cladosporium, Chaetomium, Rhizopus/Mucor,
Alternaria, Ulocladium, and Basidiomycetes. Renovations to this
historic had building failed to provide adequate thermal and vapor
barriers, thus allowing moist indoor air to migrate into the building
enclosure, causing condensation to develop. Mold grew on the
condensation and was dispersed throughout the courthouse, including
on furniture and files. The courthouse was closed and a new facility
was modified with low-offgassing materials, better ventilation and
air filtration, and strict building maintenance to accommodate those
occupants of the older building who had developed multiple chemical
sensitivities.

PMID: 15143857 [PubMed - indexed for MEDLINE]

**************************************************

Abstract: Identifying markers for chronic illness in pediatric
patients exposed to water damaged buildings: Linkage disequilibrium
of HLA DR, MSH, MMP9 and autoantibodies

Authors: Ritchie C. Shoemaker¹, Courtney Holt¹, Dennis House¹, HK
Hudnell²
¹Center for Research on Biotoxin Associated Illnesses, Pocomoke, Md;
²US EPA NHEERL, Research Triangle Park, NC

Background: No studies have previously identified biomarkers
adequate to create a case definition of illness associated with
exposure to water damaged buildings (WDB) in pediatric patients.
Previous work from this facility has presented a case definition of
illness in adults that includes exposure, symptoms and absence of
confounders, together with biomarkers HLA DR genotypes of the immune
response genes; deficiency of the hypothalamic immunomodulatory
hormone, alpha melanocyte stimulating hormone (MSH); excess pro-
inflammatory cytokine responses, represented by matrix
metalloproteinase-9 (MMP9), deficits in visual contrast and pituitary
hormone dysregulation. We have seen an increased incidence of
antibodies to gliadin, cardiolipin and myelin basic protein in adults
with chronic illness following exposure to WDB. Here we present data
supporting a pediatric case definition using multiple biomarkers from
66 patients with illness following exposure to WDB.

Methods: Patients under age 19 coming for treatment of chronic
illness at a specialized medical clinic provided informed consent for
evaluation and blood testing prior to initiation of definitive
therapy for presumptive chronic, biotoxin associated illness.
Symptoms were recorded and blood was sent to national high complexity
labs for analysis of HLA DR genotype, MSH, MMP9, anticardiolipins
(ACLA), antigliadins (AGA) and myelin basic protein (MBP) antibodies.
Lab parameters were compared to in-house registries of control
patients and published registries. Following treatment and
confirmation of diagnosis, cases were then analyzed by biomarker to
identify unique diagnostic features.

Results: Control populations have markedly different HLA DR genotype
distributions from cases, with relative risks for illness identified
for the same genotypes as reported previously in adults. Affected
patients had lower levels of MSH and MMP9 than controls. Marked
increase in incidence of antibodies to antigliadin IgG,
anticardiolipin IgM and myelin basic protein antibodies was found in
affected patients compared to controls. Taken together, the
combination of potential for exposure, absence of confounding
diagnoses, presence of distinctive groupings of symptoms, including
fatigue and cognitive problems identified over 85% of cases. Adding
HLA DR, MSH deficiency, AGA-IgG and ACLA-IgM increased the case
detection rate to 100%. For patients with MMP9 over 400, HLA DR and
MSH deficiency alone identified all cases.

Conclusion: Specific genetic, physiologic and neurotoxicologic
factors can be identified in pediatric patients that identify cases
of chronic illness due to exposure to WDB. Physiologic mechanisms
associated with increased production of particular autoantibodies
will require further study.