Veritox means Truth-Poison

Working to stop the institutionalized discrimination of the Toxic Mold Disabled (TMD) since 2004

The Veritox Theory

The creators of the below risk assessment model are Bruce Kelman and Bryan Hardin of Veritox, Inc.  Veritox is the registered name of the corporation they own along with four other people, Veritox®  Inc.  The word “veritox” is derived from two Latin words: “veritas” for truth and “toxicus” for poison.  Together these words mean “truth poison”

In 2003 Mr. Kelman and Mr. Hardin accepted no less than $25,000.00 from the Manhattan Institute Center for Legal Policy to publish a paper for the U.S. Chamber of Commerce Institute for Legal Reform.  Within the paper titled “A Scientific View of the Health Effects of Mold” Mr. Kelman and Mr. Hardin professed they had scientifically proven:

“Thus the notion that Toxic Mold is an insidious secret killer as so many media reports and trial lawyers would claim, is Junk Science unsupported by actual scientific study”

It is scientific fraud to make such a grandiose, unscientific, and broad claim based solely on the application of extrapolations to someone else’s actual research. Never the less, the Veritox Theory has been the mainstay of the defense in mold litigation since 2002.

Veritox, Inc. are currently serving as expert witnesses for the United States government. They were hired (again) by the Department of Justice on July 14, 2016.

THE VERITOX THEORY

(no longer promoted as a position statement of the American College of Occupational and Environmental Medicine; but still used against the sick in court and in physician educational materials by other CDC funded “nonprofit” medical associations and in toxic torts by “expert” defense witnesses.)

In single-dose in vivo studies, S. chartarum spores have been administered intranasally to mice31 or intratracheally to rats.76,77 High doses (30 x 106 spores/kg and higher) produced pulmonary inflammation and hemorrhage in both species. A range of doses were administered in the rat studies and multiple, sensitive indices of effect were monitored, demonstrating a graded dose response with 3 x 106 spores/kg being a clear no-effect dose. Airborne S. chartarum spore concentrations that would deliver a comparable dose of spores can be estimated by assuming that all inhaled spores are retained and using standard default values for human subpopulations of particular interest 78 – very small infants,† school-age children,†† and adults.††† The no-effect dose in rats (3 x 106 spores/kg) corresponds to continuous 24-hour exposure to 2.1 x 106 spores/m3 for
infants, 6.6 x 106 spores/m3 for a school-age child, or 15.3 x 106 spores/m3 for an adult.
If the no-effect 3 x 106 spores/kg intratracheal bolus dose in rats is regarded as a 1-minute
administration (3 x 106 spores/kg/min), achieving the same dose rate in humans (using the same default assumptions as previously) would require airborne concentrations of 3.0 x 109 spores/m3 for an infant, 9.5 x 109 spores/m3 for a child, or 22.0 x 109 spores/m3 for an adult.
In a repeat-dose study, mice were given intranasal treatments twice weekly for three weeks with “highly toxic” s. 72 S. chartarum spores at doses of 4.6 x 106 or 4.6 x 104 spores/kg (cumulative doses over three weeks of 2.8 x 107 or 2.8 x 105 spores/kg).79 The higher dose caused severe inflammation with hemorrhage, while less severe inflammation, but no hemorrhage was seen at the lower dose of s. 72 spores. Using the same assumptions as previously (and again ignoring dose rate implications), airborne S. chartarum spore concentrations that would deliver the nonhemorrhagic cumulative three-week dose of 2.8 x 105 spores/kg can be estimated as 9.4 x 103 spores/m3 for infants, 29.3 x 103 spores/m3 for a school-age child, and 68.0 x 103 spores/m3 for adults (assuming exposure for 24 hours per day, 7 days per week, and 100% retention of spores). The preceding calculations suggest lower bound estimates of airborne S. chartarum spore concentrations corresponding to essentially no-effect acute and subchronic exposures. Those concentrations are not infeasible, but they are improbable and inconsistent with reported spore concentrations. For example, in data from 9,619 indoor air samples from 1,717 buildings, when S. chartarum was detected in indoor air (6% of the buildings surveyed) the median airborne concentration was 12 CFU/m3 (95% CI 12 to 118 CFU/m3).80
Despite its well-known ability to produce mycotoxins under appropriate growth conditions, years of intensive study have failed to establish exposure to S. chartarum in home, school, or office environments as a cause of adverse human health effects. Levels of exposure in the indoor environment, dose-response data in animals, and dose-rate considerations suggest that delivery by the inhalation route of a toxic dose of mycotoxins in the indoor environment is highly unlikely at best, even for the hypothetically most vulnerable subpopulations.

References to Dr. Carol Rao’s Mechanistic Work, to which Bruce Kelman and Bryan Hardin of Veritox, Inc. applied their extrapolations to cast doubt of causation of disabilities caused by exposure to mycotoxins and other biocontaminants in the indoor environment are:
76. Rao CY, Brain JD, Burge HA. Reduction of pulmonary toxicity of Stachybotrys chartarum spores by methanol extraction of mycotoxins. Appl Environ Microbiol. 2000;66:2817-21.

“We provide evidence that there is a dose-related association between an acute
exposure to toxin-containing S. chartarum spores and measurable pulmonary responses. The consequences of low-level chronic exposure remain to be investigated, as does the relevance of the rodent data to human exposure.”

77. Rao CY, Burge HA, Brain JD. The time course of responses to intratracheally instilled
toxic Stachybotrys chartarum spores in rats. Mycopathologia. 2000;149:27-34.

“ We have demonstrated that a single, acute pulmonary exposure to a large quantity of Stachybotrys chartarum spores by intratracheal instillation causes severe injury detectable by bronchoalveolar lavage. The primary effect appears to be cytotoxicity and inflammation with hemorrhage. There is a measurable effect as early as 6 h after instillation, which may be attributable to mycotoxins in the fungal spores. The time course of responses supports early release of some toxins, with the most severe effects occurring between 6 and 24 h following exposure. By 72 h, recovery has begun, although macrophage concentrations remained elevated”

When linear dose, no threshold (LNT) models are misapplied toward promoting the false concept that an environmental injury is a proven figment of a person’s imagination and this is then portrayed by position statement to be the scientific understanding of thousands of learned physicians; the damages caused by the resultant mass-unawareness of a hazard and mass-discrimination of the environmentally-injured can be colossal.

People sickened by exposures to biotoxins and inflammagens often found in water damaged buildings WDB need medical attention for their physiologically-caused Idiopathic Environmental Intolerances (EI) (also known as Multiple Chemical Sensitivity (MCS)[19] or Toxicant induced Loss of Tolerance (TILT)).[20] They need help for their WDB induced Chronic Fatigue Syndrome (CFS), Fibromyalgia, and Myalgic Encephalomyelitis (ME) (also known as Chronic Inflammatory Response Syndrome from WDB Exposures (CIRS-WDB)).[21] They and environmentally-trained physicians repeatedly report newly-acquired intolerances to WDB re-exposure, to mold re-exposure, to chemicals, and to various forms of air pollution, foods and liquids (EI) after the initial not-normal exposure.  They also repeatedly report newly-acquired symptoms such as brain fog, difficulty concentrating, extreme fatigue, phantom pain, and chronic inflammation of various and multiple organs of the body, CIRS-WDB.  [22] [23]

Neither the environmentally-disabled nor society as a whole, need federally funded “nonprofit” medical trade associations such as the American College of Medical Toxicology (ACMT) [24] adding insult to injury by promoting the discriminatory false concept that the environmentally disabled are hypochondriacs and liars.

America’s children and elderly in low-income housing are the most vulnerable sub-population-victims of the spinning and lying.[35] When WDB-illnesses are not recognized as environmentally-induced, the false concept that WDBs pose no real public health threat is then used as an insidious excuse to not properly and timely remediate public housing. Occupants who complain are then labeled as liars and hysterics for saying they are gravely ill, while left to occupy WDB hazardous environments as their health declines.

The 2014 report by the National Institute of Health (NIH) entitled “Final Report, Pathways to Prevention Workshop: Advancing the Research on Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome” describes the dire adverse impact on the public when physicians are misdirected by trusted organizations.[36]

To quote from the NIH Report:

“Both society and the medical profession have contributed to ME/CFS patients feeling disrespected and rejected. They are often treated with skepticism, uncertainty, and apprehension and labeled as deconditioned or having a primary psychological disorder. ME/CFS patients often make extraordinary efforts at extreme personal and physical costs to find a physician who will correctly diagnose and treat their symptoms while others are treated inappropriately causing additional harm. Overall, the debilitating effects of ME/CFS can result in financial instability due to the consequences of the illness (e.g., the loss of employment, home)….economic burden estimated to be between $2 billion and $7 billion in the United States… results in major disability for a large proportion of the people affected.”

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[19] 1998, U.S. Congressman Bernard Sanders speaking before the House. “MCS is a chronic condition marked by heightened sensitivity to multiple different chemicals and other irritants at or below previously tolerated levels of exposure….MCS is often accompanied by impaired balance, memory and concentration.http://someoneskid.angelfire.com/boycottsbu2000/RepSandersChemicalSensitivity.html

[20] 2001 Miller CS The compelling anomaly of chemical intolerance. Ann N Y Acad Sci. 2001 Mar;933:1-23. http://www.ncbi.nlm.nih.gov/pubmed/12000012

[21] 2014 Shoemaker RC, House D, Ryan JC, Structural brain abnormalities in patients with inflammatory illness acquired following exposure to water-damaged buildings: A volumetric MRI study using NeuroQuant® Neurotoxicology and Teratology 45 (2014) 18–26 http://www.ncbi.nlm.nih.gov/pubmed/24946038

[22] 2014 Dr. Mary Ackerley “The Brain on Fire The role of toxic mold in triggering psychiatric symptoms” http://freepdfhosting.com/5e77f45ec4.pdf

[23] 2015 Mold Asbestos Connecticut “37 Health symptoms caused by moldhttp://www.asbestosmoldct.com/37-health-conditions-caused-by-mold/

[24] ACMT receives funding from the U.S. Department of Health and Human Services (HHS) Agency for Toxic Substance and Disease Registry (ATSDR) http://www.atsdr.cdc.gov/emes/partners.html & http://www.guidestar.org/FinDocuments/2013/870/460/2013-870460513-0add6264-9O.pdf [Page 9]

[25] 2006 Stone DC, Boone KB, Back-Madruga C, Lesser IM. Has the rolling uterus finally gathered moss? Somatization and malingering of cognitive deficit in six cases of “toxic mold” exposure. Clin Neuropsychol. 2006 Dec;20(4):766-85. http://www.ncbi.nlm.nih.gov/pubmed/16980261

[26] Source Watch & WSJ re: mold defense witness Paul Lees-Haley http://freepdfhosting.com/754f688a2f.pdf

[35] 2014 NRDC “Rampant Mold & Moisture Problems in NYC Public Housing” http://www.nrdc.org/ej/mold-and-moisture-in-public-housing.asp

[36] 2014 NIH “Final Report, Pathways to Prevention Workshop: Advancing the Research on ME/CFS” https://prevention.nih.gov/docs/programs/mecfs/ODP-P2P-MECFS-FinalReport.pdf

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