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    Re: MCS brought on by toxid mold

    Posted by Angie on 10/13/04

    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 Thank you for taking the time to
    read this.



    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.
    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
    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.
    choice reaction time, color discrimination, blink reflex, visual
    fields, grip, hearing,
    problem-solving, verbal recall, perceptual motor speed, and memory
    measured. Medical histories, mood states, and symptom frequencies
    were recorded
    with checklists, and spirometry was used to measure various pulmonary
    and flows. Neurobehavioral comparisons were made after individual
    were adjusted for age, educational attainment, and sex. Significant
    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
    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
    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,

    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,

    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]



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

    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.

    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.

    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

    PMID: 14612611 [PubMed - indexed for MEDLINE]


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

    Health symptoms caused by molds in a courthouse.

    Lee TG.

    Faculty of Environmental Design, The University of Calgary, Calgary,
    Alberta, Canada.

    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

    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
    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.

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