Fungal Contamination in Buildings: Health Effects Investigation Methods

Fungal Contamination in Buildings: Health Effects Investigation Methods
Fungal Contamination
in Public Buildings:
Health Effects and
Investigation Methods
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Fungal Contamination
in Public Buildings:
Health Effects and
Investigation Methods
Our mission is to help the people of Canada
maintain and improve their health.
Health Canada
Cover photo: Health Canada
Published by authority of the
Minister of Health
Également disponible en français sous le titre :
Contamination fongique dans les immeubles publics :
Effets sur la santé et méthodes d’évaluation
This publication can be made available in/on computer
diskette/large print/audio-cassette/braille upon request.
© Her Majesty the Queen in Right of Canada, 2004
Cat. H46-2/04-358E
ISBN 0-662-37432-0
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A preliminary version of this document was drafted by:
J. David Miller, Health Canada
Nicolas L. Gilbert, Health Canada
Robert E. Dales, Health Canada
The following individuals provided substantial input to the
document:
Randy Angle,
Alberta Environment
Pierre L. Auger,
Direction de santé publique de Québec
Yves Brissette,
Commission de la santé et de la sécurité
au travail du Québec
Bert Brunekreef,
Universiteit Utrecht, The Netherlands
Norman King,
Direction de santé publique de Montréal-Centre
Mark Lawton,
Morrison Hershfield, Inc.
Gilles Levasseur,
Health Canada
Luc Maheux,
Health Canada
Philip R. Morey,
Air Quality Sciences, inc., USA
Tedd Nathanson,
Public Works and Government Services Canada
Richard C. Summerbell,
Centraalbureau voor Schimmelcultures,
The Netherlands
Editing
Lynn Andrews
Judith Whitehead
2
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Fungal Contamination in Public Buildings:
Health Effects and Investigation Methods
Table of Contents
Abstract
Preamble
.........................................................................4
.........................................................................5
1.
Introduction......................................................................7
1.1 Indoor Air as a Public Health Issue .......................9
1.2 What Is Mold? ..........................................................9
2.
Health Effects of Indoor Molds....................................11
2.1 Epidemiological Studies of
Respiratory Illness ..................................................13
2.1.1 Cross-sectional studies.................................13
2.1.2 Case-control studies.....................................21
2.1.3 Building investigations ................................26
2.1.4 Cohort studies ..............................................27
2.2 Effects of Molds in Sensitive Groups ...................27
2.2.1 Pulmonary hemorrhage ..............................27
2.2.2 Invasive mycoses .........................................28
2.2.3 Allergic bronchopulmonary mycoses
and allergic fungal sinusitis.........................29
2.3 Animal Studies .......................................................29
2.4 Discussion................................................................31
2.4.1 Summary of findings ...................................31
2.4.2 Limitations....................................................31
2.4.2.1 Exposure assessment......................31
2.4.2.2 Outcome assessment .....................32
2.4.2.3 Confounding factors ......................32
2.4.2.4 Bias ..................................................32
2.4.2.5 Study design ...................................33
2.4.3 Conclusion ...................................................33
3.
Investigation of Fungal Contamination of the
Non-industrial Workplace.............................................35
3.1 Background .............................................................37
3.2 General Principles ..................................................37
3.3 Objectives of a Mold Investigation .....................38
3.4 Methodological Considerations ............................40
3.4.1 Informed inspection ....................................40
3.4.2 Culturable air samples ................................40
3.4.3 Sticky surface samplers ...............................41
3.4.4 Documentation of
visually moldy area......................................41
3.4.5 Mycological analysis of bulk samples .......42
3.4.6 Microscopic techniques ..............................42
3.5 Conclusion ..............................................................43
References
.......................................................................44
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Abstract
The word “mold” is a non-scientific term that in popular
parlance generally refers to members of a few dozen filamentous fungi. Mold growth on building surfaces not only
damages these surfaces, but also affects air quality as intact
spores, as well as spore and mycelial fragments, are dispersed in the air. These can be inhaled depending on their
size and concentration. Exposure to mold is associated
with increased rates of respiratory disease.
This document is a revision of an earlier version published
by Health Canada and the Federal-Provincial Advisory
Committee on Environmental and Occupational Health
(CEOH) in 1995. The intent is to update the information
and to reconcile certain practical aspects of the document
with newer publications from the American Conference of
Governmental Industrial Hygienists (ACGIH), the
American Industrial Hygiene Association (AIHA) and
other cognizant authorities. The purpose of this document
is to assist front-line public health workers in the management of potential health risks associated with fungal contamination in public buildings. The report consists of two
parts:
1. A review on health effects of indoor molds
2. A guide for the investigation of mold contamination
in non-industrial workplaces
1. Health Effects of Indoor Molds
The 1995 review concluded that “. . . epidemiological
studies have consistently detected an association with respiratory symptoms and home dampness and mold growth,
but causality in these studies has not been established.”
The purpose of this section is to update the CEOH document by reviewing the research published from 1995 to
2001 on health effects of exposure to molds in residences
and non-industrial workplaces (mostly office buildings and
schools), and to determine whether the current evidence
warrants more definitive conclusions.
Major findings from this review are:
n
n
4
Eight cross-sectional studies investigated the relationship between indoor mold and respiratory, allergic or
irritation symptoms, four of which found significant
association between mold exposure and either
physician-diagnosed asthma or asthma-related
symptoms (cough, wheezing or breathlessness).
Seven case-control studies investigated the relationship between mold and asthma, most relying only on
self-reports to assess both mold exposure and health
outcomes. One of these studies found a significant
association between “mold or dampness” and asthma;
another found a significant association between mold
and asthma but did not assess dampness; three found
significant associations between mold and asthma (one
of them after controlling for dampness) but not
between dampness and asthma; and two found significant associations between dampness and asthma, but
not between mold and asthma.
n
To date, no cohort studies have been published on the
association between residential mold exposure and
asthma, although a published study has found an association between mold exposure at school and childhood asthma. There is presently an ongoing cohort
study in Prince Edward Island, Canada.
n
Several experimental studies with animal models
exposed to fungal cells, antigens or constituents have
found effects similar to those observed in humans in
epidemiological studies, such as eosinophilia and
increased serum IgE.
Several of the studies reviewed were limited by the methods used: exposure and outcome assessment based on selfreporting; no quantitative exposure assessment (and therefore no determination of a dose–response relationship);
possible confounding by other biological agents; and
potential response bias.
Only in a few studies reported to date has an independent
effect of mold on asthma and upper respiratory health
been demonstrated. Therefore, from epidemiologic data
alone, it is difficult to assess the population health consequences of the material growth of indoor molds. It is
known, however, that exposure to fungi in occupational
environments causes allergic and toxic diseases. Adverse
effects of fungi have also been seen in inhalation studies
using animal models. Therefore, further investigation of
health effects of indoor fungi using improved exposure
and health outcome assessment methods is needed to
resolve uncertainties. As established by the CEOH in
1995, current knowledge indicates the need to prevent
damp conditions and mold growth and to remediate any
fungal contamination in buildings.
2. Investigation of Fungal Contamination
in the Non-Industrial Workplace
It cannot be emphasized enough that the best way to manage mold growth is to prevent it before it occurs. The
essential elements of a prevention strategy are control of
moisture, timely remediation of any water leakage, and
adequate maintenance of heating, ventilation and air conditioning (HVAC) systems.
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Fungal Contamination in Public Buildings:
Health Effects and Investigation Methods
The goals of a mold investigation are to:
n
establish the cause, nature and extent of fungal contamination;
n
assess the risk of adverse effects on the health of
building occupants;
n
manage the microbial problem(s); and
n
return the building to a satisfactory level of performance.
The first step in investigating a building for microbial contaminants is an informed inspection. Mold contamination
can arise from condensation, floods and various types of
leaks. Investigation of mold problems requires a thorough
knowledge of the design of the building envelope and the
types of failures that result in condensation and water
leaks. Where there is probable cause to believe that there
is appreciable mold behind wall cavities, physical inspections should be performed by opening up the hidden area.
Air sampling is appropriate either during or following the
inspection. The main purpose of such sampling is to identify contamination that would not be visible without
destructive testing and to document air contamination. Air
samples should be taken during normal activity in the
building, while the ventilation system is operational. They
should be collected simultaneously inside and outside the
building to enable indoor–outdoor comparisons. The basis
of the current methods for interpreting the results of air
sampling is a comparison of the diversity of the fungi
inside with outdoor air samples.
Sticky surface samplers are increasingly used in mold
investigations. Advantages of data from properly collected
and analyzed sticky surface samples are twofold: the
results are available within a day and in situations when
there is a high percentage of non-viable spores in the air,
the data are more reliable.
Preamble
In 1993, the Federal-Provincial Advisory Committee on
Environmental and Occupational Health (CEOH)
released Indoor air quality in office buildings: a technical guide.
This report provided guidance on methods for investigating buildings for air quality problems, including molds. A
subsequent report from the same committee, Fungal
Contamination in Public Buildings: A Guide to Recognition and
Management (1995), provided information on health implications of molds in buildings and a step-by-step protocol
for the investigation and interpretation of indoor fungal
contamination.
The purpose of this current document is to update the
Fungal Contamination in Public Buildings report in view of
the large amount of research reported since 1995 on
health effects of mold damage in the built environment, as
well as on methods for investigating buildings for such
damage. This report is not, therefore, intended to replace
the Technical Guide, but to provide additional information
to those responsible for the investigation and management
of fungal contamination in office buildings, schools and
other non-industrial workplaces.
Consistent with the 1995 report, this updated review of
health effects indicates that living or working in a building
with material mold damage is harmful to health. Therefore, indoor mold growth in buildings should be prevented by appropriate control of moisture sources and by
timely remediation of water damages. Mold growing in
buildings should also be removed under safe conditions
using established remediation protocols.
A significant difference between the two documents is the
greater emphasis on the general principles of investigation
in the current report. As new building investigation techniques become validated, the general principles described
here can be used as a framework for their application.
Once the investigation is completed, fungal damage
should be expeditiously remediated using state-of-the-art
protocols such as those developed by the New York City
Department of Health and the ACGIH. As well, quality
assurance should be carried out according to standard protocols such as those of the AIHA.
Communication with buildings managers and occupants
should be maintained throughout the investigation.
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5
1. Introduction
Photo: Canada Mortgage and Housing Corporation (CMHC)
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1.1
Indoor Air as a Public Health Issue
The potential impacts of indoor air contamination on
human health have received considerable public attention
in recent years. This is especially true in Canada, and
other countries with cold weather, where people spend
most of their time indoors. Indoor air can be contaminated by pollutants released from carpets and building materials, cleaning chemicals, tobacco smoke, cooking and
heating, as well as biological contaminants such as dust
mite and animal allergens (derived from skin, saliva and
urine) and molds. This report discusses only one aspect of
this complex array of contaminants: mold. Much of what
is known about the population health effects of biological
contaminants in indoor environments comes from studies
of people living in damp homes.
Living in damp houses is associated with increased rates of
disease, and the cause is believed to be exposure to biological contaminants (Institute of Medicine 2000). Occupants in houses that have dampness problems are at
greater risk of exposure to mold, dust mites and bacterial
endotoxins. Lower socio-economic status has been associated with higher prevalence of respiratory disease (Dales
et al. 2002). In most countries, poverty translates into living in substandard housing that leaks water and air, and is
difficult to heat. When houses are difficult or expensive to
heat or cool, the air in some rooms is often not conditioned. This leads to moisture accumulation (condensation) on cold surfaces. Depending on the surfaces and
degree of house cleaning, contaminants accumulate and
airborne particulate concentrations will vary accordingly.
Due to complex exposures, however, the attributable risk
to each of the biological contaminants discussed here
remains unknown. This alone makes it difficult to assign
tolerable exposure values.
In addition, outdoor-source fine particles (PM2.5) can be
higher indoors than outdoors. Houses near sources of outdoor air pollution (e.g. vehicular traffic) are at greater risk
of increased indoor concentrations of particulate matter
and volatile organic compounds (VOCs).
Among indoor air contaminants, mold is a cause of
increasing concern, with many epidemiological studies
and case reports linking mold to a wide range of adverse
effects on respiratory health.
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1.2
What Is Mold?
The fungus kingdom consists of eukaryotic organisms.
Fungi are subdivided into four different phyla based on
their reproduction mode: ascomycetes, basidiomycetes,
zygomycetes and mitosporic fungi.
The word “mold” is a non-scientific term that in popular
parlance generally refers to members of a few dozen filamentous fungi. Such fungi are often visible as colonies on
food and building materials, appearing on close inspection
as multicellular filaments called hyphae. Mold growth on
building material surfaces can influence air quality
because both spores and mycelial fragments are dispersed
into the air and can be inhaled, depending on their size.
The spores of fungi have a large size range: 1 to 50 µm.
Furthermore, the degree of hydration of spores, a consequence of the prevailing relative humidity, affects this
range (Madelin and Johnson 1992). Particles at the lower
end of the size range (less than 10 µm) can reach the alveoli; others may be swallowed. There is some variation
with age: lower airway deposition for 5 µm particles is six
times higher in newborns than in adults (Phalen and
Oldham 2001). The average aerodynamic diameter of a
number of spore types is listed in Table 1. The average
sizes of some spores are well within the respirable range
(<10 µm); others such as Stachybotrys chartarum appear to
be too large to penetrate into the lungs. However, there is
considerable variation not represented by the average. For
example, even though the average aerodynamic diameter
of Stachybotrys spores is too large to penetrate into the
lungs, approximately one third of the spores are within the
respirable range (Sorenson et al. 1996). Similar data for
some strains of Cladosporium cladosporioides, Penicillium
viridicatum and P. chrysogenum showed a large range in
spore sizes whereas most spores of P. commune, Aspergillus
versicolor, A. ustus, A. niger and A. sydowii were of similar
dimensions (Miller and Young 1997). As noted, mycelial
fragments are also typically present in indoor air. These
are usually of respirable size. The number of fragments
compared to the number of spores present is highly variable, but typically represent a few percent of the fungal
particles present. It is known that mycelial fragments of
some species contain different allergens than those present
in spores of the same species (Górny et al. 2002).
9
Table 1.
Spore size of various fungi determined by
cascade impaction and microscopy
Table 2.
Common fungi from
mold-damaged building materials
Average aerodynamic diameter
Axial dimensions
µm
µm
Aspergillus
fumigatus
2.2
2.2-2.3
Cladosporium
cladosporioides
2.3
(2.0-3.5) x (2.0-2.5)
Paecilomyces
variotii
2.7
2.9 x 1.3
Species
Penicillium
chrysogenum
2.6
Memnoniella
echinata
4.8
Stachybotrys
chartarum
5.6
Alternaria alternata
Memnoniella echinata
Aspergillus sydowii
Paecilomyces variotii
Aspergillus versicolor
Penicillium aurantiogriseum
Chaetomium globosum
Penicillium chrysogenum
Cladosporium cladosporioides
Penicillium commune
Cladosporium sphaerospermum
Penicillium citrinum
Eurotium herbariorum
Stachybotrys chartarum
Eurotium repens
Ulocladium chartarum
2.5 x 2.5
(Adapted from Flannigan et al. 2001).
(After Madelin and Johnson 1992; Sorenson et al. 1996).
Three features of mold biochemistry are of special interest
in terms of human health. First, mold cell wall contains
(1->3)-ß-D-glucan, a compound with inflammatory properties. Second, spores and mycelial fragments contain
allergens (Górny et al. 2002), few of which have been
chemically characterized. Many of the known fungal allergens are serine proteases, or proteins, which are present in
fairly high concentrations in the spores. These have been
described mainly from work done in phylloplane species
and Aspergillus fumigatus (Horner et al. 1995). Third, the
Aspergillus versicolor
spores of some species contain low molecular weight
chemicals that are cytotoxic or have other toxic properties
(e.g. satratoxins produced by Stachybotrys chartarum). Some
molds, such as Aspergillus fumigatus, can cause opportunistic infection in immunocompromised individuals and
severe allergic diseases in people with underlying respiratory conditions, such as asthma or cystic fibrosis (Burge
2000). Fungi commonly found in moldy building materials are shown in Table 2.
Penicillium chrysogenum
Stachybotrys chartarum
Photos: Centraalbureau voor Schimmelcultures, Koninklijke Nederlandse Akademie van Wetenschappen, The Netherlands.
10
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Fungal Contamination in Public Buildings:
Health Effects and Investigation Methods
2. Health Effects of Indoor Molds
Photo: Dr. Amanda Wheeler
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Since 1982, in Europe and North America, approximately
30 studies have been conducted on the association
between dampness, mold and respiratory health in residential housing. Studies in the United States and Canada
have involved the largest number of people. A study of
the respiratory health of 4,600 children from six cities in
the northeast United States demonstrated that the presence of mold and dampness in their homes was correlated
to several respiratory symptoms as well as a number of
non-specific symptoms. The effect on the children was of
similar dimension to parental smoking (Brunekreef et al.
1989). Two studies involving 15,000 children and 18,000
adults from 30 communities in Canada came to similar
conclusions. The authors suggested that a non-allergenic
mechanism may be involved since there was no effect
modification by reported atopy and asthma. A dose–effect
relationship was also seen in that more visible mold yielded more symptoms. Overall, the mold contamination was
associated with a 50% relative increase in asthma and a
60% increase in upper respiratory disease (Dales et al.
1991a, 1991b). Data from a further 13,000 children from
24 cities across the United States (19 cities) and Canada
(5 cities) show the same pattern (Spengler et al. 1994). The
upper boundary attributable risk for mold-caused asthma
in Canada was estimated at 20% (Dekker et al. 1991). The
health effects of fungal contamination in housing remain
significant even after adjustment for socio-economic factors, pets, household smokers, endotoxins and dust mites
(Dales and Miller 1999; Dales et al. 1999).
A review published in 1995 by Health Canada and the
Federal-Provincial Advisory Committee on Environmental
and Occupational Health (CEOH) concluded that “. . .
epidemiological studies have consistently detected an association with respiratory symptoms and home dampness
and mold growth, but causality in these studies has not
been established” (CEOH 1995a). The evidence linking
exposure to indoor molds with adverse respiratory outcomes has also been reviewed by Verhoeff and Burge
(1997). More recently, the US National Academy of
Sciences Institute of Medicine released a report on asthma
entitled Clearing the Air: Asthma and Indoor Air Exposures.
The panel found that there was insufficient evidence on a
population health basis for the association between indoor
residential molds and the development of asthma, but that
indoor mold was associated with exacerbation of asthma
in mold-sensitized individuals, and exposure may be associated with respiratory symptoms. The percentage of
mold-sensitized asthmatics is not known; estimates range
up to 40% (Institute of Medicine 2000).
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The purpose of this section is to update the review conducted by the Federal-Provincial Advisory Committee on
Environmental and Occupational Health (CEOH) in 1995
by reviewing the research published since then on health
effects due to exposure to molds in residences and nonindustrial workplaces (mostly office buildings and schools),
and to determine whether the current evidence warrants
more definitive conclusions. Following a summary of studies published since 1995 (section 2.1), some potential
effects of molds in sensitive sub-populations are discussed
(section 2.2), followed by an overview of the experimental
studies on respiratory effects of molds (section 2.3) and a
discussion of the evidence linking mold exposure to
adverse health outcomes (section 2.4).
Health problems, such as hypersensitivity pneumonitis
(HP) and organic dust toxic syndrome (ODTS) identified
in industrial and agricultural settings due to greater exposure to molds (and, in some instances, other biological
contaminants such as thermophilic actinomycetes), will
not be discussed here.
2.1
Epidemiological Studies of
Respiratory Illness
In order to review recent cross-sectional and cohort studies on health effects of indoor molds, Medline was
searched using the following keywords: fungi, or mold, or
mold and respiratory tract diseases. Articles published in
1995 or later pertaining to cross-sectional, cohort or casecontrol studies assessing the association between indoor
exposure to molds (visible mold growth or airborne fungal
cell counts) and asthma or related respiratory symptoms
were included in the review. Studies with no mold exposure variable (e.g. those considering only dampness) and
prevalence studies with no measure of association were
excluded.
2.1.1
Cross-sectional studies
Cross-sectional studies are studies in which outcomes (diseases) and exposures are assessed at one point of time.
Eight cross-sectional studies, summarized in Table 3,
investigated the relationship between indoor mold and
respiratory, allergic or irritation symptoms, and four found
significant association between mold exposure and either
physician-diagnosed asthma or asthma-related symptoms
(cough, wheezing or breathlessness).
13
Table 3.
Cross-sectional studies on respiratory and allergic effects of exposure to indoor molds, 1995 to 2001
Country
Study population (n)
Data collection method
Exposure
Canada
School children,
mean age = 10
(n = 403)
E + D: questionnaire to
parents
Mold/mildew in present home in
the past year
Canada
As above
E: dust sampling
D: questionnaire to parents
Altrnaria detected in dust
Australia
Children between 7 and 14 years
of age from 80 households
(n = 148)
E: air sampling
D: questionnaire (asthma) and
skin prick test to common
aeroallergens (atopy)
100-CFU/m3 increase in
Penicillium spores
100-CFU/m3 increase in
Aspergillus spores
Finland
Adults aged 25 to 64 years
(n = 1,460)
E + D: mail questionnaire
Visible mold OR
musty odour OR
moisture stains OR
water/moisture damage
Finland
As above, but excluding those
reporting lumbar backache or
recurrent stomachache
E + D: mail questionnaire
Visible mold OR
musty odour OR
moisture stains OR
water/moisture damage
E: exposure assessment; D: disease assessment
14
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Fungal Contamination in Public Buildings:
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Disease
OR
95% CI
Covariats adjusted for
Non-respiratory symptoms
2.25
1.26 - 4.00
Dales and Miller 1999
Irritation
1.81
1.02 - 3.24
Age, gender, parental
allergies, parental
education, pets, ETS, dust
mites, bacterial endotoxins
Cough/wheezing
1.28
0.74 - 2.23
Asthma
0.91
0.42 - 1.95
Chest illness
1.51
0.76 - 3.02
Non-respiratory symptoms
0.79
0.38 - 1.67
Dales et al., 1999
Irritation
1.05
0.51 - 2.18
Age, parental illness,
parental smoking, dust
mites
Cough/wheezing
2.00
0.84 - 4.74
Asthma
1.90
0.55 - 6.59
Chest illness
2.77
0.85 - 9.01
Asthma
1.43
1.03 - 2.00
Parental asthma, allergy
Garrett et al., 1998
Atopy (response to at
least one skin prick test)
1.48
1.10 - 1.99
Gender, parental asthma
Asthma
1.02
NS
Atopy
1.62
p < 0.001
Allergic rhinitis
1.66
p < 0.001
Cough
1.37
NS
Phlegm
1.36
p < 0.05
Rhinitis
1.69
p < 0.001
Eye irritation
1.52
p < 0.01
Lumbar backache
1.49
p < 0.01
Recurrent stomachache
1.65
p < 0.001
Atopy
1.34
NS
Allergic rhinitis
1.37
NS
Cough
1.48
NS
Phlegm
0.94
NS
Rhinitis
1.21
NS
Eye irritation
1.69
p < 0.05
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Age, gender, smoking,
education, type of dwelling
Ref.
Pirhonen et al., 1996
Pirhonen et al., 1996
15
Table 3.
Cross-sectional studies on respiratory and allergic effects of exposure to indoor molds, 1995 to 2001 (continued)
Country
Study population (n)
Data collection method
Exposure
Finland
Adults aged >= 16 years
inhabiting 310 dwellings
(n = 699)
E + D: self-administered
questionnaire
Mold present
Finland
Adults aged >= 16 years
inhabiting 310 dwellings
(n = 699)
E: homes visually inspected
Moisture present
for signs of moisture by a civil
engineer
D: self-administered questionnaire
Finland
First-year university students
aged 18 to 25
(n = 10,677)
E + D: postal questionnaire
(D validated against clinical
assessment in a sub-sample of
290 people)
Visible mold growth in dwellings in
the past year
Visible mold OR
damp stains OR
water damage in the past year
Netherlands
16
Boys aged 6 to 12
(n = 222)
E + D: questionnaire to parents
(mold growth: never, sometimes,
often, always)
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Mold growth in past 2 years
(always vs. never)
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Disease
OR
95% CI
Sinusitis
1.92
1.11 - 3.30
Bronchitis
1.98
1.13 - 3.48
Cough without phlegm
1.42
0.92 - 2.19
Cough with phlegm
1.15
0.78 - 1.69
Nocturnal cough
2.11
1.21 - 4.98
Nocturnal dyspnoea
2.33
1.09 - 4.98
Sore throat
1.46
1.03 - 2.08
Rhinitis
1.06
0.71 - 1.59
Impaired smell
1.23
0.80 - 1.91
Eye irritation
1.08
0.76 - 1.53
Bronchitis
1.68
0.95 - 2.95
Cough without phlegm
1.60
1.01 - 2.53
Cough with phlegm
1.44
1.44 - 2.19
Nocturnal cough
2.30
1.32 - 4.01
Nocturnal dyspnoea
1.58
0.74 - 3.39
Sore throat
2.40
1.56 - 3.69
Rhinitis
1.89
1.15 - 3.11
Impaired smell
1.28
0.80 - 2.06
Eye irritation
1.43
0.84 - 1.83
Asthma
2.21
1.48 - 3.28
Allergic rhinitis
1.29
1.01 - 1.66
Allergic conjunctivitis
0.95
0.68 - 1.34
Atopic dermatitis
1.31
0.96 - 1.79
Asthma
1.66
1.25 - 2.19
Allergic rhinitis
1.30
1.12 - 1.51
Allergic conjunctivitis
1.12
0.92 - 1.36
Atopic dermatitis
1.29
1.06 - 1.56
Chronic cough
3.56
0.80 - 14.10
Shortness of breath
2.26
0.54 - 9.49
Wheezing
0.95
0.16 - 5.46
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Covariats adjusted for
Ref.
Smoking, age, gender,
allergy, pets, atopic
predisposition
Koskinen et al. 1999
As above
Koskinen et al. 1999
Parental education,
smoking, ETS exposure,
pets, wall-to-wall carpets,
place of residence (form,
rural non-farm, urban),
type of residence
Kilpeläinen et al. 2001
Age, gender, parental
smoking, unvented kitchen
geysers, parental
education
Cuijpers et al. 1995
17
Table 3.
Cross-sectional studies on respiratory and allergic effects of exposure to indoor molds, 1995 to 2001 (continued)
Country
Study population (n)
Data collection method
Exposure
Netherlands (continued)
Girls aged 6 to 12
(n = 248)
E + D: questionnaire to parents
(mold growth: never, sometimes,
often, always)
Mold growth in past 2 years
(always vs. never)
Taiwan
Children aged 8 to 12
(n = 1,340)
E:+ D: questionnaire to parents
Dampness
Taiwan
Children aged 8 to 12
(n = 1,340)
E + D: questionnaire to parents
Mold growth in home
United States
Young adults aged
20 to 22 years
(n = 2,041)
E + D: self-administered postal
questionnaire
Visible mold
Water leaking
Indoor dampness
18
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Disease
OR
95% CI
Chronic cough
0.79
0.07 - 8.34
Wheezing
2.69
0.48 - 15.21
Cough
2.52
1.34 - 4.75
Phlegm
1.86
1.18 - 2.93
Wheeze
1.36
0.83 - 2.21
MD-diagnosed asthma
1.25
0.81 - 1.95
Bronchitis
1.29
0.96 - 1.73
Pneumonia
1.33
0.75 - 2.36
Allergic rhinitis
1.39
1.05 - 1.84
Cough
1.87
1.00 - 3.25
Phlegm
1.50
0.95 - 2.36
Wheeze
1.20
0.73 - 1.99
MD-diagnosed asthma
1.12
0.72 - 1.74
Bronchitis
1.68
1.26 - 2.25
Pneumonia
1.77
1.03 - 3.05
Allergic rhinitis
1.27
0.96 - 1.68
MD-diagnosed asthma
1.5
1.0 - 2.4
Current asthma
2.0
1.2 - 3.2
MD-diagnosed asthma
1.6
0.7 - 3.5
Current asthma
1.6
0.7 - 3.8
MD-diagnosed asthma
1.2
0.8 - 1.9
Current asthma
1.3
0.7 - 2.2
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Covariats adjusted for
Ref.
Age, gender, parental
education, number of
smokers in household,
gas stove
Li and Hsu 1996
As above
Li and Hsu 1996
Gender, race, education,
smoking status
Hu et al. 1997
19
n
In the Netherlands, 470 children aged 6 to 12 were
included in a survey of home environment and respiratory symptoms. Mold growth in homes in the previous two years was classified as per its frequency:
“never,” “sometimes,” “often” or “always.” Odds
ratios were adjusted for age, gender, parental smoking, unvented kitchen geysers and parental education.
The study found that neither chronic cough, shortness
of breath nor wheezing were associated with mold
growth (Cuijpers et al. 1995).
n
In Finland, 1,460 people aged 25 to 64 were included
in a survey of home environment and respiratory
symptoms. Data were collected through a mail-out
questionnaire. Odds ratios were adjusted for age, gender, smoking, education and dwelling type. Living or
having lived in a home with a dampness or mold
problem, defined as visible mold, mold smell, moisture stains or water damage, was associated with bronchitis (OR 2.04, 95% CI 1.49 to 2.78), atopy (OR 1.63,
95% CI 1.26 to 2.10), allergic rhinitis (OR 1.66, 95%
CI 1.25 to 2.19), phlegm (OR 1.36, 95% CI 1.01 to
1.85), rhinitis (OR 1.69, 95% CI 1.31 to 2.18) and eye
irritation (OR 1.52, 95% CI 1.18 to 1.96), but not
physician-diagnosed asthma (OR 1.02, 95% CI 0.60 to
1.72). Some non-respiratory, non-allergic diseases also
showed significant associations with dampness or
molds: fatigue (OR 1.81, 95% CI 1.37 to 2.39), lumbar
backache (OR 1.49, 95% CI 1.15 to 1.93) and recurrent stomachache (OR 1.65, 95% CI 1.24 to 2.20).
When data were re-analyzed after excluding “complainers,” defined as those who reported lumbar backache and/or recurrent stomachache, in order to control for reporting bias, only ORs of eye irritation and
fatigue remained significant (Pirhonen et al. 1996).
n
In Taiwan, 1,340 children aged 8 to 12 years were surveyed. Data were collected through a questionnaire to
parents. Odds ratios were adjusted for age, gender,
parental education, number of smokers in household,
and gas stove. Mold growth in homes was significantly
associated with cough (OR 1.87, 95% CI 1.00 to 3.25),
bronchitis (OR 1.68, 95% CI 1.26 to 2.25) and pneumonia (OR 1.77, 95% CI 1.03 to 3.05), but not
physician-diagnosed asthma (OR 1.12, 95% CI 0.72 to
1.74) (Li and Hsu 1996).
n
In the United States, 2,041 people aged 20 to 22 years
who had responded to a mail-out questionnaire were
included in a cross-sectional study. Data collection
was based entirely on the questionnaire. Odds ratios
were adjusted for gender, race, education and smoking status. Visible mold growth at home was associated with an increased risk of physician-diagnosed asthma (OR 1.5, 95% CI 1.0 to 2.4) and current asthma
(OR 2.0, 95% CI 1.2 to 3.2) (Hu et al. 1997).
20
n
In Australia, 80 households with 148 children aged 7
to 14 were surveyed. A detailed housing characterization was carried out, and air samples were collected.
Also, a respiratory health questionnaire was completed and skin prick tests with extracts of common aeroallergens were performed for each of the children.
The odds ratio for reported physician-diagnosed asthma with a 100-CFU/m3 increase in Penicillium spores
was 1.43 (95% CI 1.03 to 2.00), and the odds ratio for
atopy, defined as a positive response to at least one
skin prick test, with a 10-CFU/m3 increase in
Aspergillus spores was 1.48 (95% CI 1.10 to 1.99)
(Garrett et al. 1998).
n
In Finland, 699 adults aged at least 16 years were
included in a cross-sectional study. Data collection
consisted of a self-administered questionnaire followed
by an investigation by civil engineers of mold and
dampness in participants' dwellings. Odds ratios were
adjusted for smoking, age, gender, allergy, indoor pets
and atopy. The presence of mold in homes reported
by occupants was associated with increased risk of
cough without phlegm (OR 1.60, 95% CI 1.01 to
2.53), nocturnal cough (OR 2.30, 95% CI 1.32 to
4.01), sore throat (OR 2.40, 95% CI 1.56 to 3.69) and
rhinitis (OR 1.89, 95% CI 1.15 to 3.11). The presence
of molds observed by the civil engineers visiting the
house was associated with an increased risk of sinusitis
(OR 1.92, 95% CI 1.11 to 3.30), bronchitis (OR 1.98,
95% CI 1.13 to 3.48), nocturnal cough (OR 2.11, 95%
CI 1.21 to 4.98), nocturnal dyspnea (OR 2.33, 95% CI
1.09 to 4.98) and sore throat (OR 1.46, 95% CI 1.03
to 2.08) (Koskinen et al. 1999).
n
In Canada, the homes of 403 school children were
surveyed. Parents filled out a questionnaire about their
home environment and the respiratory health of their
children. Air samples were collected and analyzed for
ergosterol, viable fungi and bacterial endotoxin, while
dust samples were collected for dust mite antigen
analysis. Odds ratios were adjusted for age, gender,
parental allergies and asthma, parental education, pets
in homes and household smokers. Mold or mildew
growth in the home in the past year was associated
with irritation of eyes, nose or skin (OR 1.80, 95% CI
1.03 to 3.16), but not cough or wheezing (OR 1.36,
95% CI 0.79 to 2.33) or physician-diagnosed asthma
(OR 0.96, 95% CI 0.46 to 2.00). Additional adjustment for bacterial endotoxin and dust mites did not
change the magnitude of these associations. No significant association was found between ergosterol and
fungal cell counts, and respiratory outcomes (Dales
and Miller 1999; Dales et al. 1999).
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n
In Finland, 10,677 first-year university students aged
18 to 25 were included in a questionnaire-based survey. Exposure and outcome assessments were based
on responses. Odds ratios were adjusted for parental
education, active and passive smoking, pets, carpets,
place of residence (farm, rural non-farm or urban) and
type of residence. Visible mold in participants'
dwelling in the past year was associated with current
physician-diagnosed asthma (OR 2.21, 95% CI 1.48 to
3.28), common cold at least four times in the past year
(OR 1.48, 95% CI 1.17 to 1.88) and allergic rhinitis
(OR 1.29, 95% CI 1.01 to 1.66) (Kilpeläinen et al.
2001).
2.1.2
n
In the United Kingdom, 486 cases who had frequent
or speech-limiting wheezing in the previous 12 months,
and 475 controls, selected from participants in a previous health survey, were included in a case-control
study. Participants were aged 11 to 16 years. Exposure
classification was based on damp or mold in the children's bedroom: “none,” “damp only” and “damp
with mold.” In univariate analysis, no association was
found between damp bedroom (without mold) and
asthma (unadjusted OR 0.85, 95% CI 0.39 to 1.83),
but the presence of both dampness and mold in the
bedroom was associated with an increased risk of
wheezing (crude OR 2.20, 95% CI 1.11 to 4.43). For
the multivariate analysis, the mold/dampness variable
was dichotomized into “none” and “any mold,” and
was no longer associated with wheezing (Strachan and
Carey 1995).
n
In the United Kingdom, 102 patients with physiciandiagnosed asthma, aged 5 to 44 years and 196 population controls were interviewed by a trained interviewer about their respiratory health and their housing
conditions. After the interview, subjects were asked to
have their house inspected by a surveyor blind of
their case or control status, and 222 out of 298 participants agreed. Odds ratios were adjusted for age, gender, income, unemployment, smoking, other smokers
living in homes, and pets. When self-reported exposure was considered (283 participants included), asthma was associated with the presence of “any dampness” (OR 1.93, 95% CI 1.14 to 3.28) or “severe
dampness” (OR 5.45, 95% CI 2.81 to 10.6), with
dampness in previous home (OR 2.55, 95% CI 1.49 to
4.37), and with having moved because of dampness in
previous home (OR 2.08, 95% CI 1.02 to 4.24). When
exposure observed by the surveyor was considered,
asthma was associated with the presence of “any
dampness” (OR 3.03, 95% CI 1.65 to 5.57) and
“severe dampness” (OR 2.36, 95% CI 1.34 to 4.01),
but not with the presence of mold (OR for “severe
mold”: 1.70, 95% CI 0.78 to 3.71) (Williamson et al.
1997).
Case-control studies
In case-control studies, exposure is assessed and compared
between subjects with the disease of interest (cases), and
without this disease (controls). Nine case-control studies,
summarized in Table 4, have investigated the relationship
between mold and asthma, most of them relying only on
self-reports to assess both mold exposure and health outcomes. One of these studies found a significant association
between “mold or dampness” and asthma; another found
a significant association between mold and asthma, but
did not assess dampness; three found significant associations between mold and asthma (one of them after controlling for dampness), but not between dampness and
asthma, and two found significant associations between
dampness and asthma, but not between mold and asthma.
Interestingly, these two studies used objective criteria
rather than self-reports to assess health outcomes, and
home inspection for assessing exposure or validating the
exposure questionnaire.
n
observed by the investigator. Adjusted odds ratios
were also calculated, and were mostly lower than the
corresponding crude odds ratios. When cases with
elevated Imunoglobulin E (IgE) antibodies to molds
and/or dust mites were compared to controls without
IgE to these allergens, mold exposure observed by the
investigator was found to be associated with sensitization + physician-diagnosed asthma (crude OR 2.61,
95% CI 1.21 to 5.64) and sensitization + chronic
cough (crude OR 3.45, 95% CI 1.20 to 9.93) (Verhoeff
et al. 1995).
In the Netherlands, a nested case-control study was
carried out within a random sample of 7,632 children
aged 6 to 12 years whose parents had completed a
screening questionnaire. Cases were selected among
children with reported asthma (n=76), chronic cough
(n=81) or other respiratory conditions, for a total of
259. Controls (n=257) were selected among children
without respiratory symptoms. Data were collected
through a self-administered questionnaire to parents
and through a visit to all participants' homes by a
trained investigator blind to children's case or control
status. Crude odds ratios were calculated: reported
mold somewhere in the houses was associated with an
increased risk of chronic cough (OR 1.90, 95% CI
1.02 to 3.52), reported mold in the living room with
physician-diagnosed asthma (OR 2.95, 95% CI 1.34 to
6.52) and reported mold in the bedroom with chronic
cough (OR 3.52, 95% CI 1.55 to 8.03). No significant
association was found with the presence of mold
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21
Table 4.
Case-control studies on asthma and exposure to indoor molds, 1995 to 2001
Country
Study population
Cases/controls definition
Data collection method
Canada
Children aged 5 to 19 years
whose parents responded to a
previous survey
Cases (n = 592): physiciandiagnosed asthma AND one of
the following: attack in past year
OR asthma medication
Controls (n = 443): no history of
asthma
D + E: report by parents in a telephone interview
Austria
Children whose parents responded to a previous health survey
Cases (n = 1,782): wheezing in
the past 12 months
Controls (n = 26,966): no
wheezing in past 12 months
E + D: questionnaire to parents
Finland
Adults aged 21 to 63 years
Cases (n = 521): newly diagnosed E + D: questionnaire
asthma cases
Controls (n = 932): no previous
or current asthma
Netherlands
School children aged 6 to
12 years whose parents
completed a respiratory
symptom questionnaire
Cases (n = 76): physicianE + D: questionnaire to parents
diagnosed asthma
Controls (n = 257): no respiratory
symptoms
E: home inspection
D: questionnaire to parents
Netherlands
As above
Cases: physician-diagnosed
asthma AND IgE specific to mold
and/or dust mites
Controls: no respiratory
symptoms
E: questionnaire to parents
D: questionnaire to parents
(asthma) and blood IgE (allergy)
E: home inspection
D: questionnaire to parents
(asthma) and blood IgE (allergy)
E: exposure assessment; D: disease assessment
22
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Exposure
OR
95% CI
Mold and/or mildew in home in the past
year
1.6
1.1 - 2.3
Gender, age, gas cooking,
paternal asthma and allergies,
number of siblings
Hessel et al. 2001
Dampness or mold at home
1.43
1.24 - 1.65
Age, gender, family history of
asthma, parental
education, ETS exposure
Zacharasiewicz et al.
1999
Work
Visible mold/mold odor
1.54
1.01 - 2.32
Damp stains/paint peeling
0.84
0.56 - 1.25
Water damage
0.91
0.60 - 1.39
Visible mold/mold odor
0.98
0.68 - 1.40
Damp stains/paint peeling
1.02
0.73 - 1.41
Water damage
0.90
0.60 - 1.34
Dampness in house
1.46
0.80 - 2.64
Dampness in bedroom
1.97
0.98 - 3.95
Dampness in living room
1.16
0.51 - 2.65
Mold in house
1.57
0.84 - 2.93
Mold in living room
2.95
1.34 - 6.52
Mold in bedroom
1.88
0.74 - 4.78
Dampness in house
1.22
0.70 - 2.13
Dampness in bedroom
0.94
0.47 - 1.90
Dampness in living room
1.33
0.69 - 2.59
Mold in house
1.53
0.85 - 2.78
Mold in living room
1.83
0.81 - 4.13
Mold in bedroom
0.99
0.31 - 3.14
Dampness in house
1.95
0.89 - 4.26
Mold in house
1.93
0.85 - 4.41
Dampness in house
1.86
0.89 - 3.91
Mold in house
2.61
1.21 - 5.64
Covariates adjusted for
Ref.
Gender, age, parental atopy,
Jaakkola et al. 1992
education, smoking, ETS,
occupational exposures, pets and
all variables shown
Home
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No adjustment
(crude ORs)
Verhoeff et al. 1995
No adjustment
(crude ORs)
Verhoeff et al. 1995
23
Table 4.
Case-control studies on asthma and exposure to indoor molds, 1995 to 2001 (continued)
Country
Study population
Cases/controls definition
Data collection method
Sweden
Individuals aged 20 to 44 who
participated in a previous survey
Cases (n = 98): wheezing or
breathlessness in past year AND
bronchial hyperresponsiveness to
methacholine
Controls (n = 357): no current
asthma
E: questionnaire validated against
inspection by an occupational
hygienist in a sub-sample of
88 dwellings (mold: Cohen’s
kappa = 0.36)
D: symptoms questionnaire and
bronchial challenge test with
methacholine
Sweden
Adults aged 20 to 50 years who
responded to short respiratory
survey (n = 15,813)
Cases (n = 174): physiciandiagnosed asthma after age 16
Controls (n = 870): randomly
selected regardless of their health
status (including 35 fulfilling the
case definition)
E + D: self administered
questionnaire
United Kingdom
Children aged 11 to 16 whose
parents had responded to a
previous survey
Cases (n = 486): frequent or
speech-limiting wheezing in the
past 12 months
Controls (n = 475): no history of
asthma or wheezing
E + D: questionnaire to parents
As above, but excluding those
with “changes to bedroom as a
result of asthma or allergy”
Cases (n = 365) and
Controls (n = 463): see definition
above
As above
Cases (n = 102): hospital patients
with physician-diagnosed asthma,
aged 5 to 44 years
Controls (n = 196): population
controls matched for sex and age
within 5 years
E: questionnaire
D: hospital records (cases)
United Kingdom
E: home visits by a surveyor
(222 subjects only)
D: hospital records (cases)
24
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Exposure
OR
95% CI
Water damage or flooding
1.8
1.0 - 3.2
Dampness in the floor
4.6
2.0 - 10.5
Visible mold on indoor surfaces
1.9
0.93 - 3.8
Moldy odour
1.1
0.42 - 2.9
At least one sign of building dampness
1.8
1.1 - 3.0
Visible dampness
1.3
0.9 - 2.0
Visible mold growth
2.2
1.4 - 3.5
Visible dampness and mold growth
1.8
1.1 - 3.1
Visible mold growth
2.4
1.3 - 4.2
Dampness only
0.85
0.39 - 1.83
Dampness with mold
2.20
1.11 - 4.43
Mold
1.25
0.67 - 2.31
Age, gender, type of pillow and
quilt, age of mattress, gas
cooking, parental smoking
Any dampness
1.93
1.14 - 3.28
Serious dampness
5.45
2.81 - 10.6
Age, gender, household income,
unemployment, smoking, ETS
exposure, pets
Dampness in previous home
2.55
1.49 - 4.37
Moved because of dampness
2.08
1.02 - 4.24
Any dampness
3.03
1.65 - 5.57
Severe dampness
2.36
1.34 - 4.01
Any mold
1.35
0.79 - 2.28
Significant mold
1.70
0.78 - 3.71
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Covariates adjusted for
Ref.
Age, gender, smoking
Norbäck et al. 1999
Age, gender, smoking habits,
atopy
Thorn et al. 2001
As above + visible dampness
None (crude ORs)
Strachan and Carey
1995
Williamson et al. 1997
25
n
n
n
26
In Sweden, a nested case-control study was carried
out among individuals aged 20 to 44 who participated
in a respiratory health survey, and who agreed to
undergo a lung function examination and a bronchial
challenge test with methacholine, and to provide a
blood sample. Ninety-eight cases had current asthma,
defined as a combination of bronchial hyperresponsiveness and either wheezing or breathlessness in the
past 12 months, and 357 controls had no current asthma. Exposure assessment was based on questionnaire
data. Odds ratios were adjusted for age, gender and
smoking. Current asthma was associated with water
damage or flooding in dwellings (OR 1.8, 95% CI
1.002 to 3.2) and dampness signs on the floor (OR
4.6, 95% CI 2.0 to 10.5), and a similar but non-significant trend was found for visible mold on indoor surfaces (OR 1.9, 95% CI 0.93 to 3.8). A stratified random sample of 88 dwellings was inspected by an
occupational hygienist who recorded signs of building
dampness as requested in the questionnaire. There
was a good agreement between participants' and the
occupational hygienist's report on water damage
(Cohen's Kappa 0.40, ρ=0.001) and visible mold
(Cohen's Kappa 0.36, ρ=0.004) (Norbäck et al. 1999).
In Austria, a subset of 1,781 participants in a health
survey of children aged 6 to 9 years was used for a
case-control study. Cases were those who answered
“yes” to the question “wheezing in the past 12 months?”
and controls were those who answered “no” to that
question. Odds ratios were adjusted for age, gender,
parents' or sibling's history of asthma, parental education and exposure to environmental tobacco smoke.
Dampness or mold at home was significantly associated with wheezing (OR 1.43, 95% CI 1.24 to 1.65)
(Zacharasiewicz et al. 1999).
In Sweden, a nested case-control study was carried
out among respondents aged 20 to 50 years to a questionnaire-based survey. Cases were those who reported asthma diagnosed by a physician at age 16 or
older, and controls were randomly selected among the
survey participants. Selected participants were sent a
comprehensive questionnaire regarding their health,
their home environment and other risk factors. Odds
ratios were computed using a logistic regression controlling for gender, sex, smoking habits and atopy.
Visible mold growth in any of the six latest homes
inhabited was significantly associated with asthma
(OR 2.2, 95% CI 1.4 to 3.5), and this association
remained significant after controlling for visible dampness (OR 2.4, 95% CI 1.3 to 4.2) (Thorn et al. 2001).
n
In Canada, a nested case-control study was carried
out among children aged 5 to 19 in two communities
in Alberta. Participants were selected from among
those whose parents had responded to a mail-out
questionnaire. Five hundred and ninety-two cases
were randomly selected among those with a current
physician-diagnosed asthma, and 443 controls were
selected among those with no history of asthma. Data
on demographic, environment, medical history and
host factors were collected by telephone interviews.
Odds ratios and confidence intervals were calculated
using unconditional logistic regression, including
potential confounders: gender, age, gas cooking,
parental asthma and allergies, and number of siblings.
Exposure to indoor molds or mildew in the past year
was significantly associated with asthma (OR 1.6, 95%
CI 1.1 to 2.3) (Hessel et al. 2001).
n
In Finland, a case-control study was carried out in
adults aged 21 to 63 years. Cases were newly diagnosed asthma cases and controls had no previous or
current asthma. Odds ratios were adjusted for gender,
age, parental atopy or asthma, education, smoking,
environmental tobacco smoke exposure, pets and
occupational exposures. No association was found
between dampness or mold exposure in the home and
asthma. Conversely, visible mold or mold odour at
work was associated with a higher risk of adult-onset
asthma (OR 1.54, 95% CI 1.01 to 2.32). No such association was found between dampness or water damage, and asthma ( Jaakkola et al. 2002).
2.1.3
Building investigations
Sick building syndrome (SBS) describes a series of symptoms with no clear etiology, such as eye, nose and throat
irritation, headaches and high frequency of airway infection and cough, which are associated with a building environment. It is distinguished from building-related illnesses
(BRI) which are well-defined responses to biological,
physical or chemical exposures occurring in indoor environments (Brightman and Moss 2000). SBS and BRI
investigations were mostly cross-sectional (i.e. comparing
occupants of buildings where problems were identified to
those of “control” buildings). Some of these studies included a longitudinal component, as the health of exposed
individuals was reassessed after exposure had been
eliminated.
Some of these studies where mold contamination was
investigated, along with other exposures, are summarized
here. It should be kept in mind that because of their crosssectional design and some other methodological issues
(multiple concomitant exposures, possible bias in studies
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initiated following complaints), these studies cannot identify or demonstrate an independent association between an
exposure such as mold and dampness, and a health outcome.
n
n
n
In the United States, a health questionnaire was
administered to 53 office workers with more than
three months' employment in a water-damaged building where Stachybotrys growth was found, and to
21 office workers with similar duties, working in other
buildings. Blood samples were also collected from
every participant for immunologic tests. Employees
from the water-damaged building had a significantly
higher prevalence of lower respiratory problems (76%
vs. 43%; ρ<0.01), and eye symptoms such as burning,
irritation and blurry vision (57% vs. 19%; ρ<0.01).
There was no difference between the two groups with
respect to total white blood cell counts, but the proportion of eosinophils was marginally higher among
employees from the water-damaged building (ρ=0.06)
( Johanning et al. 1996).
In the United States, a health questionnaire was
administered to workers employed in three buildings
with severe water damage and contamination with
Aspergillus versicolor and Stachybotrys chartarum, and to
workers from two control buildings with no visible
mold growth. In total, 197 people participated in that
study. Workers from the water-damaged buildings had
a higher risk of eye itching and watering (OR 2.49,
95% CI 1.02 to 6.27), stuffy or blocked nose (OR 4.48,
95% CI 1.93 to 10.68), runny nose (OR 3.06, 95% CI
1.16 to 8.53), dry throat (OR 3.74, 95% CI 1.42 to
10.42), lethargy (OR 10.62, 95% CI 4.50 to 22.10), difficult breathing (OR 13.47, 95% CI 1.90 to 72.83), and
chest tightness (OR 10.41, 95% CI 1.46 to 62.83)
(Hodgson et al. 1998).
In Finland, 397 children from a water-damaged, moldcontaminated school (thereafter referred to as “School
E”) were compared to 192 children from a control
school where inspection revealed no mold contamination (“School C”). All participants were aged 7 to
12 years. Questionnaires were sent to parents of children from both schools before and after remediation
in School E, and a physician reviewed diagnosis and
antibiotic prescriptions in the children's medical
records. Before remediation, children from School E
had a higher risk of common cold (OR 1.51, 95% CI
1.04 to 2.20) and bronchitis (OR 2.76, 95% CI 1.11 to
6.81), but these differences disappeared after mold
remediation in School E (Savilahti et al. 2000).
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2.1.4
Cohort studies
In cohort studies, subjects classified according to their
exposure are followed over time to determine the incidence of the disease of interest. To date, no cohort studies
have been published on the association between residental
mold exposure and asthma, although a published study
has investigated the association between mold exposure at
school and childhood asthma (see below). In addition,
there is an ongoing cohort study in Prince Edward Island,
Canada.
In Sweden, a prospective study was carried out over four
years; a total of 1,347 children was surveyed twice, in
1993 and in 1997. Their mean age in 1993 was 10.3 years.
Participants were attending 39 different schools at the time
of the first survey. Total mold concentrations were determined in 1993 and 1995 and ranged from 5 to 360 cells/m3
(arithmetic mean 26 cells/m3). After adjustment for sex,
age, atopy in 1993, and smoking, the odds ratios for incident asthma (i.e. diagnosed during the follow-up period)
per 10-fold increase in total mold levels in classrooms was
1.3 (95% CI 0.5 to 3.6). Among children who were not
atopic in 1993, the odds ratio for incident asthma per 10fold increase in mold levels, adjusted for sex, age and
smoking, was 4.7 (95% CI 1.2 to 18.4) (Smedje and
Norbäck 2001).
2.2
Effects of Molds in
Sensitive Groups
Some sub-populations have been found to be at increased
risk of developing rare conditions following exposure to
molds. Exposure to extremely high mold contamination
has been associated with pulmonary hemorrhages in
infants, and increased risk of invasive mycose has been
observed in people with immune suppression.
2.2.1
Pulmonary hemorrhage
Exposure to indoor molds has been a suspected cause of
idiopathic pulmonary hemorrhage in infants and young
children. In most cases, the suspected etiologic agent was
Stachybotrys chartarum (also known as S. atra), a hydrophilic
fungus (i.e. requiring very damp conditions to grow) that
produces cellulase and is therefore able to use cellulose as
a substrate. Stachybotrys chartarum produces at least four
families of compounds: atranones, macrocyclic trichothecenes, spirolactones and cyclosporin-like compounds
(Sakamoto et al. 1993; Jarvis et al. 1995; Hinkley et al.
1999). There appear to be two chemotypes present in
North American strains: those that produce all of the
27
families of compounds and those that do not produce
tricho-thecenes, but do produce the others. Both types
appear to occur together (Nielsen et al. 2002).
In Cleveland, Ohio, 10 infants aged less than one year
were diagnosed with pulmonary hemorrhages and hemosiderosis between January 1993 and December 1994. Each
of these cases was matched for age with three controls.
Data collection was performed by a questionnaire administered to parents and sampling of molds on surfaces and
in the air. Mean concentrations of viable mold conidia in
the air were higher in houses of cases compared to
houses of controls (total viable fungi: 29,227 CFU/m3 vs.
707 CFU/m3; Stachybotrys chartarum: 43 CFU/m3 vs.
4 CFU/m3). A 10-CFU/m3 increase in the concentration
of viable Stachybotrys chartarum conidia was associated with
a significantly increased risk of acute pulmonary hemorrhage (OR 9.83, 95% CI 1.08 3×106). Nine out of
10 cases lived with smokers, compared to 16 out of
30 controls (OR 7.9, 95% CI 0.9 to 70.6), suggesting that
exposure to environmental tobacco smoke may act synergistically with the factors associated with damp buildings
(Montaña et al. 1997; Etzel et al. 1998). A review panel
mandated by the US Centers for Disease Control and
Prevention (CDC) to reassess this investigation concluded
that the methodology used to collect mold samples and to
calculate airborne counts of viable spores was inappropriate (CDC 2000).
No other published epidemiologic study has investigated
the association between exposure to S. chartarum and pulmonary hemorrhage, but cases of pulmonary hemorrhage
have been reported in infants and young children exposed
to it (Elidemir et al. 1999; Flappan et al. 1999) or to other
hydrophilic, cellulolytic fungi (Novotny and Dixit 2000).
In the Cleveland hospital where the initial outbreak
occurred, 30 infants were hospitalized with acute pulmonary hemorrhage between 1993 and 2002. Twenty-six
out of 29 infants lived in water-damaged buildings, and
25 out of 28 in homes containing toxigenic fungi
(Dearborn et al. 2002).
In 2000, the CDC created three new working groups to
develop better protocols for investigation of future clusters. Briefly, a review of patient records from the
Cleveland cases by pediatric and other specialists indicated that there were no known potential causes for the disease reported in the original studies. A clear case definition was developed should any additional clusters of infant
pulmonary hemorrhage be detected. Most of the babies
included in the original studies and subsequent infants
studied would be included by the new definition
(Dearborn et al. 2002). A second working group
28
concluded that the fungal exposure assessments in the
original study were inadequate. Several investigation techniques were described in case of future reports of clusters
of idiopathic pulmonary hemorrhage. Some of these techniques would not have been available at the time of the
original investigation (CDC 2001). A third group developed a protocol for surveillance and CDC has begun a
surveillance program in conjunction with the states
(CDC 2004).
2.2.2
Invasive mycoses
Some fungi such as Aspergillus species are ubiquitous in the
environment, and inhalation of their spores is very common. However, invasive mycoses (i.e. fungal infections)
occur mostly in immunosuppressed patients. The most
common pathogen is Aspergillus fumigatus (Bennett 1994).
The incidence of invasive mycosis is increased in AIDS
patients; an analysis of medical records of 35,232 HIVinfected patients who attended outpatients clinics in 10 US
cities between 1990 and 1998 revealed that the incidence
of invasive aspergillosis was 5.1 per 1000 (95% CI 2.8 to
7.3) in those with CD4 counts 50 to 99 cells/mm3 and
10.2 per 1000 in those with CD4 counts lower than
50 cells/mm3, compared to 1.0 per 1000 (95% CI 0.6
to 1.4) in those with CD4 counts equal to or higher than
200 cells/mm3 (Holding et al. 2000).
Several outbreaks of invasive aspergillosis have been
reported in hematology wards where neutropenic
leukemia patients were housed. The risk of invasive
aspergillosis in immunosuppressed patients was associated
with the airborne concentrations of Aspergillus spores, and
increased incidences have been observed following events
resulting in higher Aspergillus counts in the air, such as
construction or dysfunction in air filtration systems.
n
From May 1981 to October 1985, 14 bone marrow
transplant patients developed nosocomial Aspergillus
infections out of 111 patients who underwent such
transplants. Further analysis revealed that all these
cases of infection occurred among the 74 patients
housed outside a high-efficiency particulate air
(HEPA) filtered environment, while none of the
39 patients housed in a HEPA-filtered environment
developed aspergillosis. Only one of the 166 air
samples collected in the HEPA-filtered environment
(0.6%) was positive for Aspergillus, while 75 out of
466 samples collected elsewhere in the hospital
(16.1%) and 13 out of 54 samples collected outside the
hospital (24.1%) were positive (Sherertz et al. 1987).
n
In 1993, six cases of aspergillosis were identified
among the patients who attended the hematologyoncology ward of a pediatric hospital in Glasgow,
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United Kingdom, while only one case had been identified in that hospital over the five previous years. The
outbreak investigation revealed that a contaminated
vacuum cleaner used in the ward dispersed a
bioaerosol; the Aspergillus concentration close to that
vacuum cleaner was 62 CFU/m3 when it was in use,
compared to 0 to 6 CFU/m3 elsewhere in the building
(Anderson et al. 1996).
n
In the hematology-oncology ward of a Montréal hospital, the incidence of invasive aspergillosis in patients
with leukemia or bone marrow transplant identified as
neutropenic rose to 9.88 per 1000 days at risk during
construction activity ( July 1989 to August 1992), compared to 3.18 per 1000 days at risk before the construction started ( January to June 1989). Installation of
wall-mounted portable HEPA filters and implementation of other infection control measures subsequently
decreased the incidence of invasive aspergillosis to
2.91 per 1000 days at risk, even though the construction work continued (August 1992 to September
1993). The average concentration of Aspergillus in the
air during the epidemic period was 6.77 CFU/m3, and
no Aspergillus was recovered in air samples after the
installation of the HEPA filter and the implementation
of infection control measures (Loo et al. 1996).
n
In the fall of 1993, in Israel, a nosocomial outbreak of
invasive pulmonary aspergillosis occurred in leukemia
patients treated in a regular ward with only natural
ventilation during extensive hospital construction and
indoor renovation. The infection among acute leukemia patients rose to 50%, and invasive pulmonary
aspergillosis developed in 43% of acute leukemia
patients during the next 18 months despite the administration of chemoprophylaxis. After that period, a
new hematology ward was opened with an air filtration system with HEPA filters, and none of the acute
leukemia or bone marrow transplantation patients
who were hospitalized exclusively in the hematology
ward developed invasive pulmonary aspergillosis,
while 29% of acute leukemia patients who were
housed in a regular ward, because of shortage of space
in the new facility, still contracted invasive pulmonary
aspergillosis. The average Aspergillus concentration
was 0.18 spores/m3 in the new HEPA-ventilated
hematological ward, while the average concentration
in the regular ward during construction was
15 spores/m3 (Oren et al. 2001).
Community-acquired (i.e. out of hospital) opportunistic
invasive aspergillosis is not as well documented, but some
cases have been reported (Benoit et al. 2000; Chen et al.
2001). Immunosuppressed patients remain vulnerable to
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Aspergillus infections if exposed in the outpatient setting or
at home after being released from hospital (VandenBergh
et al. 1999).
2.2.3
Allergic bronchopulmonary mycoses
and allergic fungal sinusitis
Fungi can colonize the lungs or nasal cavity of patients
with underlying respiratory disease such as asthma or
chronic rhinosinusitis. This condition is referred to as allergic bronchopulmonary mycosis when occurring in the lungs,
and as allergic fungal sinusitis when taking place in the nasal
cavity. Since Aspergillus species (especially Aspergillus fumigatus) are the most common etiologic agents causing allergic bronchopulmonary mycosis, this condition is commonly referred as allergic bronchopulmonary aspergillosis, or
ABPA. Both conditions are characterized by eosinophilia
and by the presence of non-invasive fungal hyphae in sputum or in nasal mucus (Hunninghake and Richerson 1994;
Ponikau et al. 1999). Case reports have suggested a link
between fungal counts in the air and the development of
acute bronchopulmonary mycoses (Beaumont et al. 1984;
Kramer et al. 1989; Ogawa et al. 1997).
2.3
Animal Studies
Several experimental studies with animal models exposed
to fungal cells, antigens or constituents have found effects
similar to those observed in humans in epidemiological
studies, such as eosinophilia and increased serum IgE.
n
Twenty-four adult albino guinea pigs inhaled daily
8 mg of a Penicillium chrysogenum extract nebulized in
phosphate-buffered saline (PBS), and two of them
were sacrificed each week (up to 12 weeks). Twelve
other guinea pigs were handled the same way, but
received only nebulized PBS, and one of them was
sacrificed each week. No histopathological lesion was
found in control animals throughout the experiment,
but interstitial infiltrates appeared in the alveoles of
Penicillium-treated animals after four weeks, and granulomas appeared after 10 weeks. Also, specific IgM
and IgG antibodies to P. notatum were detectable in
Penicillium-treated animals after seven weeks (Alonso
et al. 1998).
n
A similar experiment carried out using a Rhizopus
nigrans extract yielded similar results (i.e. IgG antibodies to R. nigrans in serum after seven weeks, and
interstitial infiltrates four weeks and granulomas after
10 weeks in the alveoles of Rhizopus-treated animals)
(Alonso et al. 1997).
n
Male and female guinea pigs were exposed to aerosols
containing either 30 µg/m3 of (1->3)-ß-D-glucan (a
29
fungal cell component), 75 µg/m3 of Escherichia coli
lipopolysaccharide (a bacterial endotoxin), both, or
the vehicle only (controls). Animals were exposed
four hours per day, five days per week for five weeks
and then sacrificed. Cell counts were determined in
Bronchoalveolar lavage (BAL) fluid and in lung interstitium. Macrophages were increased by endotoxin
(BAL fluid ρ<0.001, interstitium ρ<0.05) and by
glucan+endotoxin (BAL fluid ρ<0.001, interstitium
ρ<0.05), but not by glucan alone. Lymphocytes were
increased in BAL fluid by endotoxin (ρ<0.05) and
glucan+endotoxin (ρ<0.01), but the highest response
was observed with glucan alone (ρ<0.001 in BAL fluid
and interstitium). Neutrophils were increased in BAL
fluid by endotoxin (ρ<0.001) and glucan+endotoxin
(ρ<0.001), but not by glucan. Eosinophils were
strongly increased by glucan in both BAL fluids and
interstitium (ρ<0.001), slightly increased by glucan+
endotoxin in BAL fluid only (ρ<0.05) and not affected
by endotoxin (Fogelmark et al. 2001).
n
C57BL/6 mice aged six to eight weeks were sensitized
to Aspergillus antigens (100 µg in 50 µl saline) three
successive days a week for three weeks, and sacrificed
after one, two or three weeks. Control mice were handled the same way, but were administered 50 µl saline
instead of the antigen solution. Total cells counts were
strongly increased in sensitized mice compared to
controls at weeks one, two and three (ρ<0.02 at each
week). The proportion of macrophages in BAL cells
remained constant at 97% over weeks in control mice,
while in Aspergillus-treated mice the proportion of
macrophages decreased (34% at week one) and the
proportion of lymphocytes, neutrophils and
eosinophils increased. The neutrophil counts in BAL
fluid reached (62.2±14.4) × 104 cells at week two and
(78.2±29.1) × 104 cells at week three in Aspergillustreated mice, compared to (0.1±0.1) × 104 cells in control mice throughout the study (ρ<0.05) (Wang et al.
1994).
n
Groups of six to nine female C57B1/6 mice were
inoculated intranasally with 50 µl saline containing
either no fungal conidia (control group), 104 nonviable (methanol-treated) conidia or 104 untreated
conidia (of which 25±5% were viable) of Penicillium
chrysogenum once a week for six weeks, and were sacrificed 24 hours after the last inoculation. P. chrysogenum
conidia were isolated from a building affected by
building-related illness. Mean total IgE levels in
serum were 804 ng/ml (SD 301 ng/ml) in controls,
833 ng/ml (SD 339 ng/ml) in animals treated with
non-viable conidia, and 2627 ng/ml (SD 1778 ng/ml)
in animals treated with viable conidia. Mean percentage of eosinophils over total peripheral white blood
30
cells were 5.3% (SD 0.8%) in controls, 7.3% (SD 1.7%)
in animals treated with non-viable cells, and 10.9%
(SD 0.9%) in animals treated with viable conidia.
Finally, mean eosinophil counts in BAL were 0.22
(SD 0.44) per 1000 BAL cells in controls, 0.5 (SD
0.55) in animals treated with non-viable conidia, and
14.17 (SD 5.91) in animals treated with untreated conidia. Total serum IgE, peripheral eosinophil count and
BAL eosinophil counts were significantly higher in the
group treated with viable conidia than in controls
(ρ<0.05) (Cooley et al. 2000).
Also, some studies found severe hemorrhagic responses
induced by Stachybotrys chartarum spores.
n
Four-day-old Sprague-Dawley rat pups were instillated
intratracheally with 1.0 to 8.0×105 intact spores (suspended in saline) per gram of body weight, similar
suspensions of spores treated with ethanol to remove
trichothecene toxins, or with saline only. Animals
were sacrificed on their 7th or 12th day of life. Cell
counts of macrophages, lymphocytes and neutrophils
were increased two-fold, five-fold, and seven-fold,
respectively, in the bronchoalveolar lavage fluid of
animals treated with 1.1×105 intact spores/g compared
to those treated with saline only or with ethanoltreated spores (ρ<0.001 for each cell type). There
was no difference between the two latter groups.
Hemoglobin concentration in BAL fluids in animals
treated with intact spores, ethanol-treated spores and
saline were 2.46±0.33 mg/ml, 1.26±0.16 mg/ml and
1.22 mg/ml, respectively; the difference between
groups was significant (ρ=0.004). The S. chartarum
strain used in this study had been isolated in the
water-damaged house of an infant that was part of the
Cleveland outbreak (Yike et al. 2002). These findings
indicate that mycotoxins (or another constituent
removed by the ethanol treatment) may be responsible for inflammatory and hemorrhagic response of the
infant lung to S. chartarum.
Other studies with rodents exposed to Stachybotrys
chartarum showed effects on lung physiology that may
be mediated by different mechanisms.
n
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Carworth Farms White mice were intranasally
instilled with 50 ml saline containing either
107 Cladosporium cladosporioides conidia per ml,
107 Stachybotrys chartarum conidia per ml, or 10-7 M of
isosatratoxin F; another group was untreated (control
group). For each treatment, groups of two to four mice
were sacrificed 0, 12, 24, 48 and 72 hours postexposure. None of the mice, regardless of treatment,
showed any apparent clinical sign of respiratory
distress or sickness. The phospholipid composition
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of lung surfactant was significantly modified from
12 hours to the end of the experiment following exposure to S. chartarum conidia and isosatratoxin, while
following C. cladosorioides exposure small changes
were observed at 48 hours post-exposure only (Mason
et al. 1998).
n
Groups of five Carworth Farms White mice were
intranasally instilled with 50 ml saline containing
either 1.4×106 Cladosporium cladosporioides conidia per
ml, 1.4×106 Stachybotrys chartarum conidia per ml, or
10 µg/ml of isosatratoxin F, or with saline only.
Animals were sacrificed after 24 hours. In vitro conversion of a biologically active form of alveolar surfactant to a biologically inactive form was significantly
higher in surfactant of S. chartarum-treated mice than
in those of all other groups, including controls; other
treatment groups were not different from controls with
respect to that end-point (Mason et al. 2001).
n
Stachybotrys chartarum spores suspended in saline were
instilled into mouse trachea, and mice were sacrificed
24 hours later. Exposure to S. chartarum induced an
overall reduction of phospholipid content in alveolar
surfactant. The relative distribution of phospholipids
across surfactant fraction and the nature of surfactant
phospholipids were also altered (McCrae et al. 2001).
n
Groups of five to six mice were inoculated intratracheally with 50 ml saline containing either 1.4×106
Cladosporium cladosporioides conidia per ml, 1.4×106
Stachybotrys chartarum conidia per ml, or 0.02 µg/ml of
isosatratoxin F, or with saline only. No difference was
observed between alveolar type II cells of control,
saline-treated or C. cladosporioides-treated animals,
while alveolar type II cells from mice treated with
either S. chartarum spores or isosatratoxin F showed
remarkable ultrastuctural changes compared to controls (Rand et al. 2002).
2.4
Discussion
2.4.1
Summary of findings
The major findings on the health effects of mold can be
summarized as follows.
n
Exposure to indoor mold is associated with an
increased prevalence of asthma-related symptoms,
such as chronic wheezing, irritative and non-specific
symptoms.
n
Studies on mold exposure and the development of
asthma yielded more conflicting results.
n
In laboratory animal studies, instillation of fungal antigens (Penicillium and Aspergillus) and fungal cell components (1->3-D-glucan) resulted in infiltration of lung
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tissues by lymphocytes, neutrophils and eosinophils in
rodents. Also in laboratory animals, instillation of
Stachbotrys spores at non-lethal levels resulted in severe
biochemical and ultrastructural changes.
n
Data published to date suggest that the association
between Stachybotrys chartarum and acute pulmonary
hemorrhage in infants cannot be excluded.
n
There is evidence from outbreak investigations and
case reports that increased concentrations of airborne
fungal spores resulting from environmental perturbations or inadequate control measures are associated
with a higher risk of invasive mycoses in immunocompromised individuals. No thorough epidemiological studies have assessed what airborne concentration
of Aspergillus spores is required to cause an infection.
2.4.2
Limitations
2.4.2.1 Exposure assessment
In most epidemiological studies on indoor mold and
health, the exposure assessment was based on participants'
self-reports. In the few studies where exposure to mold
was assessed by a member of the research team, the exposure classification was based on dichotomous questions
such as the presence or absence of dampness and/or
mold; there was no quantitative exposure assessment, and
therefore no determination of a dose–response relationship. Exceptions are the studies of Garrett et al. (1998) and
Dales et al. (1999). Also, in most cross-sectional and casecontrol studies, the mold taxa present in homes were not
identified. Mold species differ considerably, not only in
their potential to cause adverse effects to human health,
but also in the mechanisms by which they can affect
health (i.e. through releasing volatile compounds, allergens or mycotoxins) and, therefore, in the nature of effects
they can cause.
The difficulty of quantifying human exposure to mold is
thus a major obstacle in ascertaining the existence of
cause-and-effect relationships, as dose–response relationships cannot be assessed. This difficulty has led the
Institute of Medicine (2000) to conclude that “. . . standardized methods for assessing exposure to fungal allergens are essential, preferably based on measurement of
allergens rather than culturable or countable fungi . . .”
in order to obtain a clear understanding of the effects of
building-related fungi.
Quantitative measurement, rather than questionnairebased assessment, of exposure to fungi may be a promising way to improve epidemiological studies. However,
the traditional method of exposure measurement (i.e.
air sampling and culture of fungal spores) shows several
31
limitations that make their utility questionable. For example, airborne fungal spores can be sampled only over
short periods of time, while air counts of fungal spores
vary considerably over longer periods of time. Also, the
culture medium used always favours some species over
others, and some fungal taxa have the ability to inhibit the
growth of other taxa in culture media.
For all the reasons mentioned above, the determination of
surrogate markers of fungal growth, such as ergosterol and
(1->3)-ß-D-glucan, in house dust appear to be more promising (Dillon et al. 1999). Both ergosterol and (1->3)-ß-Dglucan are cell membrane constituents in fungi (Li and
Hsu 1996; Miller and Young 1997). (1->3)-ß-D-glucan has
been associated with increased peak expiratory flow (PEF)
variability in asthmatic children (Douwes et al. 2000).
There is, however, a need for further research to develop
standardized protocols for the determination of (1->3)-ßD-glucan in the environment (Dillon et al. 1999).
Determination of extracellular polysaccharides (EPS) of
Aspergillus and Penicillium in house dust is another
approach being developed for the assessment of exposure
to mold. EPS is a fungi-specific marker but, unlike glucan,
it is not suspected to be causally related to adverse effects
on respiratory health (Chew et al. 2001).
Molecular approaches have been developed for assessing
both qualitative and quantitative fungal exposure in buildings and other environments (Haugland et al. 1999). To
date, there is little practical experience with this approach.
Some research groups have proposed using animalderived antibodies to provide quantitative and qualitative
information on fungal exposure (Wijnands et al. 2000a,
2000b). Another approach to measuring fungal exposure,
advocated by the US Institute of Medicine Committee on
Asthma (Institute of Medicine 2000), is to determine
human fungal allergens or antigens. Research is under
way on this in Canada.
2.4.2.2 Outcome assessment
Objective assessment of health outcomes is another weakness of many epidemiological studies on health effects of
mold exposure, since most studies rely on subjective
assessments by questionnaires, which once again render
the drawing of firm conclusions more difficult. Objective
measures of health outcomes do exist, but incorporating
them into studies greatly increases study costs.
2.4.2.3 Confounding factors
Damp conditions favourable to mold growth are also
favourable to other biological agents known to be allergenic, such as dust mites and gram-negative bacteria.
32
Unlike mold, bacteria are not visible and, therefore, their
presence can be assessed only by air or dust sampling.
Therefore, the association observed between mold exposure and allergic responses could be explained in part by
confounding bacteria or dust mites being associated with
both the exposure to mold and the outcomes considered.
This may explain the findings, in some studies
(Williamson et al. 1997; Norbäck et al. 1999), of stronger
associations between dampness and asthma than between
visible mold and asthma. However, in a cross-sectional
study where bacterial endotoxins and dust mites were
actually measured, controlling for these other allergen levels did not affect the association between indoor mold and
respiratory symptoms (Dales and Miller 1999). Moreover,
a case-control study revealed a significant association
between mold growth and asthma after controlling for visible dampness (Thorn et al. 2001). Also, experiments in
animal models showed that mold antigens are able to
induce allergic responses in the absence of endotoxin or
other biological agents (Alonso et al. 1997, 1998; Cooley et
al. 2000).
Chemical exposures may also be confounders in at least
one of the studies summarized above. In Smedje and
Norbäck's (2001) cohort study, both airborne fungi and
formaldehyde were significant risk factors for incident
asthma, but could not be included together in multivariate
models because of their strong mutual association.
Other potential confounders in respiratory disease epidemiology, such as socio-economic status, smoking and
environmental tobacco smoke exposure, have been
controlled for in the majority of cross-sectional and casecontrol studies reviewed, and are therefore unlikely to
explain the findings.
2.4.2.4 Bias
There may be a reporting bias in some studies, as there is
an increasing awareness in the population that molds are
suspected to cause respiratory health effects. People with
mold problems may pay more attention to symptoms
experienced by their children or themselves. This is likely
to have occurred in the Finnish cross-sectional study that
found an association between mold and backaches and
stomachaches (Pirhonen et al. 1996). As well, people with
respiratory health problems may pay more attention to
the presence of mold, as physicians investigating asthma
or other respiratory diseases commonly ask patients if
they have been exposed to mold or dampness, but this
bias was eliminated in many studies by having houses
inspected by an investigator blind of participants' case or
control status. In the Williamson et al. (1997) case-control
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study, where the possibility of such a bias was reduced by
a case or control classification based on hospital records
and exposure assessment based on home visits, an odds
ratio of 1.7 (but non-significant) was found between severe
dampness and asthma.
2.4.2.5 Study design
To our knowledge, only one cohort study was published
on health effects of indoor, non-occupational exposure to
molds (Smedje and Norbäck 2001). At the time of writing,
another cohort study is being conducted in Canada, the
Prince Edward Island infant health study. The evidence
linking mold to health effects arises mostly from crosssectional and case-control studies. These two designs are
generally considered weaker than cohort studies for investigating the etiology of disease, since it is difficult to ascertain that the suspected cause actually preceded the disease
under study. However, though asthma and allergy are
chronic conditions, asthma symptoms can improve when
exposure to allergens and/or irritants that induce bronchoconstriction is removed. A cross-sectional or case-control
study finding an association between “mold and/or dampness” and chronic wheezing does not demonstrate that
mold has caused the onset of asthma, but it may indicate
that either mold or dampness induces respiratory symptoms in asthmatics (assuming, of course, that both exposure and outcome assessments are accurate; see previous
sections). On the other hand, cohort studies of home
indoor environments and respiratory/allergic diseases
(preferably with objective assessment of exposure and outcome, such as home inspection and physical assessments)
are needed to ascertain the existence of a causal link
between mold and respiratory diseases.
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2.4.3
Conclusion
As seen in section 2.4.1, several studies have found significant associations between exposure to mold and/or dampness, and irritative and non-specific respiratory symptoms,
as well as the exacerbation and development of respiratory diseases such as asthma. Due to limitations in the
assessment of both exposure and outcomes, and since in
almost all studies to date an independent effect of mold
could not be isolated from that of other contaminants
associated with dampness, epidemiologic data alone are
insufficient to conclude that indoor mold causes respiratory disease. However, such a causal link is highly plausible
in view of the fact that exposure to fungi in occupational
environments causes allergic and toxic disease and that
adverse effects of fungi have also been seen in inhalation
studies using animal models.
In the hospital setting, airborne exposure to certain fungi
is associated with an increased risk of fungal infection in
immunocompromised individuals.
Although further investigation of health effects of indoor
fungi by means of improved exposure and health outcome
assessment methods are needed to resolve uncertainties,
current knowledge supports the need to prevent damp
conditions and mold growth and to remediate any fungal
contamination in buildings.
33
3. Investigation of
Fungal Contamination
of the Non-Industrial Workplace
Photo: Architectural Diagnostics Ltd.
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35
3.1
Background
3.2
General Principles
A safe workplace is mandated by law in Canada under
various legislative frameworks. These include Section 12
of the Hazardous Products Act1, the Canada Labour Code, the
Transportation of Dangerous Goods Act, provincial occupational health and safety acts, and related regulations. It is
essential to have in place an operating procedure that will
protect the health and safety of occupants2, as well as the
workers performing their duties in the investigation of possible fungal contamination in public buildings3 (CEOH
1995a). Analyses of the legislative framework for indoor
air quality (IAG) in Canada illustrated its variable nature
and described the case law that might apply (Beaudry
1999; Morton and Kassirer 2000).
Indoor air quality investigations4 can begin in several
ways. Some building owners or managers conduct regular
air quality audits to detect problems before they can potentially affect occupants. At the other end of the spectrum
are investigations which occur as a result of acute reactions from individuals entering a building. Appropriate
measures should be taken when an investigation is
prompted by health complaints. It is important to involve
specialists with recognized professional training and experience to investigate potential mold problems in public
buildings using methods documented by the ACGIH
(1999) and the American Industrial Hygiene Association,
or AIHA (Dillon et al. 1996).
Recent reviews indicated that there is no specific regulatory mention of most contaminants present in residential or
office indoor air (CEOH 1989, 1995). As is the case with
other indoor air contaminants, the legal framework for
mold is mainly based on regulations that suggest or
require the adherence to the advice of cognizant authorities, including CEOH, the American Society of Heating
Air-Conditioning & Refrigerating Engineers Standard 62,
and the ACGIH Threshold Limit Values (TLVs), as well
as determinations or policies of provincial and territorial
labour and health departments. In addition, health and
safety requirements in legislation impose some obligations
to industrial hygienists, professional engineers, physicians
and other health professionals to act in accordance with
the best interests of occupants. This should be done in
accordance with the policies of the designated Medical
Officer of Health or Public Health Directors for the area
concerned and/or Health Canada for federal jurisdictions.
In HVAC systems, humidifiers, dirty filters and accumulated debris in ducts subject to condensation or leaks can
all be sources of building-associated mold. Spores can be
blown out of ducts in a periodic fashion. Fungi can be
released when occupied spaces adjacent to contaminated
wall cavities, elevator shafts or faulty sewer drains are
depressurized. Release from these sources can be affected
by air infiltration rates and pressure differentials resulting
from wind and thermal loading (weather) and unbalanced
ventilation or exhaust systems. Distribution of fungi from
carpets or surface contamination is affected by activity in
the occupied space and the intensity of cleaning.
It cannot be emphasized enough that the best way to manage mold growth is to prevent it before it occurs. The
essential elements of a prevention strategy are the control
of moisture, the timely remediation of any water leakage,
and adequate maintenance of heating, ventilation and air
conditioning (HVAC) systems (Lavoie and Lazure 1994;
Flannigan and Morey 1996).
1.
Which established the Workplace Hazardous Materials
Information System (WHMIS).
2.
In section 3, “occupants” means individuals present in public buildings, including workers, students, visitors and the
general public.
3.
In section 3, “public building” means any building accessible to the public (e.g. office building, school, store).
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If required, laboratory tests must be done using appropriate methods and by qualified and experienced professionals. Commercial laboratories should demonstrate successful performance in the AIHA Environmental
Microbiology Proficiency Analytical Testing (EMPAT)
program and preferably be an Environmental Laboratory
accredited by the Standards Council of Canada (SCC),5 or
ISO or Good Laboratory Practice (GLP) certification.6
4.
In section 3, “investigation” means the process of appropriately trained individuals entering the building to conduct
inspection, sampling, documentation and production of
reports.
5.
The Standards Council of Canada (SCC) offers environmental laboratory accreditation in partnership with the
Canadian Association for Environmental Analytical
Laboratories (Inc.) (CAEAL). CAEAL is a not-for-profit
association of public and private sector laboratories.
6.
Good Laboratory Practice (GLP) refers to compliance with
a series of guidelines, developed by the Organisation for
Economic Co-Operation and Development (OCED),
regarding laboratory facilities, standard operating procedures (SOPs), quality assurance and reporting. GLP certication is granted by a number of agencies around the world,
including the US Food and Drug Administration.
37
There are also university and governmental laboratories
with highly qualified specialists in mold identification that
can provide reliable data; however, they must be required
to use recognized methods. Canada Mortgage and
Housing Corporation (CMHC) attempts to maintain a list
of laboratories that have provided services for the
Government of Canada. Provincial officials in Health or
Labour Departments may also be able to provide recommendations. All reasonable steps must be taken to ensure
that no action during the investigation or remediation7
process results in further contamination of the building or
increased risk for occupants or the public. Finally, the provision of reliable and timely information to occupants is a
critical aspect of any IAQ investigation because of the
need for individuals in one of the potential risk groups to
be informed in the event of a microbiological problem in
their workplace or education facility.
3.3
Factors to consider when addressing a potential mold problem
1.
It is important to focus on the problem as quickly as
possible to allow the investigating team to provide
clear answers to the occupants, managers and health
providers about the state of the building. For reasons
discussed in section 3.4, mold problems very often
result from chronic moisture problems. If exposure
has reached the point where health complaints have
been made, it has typically taken years for this to
occur. Since there is some mold on materials in all
buildings, determinations must be made regarding the
nature and extent of the contamination and who is
exposed.
2.
The first step in a mold investigation is an informed
inspection during or after which air samples may be
taken (see 3.4.1). Investigators must decide whether
there is a possible hidden contamination, including in
the HVAC system or wall cavities (Miller 1993). In
such cases, air samples are especially useful. Air samples collected using methods that require the culturing
of viable spores are often sensitive even to subtle
problems, and provide results after 7 to 10 days. In
contrast, non-viable (sticky surface) samples are
generally less sensitive, but provide data within 24 to
48 hours. All samples should be taken according to
the methods described in the AIHA Field Guide
(Dillon et al. 1996).
3.
After air samples are taken, floors and other surfaces
where dust may accumulate should be cleaned with a
high efficiency particle arresting (HEPA) vacuum.
With few exceptions, most exposure to mold spores
arises from people moving around in the occupied
space which stirs up settled dusts. Cleaning will, in
most cases, immediately reduce exposure while the
investigation process continues. If there are people in
the building, the decision of whether or not to take air
samples should be made quickly so cleaning can
proceed.
4.
As the nature and extent of the contamination
become known, this information needs to be given to
occupants. Among other things, this permits those
with special sensitivities to unusual airborne mold
exposures to consult with a medical professional about
whether they should remain in the building, or not.
5.
An accurate survey of the extent of the contamination
and moisture or damage is required to document and
remediate the affected area. There are three purposes
for this important step: (a) the complexity of the
removal process depends on the affected area
(ACGIH 1999; New York City Department of Health
2000); (b) there is evidence that the potential for
health effects among occupants depends on the area
Objectives of a
Mold Investigation
As noted above, the intensity and complexity of mold
investigations vary according to the size and nature of the
building, whether an air quality audit is being conducted
or whether the investigation is a response to a health complaint. The benchmark is the CEOH (CEOH 1989,
1995a, 1995b) advice to minimize exposure to fungi, that
there are population health effects of mold and dampness
and that there are risk groups. The goals are to define and
manage the microbial problem(s) and return the building
to a satisfactory level of performance. Air quality investigations for audit purposes are not considered here.
The following discussion refers to an incident in which a
health complaint has been made and initial evidence
shows that mold might be one of the potential issues.
The goals of such investigations are to:
n
establish the cause, nature and extent of fungal
contamination;
n
assess the risk of adverse effects on the health of
occupants;
n
manage the microbial problem(s); and
n
return the building to a satisfactory level of performance.
7.
“Remediation” includes both the thorough cleaning of any
mold growing in the building and correcting the building
defect that led to mold growth (excessive humidity, water
leaking, or water infiltration from the outside).
38
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of mold contamination; and (c) the quality assurance
process for the remediation depends in part on the
thoroughness of the investigation (AIHA 2001).
During the investigation stage, dust control (e.g.
misting and using a HEPA vacuum) is required
when making small investigative openings in walls
(< 0.1 m2) adjacent to occupied space. Larger inspection holes, especially where mold contamination has
been determined to be extensive, requires containment or other protective measures if the space is to be
re-occupied before doing repairs. The survey should
also assess the degree of connection of the discovered
mold to the living/working space. The documentation
step can be eliminated if the building has been
unoccupied.
6.
In documenting the nature and extent of the mold
observed, there are several reasons for determining
the fungal species present. The first reason is to verify
that the damage seen is really fungal in nature. Sometimes dirt or other deposits on surfaces in buildings or
HVAC diffusers are not building-associated mold. It
can also be useful to know what environmental conditions have led to mold growth. The species of mold
present can provide valuable clues. Molds that grow
under damp conditions are different from those that
grow under very wet conditions. This might help in
identifying sources of water that might not be obvious.
For example, the finding of a wet-loving buildingassociated mold near a window frame might suggest a
significant leak around the window or a condensation
problem in the wall cavity. The finding of a damploving mold behind a chest of drawers on an outside
wall might suggest inadequate ventilation or insulation. In addition, the occupants' medical professional
may find it useful to have a list of the dominant fungi
present.
7.
Fungal damage should be quickly remediated using
the protocols outlined in the New York City
Department of Health Guidelines (2000) and ACGIH
guidelines (1999; Chapter 15) (ACGIH 1999; New
York City Department of Health 2000) and quality
assurance process used (AIHA 2001). These are similar to those outlined in the CEOH Guide (1995a).
Note that the primary method to assure that mold
remediation has been done properly is confirmation
that the causal water or moisture sources have been
identified and eliminated. Repairing mold damage in
an exterior wall where it has been determined that
there is a good air barrier can typically be done without additional protective measures. The air barrier
should normally be sufficient to prevent the ingress of
mold spores indoors. It is important to note, however,
that construction, demolition and repairs all result in
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the release of construction dusts and other debris. It is
generally not appropriate to permit the space to be
occupied when construction is actively under way.
Measures to protect contents from settled dusts during
repairs, plus HEPA cleaning after repairs, are additional steps potentially required for re-occupancy,
depending on the nature and extent of the damage
and repairs. Containment of dust and spores using
negative pressure and isolation of the remediation
area is a prudent practice. There is no public health
reason to contain the outside of a building in the
situation where remediation is being done from the
exterior. A possible exception is when the exterior
walls are in a semi-enclosed space (e.g. a stairwell).
8.
The risk of health consequences from mold exposures
arising from mold-damaged building materials varies
with the degree of isolation from the occupied space.
Considering construction methods and climates in
Canada, exposure risk from greatest to least would be
growth: (a) on surfaces exposed to occupied space;
(b) on interior walls or floor cavities (especially if
there are ducts); (c) in exterior walls with poor air
barriers; (d) in exterior walls outboard of a good air
barrier; and (e) in attic space or roof space above an
air barrier. If the mold damage is in the ventilation
system, immediate steps are required to stop the
spread of contamination. If the contamination is on
the surface of walls, ceilings or floors exposed to the
occupied space, immediate steps are required to contain the mold-damaged areas. Options to consider are
the use of polyethylene barriers either with or without
depressurization. If the contamination is mainly in
demising wall cavities, access to highly damaged areas
of the building should be restricted until remediation
is complete. In the remaining areas, professional
judgment will have to be made on the potential to
introduce contamination into the occupied spaces
until repairs are complete. Additional steps to consider include regular HEPA cleaning with some air
monitoring to ensure the effectiveness of the cleaning.
A team to manage the remediation and repair process
needs to be created. The remediation and repair work
should be closely monitored to ensure its effectiveness, and quality assurance and compliance testing
should be incorporated.
9.
Typically, all porous materials on which there has
been fungal growth must be safely and effectively
removed, followed by a thorough particulate cleaning
by crews appropriately trained in dust control.
Surfaces that collect large amounts of settled dusts and
spores, including carpets and ceiling tiles, may also
need to be removed. These are difficult to clean and
there are no accepted methods of verifying that they
39
have been adequately cleaned. Factors to consider in
making the decision to remove remaining porous
surfaces in mold-damaged areas include the nature,
extent and duration of the mold problem in the building. As remediation proceeds, exposed areas must be
checked for any remaining mold damage revealed
during demolition. Semi-porous materials on which
mold growth has occurred can be cleaned if they are
structurally sound, and must be replaced if they are
not. Dusts on non-porous surfaces can usually be
cleaned using methods appropriate for the given
material.
If the contamination was extensive (i.e. on the upper
end of the remediation categories defined by ACGIH
[1999] or New York City Department of Health
[2000]), settled dust samples should be collected after
remediation. The purpose of this step is to provide
documentation that the affected areas have been
thoroughly cleaned. The dry weight of settled dust
collected/m2 should be measured according to the
guidance from the AIHA (2001). When the molddamaged materials have been removed and the affected area thoroughly cleaned with a HEPA vacuum,8
the building can be treated like a normal construction
site for the build-back.
After the repairs have been completed, air samples
taken one or two weeks after the ventilation system
has been running normally can be useful as a last
measure of the success of the steps taken.
3.4
Methodological Considerations
Microbiological sampling during a building investigation
for mold-related problems is complicated. Several cognizant authorities have published guidance on this topic.
For example, the AIHA published a Field Guide of consensus methods for microbiological sampling (Dillon et al.
1996). The ACGIH has published a comprehensive manual on microbiological problems of buildings, including
chapters on investigation and remediation that recognize
the AIHA manual as a source for sampling methods
(ACGIH 1999). Details on some of the procedures can
also be found in Flannigan, Samson and Miller (Flannigan
et al. 2001). The US Environmental Protection Agency
(EPA) has also published mold remediation guidance for
public buildings (USEPA 2001) and for homes (USEPA
2002).
8.
40
Residual dust should be reduced to as low as can reasonably
be achieved. This has been defined as less than 100 mg dry
weight/m2 on smooth surfaces in a number of cognizant
authority documents (ACGIH 1999; AIHA 2001).
The goals of any investigation are to establish the cause,
nature and extent of fungal contamination and to assess
the risk of adverse effects on the health of occupants.
3.4.1
Informed inspection
The first step in investigating a building for microbial
contaminants is an informed inspection. This should be
performed by someone with engineering or architectural
knowledge of moisture problems in buildings, considering
the type of building under investigation. The investigation
of large public buildings requires a different skill set than a
house. Mold contamination can arise from condensation,
floods and various types of leaks. Inspection of mold
problems requires a thorough knowledge of the design of
the building envelope and of the types of failures that
result in condensation and water leaks. The physical investigation of molds in both public and domestic buildings
requires considerable expertise in the design, construction
and operation of these structures. Informed inspection
checklists suitable for residential housing have been
developed by CMHC (1993) and by Public Works and
Government Services Canada (Davidge et al. 1992) and
the USEPA (USEPA and USDHHS 1991) for public
buildings.
Air sampling is not appropriate unless a thorough building
inspection is done either on a concurrent basis or before
sampling. Sampling is done to identify contamination that
is not visible without destructive testing and to document
air contamination. Similarly, after sample results are
obtained, the data must be compared with the information
obtained during the physical inspections. “Are the results
plausible?” is a question that must always be asked and
answered to properly assess the risk of false negative and
false positive results for mold contamination. Additionally,
documentation of the sources and nature of the contamination allows a failure analysis to be done on the building
(or HVAC system). This will assist in developing costeffective investigation strategies and ultimately any
remedial action necessary.
3.4.2
Culturable air samples
Air samplers collect fungal propagules either on agar
media or in aqueous suspensions. Such samples provide
information on culturable or “viable” propagules in air. It
is important to consider that existing air-sampling techniques underestimate the true airborne concentrations of
fungal spores for several reasons. The number of fungal
propagules determined by culture are substantially less (by
1% to 50%) than those determined by direct methods;
however, this varies between species. Different species of
fungi have different growth requirements so the use of any
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medium produces different recoveries. The spores of fungi
decline in viability with time; the spores of some species
remain viable for years and for other species for months.
Some species grow very fast or are aggressive in culture
and produce antifungal agents that can affect the growth
of other species present in culture. The variability of spore
clouds in the air in a building with active mold growth is
much larger than the precision of available sampling
methods. Air sampling is useful for investigating large
buildings for mold contamination and must be considered
if the investigation was prompted by health complaints.
It is seldom possible to take enough samples to conduct
rigorous statistical analyses, but statistical principles need
to be considered when determining the number of samples to be taken (ACGIH 1999). Careful consideration
must be given as to how and where each sample is to be
taken.
Air samples should be taken during normal activity in the
building, while the ventilation system is operational.
Factors to consider include taking samples in a given
space and allowing one or two hours between duplicates
(e.g. go around each floor of the building in one direction,
go up each level and then down, morning and afternoon,
etc.). This technique takes into consideration the variability of airborne spore concentrations over time and with
different activities, as well as varying thermal and wind
loads. Air samples should not be taken when it is raining.
Rain has a transient effect on the microbial populations in
outdoor air that can result in a reduction of the sensitivity
of the indoor–outdoor comparison. The number of outdoor air samples should in principle be equal to the number taken indoors. Since this is seldom practical, there
needs to be at least between three and six samples taken
outdoors during the period(s) when the indoor sampling is
under way. These need to be taken above grade to avoid
collecting windblown soil particles containing fungi which
can affect the comparison of the indoor–outdoor diversity.
It is recommended that outdoor air samples be collected
as close to the air intake as possible or facing into the
wind on the building roof. Other considerations can be
found in the AIHA Field Guide (Dillon et al. 1996) and
the ACGIH bioaerosols manual (ACGIH 1999).
The basis of the current methods for interpreting the
results of air sampling is a comparison of the diversity of
the fungi inside with outdoor air samples, taking into
account indicator species and species with poor recoveries
on agar media such as Stachybotrys chartarum (CEOH
1995a; Dillon et al. 1996; ACGIH 1999). There is a shifting array of fungal species in outdoor air as the season
progresses. Average numbers of total propagules in July
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range from 20,000 per m3. to peak levels of twice that
value. In the absence of snow cover, total Aspergillus/
Penicillium comprise <1% of the total fungal spores present
in outdoor air. When there is snow cover, the total number of fungal spores decreases, and the proportion of
Aspergillus/Penicillium therefore increases to 10% to 20%.
The advantage of properly collected and analyzed viable
air samples is that the data can be used to detect signs of
the early stages of a mold problem, as well as growths in
wall cavities or ventilation ducts (where dilution by outside air limits the sensitivity of the analysis).
3.4.3
Sticky surface samplers
Sticky surface samplers such as Zefon Air-O-CellTM,
AllergencoTM and BurkhardTM are increasingly used in
IAG investigations. There is little published information
on their comparative quantitative and qualitative performance (Dillon et al. 1996). However, some studies have provided information on the cut points of these samplers
(Aizenberg et al. 2000). A limitation of these methods is
the skill of the microscopist in counting fungal propagules
in a field containing debris of various kinds.
Advantages of data from properly collected and analyzed
sticky surface samples include the fact that the results are
available within a day and in situations when there is a
high percentage of non-viable spores in the air, the data
are more reliable.
3.4.4
Documentation of visually moldy area
Within the informed inspection component of the overall
investigation, detailed notes of the amounts of mold visible should be noted on the appropriate perspective of the
building plans. The moldy areas should be drawn on the
plan with sufficient accuracy to permit an estimation of
the number of square metres of mold.
Bulk samples might be collected from the visibly moldy
building materials to delimit the affected areas by examining the materials for fungal growth. A small amount of
material can be scraped off the surface and examined
under the microscope and/or plated on agar media.
Usually, the colour of visibly moldy material comes from
conidia, ascocarps, pycnidia and, in the case of melanized
fungi, the mycelia. Conidia that are not visible to the
naked eye, but present on building materials may still
have the potential to affect the air quality of the occupied
space.
Where there is probable cause to believe that there is
appreciable mold behind wall cavities, physical inspections
41
should be performed by opening up the hidden area.
Factors to consider include whether there is insulation in
the walls and what kind of water damage has occurred.
For example, if there has been a pipe burst, flood, fire
storm or evident problems with the cladding or windows,
all affected areas can be reasonably suspected of having
been affected and need to be examined for mold damage.
The informed inspection and/or air samples can be useful
in determining whether destructive testing is required.
Methods range from sawing the bottom 0.3 metre off one
side of interior walls to using a keyhole saw and a boroscope (AIHA 2001). Such destructive testing should be
done with source control HEPA vacuums (e.g. near the
saw) or under simple containment, using all appropriate
respiratory protection required (ACGIH 1999).
3.4.5
Mycological analysis of bulk samples
Bulk samples refer to physical, destructive samples of
building materials. Dilution plating methods are selective
and do not provide direct information on the fungi growing on the damaged material versus dormant organisms
that might have settled out from the air. Dilution plating
involves taking an amount of a powered material (e.g.
ground wallboard, settled dust) and suspending it in an
appropriate diluent. This is then further diluted in 10-fold
steps and aliquots are plated on agar media at least in triplicate, followed by spreading the liquid evenly over the
surface, incubating and counting the colonies that emerge.
Representative colonies are then transferred to agar media
appropriate to identify the species present. The strength of
this method is that a picture of the diversity of species
present can be obtained.
Small pieces of building materials collected (ca. 0.5 g) can
be plated on different agar media. These are incubated
and the colonies that grow out are counted and transferred
for identification. The advantage of this method is that the
colonies that first emerge from moldy building material
are likely to be the most reflective of those active in the
damaged material.
3.4.6
Microscopic techniques
Samples of moldy building materials that are plated by
either method should also always be mounted in lactophenol cotton blue or other appropriate stain and examined
by microscopy to determine the presence of organisms
that might not be viable. This allows a comparison to be
made between viable and non-viable cultures. This will
provide information on the dead fungi present on damaged material to be obtained, thus helping prevent false
negative results. (Dead fungal spores still contain allergens
and toxins.) If the majority of the fungi are found to be
dead on a moldy item, the water event probably occurred
months to years ago.
There are two basic techniques to examine moldy surfaces
by microscopy: tape samples and mounting scrapings of
the mold-damaged area collected in small plastic bags or
vials. Tape samples are made by pressing the affected surface with good quality cellophane tape. If scrapings are
available, they can be mounted on slides and examined;
they can also be cultured whereas the tape samples cannot. As with all microscopic methods, large dark spores
are easier to see and, depending on the skill of the microscopist, small hyaline spores are often overlooked. The
taxonomic information obtained is limited.
In the absence of regular HEPA vacuum cleaning, mycological analysis of settled dust samples has value in identifying a problem that might be seasonal or due to factors
not present at the time of the investigation (ACGIH 1999).
For example, condensation around perimeter induction
units, which leads to wet carpets, occurs only in the summer. Investigation of occupant complaints may occur
when the carpet is not wet. As is the case for air samples,
interpretation of dust samples is appropriately made by
analysis of the fungal diversity, but is less straightforward
(Dillon et al. 1996; ACGIH 1999).
42
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Fungal Contamination in Public Buildings:
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3.5
Conclusion
The guidance offered above on remediation and inspection emphasizes the need to use investigators who are
qualified and experienced in this aspect of engineering
and industrial hygiene. Because there is considerable variation in construction methods used and in climates across
Canada, such investigations cannot be standardized in
detail.
The guidance on mold sampling has emphasized that sampling is often a necessary part of investigation for public
buildings and less useful for house dwellings.9 Sampling
should be done by qualified and experienced investigators
using laboratories with demonstrated proficiency.
As noted in most current documents concerning mold in
buildings, prevention is key. Prompt attention to condensation and water leaks in the building fabric, and wet
building materials (resulting from plumbing or other
causes, such as flood or storm damage) will eliminate the
growth of mold and prevent the increase of other contaminants, such as house dust mites in the built environment.
Such preventive actions are relatively inexpensive compared to the costs associated with remediation of mold
problems in buildings. The value of prevention appears
even more obvious when one takes into account health
problems that may be avoided.
9.
CMHC has posted a discussion of the merits of mold sampling in single family dwellings on its Web site:
http://www.cmhc-schl.gc.ca
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43
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