DOCTORS REPORT
This family acquired a typical biotoxin-associated illness, following exposure and re-exposure to the indoor air environment of their residence, a double wide trailer, installed on their land. I have written briefly to you on 5/11/07; now that their lab results are all in, I can discuss their case with reasonable medical certainty. This family was well before moving into the trailer in July 1998. Their illness began almost immeadiately, through discovery of the evidence of water intrusion, and microbial growth is delayed. The descriptions provided to me by this family, of the construction defects, are consistent with the environmental reports provided to me; there were multiple reasons why there was excessive moisture in the interior environment of the residence. The excessive moisture is the source of the amplified microbial growth in the residence.
They leave the residence 11/21/02. Their symptoms show minimal improvement with removal from exposure; they remain ill until definitive treatment was prescribed here after their office visits of 4/02/07.
It is my opinion, to a reasonable degree of medical certainty, that the well documented physiologic abnormalities, together with the symptoms complex of this family, recorded before treatment with my protocols, are solely caused by the exposure to multiple toxigenic elements, including fungi that were present in their residence. They never should have been exposed to an indoor environment with ongoing sources of water intrusion.
I will call their illness complex, "Mold Illness", as a shortened versionof the phrase, a chronic, biotoxin associated illness, caused by exposure to the interior environment of a building with water damage, (WDB), that contains amplified growth of microbes, including, but not limited to fungi, that are toxigenic and/or elicit a pro-inflammatory innate immune response.
Given the time that has elapsed since the onset of their illness to definitive delineation of their deranged physiology, caused by their residence exposures, it is more likely than not, that they have sustained permanent physiologic impairment.
Given the chronicity of their illness since 1998, when the were exposed to their new residence, without change in symptoms, with absence of use of treatment protocols, designed to treat the innate immune response abnormalities seen in mold illness patients, up until now, and removal from exposure, we may conclude that, (1) self-healing did'nt occur; (2) only the residence made them ill; and (3) given their rapid improvement coinciding only with institution of therapy with an orally administered, non-absorbable anion binding resin, cholestyramine (CSM), and with exposure to all other environments, except for the doublewide, that their illness could only have resulted from exposure to toxigenic elements found in the water-damaged-building (WDB), that was their residence.
The abscence of thorough environmental testing data provided by this family, despite the history of environmental testing, does not change my opinion in this case for several reasons. First, testing does not confirm human illness; only documentation of the illness as will be discussed, can do that. Second, prescence of illness is independent of whatever testing may have been used, as shown in slides from the appendices to this report. Third, prescence of a history of water intrusion, prescence of musty smells and visible mold, all support the concept that the residence was contaminated.
There is no evidence that they had any non-residential exposures that are confounders of their diagnosis.
Given the duration of their illness and the magnitude of the multiple corroborating laboratory studies obtained to date, at their office visits here, I can predict that they will suffer permanent sequelae from their residential exposures. The chronic inflammatory illness they have is progressive; it did not simply vanish with the use of time, (as we have already seen), and therapies beyond the initial use of CSM alone are required. A second step in sequential therapy is currently underway, with additional lab testing pending at the end of this month.
I have included references for your use. This report will include data generated by my 9 year experience, treating over 4300 mold illness patients, as well as multiple peer-reviewed papers from our group, as well as the multiple invited academic presentations I have made over the last 9 years.
I note the abscence of complete environmental sampling performed in this case. It is not unusual to find that sampling efforts that are commissioned, and therefore paid for, will not be as comprehensive as one, looking back on what was done in the past, might like. Ample evidence of amplified microbial growth is present in this case; this is the necessary requirement of the first tier of the case definition, as will be discussed. The illness of this family is one caused by exposure to the complex biological mixture found in WDB. No one can say that the illness of this family, is simply due to production of mycotoxins by toxigenic fungi alone. That these kinds of organisms were present in the home is not questioned; the illness is due to the effectsof exposure to these kinds of organisms, and to other imflammagens present in the WDB. Not only are there multiple other sources of inflammatory responses, but other organisms are toxigenic as well, some synergistically, so with "Stachybotrys", for example, especially actinomycetes and gram negative bacteria. The role of endotoxin-producing bacteria in WDB is given less "press" than fungi, but bacteria is are significant participants in the complex biological mixture that we see in WDB, and are also implicated in a synergistic role with fungi. Further, we cannot discount the role of beta glucans, as initiators of inflammatory reponses in chronically exposed patients. Indeed, the US Centers for Disease Control and Prevention (CDC), have published their concerns regarding mycotoxins, endotoxins and beta glucans; each are commonly found when proper testing is done on WDB, in that each different substance is associated with human illness, (Rao C. and Brown C., et al, Applied and Environmental Microbiology, March 2007).
This family meets all criteria for a peer-reviewed, published, case defintion for mold illness. They had the potential for exposure to water damaged buildings (WDB), as evidenced by a long history of water intrusion, visible mold growth and prescence of musty smells.
It is my opinion to reasonable degree of certainty that not only did this family suffer chronic disease as a result of their exposure to the WDB, but also it is my opinion to a reasonable degree of medical certainty, that their illness was a result of gradually developing injury caused by exposure to toxigenic organisms, including, but not limited to, toxigenic fungi.
The syndrome that affects this family is a biotoxin associated illness, that has been given many names, including Sick Building Syndrome (SBS). The term "mold illness" used herein to apply to their illness, as reviewed earlier, does not imply that the only toxigenic organisms present were fungi; other toxigenic genera were involved as well, including actinomycetes, bacteria and mycobacteria.
We have statistical certainty, that the likelihood that this family could have aquired their illness from some other source other than the residence, has a probability of p <0.0000000001. What that infinitesimally small number means,is that it is inherently absurd, not to mention illogical, to think that the illness of this family is not due to exposure to the indoor environment in their residence. The odds that something other than the residence was responsible for the illness of these patients, is so low, as to become essentially incalculable. Added to that infintesimally small number, calculated for one person, is the epidemiologic reality that all of the family is ill, each with a syndrome that meets the criteria for a positive case identification in each. The likelihood that these patients could have developed illness independently is exponentially less likely compared to the probability that they shared a common source of exposure that is causitive of their illness.
The illness of this family is identical in concept to the illness of thousands of other biotoxin-associated illness patients. Once the inflammatory abnormalities initiated by the biotoxin exposure progresses, a final common pathway of illness is identified that generalizes to all sources of biotoxin asscociated illness, particularly mold illness.
The understanding of the physiology of mold illness has resulted from treatment of thousands of patients, noting changes in symptoms and biomarkers with particular specific interventions. This prescence of understanding stands in clear contradistinction to the lack of experience in actual mold illness of non-treating physicians or non-physicians.
We know that the frequency of mold illness susceptible patients approximates 24% of the normally distributed population. Almost a quarter of the normal populationis genetically susceptible to "chronic" mold illness. three quarters isn't.
We also know from years of experience of thousands of patients, that certain HLA DR haplotypes, found in leass than 4% of the population, comprise over 88% of the most affected patients, who typically have the worst clinical parameters and worst outcome. These haplotypes, called the "dreaded", are 4-3-53 and 11/12-3-52B. (Of these 4 family members, father, mother & 2 sons; the mother has the 4-3-53, the father and oldest son has the 12-3-52-B). For an individual patient, gene frequency in a large population becomes of seconday importance; however, knowing the genetic susceptibility of a given patient is enourmously helpful for the treating physician. Our experience has shown that even after successful acute phase treatment, patients with genetic susceptibility are subject to a dramatically increased risk, of the reacquisition of illness, following any subsequent exposure to WDB/Mold. The greatest susceptibility to repeat acqusition of illness is seen in those patients with the dreaded haplotypes.
If you look for something in the wrong place you wont find it. If you look for an object in the dark with a hammer instead of a flashlight, you won't see it. Indeed, if a mold illness patient has an allergy to mold, that allergy is an illness, that is in addition to the mold illness. "It is not a substitute". Allergy to mold is not mold illness. Allergy involves the arm of the immune response called acquired immunity. Mold illness involves innate immunity, not acquired immunity.
In this case, even if we didn't have the pervasive lab abnormalities and prescence of firm confirmation of case, which we do have, we need to add the additional weight that comes from the importance of the epidemiology; we have a common source of exposure and common illness known to be caused by such exposure in this family. Furthermore, the illness features shared by all of this family are not found in any of those without such exposure.
Before this familys office visit, the family had their medical histories furnished to our office, upon arrival, any new updated medical history was taken, they had physical exams, VCS/Visual Contrast Testing performed, with pulmonary functions, electrocardiogram and pulse oximetry performed. My office performed the needed blood draws and I ordered a comprehensive battery of laboratory tests for the entire family. No lab test known will diagnose mold illness by itself; the diagnosis is made by use of a standard, all encompassing process of medicine. The lab results of this family confirmed the intitial clinical impression that they were each a "case", with an illness caused by an exposure to biotoxins and sources of inflammatory reponses made by toxigenic organisms present in the residence. The number of lab abnormalities and diversity of sources of the physiologic disturbances they had were signifigant. They had abnormalities in multiple arms of the inflammatory cascade seen in mold illness patients, and not seen in patients who don't have biotoxin illness, including food allergy, and depression, for example.
This family is no different from my thousands of cases of mold illness; they are primed for subsequent illness acquired, following exposure to any WDB, solely caused by exposure to the indoor air environment of the residence. What this means, is that because of the illness that this family acquired from their residence, their life will be forever changed. They will need to find safety in a "bubble", such that they must avoid exposure to other WDB, and take protective medication if they are re-exposed.
In my opinion, this family will need ongoing medical care for the predictable future, to ensure that they wont suffer any additional mold illness following exposure to another WDB, as would happen, given their prior mold illness. To date, there are no therapies available for mold illness patients, that can correct the increased susceptibility to illness caused by re-exposure. I must emphasize, that newer modalities for treatment of mold illness may cause me to reassess these current care guidelines.
Progressive biotoxin effects masquerade as a wide range of other ailments-ranging from "flu-like-illness" to "chronic-fatigue-syndrome". Because the science of mold illness is relatively recent, the public is almost always unaware of the correct source of health symptoms caused by exposure to water-damaged buildings. Some cell and neural damage is asymptomatic. For 76% of persons, self-healing would occur following exposure. The others, if ill, would not self-heal in the abscence of intervention. Immunocompromised or genetically susceptible members pf the public would be particularly at risk, not only for toxicity, but, as is well established, though uncommon, for systemic fungal infections.
Since October 2002, there have been remarkeable changes in the opinions of "expert" panels regarding mold illness. Before that time "mold illness", wasn't accepted as a unique illness.
Recent treatment protocols have shown significant benefit in patients with illnesses essentially identical to this family. We see reduction of symptoms by over 75% in over 92% of 3800 patients treated. Those with improvement, less than 75% often are those with two particular HLA DR genotypes, representing the immune response genes, including the 4-3-53, and the 11-3-52B, or those with particular massive cytokine responses, sufficient to prevent a "re-setting" of normal cytokine physiology.
After having considered this family's past medical history, and absent any other confounding occupational or residence exposures, and after viewing their results of their comprehensive lab evaluation, and then comparing those factors to the current grouping of abnormalities, one can disregard hypothetical diagnoses in a differential list, as any physician who actually treats mold illness knows.
As Fisk and the IOM have discussed, exposure to damp buildings and the microbial growth fomented by such dampness clearly will add to the burden of asthma. If Fisk is right that 21% of asthma is due to exposure to moldy environments, then we must ask, what additional percentage of patients with allergies are worsened by such exposure. No reasonable man will deny that allergy to molds causes persistent health symptoms with ongoing exposure. Having discussed allergy briefly, I will emphasize that it is clear, that this family's symptoms are consistent with chronic, bio-associated illness, meeting the case definition which I used in a peer-reviewed paper presented to the 5th International Conference on Bioaerosols, Fungi, Bactieria, Mycotoxins and Human Health on September 10, 2003 in Saratoga springs, NY. This study design (called ABB AB) is more powerful than a cross-section study in that it gives longitudinl before and after events in three types of interventions, including three prospective studies, using the patient as his own control and providing proof of causation of illness.
