Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter.
Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 90
3
Exposure Assessment
INTRODUCTION
Assessments of exposure to environmental agents in indoor air play a
central role in epidemiologic studies that seek to characterize population
risks, in screening studies aimed at identifying individuals at risk, and in
interventions designed to reduce risk. Because of the central importance of
exposure assessment, there is a need to understand the strengths and limita-
tions of the approaches that are available to assess exposures in those
contexts. Indoor dampness may be associated with some respiratory health
effects (Chapter 5), and a causal role for microorganisms has been sug-
gested. However, the specific roles of infectious and noninfectious microor-
ganisms and their components in diseases related to indoor environments
are poorly understood. The lack of knowledge regarding the role of micro-
organisms in the development and exacerbation of those diseases is due
largely to the lack of valid quantitative exposure-assessment methods and
knowledge of which specific microbial agents may primarily account for
the presumed health effects. In most studies, exposure is assessed by means
of questionnaires, and relatively few studies have attempted to measure
exposure to microorganisms.
Indoor environments contain a complex mixture of live (viable) and
dead (nonviable) microorganisms, fragments thereof, toxins, allergens, mi-
crobial volatile organic compounds (MVOCs), and other chemicals. Sensi-
tive and specific methods are available for the quantification of some bio-
logic agents, such as endotoxins, but not for others. Many of the newly
90
OCR for page 91
EXPOSURE ASSESSMENT 91
developed methods--for example, measurement of microbial agents, such
as (13)-glucans or fungal extracellular polysaccharides (EPSs)--have
not been well validated and are not commercially available. Even for some
well-established methods, such as the Limulus amebocyte lysate (LAL) as-
say for measuring bacterial endotoxins, substantial variations in exposure
assessment between laboratories have been demonstrated (Chun et al., 2000;
Reynolds et al., 2002; Thorne et al., 1997). It is known that the con-
ditions of storage and transport of bioaerosol samples and extraction of
dust samples may affect the activity of some biologic agents, such as endo-
toxins, and thus their measured concentrations, but those conditions are not
often addressed (Douwes et al., 1995; Duchaine et al., 2001; Thorne et al.,
1994). Finally, there may be biologic agents whose health effects have not
been identified. Microbial exposure assessment in the indoor environment
is therefore associated with large uncertainties, which potentially result in
large measurement errors and biased exposureresponse relationships.
This chapter focuses on exposure assessment of microorganisms and
microbial agents that occur in damp indoor environments. It discusses
issues related to dampness in general only briefly.
DEFINITIONS
Exposure1
Two classes of exposure measures can be distinguished: the theoreti-
cally ideal (and typically unknown) risk-relevant exposure metric (ERR) that
represents the individual breathing-zone concentration of an agent of inter-
est over a period that is relevant to the risk of developing the health out-
come of interest and the practical and available exposure surrogate that
correlates to some extent with the ERR. When used without qualification in
this report, exposure refers to surrogate exposure measures.
The ERR is the theoretical measure of exposure that best represents the
risk of adverse health consequences. Researchers often do not know enough
about the specific pathogenesis of indoor-related diseases to identify the
appropriate ERR confidently. One possible ERR for the exacerbation of asthma,
for example might be a short-term average that captures peak agent expo-
sures in the breathing zone immediately before the exacerbation. Relevant
averaging times might range from about 20 min to 48 hours.
Direct exposure surrogates include personal monitoring involving the
measurement of agent concentrations with monitors carried by individual
subjects. These offer more proximal measures of individual exposure than
1This section is derived from Clearing the Air (IOM, 2000), pages 5154.
OCR for page 92
92 DAMP INDOOR SPACES AND HEALTH
do the indirect approaches, but usually at the expense of sample size or
ability to characterize long-term exposures. Indirect measures include envi-
ronmental area monitoring (airborne or dust sampling), recall question-
naires, real-time diaries, and biologic response markers (IgG against fungal
antigens, for example). These approaches tend to be more practical in large-
scale studies and often are better suited to long-term exposure characteriza-
tion than are direct measures.
Exposure Mechanisms
Inhalation is usually presumed to be the most important mechanism of
exposure to fungi and other dampness-related microbial agents in indoor
environments. It is also generally believed that the most harmful agents are
within particles, such as fungal spores; however, although this has been the
general assumption, recent studies have identified hyphal fragments (Górny
et al., 2002) and dust (Englehart et al., 2002) as potential carriers of harm-
ful agents. This section briefly discusses the process of exposure; it focuses
on exposures to fungal spores, but the same exposure mechanisms and
associated questions apply to other microbial particles of similar size.
Fungal growth occurs on indoor surfaces--including surfaces in heat-
ing, ventilating, and air-conditioning systems--and an inhalation exposure
to a fungal spore requires that the spore be initially aerosolized at the site of
growth and transported to the inhaled parcel of air. Some fungi actively
(forcibly) discharge spores into the air (Burge, 2000). In other cases, the
initial aerosolization is likely to be caused by indoor air movements or
physical disturbances caused by people. After initial aerosolization, a spore
may be transported by air motion to the inhaled air parcel.
Most fungal spores have aerodynamic diameters of 210 µm (American
Thoracic Society, 1997) and deposit quickly on indoor surfaces because of
gravitational settling. For example, a 10-µm particle with unit density will
fall 1 meter in 5.5 minutes in still air, and a 5-µm particle will fall 1 meter
in 21 minutes (Hinds, 1982). Because the deposition rates of these large
particles caused by gravitational settling exceed typical ventilation and fil-
tration rates in houses,2 most spores deposit on indoor surfaces after aero-
solization. The deposition of spores is confirmed by their detection in dust
samples taken from a broad array of indoor surfaces, including surfaces
that are too dry to support fungal growth.
2Deposition on surfaces will cause 5-µm-aerodynamic-diameter particles to be removed
from indoor air at a rate equivalent to 1.55 air changes per hour of ventilation (Thatcher et
al., 2001). For a 10-µm particle, removal by deposition may be as high as the equivalent of 10
air changes per hour of ventilation. Thus, in most buildings, deposition on surfaces is the
largest removal process for particles of 510 µm.
OCR for page 93
EXPOSURE ASSESSMENT 93
Once deposited, spores can be resuspended by disturbances, such as
walking and cleaning. Thus, the inhalation-exposure process for fungal
spores (and other microbial particles of similar size) may be largely a conse-
quence of resuspension. Thatcher and Layton (1995) have shown that re-
suspension occurs predominantly for particles larger than 1 µm and that the
amount of resuspension increases with particle size. In experiments, such
activities as walking, sitting, and house-cleaning increased air concentra-
tions of 5- to 10-µm particles by a factor of 1.511. The surface properties
of spores may affect their adherence to surfaces and the probability of their
resuspension. There is evidence that human activities, including particle
resuspension, cause a "personal cloud" of particles, whereby people's expo-
sures to particles exceed those indicated by measurements at a fixed loca-
tion (Özkaynak et al., 1996). The same personal cloud would be expected
for fungal spores. The spores that deposit on surfaces can also be trans-
ported to other locations by tracking, for example, sticking to shoes and
then detaching at another location.
Many of the above comments also apply to the process of inhalation
exposure to fungal spores that are transported to the indoors from
outdoors. Those spores can be brought into a building with outdoor air
by natural ventilation through open windows and by air infiltration
through unintentional cracks and holes in the building envelope and can
be tracked in by people and pets. Once they are inside, the processes of
spore settling, resuspension, and tracking would be expected to influence
inhalation exposures as they do exposure to fungal spores from indoor
sources.
Because spores and other components of molds are present on indoor
surfaces and people have contact with these surfaces, exposures to fungal
agents may occur through dermal contact and transport of lipid-soluble
chemicals through the skin. In addition, incidental ingestion of fungal con-
stituents on surfaces and in household dust may occur as a consequence of
hand-to-mouth activity. Exposures via dermal contact or ingestion are
known to be important for some chemicals and for lead. Infants are gener-
ally affected more than adults because of their contact with floors and their
high level of hand-to-mouth activity. However, the significance of those
routes of exposure to indoor fungi and other dampness-related microbial
pollutants is not known.
In summary, the entire process of fungal-spore aerosolization, trans-
port, deposition, resuspension, and tracking, all of which determine inhala-
tion exposure, is poorly understood. A better understanding of the process
would enable a better assessment of exposures and might elucidate better
means of reducing them. The significance of exposures to fungi in normal
indoor environments through dermal contact and ingestion is also not well
understood.
OCR for page 94
94 DAMP INDOOR SPACES AND HEALTH
Dose3
Dose is the amount of an agent that is absorbed or deposited in the
body of an exposed organism at a given time (NRC, 1991). Internal dose
is the amount of an agent that is absorbed into the body, whereas biologi-
cally effective dose is the amount of an agent or its metabolites that inter-
acts with a target site.
The primary determinants of where an inhaled gas, such as an MVOC,
makes contact with the respiratory system are its solubility and reactivity.
Reactive gases tend to reach the upper respiratory system. The primary
determinant of deposition of airborne particles is the aerodynamic particle
diameter (dae). Aerodynamic particle diameter, as distinct from physical
diameter, determines the motion of particles in air. The dae of a particle is
defined as the diameter of the unit density sphere that has the same terminal
settling velocity as the particle of interest (ICRP, 1994). Particles with dae
larger than 15 µm are captured preferentially (but not exclusively) in the
upper respiratory tract (nose and throat). Particles with dae of 2.515 µm
enter the lungs but tend to deposit in the upper conducting airways, where
their mass and high velocities favor inertial impaction. Because they lack
inertia, smaller particles move with the inhaled air stream into the alveolar
region, where they may or may not deposit. The fraction of particles that
deposit in the deep lung increases with decreasing dae below 0.5 µm because
of the high diffusion constants of very small particles.
The role of particle density in determining dae is critical. A spherical
particle with a physical diameter of 16 µm but a density of 0.1 will behave
aerodynamically like a 5-µm water droplet. That property helps to explain
the ability of large-diameter, low-density pollen grains to penetrate and
deposit in the lung. Once deposited in the lungs, airborne agents may react
with biomolecules, be absorbed into the blood, or be cleared from the
lungs. From the viewpoint of indoor-related symptoms and diseases, the
relevant sites and nature of interactions between inhaled agents and the
human body remain uncertain, and this uncertainty limits our ability to
define biologically effective dose in this context. It is important to note that
all measures of dose, like those of exposure, can be viewed as surrogates of
the theoretical risk-relevant dose measure.
SAMPLING STRATEGIES
Several strategies are available for exposure assessment conducted for
risk-assessment purposes.4 In epidemiology, questionnaires are the most
3This section is derived from Clearing the Air (IOM, 2000), pages 5556.
4Sampling strategies or diagnostic tools to assess whether a building has dampness or mold
problems or to assess potential sources of exposure are discussed separately in Chapters 2 and 6.
OCR for page 95
EXPOSURE ASSESSMENT 95
commonly-used instrument for gathering exposure information (for ex-
ample, by asking about the presence of dampness or visible mold in the
home). For individual patients with suspected indoor-related health prob-
lems, a home visit by an occupational hygienist with experience in this field
may be the method of choice. Alternatively, personal or environmental
monitoring can be used to measure agents of interest in the home. The latter
approach has the potential to result in a more valid and accurate exposure
assessment; however, this depends heavily on the chosen sampling strategy,
which in turn depends on many factors, including
· Specific disease or symptoms.
· Acute vs chronic health outcomes (for example, disease exacerbation
vs disease development).
· Population vs patient-based approach.
· Suspected exposure variation in time and space and between con-
trols and cases.
· Available methods to measure individual agents.
· Costs of sampling and analyses.
For indoor-associated health problems, many exposures have to be
considered because it is often not clear which specific microorganisms or
agents cause symptoms or diseases. In fact, studies are often conducted with
the specific aim of assessing which exposures may contribute to the devel-
opment of symptoms. However, in practice, the funding and availability of
methods of measuring specific agents (many methods are not commercially
available and are applied only in research settings) severely limit the poten-
tial to measure all agents of interest.
Settled Dust vs Airborne Measurements
Indoor exposure assessment may use air or surface sampling or both.
Swab samples can be taken, but they have limited value in quantitative
exposure assessment and are usually used only as a diagnostic tool to
characterize whether buildings have dampness- or mold-related problems
(see Chapter 6).
In most studies, dust samples from dust reservoirs, such as living-room
and bedroom floors and mattresses, are collected for analysis of microbial
content (with or without prior sieving or extraction). A theoretical advan-
tage of settled-dust sampling is the presumed time integration that occurs in
the deposition of bioaerosols on surfaces. Surface sampling may thus be the
method of choice for assessing the association between exposure and the
development of chronic conditions, such as asthma. The method is fast,
easy, and inexpensive, using only a vacuum cleaner and filters or nylon
OCR for page 96
96 DAMP INDOOR SPACES AND HEALTH
sampling bags to collect dust, so it is particularly useful in large epidemio-
logic studies (focusing on chronic diseases), in which airborne measure-
ments often are not feasible. One example in which this method is widely
applied is the routine measurement of settled dust allergens. Allergen con-
centrations are usually expressed in units of allergen per gram of dust.
One limitation of the common practice of reporting concentrations of
allergen or specific microbial agents per gram of dust collected should be
noted: by dividing by total amount of dust collected, this expression of
exposure does a poor job of characterizing the total burden of a specific
agent in a building. For example, homes A and B could have the same
amount of an agent (fungal allergen, endotoxin, viable microorganisms, or
the like) per gram of dust by the conventional measure, whereas home A
might have 10 times more dust than home B, so the average exposure of
occupants of home A could be 10 times that of occupants of home B. For
exposure-assessment purposes, it may therefore be more accurate to ex-
press exposure as floor-dust concentration per square meter sampled than
as concentration per gram of sampled dust.
It is critical that surface sampling procedures be standardized so that
sample results can be compared between sampling sessions. This requires
standardization with regard to the selection of the sampling location, the
technique of vacuuming, vacuum suction and the duration of sampling.
Provided that sampling procedures are standardized, sampling of settled
dust is reproducible as has been demonstrated for samples taken repeatedly
over time (Heinrich et al., 2003).
Although surface sampling has advantages in many situations (particu-
larly when a proxy of long-term average exposure is required), airborne
measurements may be more desirable in others. Airborne measurements
allow fluctuations in exposure to be assessed over the course of a week, a
day or even hours; this can be essential in studying acute adverse effects
such as daily lung-function changes with such metrics as FEV1 (forced
expiratory volume in 1 sec) or PEF (peak expiratory flow). Airborne sam-
pling is also likely to capture the more appropriate dust fraction; that is,
inhalable particles. Chew et al. (2003) propose that reservoir dust and air
sampling represent different types of potential exposure to residents, sug-
gesting that collection of both air and dust samples may be essential. How-
ever, airborne concentrations of specific agents are generally low in the
residential indoor environment, and for many laboratory-based methods
analytic sensitivity is not sufficient, so short-term airborne sampling is
impossible for most agents. "Aggressive air sampling" has been suggested
to overcome the problem of low indoor-air concentrations under "routine"
conditions (IOM, 1993; Rylander, 1999; Rylander et al., 1992). Aggressive
sampling involves activities intended to encourage the generation of bio-
logic aerosols during sampling by agitating floor dust with devices that
OCR for page 97
EXPOSURE ASSESSMENT 97
mimic people walking on carpets (Buttner et al., 2002) or by rapping on
ventilation ducts (Dillon et al., 1999). Its usefulness in exposure assessment,
however, is not clear. Viable microorganisms in the air can be identified
with great sensitivity, provided that one is able to capture them alive and
select a medium that can support their growth so that they can be measured
under normal circumstances with methods for airborne sampling. How-
ever, sampling of viable microorganisms in the air with culture techniques
will provide at best a "snapshot" of current exposure, given the high vari-
ability of microbial concentrations, the episodic nature of emissions from
some microbial agents, and the relatively short sampling time allowed for
this method. Thus, assessing the "true exposure" (ERR) requires many sam-
ples and is not possible in most population studies.
In summary, airborne measurements may be a good indicator of expo-
sure from a theoretical point of view, particularly for assessing acute short-
term exposures, but detection problems limit their use for most biological
agents in practice. Surface sampling is often the only alternative. When
long-term exposures are being assessed, surface sampling may have an
additional advantage over airborne measurements in that airborne mea-
surements require a much larger number of samples to be taken because of
the expected large variation in airborne concentrations. Nonetheless, it
should be stressed that surface sampling is crude and is expected to yield a
poor surrogate of airborne concentrations and the theoretical risk-relevant
dose measure. Results of surface sampling as a measure of exposure should
be interpreted with caution (Chew et al., 1996).
Personal vs Area Sampling
Assuming that airborne sampling is the desirable choice in a particular
situation, personal measurements best represent the current airborne ERR.
Therefore, personal sampling is preferred to area sampling. Modern sam-
pling equipment is now sufficiently light and small to use for personal
sampling, and several studies of chemical air pollution have demonstrated
its feasibility in both the indoor and outdoor environments (Janssen et al.,
1999, 2000). However, practical constraints may make personal sampling
impossible: it might be too cumbersome for the study subjects, or there
might be no portable equipment to make the desired measurements (such as
measurements of viable microorganisms).
If personal sampling is not possible, area sampling can be applied to
reconstruct personal exposure with the "microenvironmental model" ap-
proach.5 The microenvironmental model of human exposure is widely ac-
5Addressed in greater detail in Clearing the Air (IOM, 2000), page 54, from which this
discussion is derived.
OCR for page 98
98 DAMP INDOOR SPACES AND HEALTH
cepted for environmental exposure assessment (Sexton and Ryan, 1988). In
that model, exposure of a person to an airborne agent is defined as the time-
weighted average of agent concentrations encountered as the person passes
through a series of microenvironments. However, exposures to microbial
agents--such as particulate allergens, endotoxins, and fungal spores--often
occur episodically because of inadvertent disturbance and resuspension of
reservoirs of biologic agents by human activities (vacuum cleaning, han-
dling of bedding, and the like) or because of mold blooms. Those episodic
exposure patterns are not likely to be accurately captured by environmental
area samplers. In addition, it is practically impossible to measure all the
relevant microenvironments. Given those uncertainties, personal sampling
is, despite some practical problems, a preferred method.
When, Where, and How Often to Sample
To the extent to which it is possible, samples should be taken to
represent ERR at the appropriate time. In the case of acute effects, expo-
sure measurements taken shortly (up to 8 or 12 hours) before the effects
take place would clearly be the most useful. However, it is not always
possible to collect such information. Personal sampling is preferable, but
if it cannot be performed, ambient sampling can be conducted where the
person in question spends the most time. If air sampling is impossible for
the reasons mentioned above, settled-dust samples can be taken in the same
areas.
The case of chronic effects is more complicated because ideally expo-
sure should be assessed before the occurrence of the effects and preferably
at the time that is biologically most relevant, that is, when the exposure is
thought to be the most problematic (such as when fungi are releasing
spores) or when subjects are most susceptible to exposure. That is possible
only in longitudinal cohort studies, and even then it often is not clear when
people are most susceptible to the exposure of interest, although it is gener-
ally assumed that early childhood is the most relevant period for allergens.
Cohort studies, however, are time-consuming and expensive. Most often,
case-control studies are conducted; in these studies, exposure can be as-
sessed only retrospectively. Settled-dust sampling (which is reviewed in
Macher, 2001a,b) may be the best option because microbial agents in house
dust appear to be relatively stable over long periods, and current concentra-
tions may be a reasonable proxy for past exposures, assuming that the
subjects have not moved homes or substantially changed the home condi-
tions. It is not clear which sampling site best represents exposure; therefore,
often a combination of bedroom and living-room floor dust samples and
mattress dust samples is taken, sometimes including samples from the
kitchen floor.
OCR for page 99
EXPOSURE ASSESSMENT 99
For risk-assessment purposes, measures of exposure need to be both
accurate and precise so that the effect of exposure on disease can be estimated
with minimal bias and maximal efficiency. Therefore, exposure must be
assessed with a minimal measurement error. Precision can be gained (that is,
measurement error can be reduced) by increasing the number of samples
taken in each home. In population studies, repeated sampling within the
home as a proxy for within-subject variation in exposure is particularly
effective for exposures that are known to vary widely in the home relative to
the variation observed between homes. If the within-home variation is smaller
than the between-home variability, however, repeated sampling will not sig-
nificantly reduce the measurement error, and one or a few samples will be
sufficient. If within- and between-home variations are known (from previous
surveys or pilot studies, for example), the number of samples required to
obtain a given reduction in risk-estimate bias can be computed in the man-
ner described by Cochran (1968). A within-home to between-home variance
ratio of 3:1 to 4:1--which is not uncommon in airborne sampling of viable
microorganisms--implies that 2736 samples per home are required to esti-
mate the average exposure reliably for an epidemiologic study with no more
than a 10% bias in the relationship between some health end point and the
exposure (Heederik and Attfield, 2000; Heederik et al., 2003).
Studies that include repeated measurements are scarce, so within-home
and between-home variation cannot be accurately assessed. However, data
are available on some agents. For example, it is well known that the con-
centration of total airborne viable fungi varies widely within a building
even over very short periods (Hunter et al., 1988; Verhoeff et al., 1994).
Viable mold counts in house-dust samples taken from the same location
within a 6-week interval also showed very poor reproducibility (Verhoeff et
al., 1994). In the same study, the variation in isolated genera and species
between duplicate samples was even more substantial, with a very high
within-home to between-home variance ratio of 3:1 to 4:1. More recently,
that was confirmed in another study focusing on dustborne concentrations
(Chew et al., 2001). It was demonstrated further that measurements of
markers of fungal exposure in house dust, such as fungal EPSs were more
reproducible, with an estimated within-home to between-home variance
ratio of only 0.5:1. The estimated within-home variation of (13)-glucans
and total culturable fungi was similar to the betweenhome variations, with
ratios close to 1:1. Endotoxin concentrations in house dust in 20 homes in
the United States measured repeatedly during a period of 12 months were
significantly correlated (r = 0.76 for bed dust and 0.40 for bedroom-floor
dust); this suggests average to good reproducibility for this measure (Park et
al., 2000). In addition, a much larger study in Germany involving repeated
dust sampling in 745 homes with a median interval of 7 months between
first and second sampling periods showed that allergen (mite and cat) and
OCR for page 100
100 DAMP INDOOR SPACES AND HEALTH
endotoxin concentrations were well correlated over time, with crude corre-
lation coefficients of 0.650.75 for the allergens and 0.59 for endotoxins
(Heinrich et al., 2003). Viable-spore counts were, however, very poorly
correlated--a correlation coefficient of only 0.06. On the basis of that
limited experience, within-home variability of indoor-air concentrations of
biologic agents are expected to be generally high and within-home variabil-
ity of concentrations of these components in settled house dust generally
low (compared with between-home variation). An exception is viable mi-
croorganisms, the concentration of which is highly variable in both indoor
air and settled dust.
Little is known about spatial variation--that is, variation in concentra-
tions between sampling locations at the same site, such as, in the case of
surface sampling, on the same floor or bed. For example, studies have
shown that house dust mite and cat allergen distribution is highly variable
in settled dust (Hirsch et al., 1998; Loan et al., 2003). Expression as aller-
gen mass did not reduce this variability (Hirsch et al., 1998). Isolated
sampling of settled dust thus does not necessarily characterize the total
burden of a specific agent in a building. However, in the case of floor dust,
samples taken from the center of the room (as is commonly done in studies)
have been shown to yield concentrations very similar to the mean concen-
tration level for the whole floor, indicating that a single sample taken in this
manner may be representative (Loan et al., 2003). Similar studies for other
microbial agents have not yet been conducted.
Thus, because only sparse data are available on variation in exposure
to biologic agents in the home environment, it is not possible to recommend
how many samples should be taken to produce an accurate assessment of
the ERR. However, there is a strong suggestion that airborne concentrations
are characterized by high variability over time, an indication that one sample
per home is unlikely to be sufficient even when acute health effects are
being considered, because variations in exposure occur over very short
periods. Measurements of specific microbial agents in house dust generally
appear to vary less and seem stable even over relatively long periods (up to
12 months and perhaps even longer), so one or a few samples may be
sufficient. If only one floor sample is to be collected, research suggests that
it be taken from the center of the floor (in front of a couch or a chair); for
mattresses, the whole mattress should be sampled. Although measurements
of dust can be more precise, it is not clear how well they represent airborne
exposure. Measurements of viable microorganisms vary greatly over time
regardless of whether they are sampled in air or in floor or bed dust, and
many samples might be required.
In most circumstances, the only reason to go to the expense to measure
specific taxa or the presence of glucan, ergosterol and the like is for the
purposes of research into the health effects of exposure to those agents.
OCR for page 114
114 DAMP INDOOR SPACES AND HEALTH
in buildings with mold problems ranged from about 10 to more than
100 ng/m3 according to an LAL assay of (13)-glucans in airborne dust
samples that were generated by rigorous agitation of settled dust in those
buildings (Rylander, 1999). Exposures in buildings that had no obvious
mold problems were close to 1 ng/m3. In the Netherlands and Germany,
mean (13)-glucans concentrations in house dust determined with a spe-
cific enzyme immunoassay were highly comparable at around 1,0002,000
µg/g of dust and 5001,000 µg/m2 (Chew et al., 2001; Douwes et al., 1996,
1998, 2000; Gehring et al., 2001). Samples were also taken in homes that
were not selected specifically on the basis of mold problems and were
analyzed in the same laboratory with identical procedures. No airborne
samples were taken.
EVALUATION OF EXPOSURE DATA
No health-based recommended exposure limits for indoor biologic
agents exist, and this makes the interpretation of exposure difficult, par-
ticularly in case studies. Strategies to evaluate exposure data (either quanti-
tatively or qualitatively) should include comparison of exposure data with
background concentrations or, better, a comparison of exposures between
symptomatic and nonsymptomatic subjects. A quantitative evaluation in-
volves comparing exposures, whereas a qualitative evaluation could consist
of comparing species or genera of microorganisms in different environ-
ments. Because of differences in climatic and meteorological conditions and
differences in measurement protocols used in various studies (viable versus
non-viable microorganism sampling, sampler type, analysis, and so on),
reference material from the literature can seldom be used. Thus, to draw
valid conclusions, it is important in each study to include measurements in
indoor environments of subjects without symptoms. Furthermore, interpre-
tations of airborne sampling should be based on multiple samples because
spacetime variability in the environment is high. Finally, the proper inter-
pretation of exposure results requires detailed information about sampling
and analytic procedures (including quality control) and knowledge of the
potential problems associated with those procedures.
It is not possible to reach a general conclusion on whether total fungal
counts represent a meaningful measure of exposure for indoor-related health
effects. In cases where health outcomes have established links to a specific
agent or microorganism, it is appropriate to focus on measurement of that
agent or microorganism. If, on the other hand, agents such as (13)-
glucans are involved, then a total fungi count may be a relevant measure as
almost all fungi contain (13)-glucans. Given the present state of knowl-
edge, it may be appropriate to make both specific and total fungi measures
when this is possible.
OCR for page 115
EXPOSURE ASSESSMENT 115
Further, it is currently not clear whether fungal counting methods do
a better job of characterizing a person's or population's true exposure
than the traditionally-applied culture methods: this is largely dependent
on the aim of the study, the specific health outcome(s) of interest, and the
nature and source of the exposure. For some health outcomes--those
involving allergic sensitization, for example--the identity of the microbial
agent may be as important as the amount of agent present. These gaps in
the knowledge base create a potential for misinterpretation and misuse of
results that must be kept in mind whenever sampling is conducted. More
research is needed to further our understanding of which exposure assess-
ment methods are most relevant in assessing health risks from indoor
exposures. General recommendations with regard to exposure assessment
methods for the purpose of risk assessment can therefore not be given,
particularly since indoor-related symptoms or diseases may be caused by
multiple exposures.
FINDINGS, RESEARCH NEEDS, AND RECOMMENDATIONS
Based on the review of the papers, reports and other information pre-
sented in this chapter, the committee has reached the following findings and
recommendations, and has identified the following research needs regard-
ing exposure assessment for damp indoor environments.
· The evaluation of exposure characterization results should, when-
ever possible, be based on:
-- Comparison of exposure data with background concentrations
or, better, a comparison of exposures between symptomatic and nonsympto-
matic subjects.
-- Multiple samples, because spacetime variability in the environ-
ment is high.
-- Detailed information about sampling and analytic procedures (in-
cluding quality control) and knowledge of the potential problems associ-
ated with those procedures.
· The lack of knowledge regarding indoor microbial exposures and
related health problems is due primarily to a lack of valid quantitative meth-
ods for assessing exposure.
· There are several methods for measuring and characterizing fungal
populations, but methods for assessing human exposure to fungal agents
are poorly developed. Part of the difficulty is related to the large number of
fungal species that are measurable indoors and the fact that fungal allergen
content and toxic potential varies among species and among morphologic
forms within species. In addition, the most common methods for fungal
assessment--counting cultured colonies and identifying and counting
OCR for page 116
116 DAMP INDOOR SPACES AND HEALTH
spores--have variable and uncertain relationships to allergen, toxin, and
irritant content of exposures.
· Existing exposure assessment methods for fungal and other micro-
bial agents need rigorous validation and further refinement to make them
more suitable for large-scale epidemiologic studies. This includes standard
ization of protocols for sample collection, transport of samples, extraction
procedures, and analytical procedures and reagents. Such work should re-
sult in concise, internationally accepted protocols that will allow measure-
ment results to be compared both within and across studies.
· Research is needed to develop improved exposure assessment meth-
ods, particularly methods based on nonculture techniques and techniques
for measuring constituents of microorganisms--allergens, endotoxins,
(13)-glucans, fungal extracellular polysaccharides (EPSs), fungal spores,
other particles and emissions of microbial origin. These needs include:
-- Further improvement of light and portable personal airborne ex-
posure measurement technology.
-- More rapid development of measurement methods for specific
microorganisms that use DNA-based and other technology.
-- Rapid and direct-reading assays for bioaerosols for the immediate
evaluation of potential health risks.
· Application of the new or improved methods will allow more valid
exposure assessment of microorganisms and their components, which
should facilitate more-informed risk assessments.
REFERENCES
Åberg N, Sundell B, Eriksson B, Hesselmar B, Åberg B. 1996. Prevalence of allergic diseases
in school children in relation to family history, upper respiratory infections, and residen-
tial characteristics. Allergy 51(4):232237.
ACGIH (American Conference of Governmental Industrial Hygienists). 1999. Bioaerosols:
Assessment and Control. Macher JM, ed. Cincinnati, OH: American Conference of
Governmental Industrial Hygienists.
Adler CM. 2002. Mycotoxins: characteristics, sampling methods, and limitations. ENVIRO-
CHECK, Inc. Winter 20022003. http://www.envirocheckonline.com/docs/mycotoxins.pdf.
accessed June 16, 2003.
Aketagawa J, Tanaka S, Tamura H, Shibata Y, Sait H. 1993. Activation of limulus coagula-
tion factor G by several (13)--D-glucans: comparison of the potency of glucans with
identical degree of polymerization but different conformations. Journal of Biochemistry
113:683686.
Alvarez AJ, Buttner MP, Toranzos GA, Dvorsky EA, Toro A, Heikes TB, Mertikas-Pifer LE,
Stetzenbach LD. 1994. Use of solid-phase PCR for enhanced detection of airborne mi-
cro-organisms. Applied Environmental Microbiology 60:374376.
American Thoracic Society. 1997. American Thoracic Society Workshop, Achieving Healthy
Indoor Air. American Journal of Respiratory and Critical Care Medicine 156(Supple-
ment 3):534564.
OCR for page 117
EXPOSURE ASSESSMENT 117
Andriessen J, Brunekreef B, Roemer W. 1998. Home dampness and respiratory health status
in European children. Clinical and Experimental Allergy 28:11911200.
Bang FB. 1956. A bacterial disease of Limulus polyphemus. Bulletin of the John Hopkins
Hospital 98:325350.
Bechtel DH. 1989. Molecular dosimetry of hepatic aflatoxin B1-DNA adduct: linear correla-
tion with hepatic cancer risk. Regulatory Toxicology and Pharmacology 10(1):7481.
Bischof W, Koch A, Gehring U, Fahlbusch B, Wichmann HE, Heinrich J. 2002. Predictors of
high endotoxin concentrations in the settled dust of German homes. Indoor Air 12:29.
Braun-Fahrländer C, Riedler J, Herz U, Eder W, Waser M, Grize L, Maisch S, Carr D,
Gerlach F, Bufe A, Lauener RP, Schierl R, Renz H, Nowak D, von Mutius E, Allergy and
Endotoxin Study Team. 2002. Environmental exposure to endotoxin and its relation to
asthma in school-age children. New England Journal of Medicine 347(12):869877.
Brunekreef B. 1992. Damp housing and adult respiratory symptoms. Allergy 47(5):498502.
Brunekreef B, Groot B, Rijcken B, Hoek G, Steenbekkers A, de Boer A. 1992. Reproducibility
of childhood respiratory symptom questions. The European Respiratory Journal 5(8):
930935.
Burge HA. 2000. The fungi. In: Indoor Air Quality Handbook. JD Spengler, JM Samet, JF
McCarthy, eds. New York: McGraw-Hill.
Burge HA, Pierson DL, Groves TO, Strawn KF, Mishra SK. 2000. Dynamics of airborne
fungal populations in a large office building. Current Microbiology 40:1016.
Burrell R, Rylander R. 1981. A critical review of the role of precipitins in hypersensitivity
pneumonitis. European Journal of Respiratory Diseases 62(5):332343.
Buttner MP, Cruz-Perez P, Stetzenbach LD. 2001. Enhanced detection of surface-associated
bacteria in indoor environments by quantitative PCR. Applied Environmental Microbi-
ology 67(6):25642570.
Buttner MP, Cruz-Perez P, Stetzenbach LD, Garrett PJ, Lutke AE. 2002. Measurement of
airborne fungal spore dispersal from three types of flooring materials. Aerobiologia
18(1):111.
Chew GL, Muilenberg ML, Gold D, Burge HA. 1996. Is dust sampling a good surrogate for
exposure to airborne fungi? Journal of Allergy and Clinical Immunology 97:419.
Chew GL, Douwes J, Doekes G, Higgins KM, Strien R, Spithoven J, Brunekreef B. 2001.
Fungal extracellular polysaccharides, (13)-glucans, and culturable fungi in repeated
sampling of house dust. Indoor Air 11:171178.
Chew GL, Rogers C, Burge HA, Muilenberg ML, Gold DR. 2003. Dustborne and airborne
fungal propagules represent a different spectrum of fungi with differing relations to
home characteristics. Allergy 58(1):1320.
Chun DT, Chew V, Bartlett K, Gordon T, Jacobs RR, Larsson BM, Larsson L, Lewis DM,
Liesivuori J, Michel O, Milton DK, Rylander R, Thorne PS, White EM, Brown ME.
2000. Preliminary report on the results of the second phase of a round-robin endotoxin
assay study using cotton dust. Applied Occupational and Environmental Hygiene 15:
152157.
Cochran WG. 1968. Errors of measurement in statistics. Technometrics 10:637666.
Croft WA, Jastromski BM, Croft AL, Peters HA. 2002. Clinical confirmation of trichothecene
mycotoxicosis in patient urine. Journal of Environmental Biology 23(3):301320.
Cruz-Perez P, Buttner MP, Stetzenbach LD. 2001a. Specific detection of Aspergillus fumi-
gatus in pure culture using quantitative polymerase chain reaction. Molecular and Cellu-
lar Probes 15:8188.
Cruz-Perez P, Buttner MP, Stetzenbach LD. 2001b. Specific detection of Stachybotrys charta-
rum in pure culture using quantitative polymerase chain reaction. Molecular and Cellu-
lar Probes 15:129138.
OCR for page 118
118 DAMP INDOOR SPACES AND HEALTH
Cuijpers CE, Swaen GM, Wesseling G, Sturmans F, Wouters EF. 1995. Adverse effects of the
indoor environment on respiratory health in primary school children. Environmental
Research 68(1):1123.
Curtis L, Ross M, Persky V, Scheff P, Wadden R, Ramakrishnan V, Hryhorczuk D. 2000.
Bioaerosol concentrations in the quad cities 1 year after the Mississippi river floods.
Indoor and Built Environment 9(1):3543.
Dales RE, Miller D. 1999. Residential fungal contamination and health: microbial cohabi-
tants as covariates. Environmental Health Perspectives 107(Supplement 3):481483.
Dales RE, Burnett R, Zwanenburg H. 1991. Adverse health effects among adults exposed
to home dampness and molds. American Review of Respiratory Disease 143(3):505
509.
Dales RE, Miller D, McMullen E. 1997. Indoor air quality and health: validity and determi-
nants of reported home dampness and moulds. International Journal of Epidemiology
26:120125.
Dillon HK, Heinsohn PA, Miller JD, eds. 1996. Field Guide for the Determination of Biologi-
cal Contaminants in Environmental Samples. Fairfax, VA: American Industrial Hygiene
Association.
Dillon HK, Miller JD, Sorenson WG, Douwes J, Jacobs RR. 1999. A review of methods
applicable to the assessment of mold exposure to children. Environmental Health Per-
spectives 107(Supplement 3):473480.
Douwes J, Versloot P, Hollander A, Heederik D, Doekes G. 1995. Influence of various dust
sampling and extraction methods on the measurement of airborne endotoxin. Applied
Environmental Microbiology 61:17631769.
Douwes J, Doekes G, Montijn R, Heederik D, Brunekreef B. 1996. Measurement of (13)-
glucans in the occupational and home environment with an inhibition enzyme immu-
noassay. Applied Environmental Microbiology 62:31763182.
Douwes J, Doekes G, Heinrich J, Koch A, Bischof W, Brunekreef B. 1998. Endotoxin and
(13)-glucan in house dust and the relation with home characteristics: a pilot study in
25 German houses. Indoor Air 8:255263.
Douwes J, van der Sluis B, Doekes G, van Leusden F, Wijnands L, van Strien R, Verhoeff A,
Brunekreef B. 1999. Fungal extracellular polysaccharides in house dust as a marker for
exposure to fungi: relations with culturable fungi, reported home dampness and respira-
tory symptoms. Journal of Allergy and Clinical Immunology 103:494500.
Douwes J, Zuidhof A, Doekes G, van der Zee S, Wouters I, Boezen HM, Brunekreef B. 2000.
(13)--D-glucan and endotoxin in house dust and peak flow variability in children.
American Journal of Respiratory and Critical Care Medicine 162:13481354.
Douwes J, Pearce N, Heederik D. 2002. Does bacterial endotoxin prevent asthma? Thorax
57:8690.
Duchaine C, Thorne PS, Mériaux A, Grimard Y, Whitten P, Cormier Y. 2001. Comparison of
endotoxin exposure assessment by bioaerosol impinger and filter sampling methods.
Applied Environmental Microbiology 67(6):27752780.
Eduard W, Heederik D. 1998. Methods for quantitative assessment of airborne levels of non-
infectious micro-organisms in highly contaminated work environments. American In-
dustrial Hygiene Association Journal 59:113127.
Eduard W, Sandven P, Johansen BV, Bruun R. 1988. Identification and quantification of
mould spores by scanning electron microscopy (SEM): analysis of filter samples col-
lected in Norwegian saw mills. Annals of Occupational Hygiene 31(Supplement 1):447
455.
OCR for page 119
EXPOSURE ASSESSMENT 119
Eduard W, Sandven P, Levy F. 1992. Relationships between exposure to spores from Rhizo-
pus microsporus and Paecilomycetes variotti and serum IgG antibodies in wood trim-
mers. International Archives of Allergy and Immunology 97:274282.
Englehart S, Loock A, Skutlarek D, Sagunski H, Lommel A, Färber H, Exner M. 2002.
Occurrence of toxigenic Aspergillus versicolor isolates and sterigmatocystin in carpet
dust from damp indoor environments. Applied and Environmental Microbiology 68(8):
38863890.
Engvall K, Norrby C, Norbäck D. 2001. Asthma symptoms in relation to building dampness
and odour in older multifamily houses in Stockholm. International Journal of Tubercu-
losis and Lung Disease 5(5):468477.
Evans J, Hyndman S, Stewart-Brown S, Smith D, Petersen S. 2000. An epidemiological study
of the relative importance of damp housing in relation to adult health. Journal of Epide-
miology and Community Health 54:677686.
Gehring U, Douwes J, Doekes G, Koch A, Bischof W, Wichmann HE, Heinrich J. 2001.
(13)-glucan in house dust of German homes related to culturable mold spore counts,
housing and occupant characteristics. Environmental Health Perspectives 109:139144.
Gehring U, Bischof W, Fahlbusch B, Wichmann HE, Heinrich J. 2002. House dust endo-
toxin and allergic sensitization in children. American Journal of Respiratory and Criti-
cal Care Medicine 166(7):939944. [Erratum: American Journal of Respiratory and
Critical Care Medicine (2003) 167(1):91.]
Gereda JE, Leung DYM, Thatayatikom A, Streib JE, Price MR, Klinnert MD, Liu AH. 2000.
Relation between house-dust endotoxin exposure, type 1 T-cell development, and aller-
gen sensitization in infants at high risk of asthma. Lancet 355(9216):16801683.
Górny RL, Reponen T, Willeke K, Schmechel D, Robine E, Boissier M, Grinshpun SA. 2002.
Fungal fragments as indoor air biocontaminants. Applied and Environmental Microbiol-
ogy 68(7):35223531.
Grinshpun SA, Willeke K, Ulevicius V, Juozaitiis A, Terzieva S, Donnelly J, Stelma GA,
Brenner K. 1997. Effect of impaction, bounce and reaerosolization on collection effi-
ciency of impingers. Aerosol Science and Technology 26(4):326342.
Haugland RA, Heckman JL, Wymer LJ. 1999. Evaluation of different methods for the extrac-
tion of DNA from fungal conidia by quantitative competitive PCR analysis. Journal of
Microbiological Methods 37(2):165176.
Heederik D, Attfield M. 2000. Characterization of dust exposure for the study of chronic
occupational lung disease--a comparison of different exposure assessment strategies.
American Journal of Epidemiology 151(10):982990.
Heederik D, Douwes J, Thorne PS. 2003. Biological Agents--evaluation. In: Modern Indus-
trial Hygiene. J Perkins, ed. Cincinnati, OH: ACGIH.
Heinrich J, Hölscher B, Douwes J, Richter K, Koch A, Bischof W, Fahlbusch B, Kinne R,
Wichmann HE. 2003. Reproducibility of allergen, endotoxin and fungi measurements in
the indoor environment. Journal of Exposure Analysis and Environmental Epidemiology
13:152160.
Hinds WC. 1982. Aerosol Technology. New York: John Wiley and Sons.
Hirsch T, Kuhlisch E, Soldan W, Leupold W. 1998. Variability of house dust mite allergen
exposure in dwellings. Environmental Health Perspectives 106(10):659664.
Hirvonen MR, Ruotsalainen M, Roponen M, Hyvärinen A, Husman T, Kosma V-M,
Komulainen H, Savolainen K, Nevalainen A. 1999. Nitric oxide and proinflammatory
cytokines in nasal lavage fluid associated with symptoms and exposure to moldy build-
ing microbes. American Journal of Respiratory and Critical Care Medicine 160:1943
1946.
OCR for page 120
120 DAMP INDOOR SPACES AND HEALTH
Hu F, Persky V, Flay B, Phil D, Richardson PH. 1997. An epidemiological study of asthma
prevalence and related factors amoung young adults. Journal of Asthma 34(1):6776.
Hunter CA, Grant C, Flannigan B, Bravery AF. 1988. Mould in buildings: the air spora of
domestic dwellings. International Biodeterioration & Biodegradation 24:81101.
Hyvärinen A, Reponen T, Husman T, Nevalainen A. 2001. Comparison of indoor air quality
in mold problem and reference buildings in subarctic climate. Central European Journal
of Public Health 9(3):133139.
ICRP (International Commission on Radiological Protection). 1994. ICRP 66: Human Respi-
ratory Tract Model for Radiological Protection. Annals of the ICRP 24(13).
Immonen J, Laitinen S, Taskinen T, Pekkanen J, Nevalainen A, Korppi M. 2002. Mould-
specific immunoglobulin G antibodies in students from moisture and mould-damaged
schools: a 3-year follow-up study. Pediatric Allergy and Immunology 13:125128.
IOM (Institute of Medicine). 1993. Indoor Allergens: Assessing and Controlling Adverse
Health Effects, Washington, DC: National Academy Press.
IOM. 2000. Clearing the Air: Asthma and Indoor Air Exposures. Washington, DC: National
Academy Press.
Jaakkola MS, Nordman H, Piipari R, Uitti J, Laitinen J, Karjalainen A, Hahtola P, Jaakkola
JJ. 2002. Indoor dampness and molds and development of adult-onset asthma: a pop-
ulation-based incident case-control study. Environmental Health Perspectives 110(5):
543547.
Jaffal AA, Banat IM, El Mogleth AA, Nsanze H, Bener A, Ameen AS. 1997. Residential
indoor airborne microbial populations in the United Arab Emirates. Environment Inter-
national 23(4):529533.
Janssen NAH, Hoek G, Harssema G, Brunekreef B. 1999. Personal exposure to fine particles
in children correlates closely with ambient fine particles. Archives of Environmental
Health 54:95101.
Janssen NAH, de Hartog JJ, Hoek G, Brunekreef B, Lanki T, Timonen KL, Pekkanen J. 2000.
Personal exposure to fine particulate matter in elderly subjects: relation between per-
sonal, indoor, and outdoor concentrations. Journal of the Air & Waste Management
Association 50:11331143.
Jedrychowski W, Flak E. 1998. Separate and combined effects of the outdoor and indoor
air quality on chronic respiratory symptoms adjusted for allergy among preadolescent
children. International Journal of Occupational Medicine and Environmental Health
11(1):1935.
Karlsson K, Malmberg P. 1989. Characterization of exposure to molds and actinomycetes in
agricultural dusts by scanning electron microscopy, fluorescence microscopy and the
culture method. Scandinavian Journal of Work, Environment, and Health 15:353359.
Khan AA, Cerniglia CE. 1994. Detection of Pseudomonas aeruginosa from clinical and envi-
ronmental samples by amplification of the exotoxin A gene using PCR. Applied Envi-
ronmental Microbiology 60:37393745.
Kilpeläinen M, Terho EO, Helenius H, Koskenvuo M. 2001. Home dampness, current aller-
gic diseases, and respiratory infections among young adults. Thorax 56(6):462467.
Koskinen OM, Husman TM, Meklin TM, Nevalainen AI. 1999. The relationship between
moisture or mould observations in houses and the state of health of their occupants.
European Respiratory Journal 14(6):13631367.
Lange JL, Thorne PS, Lynch NL. 1997. Application of flow cytometry and fluorescent in situ
hybridization for assessment of exposures to airborne bacteria. Applied Environmental
Microbiology 63:15571563.
Lee SC, Chang M, Chan KY. 1999. Indoor and outdoor air quality investigation at six
residential buildings in Hong Kong. Environment International 25(4):489496.
OCR for page 121
EXPOSURE ASSESSMENT 121
Li CS, Hsu CW, Tai ML. 1997. Indoor pollution and sick building syndrome symptoms
among workers in day-care centers. Archives of Environmental Health 52(3):200207.
Loan R, Siebers R, Fitzharris P, Crane J. 2003. House dust-mite allergen and cat allergen
variability within carpeted living room floors in domestic dwellings. Indoor Air 13(3):
232236.
Macher JM. 2001a. Review of methods to collect settled dust and isolate culturable microor-
ganisms. Indoor Air 11(2):99110.
Macher JM. 2001b. Evaluation of a procedure to isolate culturable microorganisms from
carpet dust. Indoor Air 11(2):134140.
Macher JM, Huang FY, Flores M. 1991. A two-year study of microbiological indoor air
quality in a new apartment. Archives of Environmental Health 46(1):2529.
Macneil L, Kauri T, Robertson W. 1995. Molecular techniques and their potential applica-
tion in monitoring the microbiological quality of indoor air. Canadian Journal of Micro-
biology 41(8):657665.
Michel O, Ginanni R, Duchateau J, Vertongen F, Le Bon B, Sergysels R. 1991. Domestic
endotoxin exposure and clinical severity of asthma. Clinical and Experimental Allergy
21:441448.
Michel O, Kips J, Duchateau J, Vertongen F, Robert L, Collet H, Pauwels R, Sergysels R.
1996. Severity of asthma is related to endotoxin in house dust. American Journal of
Respiratory and Critical Care Medicine 154:16411646.
Miller JD, Young JC. 1997. The use of ergosterol to measure exposure to fungal propagules
in indoor air. American Industrial Hygiene Association Journal 58:3943.
Milton DK, Alwis KU, Fisette L, Muilenberg M. 2001. Enzyme linked immunosorbent assay
specific for (16) branched, (13)--D-glucan detection in environmental samples. Ap-
plied and Environmental Microbiology 67(12):54205424.
Miraglia M, Brera C, Colatosti M. 1996. Application of biomarkers to assessment of
risk to human health from exposure to mycotoxins. Microchemical Journal 54(4):472
477.
Mohamed N, Ng'ang'a L, Odhiambo J, Nyamwaya J, Menzies R. 1995. Home environment
and asthma in Kenyan schoolchildren: a case-control study. Thorax 50(1):7478.
Nafstad P, Ųie L, Mehl R, Gaarder P, Lodrup-Carlsen K, Botten G, Magnus P, Jaakkola J.
1998. Residential dampness problems and symptoms and signs of bronchial obstruction
in young Norwegian children. American Journal of Respiratory and Critical Care Medi-
cine 157:410414.
Nevalainen A. 1989. Bacterial aerosols in indoor air. (doctoral dissertation). Publications of
the National Public Health Institute A3/1989, Kuopio, Finland.
Nevalainen A, Pasanen A-L, Niininen M, Reponen T, Kalliokoski P. 1991. The indoor air
quality in Finnish homes with mold problems. Environment International 17:299302.
NRC (National Research Council). 1991. Human Exposure Assessment for Airborne Pollut-
ants. Washington, DC: National Academy Press.
Özkaynak H, Xue J, Spengler J, Wallace L, Pellizzari E, Jenkins P. 1996. Personal exposure to
airborne particles and metals: results from the Particle TEAM Study in Riverside, Cali-
fornia. Journal of Exposure Analysis and Environmental Epidemiology 6(1):5778.
Parat S, Perdrix A, Fricker-Hidalgo H, Saude I. 1997. Multivariate analysis comparing micro-
bial air content of an air-conditioned building and a naturally ventilated building over
one year. Atmospheric Environment 31:441449.
Park JH, Spiegelman DL, Burge HA, Gold DR, Chew GL, Milton DK. 2000. Longitudinal
study of dust and airborne endotoxin in the home. Environmental Health Perspectives
108:10231028.
OCR for page 122
122 DAMP INDOOR SPACES AND HEALTH
Park JH, Gold DR, Spiegelman DL, Burge HA, Milton DK. 2001. House dust endotoxin and
wheeze in the first year of life. American Journal of Respiratory and Critical Care
Medicine 163(2):322328.
Pastuszka JS, Paw UKT, Lis DO, Wlazl /o A, Ulfig K. 2000. Bacterial and fungal aerosol in
indoor environment in Upper Silesia, Poland. Atmospheric Environment 34(22):3833
3842.
Pena J, Ricke SC, Shermer CL, Gibbs T, Pillai SD. 1999. A gene amplification-hybridization
sensor based methodology to rapidly screen aerosol samples for specific bacterial gene
sequences. Journal of Environmental Science and Health Part A--Toxic/Hazardous Sub-
stances & Environmental Engineering 34(3):529556.
Pirhonen I, Nevalainen A, Husman T, Pekkanen J. 1996. Home dampness, moulds and their
influence on respiratory infections and symptoms in adults in Finland. European Respi-
ratory Journal 9(12):26182622.
Platt SD, Martin CJ, Hunt SM, Lewis CW. 1989. Damp housing, mould growth, and symp-
tomatic health state. British Medical Journal 298(6689):16731678.
Platts-Mills TAE, Chapman MD. 1987. Dust mites: immunology, allergic disease, and envi-
ronmental control. Journal of Allergy and Clinical Immunology 80:755775.
Platts-Mills TAE, de Weck AL. 1989. Dust mite allergens and asthma--a worldwide problem.
Journal of Allergy and Clinical Immunology 83:416427.
Price JA, Pollock I, Little SA, Longbottom JL, Warner JO. 1990. Measurement of airborne
mite antigen in homes of asthmatic children. Lancet 336:895897.
Reynolds S, Thorne P, Donham K, Croteau EA, Kelly KM, Lewis D, Whitmer M, Heederik
D, Douwes J, Connaughton I, Koch S, Malmberg P, Larsson BM, Milton DK. 2002.
Interlaboratory comparison of endotoxin assays using agricultural dusts. American In-
dustrial Hygiene Association Journal 63:430438.
Rizzo MC, Naspitz CK, Fernandez-Caldas E, Lockey RF, Mimica I, Sole D. 1997. Endotoxin
exposure and symptoms in asthmatic children. Pediatric Allergy and Immunology 8(3):
121126.
Roponen M, Kiviranta H, Seuri M, Tukiainen H, Myllykangas-Luosujärvi R, Hirvonen MR.
2001. Inflammatory mediators in nasal lavage, induced sputum and serum of employees
with rheumatic and respiratory disorders. European Respiratory Journal 18:542548.
Roponen M, Toivola M, Alm S, Nevalainen A, Jussila J, Hirvonen MR. 2003. Inflammatory
and cytotoxic potential in the airborne particle material assessed by nasal lavage and cell
exposure methods. Inhalation Toxicology 15(1):2338.
Ross MA, Curtis L, Scheff PA, Hryhorczuk DO, Ramakrishnan V, Wadden RA, Persky VW.
2000. Association of asthma symptoms and severity with indoor bioaerosols. Allergy
55:705711.
Rylander R. 1999. Indoor air-related effects and airborne (13)--D-glucan. Environmental
Health Perspectives 107(Supplement 3):501503.
Rylander R, Persson K, Goto H, Yuasa K, Tanaka S. 1992. Airborne ,1-3-glucan may be
related to symptoms in sick buildings. Indoor Environment 1:263267.
Sabbioni G, Wild CP. 1991. Identification of an aflatoxin G1-serum albumin adduct and its
relevance to the measurement of human exposure to aflatoxins. Carcinogenesis 12(1):
97103.
Sexton K, Ryan PB. 1988. Assessment of Human Exposure to Air Pollution: Methods, Mea-
surements, and Models. In: Air Pollution, the Automobile, and Public Health. AY
Watson, RR Bates, D Kennedy, Eds. Sponsored by the Health Effects Institute, Cam-
bridge, MA. Washington, DC: National Academy Press.
OCR for page 123
EXPOSURE ASSESSMENT 123
Sonesson A, Larsson L, Fox A, Westerdahl G, Odham G. 1988. Determination of environ-
mental levels of peptidoglycan and lipopolysaccharide using gas chromatography-mass
spectrometry utilizing bacterial amino acids and hydroxy fatty acids as biomarkers.
Journal of Chromatography 431(1):115.
Sonesson A, Larsson L, Schütz A, Hagmar L, Hallberg T. 1990. Comparison of the Limulus
Amebocyte Lysate Test and gas chromatography-mass spectrometry for measuring lipo-
polysaccharides (endotoxins) in airborne dust from poultry-processing industries. Applied
Environmental Microbiology 56:12711278.
Strachan DP, Carey I. 1995. Home environment and severe asthma in adolescence: a popula-
tion based case-control study. British Medical Journal 311:10531060.
Strachan DP, Flannigan B, McCabe EM, McGarry F. 1990. Quantification of airborne moulds
in the homes of children with and without wheeze. Thorax 45(5):382387.
Szponar B, Larsson L. 2000. Determination of microbial colonisation in water-damaged build-
ings using chemical marker analysis by gas chromatography-mass spectrometry. Indoor
Air 10:1318.
Szponar B, Larsson L. 2001. Use of mass spectrometry for characterising microbial communi-
ties in bioaerosols. Annals of Agricultural and Environmental Medicine 8(2):111
117.
Tariq S, Matthews SM, Stevens M, Hakim EA. 1996. Sensitization to Alternaria and Cla-
dosporium by the age of 4 years. Clinical and Experimental Allergy 26:794798.
Taskinen TM, Laitinen S, Nevalainen A, Vepsäläinen A, Meklin T, Reiman M, Korppi M,
Husman T. 2002. Immunoglobulin G antibodies to moulds in school-children from
moisture problem schools. Allergy 57:916.
Thatcher TL, Layton DW. 1995. Deposition, resuspension, and penetration of particles within
a residence. Atmospheric Environment 29(13):14871497.
Thatcher, TL, McKone TE, Fisk WJ, Sohn MD, Delp WW, Riley WJ, Sextro RG. 2001.
Factors affecting the concentration of outdoor particles indoors (COPI): Identification of
data needs and existing data. LBNL-49321. Berkeley, CA: Lawrence Berkeley National
Laboratory Report.
Thorne PS, Lange JL, Bloebaum PD, Kullman GJ. 1994. Bioaerosol sampling in field studies:
can samples be express mailed? American Industrial Hygiene Association Journal 55:
10721079.
Thorne PS, Reynolds SJ, Milton DK, Bloebaum PD, Zhang X, Whitten P, Burmeister LF.
1997. Field evaluation of endotoxin air sampling assay methods. American Industrial
Hygiene Association Journal 58:792799.
Van Emon JM, Reed AW, Yike I, Vesper SJ. 2003. Measurement of StachylysinTM in serum to
quantify human exposures to the indoor mold Stachybotrys chartarum. Journal of Oc-
cupational and Environmental Medicine 45(6):582591.
Verhoeff AP, van Reenen-Hoekstra ES, Samson RA, van Strien RT, Brunekreef B, van Wijnen
JH. 1994. Fungal propagules in house dust. I. Comparison of analytic methods and their
value as estimators of potential exposure. Allergy 49:533539.
Verhoeff AP, van Strien RT, van Wijnen JH, Brunekreef B. 1995. Damp housing and child-
hood respiratory symptoms: the role of sensitization to dust mites and molds. American
Journal of Epidemiology 141:103110.
Waegemaekers M, van Wageningen N, Brunekreef B, Boleij JS. 1989. Respiratory symptoms
in damp homes. A pilot study. Allergy 44(3):192198.
Wever-Hess J, Kouwenberg JM, Duiverman EJ, Hermans J, Wever AM. 2000. Risk factors
for exacerbations and hospital admissions in asthma of early childhood. Pediatric
Pulmonology 29(4):250256.
OCR for page 124
124 DAMP INDOOR SPACES AND HEALTH
Willeke K, Lin X, Grinshpun SA. 1998. Improved aerosol collection by combined impaction
and centrifugal motion. Aerosol Science and Technology 29(5):439456.
Williamson IJ, Martin C, McGill G, Monie RDH, Fennery AG. 1997. Damp housing and
asthma: a case-control study. Thorax 52(3):229234.
Wood RA, Eggleston PA, Lind P, Ingemann L, Schwartz B, Graveson S, Terry D, Wheeler B,
Adkinson NF Jr. 1988. Antigenic analysis of household dust samples. The American
Review of Respiratory Disease 137(2):358363.
Yang CY, Tien YC, Hsieh HJ, Kao WY, Lin MC. 1998. Indoor environmental risk factors
and childhood asthma: a case-control study in a subtropical area. Pediatric Pulmonology
26(2):120124.
Zock JP, Jarvis D, Luczynska C, Sunyer J, Burney P. 2002. Housing characteristics, reported
mold exposure, and asthma in the European Community Respiratory Health Survey.
Journal of Allergy and Clinical Immunology 110(2):285292.