Taskinen, TM et al. “Immunoglobulin G Antibodies to Molds in Schoolchildren 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 based on 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
centre 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 centres 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 suggest 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 Aspergillus 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
mould’s species may represent the primary cause of the workers’ symptoms
and abnormal breathing tests.
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.
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
Schoolchildren 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
centre 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 centres 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 suggest 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 Aspergillus 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
mould’s 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.