Scientific Studies

Numerous Studies have been documented as to the exposural links in Water Damaged Buildings and associated health issues from mould exposure

Clinical medicine and the budding science of indoor mold exposure-Stephen J. Genuis ? Faculty of Medicine at the University of Alberta, Canada

Recent research and increasing discussion in the medical literature have brought attention to public health concerns associated with mold exposure. Many kinds of mold and their mold-associated products have the potential to disrupt human molecular biochemistry and physiology, resulting in various types of acute and chronic affliction. As environmental health has not been a focus for medical education, some clinicians are not fully aware of the scope of mold-related health problems and are inadequately equipped to investigate and manage possible cases of mold exposure.

As a result, manifestations of mold-related illness often remain misdiagnosed and ineffectually treated. It is important for physicians to be aware of the pathogenesis, the manifestations, the investigations and the management of possible mold exposure. An overview of mold-related health problems and two case histories are presented for consideration (READ MORE) See attached article

Taskinen, TM et al. “Immunoglobulin G Antibodies to Molds in School-children From Moisture Problem Schools.”Allergy 2002; 57 (1) 9-16.

Summary: Children attending moisture damaged schools and those attending schools without moisture damage could not be differentiated by blood levels of antibodies (IgG). Only 6 of the 133 children had positive skin prick tests to mold while only 7 of 54 children had elevated IgE antibodies to mold. Although children attending the moisture damaged schools had more respiratory symptoms, they could not be distinguished from their counterparts attending schools without moisture damage on the basis of any of the blood tests.

Comments: Many studies have shown that individuals occupying damp or water damaged building have more respiratory symptoms and illnesses. The mechanism does not appear to be mediated by IgG or IgE antibodies. Current blood test cannot distinguish individuals who have occupied mouldy buildings from those who have not occupied mouldy buildings.

 

 

Salvilahti R, Uitti J, Laippala P, Husman T, Roto, P. “Respiratory Morbidity Among Children Following Renovation of a Water-Damaged School.”Archives of Environmental Health; 55 (6) 405-411.

Summary: This study again found that attendance at a moisture-damaged building was associated with an increase in respiratory symptoms and infections. Although their initial information was based on self- reporting of symptoms (which could involve bias) medical records from the local health center confirmed the increase in respiratory diagnoses and treatment with antibiotics among the children attending the moisture-damaged school. They continued to follow these children after remediation of the water damage in their school. The number of respiratory symptoms and infections decreased during the year after the remediation.

Comments: This is one of the few studies to have objective information (medical diagnoses and antibiotic treatment) to corroborate the increase in respiratory symptoms of individuals occupying a moisture-damaged building. This also appears to be the only study to follow the occupants of this building and the control building for a year after remediation of the building. Note that although mold is present in water damaged buildings mold has not been proven to be the cause of the increased respiratory illness.

2.Zureik, M et al. “Sensitization to Airborne Moulds and Severity of Asthma: Cross Sectional Study From European Community Respiratory Health Survey.” British Medical Journal 2002; 325: 1-7.

Summary: This study identified 1132 adults with current asthma from a survey of 30 medical centers in 11 countries (Europe, Australia, New Zealand and the United States) and tested them for severity of their asthma and their allergy to mold and other common allergens. Allergy to molds was less common than allergy to cat, pollen or dust mites. However, only allergy to mold and dust mites correlated with the severity of asthma.

Comments: Other studies have shown that asthmatics living in damp housing have more asthma attacks than those living in drier buildings. This study identifies allergy to molds and dust mites as risk factors for increased severity of asthma. Since both molds and dust mites need moisture levels to grow, these findings are consistent. This study increases the association between worsening of asthma and time spent in mouldy (damp) buildings although it does not prove that the mold is the direct cause of the worsening of the asthma. Individuals with asthma should minimize their time spent in damp buildings and owners of buildings should respond promptly to water damage in buildings.

3.Barnes C, Buckley S, Pacheco F, Portnoy J. “IgE-reactive Proteins From Stachybotrys Chartarum.”Annals of Allergy, Asthma & Immunology 2002; 89: 29-33

Summary: Plasma from 132 healthy blood donors was tested for antibodies to Stachybotrys chartarum. Using enzyme immunoassay 65 of 132 samples tested contained IgG antibodies to S. chartarum and 13 of 139 samples contained IgE antibodies to S. chartarum. The authors conclude that exposure and sensitivity to S. chartarum is much more widespread than previously recognized.

Comments: The authors admit that the positive tests could represent cross reactivity where antibodies formed to some other mold or non-mold protein reacted with the material from the Stachybotrys. This information means that measurement of antibody levels to Stachybotrys will not be useful to detect recent exposure to Stachybotrys. The IgE antibodies to S. Chartarum suggests that this fungus may be a cause of allergic reaction. Previous reports suggested that allergy to S. Chartarum did not develop or was extremely rare.

4.Vesper SJ, Vesper MJ. “Stachylysin May be a Cause of Haemorrhaging in Humans Exposed to Stachybotrys Chartarum.”Infection and Immunity 2002; 70: 2065-2069.

Summary: Stachylysin, a mycotoxin produced by Stachybotrys chartarum, was isolated and found to produce vascular leakage when injected into Lumbricus terrestis (earth worms). “Seven of eight strains of S. chartarum isolated from homes of infants with pulmonary hemorrhage (PH) in Cleveland, Ohio, and the strain from the lung of an infant with PH in Texas produced stachylysin in tryptic soy broth (TSB), whereas only one out of eight strains isolated from control homes produced stachylysin.” If sheep’s blood was added to the TSB, then all strains produced stachylysin. The authors conclude that their results support the hypothesis that stachylysin may be one agent responsible for haemorrhaging in humans.

Comments: Not all strains of S. chartarum produce specific mycotoxins when growing on water damaged building materials. The results obtained in the laboratory also may not reflect what was happening when the fungus was growing in the building. These results do provide a possible explanation for the low incidence of pulmonary hemorrhage in infants compared to the total number of buildings that have significant growth of S. chartarum. It may be that relatively few strains of S. chartarum can produce this mycotoxin when growing on the nutrients found in typical buildings. These results still do not provide proof that a mycotoxin from S. chartarum caused the pulmonary hemorrhage. No evidence has been presented to date that enough of any mycotoxin was or could have been airborne to cause the pulmonary haemorrhaging. Most mycotoxins are attached to spores so that spores must be airborne for exposure to the mycotoxin to occur. Most spores of S. chartarum are large (heavy) and sticky so that they do not tend to remain in air very long, especially when the substrate (paper or wood) is wet. When the building materials and the mold become drier more spores may become airborne.

5.Centers for Disease Control. “Update: Pulmonary Hemorrhage/ Hemosiderosis among Infants – Cleveland, Ohio, 1993-1996.”
Morbidity and Mortality Weekly Report 2000. 49: 180-184 (Also published in JAMA. April 19, 2000; 283: 1951-1953.)

Summary: The CDC conducted a review of the original research both internally with the CDC and by outside experts. “Both groups of reviewers recognized limitations that precluded drawing conclusions about clinical or etiologic ties to IPH (Idiopathic Pulmonary Hemosiderosis).”

Comments: This rebuttal has been misquoted in both the medical and lay press. The report from the CDC did not say that Stachybotrys chartarum did not cause the pulmonary hemorrhage in these infants. Rather the CDC report stated that the cause of the pulmonary hemorrhage was proven to be due to exposure to Stachybotrys chartarum. Although there clearly were flaws in the initial study, the CDC’s rebuttal appeared to have political overtones. The reviewers seemed to ignore additional information that was supplied by the researchers. Additionally the CDC declined to investigate additional reports of pulmonary hemorrhage in infants in other cities. What is puzzling to those who monitor this issue is why pulmonary hemorrhage is quite rare among infants if it is caused by exposure to fungi. Many homes have water damage and significant fungal growth and yet pulmonary hemorrhage remains quite rare. This suggests that multiple factors may be involved in causing pulmonary hemorrhage.

6.Elidemir O, Colasurdo G, Rossmann S. “Isolation of Stachybotrys From the Lung of a Child with Pulmonary Hemosiderosis.” Paediatrics 1999; 104: 964 – 966.

Summary: A 7-year old boy was diagnosed with pulmonary Hemosiderosis (chronic bleeding in the lung) and Stachybotrys chartarum was cultured from fluid removed from his lungs. He had been well until age 5 when his family moved into a house that experienced severe flood damage. The house was being repaired in stages by his family but still had significant contamination with Stachybotrys chartarum, as well as Penicillium and Aspergillis species. After a short time in the house he developed pneumonia followed by a chronic, non-productive cough, intermittent, low-grade fever and decreased appetite. No one who lived in the house smoked cigarettes. After diagnosis he lived in another house for 2 months until his damaged house was repaired. His symptoms resolved and he was symptom-free 10 months after diagnosis.

Comments: While this is only one case report it provides strong evidence that Stachybotrys chartarum inhaled from one’s home can cause pulmonary disease similar to the pulmonary hemorrhage identified in the Cleveland infants. Although Stachybotrys chartarum as well as other fungi was identified in the house no air sampling is reported. At this time there is no information regarding the level of airborne exposure that is necessary to cause disease. This report adds to the evidence that living in mouldy environments can be injurious to one’s health. It is also interesting to note that the house was successfully remediated.

Flappan, SM, Portnoy J, Jones P, Barnes C. “Infant Pulmonary Hemorrhage in a Suburban Home with Water Damage a Mold (Stachybotrys atra (chartarum)).” Environmental Health Perspectives, 1999; 107: 927-930.

Summary: A 1-month old infant developed vomiting and irritability followed by progressive respiratory distress requiring intubation and mechanical ventilation. Bleeding from the lungs occurred and analysis of lung fluids identified Hemosiderosis indicating that the bleeding was chronic. The infant recovered fully. An investigation of the home in which the infant was living revealed water damage due to a leaking roof. Stachybotrys chartarum and other mold species were found in the air in the infant’s room and in the paper-faced gypsum board in the closet of that room.

Comments: Unlike the older homes in the Cleveland series, this home was only 15 years old and located in a suburb. No fungi were identified within the infant’s lung. No tests were diagnostic of exposure to Stachybotrys chartarum. Infants under 1 year of age may be more susceptible to bleeding in the lungs regardless of the cause. Although in most cases it currently is not possible to determine if fungal spores and chemicals produced by molds have entered an individual’s lungs, the association between significant fungal growth within the home environment and illness in infants is growing.

7. Hodgson MJ et al. “Building-Associated Pulmonary Disease from Exposure to Stachybotrys chartarum and Aspergillus versicolor.” Journal of Occupational Environmental Medicine, 1998; 40: 241-249.

Summary: The authors investigated a courthouse and associated office buildings with known moisture problems where the workers had been complaining since initial occupancy two years earlier. Water damaged building materials were contaminated with several fungal species. A questionnaire was administered to the occupants of the damaged buildings and to workers in a “control” building. Some workers also had pulmonary functions tests (breathing tests). The workers in the problem buildings had many more complaints (both respiratory and non-specific) than did workers in the control buildings. Some workers showed a small decrease in their breathing capacity during the course of their workday in the contaminated building. The authors conclude that toxins from one or a combination of the molds species may represent the primary cause of the workers’ symptoms and abnormal breathing tests.

Comment: The title of the article makes it appear that the research proved that fungal exposure caused the building-associated pulmonary disease. The text in the article more accurately states “associated with” rather than “caused by.” Clearly some of the workers had asthma that was made worse by being in the building. This is an allergic process that does not require the presence of fungal toxins. However, most of the findings are based on the subjective reports of the workers who knew that there were moisture problems in the buildings. “No obvious contamination was noted on casual review of the control buildings, but no formal evaluation was undertaken of air quality.” The assumption was made that the control buildings were okay or better than the study buildings because the workers there did not have complaints and a casual review of the building did not identify problems.

Unhappy workers or employees in buildings with known physical problems are more likely to have complaints and symptoms than those working in buildings without those problems. We do not know if the case and control buildings had significant differences in indoor air quality. We are asked to assume that this is the case but then conclude that differences in air quality account for the differences in symptoms. This is not a sound basis for research.

While asthma can be exacerbated by specific fungal allergens it can also be worsened by exposure to high particulate levels or chemicals. The simultaneous occurrence of mold in a building and an increased number of occupant complaints is not proof that the mold is the cause of the complaints. However, this lack of proof of cause and effect is not a justification for delays in remediating mold and repairing defects that permit wetting of building materials. Enough studies conducted throughout the world have documented that occupants of damp buildings have more respiratory problems than occupants of dry buildings. We do not have to establish exactly what it is in damp buildings that cause illness to conclude that dry buildings are better for the occupants’ health. On the other hand good scientific studies are necessary to establish specific cause and effect.

 

 

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