Re: MCS brought on by toxid mold
Posted by ff on 10/14/04
I think Mary gave you some good advice, and as far as the insults, you
should have been posting a year ago when the Wrath of Mary was common.
Basically, we/you may sound irrational, and we need to take a hard look
at that. If you want to prent the issue, I say drop phrases like get-a-
piece-of-the-pie, crazy, hypochondriac, i.e. present your case in a way
that gives credibility to what you say (I say this, realizing that I
may be an offender as well).
On 10/13/04, Angie wrote:
> 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 email@example.com. Thank you for taking the time to
> read this.
> 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
> 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
> 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. firstname.lastname@example.org
> 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
> 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. email@example.com
> 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&37; of cases.
> HLA DR, MSH deficiency, AGA-IgG and ACLA-IgM increased the case
> detection rate to 100&37;. For patients with MMP9 over 400, HLA DR
> 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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