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5
Dampness, Moisture, and Flooding
INTRODUCTION
This chapter addresses indoor environmental quality (IEQ) problems
associated with moisture, condensation, and inundation and the possible
effects of climate change on these problems. There is an extensive litera-
ture on the effects of indoor dampness on health, including an Institute of
Medicine (IOM) report (IOM, 2004) that remains salient and is drawn on
heavily in this chapter. The committee did not attempt to re-examine all
the scientific evidence considered in the IOM report and other efforts—an
undertaking beyond the scope of this study—but instead highlights their
findings and other research relevant to the consideration of the health ef-
fects of alterations in IEQ induced by climate change.
The chapter’s focus is on fungi1 and bacteria—microbial agents that
grow in the presence of water—and products of damaged building materi-
als. They produce biologic and chemical emissions that can lead to irritant,
allergic, other immunologic, or toxic responses. Other chapters address
some issues relevant to occupants’ exposures to those emissions. Ventila-
tion, which is discussed in Chapter 8, has an effect on exposure: levels of
indoor contaminants are higher in spaces that have lower air-exchange
1 Fungi have eukaryotic cells as do animals and plants but are a separate kingdom. Most
consist of masses of filaments, live off dead or decaying organic matter, and reproduce by
spores. Visible fungal colonies found indoors are commonly called mold (mould), sometimes
mildew. This report, following the convention of earlier IOM reports and much of the litera-
ture on indoor environments, uses the terms fungus and mold interchangeably to refer to the
microorganisms.
133
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134 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
rates. Some microbial agents also cause infections (this topic is addressed
in Chapter 6).
CLIMATE CHANGE AND INDOOR DAMPNESS AND FLOODING
The effects of climate change on moisture indoors are driven by several
factors, including extreme weather events, local changes in temperature and
humidity, and the adaptations that occupants make and mitigation strate-
gies that they use in response to changed environmental conditions.
The US Global Change Research Program notes that increases in air
temperatures and increased frequency and intensity of heavy downpours
have already been observed in the United States and that likely future
changes “include more intense hurricanes with related increases in wind,
rain, and storm surges” (USGCRP, 2009). Extreme weather conditions may
lead to breakdowns in building envelopes followed by sudden infiltration of
water into indoor spaces. Dampness problems and water intrusion create
conditions favorable to the growth of fungi and bacteria and may cause
building materials to decay or corrode and lead to off-gassing of chemicals.
In areas where the climate is warm and humid for more months of the
year, air conditioning will be used more often. Well-designed and properly
operating heating, ventilation, and air conditioning (HVAC) systems can
ameliorate humid conditions; poorly designed or maintained systems may
introduce moisture and create condensation on indoor surfaces.2 Mold-
growth prevention and remediation may also introduce fungicides and
other agents into the indoor environment, which can lead to adverse expo-
sures of occupants.
Flooding as a result of extreme weather events can have profound
health and economic effects. In 2010, there were 103 flood-related fatali-
ties in the United States, a significantly higher number than the 10-year
average of 71 measured between 2001 and 2010 (National Oceanic and
Atmospheric Administration, 2011). In that same year, floods were part of
six of the seven most costly insurance loss events in the United States; events
that were responsible for $6.3 billion in losses (Swiss Re, 2011). Jonkman
and colleagues (2009) estimate that two-thirds of the 771 known fatalities
of Hurricane Katrina were the direct result of flooding and that additional
fatalities were associated with flood-related circumstances including lack of
access to potable water or medical services and exposure to extreme heat
as a result of power outages.
Altered climatic conditions will not introduce new dampness problems
into the indoor environment but may make existing problems more wide-
2 This topic is addressed in Chapter 7.
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DAMPNESS, MOISTURE, AND FLOODING
spread and more severe and thus increase the urgency with which preven-
tion and interventions must be pursued.
INDOOR DAMPNESS
Almost all buildings experience excessive moisture, leaks, or flooding at
some point. Research regarding the sources and causes of indoor dampness
was addressed in detail in a previous IOM report (2004), which described
how and where buildings become wet; reviewed the signs of dampness,
how dampness is measured, and what is known about its prevalence and
characteristics, such as severity, location, and duration; discussed the risk
factors for moisture problems; reviewed how dampness influences indoor
microbial growth and chemical emissions; cataloged the various agents
that may be present in damp environments; and addressed the influence of
building materials on microbial growth and emissions. That effort’s findings
are briefly summarized below.
Dampness—a term used to describe a variety of moisture problems,
including high relative humidity, condensation, water ponding, and other
signs of excess moisture or microbial growth—is prevalent in residential
housing. The prevalence and significance of dampness are less well under-
stood in nonresidential structures, such as office buildings and schools, than
in residential buildings.
There is no single cause of excessive indoor dampness, and the primary
risk factors for it differ among climates, geographic areas, and building
types. The prevalence of dampness problems appears to increase as build-
ings age and deteriorate, but some modern construction techniques and
materials and the presence of air-conditioning can increase the risk of
dampness problems. The prevalence and nature of these problems suggest
that what is known about their causes and prevention is not consistently
applied in building design, construction, maintenance, and use.
DAMPNESS AND HEALTH
Efforts to quantify the effects of indoor environmental factors on hu-
man health often rely on markers of dampness indoors to characterize
risk. This approach reflects recognition that indoor moisture is associated
with adverse health outcomes and that exposures to emissions from mold,
bacteria, and damaged materials increase when indoor environments are
chronically wet or damp.
There have been three large-scale reviews of the relationship between
indoor dampness and human health in the past decade. In 2004, IOM is-
sued Damp Indoor Spaces and Health. The World Health Organization
(WHO) released WHO Guidelines for Indoor Air Quality: Dampness and
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136 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
Mould in 2009, and researchers involved in the WHO effort updated and
expanded that review in 2011 (Mendell et al., 2011).
The IOM report reviewed literature published up to late 2003 on a
wide array of health effects. Among the major findings were that sufficient
evidence existed for associating the presence of mold or other agents in
damp buildings with nasal and throat symptoms, cough, wheeze, asthma
exacerbation, and hypersensitivity pneumonitis in susceptible persons. The
committee responsible for the IOM report concluded that limited or sugges-
tive evidence existed for associating exposure to damp indoor environments
with shortness of breath, asthma, and, in otherwise healthy children, lower
respiratory disease. Tables 5-1 and 5-2 summarize the report’s conclusions,
and Box 5-1 summarizes the categories used to classify the strength of the
evidence.
The WHO guidelines covered literature published up to July 2007
(WHO, 2009). Their authors took the same approach to evaluating and
categorizing evidence for dampness as was used in the IOM report but ex-
TABLE 5-1 Summary of Findings Regarding the Association Between
Health Outcomes and Exposure to Damp Indoor Environmentsa
Sufficient Evidence of a Causal Relationship
(no outcomes met this definition)
Sufficient Evidence of an Association
Upper respiratory (nasal and throat) tract Wheeze
symptoms Asthma symptoms in sensitized persons
Cough
Limited or Suggestive Evidence of an Association
Dyspnea (shortness of breath) Asthma development
Lower respiratory illness in otherwise
healthy children
Inadequate or Insufficient Evidence to Determine Whether an Association Exists
Airflow obstruction (in otherwise healthy Skin symptoms
persons) Gastrointestinal tract problems
Mucous membrane irritation syndrome Fatigue
Chronic obstructive pulmonary disease Neuropsychiatric symptoms
Inhalation fevers (nonoccupational Cancer
exposures) Reproductive effects
Lower respiratory illness in otherwise Rheumatologic and other immune diseases
healthy adults
Acute idiopathic pulmonary hemorrhage
in infants
a The categories of evidence are summarized in Box 5-1 and explicated in Damp Indoor
Spaces and Health (IOM, 2004).
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DAMPNESS, MOISTURE, AND FLOODING
TABLE 5-2 Summary of Findings Regarding the Association Between
Health Outcomes and the Presence of Mold or Other Agents in Damp
Indoor Environmentsa
Sufficient Evidence of a Causal Relationship
(no outcomes met this definition)
Sufficient Evidence of an Association
Upper respiratory (nasal and throat) tract Wheeze
symptoms Asthma symptoms in sensitized persons
Cough
Hypersensitivity pneumonitis in
susceptible persons
Limited or Suggestive Evidence of an Association
Lower respiratory illness in otherwise
healthy children
Inadequate or Insufficient Evidence to Determine Whether an Association Exists
Dyspnea (shortness of breath) Skin symptoms
Asthma development Gastrointestinal tract problems
Airflow obstruction (in otherwise healthy Fatigue
persons) Neuropsychiatric symptoms
Mucous membrane irritation syndrome Cancer
Chronic obstructive pulmonary disease Reproductive effects
Inhalation fevers (nonoccupational Rheumatologic and other immune diseases
exposures)
Lower respiratory illness in otherwise
healthy adults
Acute idiopathic pulmonary hemorrhage
in infants
a The categories of evidence are summarized in Box 5-1 and explicated in Damp Indoor
Spaces and Health (IOM, 2004).
amined a larger set of health outcomes. Their analysis supported the IOM
report findings that there was sufficient evidence to conclude that there
is an association between indoor dampness-related agents3 and asthma
exacerbation, upper respiratory tract symptoms, cough, and wheeze. In
addition, they determined that two outcomes not evaluated in the IOM
report—current asthma and respiratory infections—and two outcomes that
had been placed in the category of limited or suggestive evidence—asthma
development and dyspnea (shortness of breath)—merited inclusion in the
sufficient evidence category. Evidence regarding allergic rhinitis, bronchitis,
3Defined by the authors as “evidence of visible water damage, visible mold, mold odor, or
similar related factors.”
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138 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
BOX 5-1
Summary of the Categories of Evidence Used in
Damp Indoor Spaces and Health (IOM, 2004)
Sufficient Evidence of a Causal Relationship
Evidence is sufficient to conclude that a causal relationship exists between the
agent and the outcome. That is, the evidence fulfills the criteria for “sufficient evi-
dence of an association” and, in addition, satisfies the following criteria: strength
of association, biologic gradient, consistency of association, biologic plausibility
and coherence, and temporally correct association.
Sufficient Evidence of an Association
Evidence is sufficient to conclude that there is an association. That is, an as-
sociation between the agent and the outcome has been observed in studies in
which chance, bias, and confounding can be ruled out with reasonable confidence.
Limited or Suggestive Evidence of an Association
Evidence is suggestive of an association between the agent and the outcome
but is limited because chance, bias, and confounding cannot be ruled out with
confidence.
Inadequate or Insufficient Evidence to Determine Whether an Association
Exists
The available studies are of insufficient quality, consistency, or statistical power
to permit a conclusion regarding the presence of an association. Alternatively, no
studies exist that examine the relationship.
and eczema—which had not been separately evaluated in the IOM report—
was deemed limited or suggestive.
Mendell and colleagues carried the WHO review forward to late 2009.
On the basis of their examination of previously available and newly pub-
lished evidence, they raised bronchitis, allergic rhinitis, eczema, and ever-
diagnosed asthma (that is, without regard to whether there was a current
diagnosis of asthma) to the sufficient-evidence category. Epidemiologic re-
search also yielded limited or suggestive evidence of an association between
dampness-related agents and the “common cold” and “allergy/atopy.”
The sections that follow provide some background on asthma, other re-
spiratory ailments, and other conditions mediated by an immune response.
They also highlight some of the recent literature on those health outcomes.
Asthma is a prominent public-health concern because of rising rates and
substantial effect on health, productivity, and health-care costs, but other
immunologic conditions related to dampness are also problematic and may
increase if sustained high levels of indoor moisture become more common
(Mudarri and Fisk, 2007).
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DAMPNESS, MOISTURE, AND FLOODING
Asthma and Other Respiratory Ailments
In the United States, asthma from all causes increased in frequency
and severity in the two decades from 1980 to 2000. From 1980 to 1996,
the prevalence of asthma increased by 74%, and the incidence from 1.2
per 1,000 per year to 4.7 per 1,000 per year (Mannino et al., 2002). An
assessment of annual asthma incidence in the total US population, using
the National Health Interview Survey (NHIS) data for 1980–1996, esti-
mated that 7.2–12.4% of those with prevalent asthma noted an onset in
the preceding year (Rudd and Moorman, 2007). Data from the NHIS, the
National Ambulatory Medical Care Survey, the National Hospital Ambula-
tory Medical Care Survey, the National Hospital Discharge Survey, and the
National Vital Statistics System indicated that an estimated 8.2% of adults
in the United States reported current asthma and that 4.2% of adults had
at least one asthma attack in the previous year (Akinbami, 2011).
Efforts to estimate the burden of asthma that can be attributed to damp
indoor spaces are limited by a lack of data on the prevalence of dampness
indoors and by the absence of consistent occupational or environmental
information on cases of asthma. Reviews estimate that one-fifth of current
asthma in the United States is attributable to dampness in homes (Fisk et
al., 2007) and that new-onset asthma or asthma-like symptoms may occur
more frequently in people who are exposed to moisture or mold at home
or at work (Sahakian et al., 2008). One study of office workers who oc-
cupied a water-damaged office building at a particular time documented an
asthma incidence rate more than 7 times higher after occupancy than in the
years before occupancy (1.9/1,000 person-years before building occupancy;
14.5/1,000 person-years after) (Cox-Ganser et al., 2005). Later analysis of
that workforce with regard to exposure to mold, measured as culturable
fungi and ergosterol concentrations in floor dust, demonstrated an excess
risk of new-onset asthma at higher levels of exposure (Park et al., 2008).
Papers published since Mendell et al. (2011) completed their litera-
ture review in late 2009 have tended to support the conclusions drawn by
them. A 2010 study of possible cases of occupational asthma in Finland
determined that exposure to dampness and mold in the workplace was
associated with new-onset adult asthma and aggravated the symptoms of
asthmatics (Karvala et al., 2010). Nguyen and colleagues’ analysis of the
results of The National Asthma Survey—New York State found that there
was a positive relationship between asthma symptoms, mold, and humid-
ity in households that had at least one asthmatic adult or child (Nguyen
et al., 2010).
A study in three urban cities in Korea established that students experi-
enced higher levels of wheezing in classrooms that were damp, had visible
mold growth, or had water damage (Kim et al., 2011). Sun et al. (2010)
examined allergic symptoms, including wheezing, in students living in dor-
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140 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
mitories in Tianjin University, China, during the 2006–2007 school year.
The students reported more moisture accumulation and moldy odors and
higher levels of wheezing and rhinitis in summer than winter months. In
contrast, Holme and colleagues’ study of children in Sweden did not find
an association between visible signs of dampness and spore concentration
in indoor air or a relationship between spore concentrations and children’s
allergy and asthma symptoms (Holme et al., 2010).
Other Immunologic Conditions
Epidemiologic studies have shown that some immunologic outcomes
in addition to asthma may be related to moisture incursion in buildings.
Sarcoidosis is more frequent in occupants of water-damaged buildings
(Cox-Ganser et al., 2005; Laney et al., 2009; Newman et al., 2004), includ-
ing school buildings (Dangman et al., 2005). It is important to note that in
each of the cited investigations of sarcoidosis, the researchers documented
increases in asthma and asthma-like symptoms.
It is biologically plausible that exposure to bacteria (notably the en-
dotoxin that is a cell-wall component of some bacteria) and fungi that are
often present in damp indoor environments could trigger immune responses
that lead to inflammation. Experimental studies have demonstrated that
common microbial constituents of damp indoor environments can be po-
tent inducers of inflammatory responses (Hirvonen et al., 2005). Research-
ers believe that granuloma formation in sarcoidosis is in response to an
unidentified antigenic stimulus that induces a local Th1-cell–mediated im-
mune response (DuBois et al., 2003). Chronic stimulation of macrophages
causes the continuing release of inflammatory cytokines (IL-2, IL-12, IFN-
c, and TNF-α), which leads to accumulation of Th1 cells at the site of
inflammation. That immunologic cycling contributes to expansion of the
granuloma structure (Richie, 2005).
Autoimmune diseases occur when a person mounts a specific immune
response to self antigens that leads to tissue damage. Autoimmune dis-
eases are often progressive and debilitating. The burden of autoimmune
diseases in the United States is substantial: they affect an estimated 8%
of the total population (Fairweather et al., 2008) and disproportionately
affect females—more than three-fourths of cases of autoimmune diseases
are in women (Dooley and Hogan, 2003; Gleicher and Barad, 2007;
Jacobson et al., 1997). In a 2008 review, Fairweather et al. (2008) describe
autoimmune diseases as the third-most common category of disease after
cancer and cardiovascular disease in the United States. The role of envi-
ronmental and occupational exposures is poorly defined (Gold et al., 2007),
but exposure to external antigens may trigger and support an autoimmune
inflammatory response (Münz et al., 2009), and joint symptoms and dis-
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DAMPNESS, MOISTURE, AND FLOODING
eases have been associated with microbial exposures related to moisture
damage (Luosujärvi et al., 2003).
SPECIFIC DAMPNESS-RELATED CONTAMINANTS
The principal indoor dampness-related agents that affect health are
thought to be molds and bacteria that amplify in the presence of water
and products of damaged building materials. As the Damp Indoor Spaces
and Health report (IOM, 2004) notes, mold spores are regularly found in
indoor air and on surfaces and materials; no indoor space is free of them.
There are many species and genera, and those most typically found indoors
vary in geographic area, climate, season, and other factors. The availabil-
ity of moisture is the primary factor that controls mold growth indoors.
Although much attention is focused on mold growth indoors, it is not the
only dampness-related microbial agent. Mold growth is often accompa-
nied by bacterial growth. Some research on fungi and bacteria focuses on
specific components that may be responsible for particular health effects:
hyphal (filament) fragments of fungi, protein allergens of microbial origin,
structural components of fungal and bacterial cells, and such products as
microbial volatile organic compounds (MVOCs) and mycotoxins. Release
of those components depends on many physiologic and environmental fac-
tors. Dampness can also damage building materials and furnishings, causing
or exacerbating the release of chemicals and other nonbiologic particles.
The following sections summarize information on those agents and
some of the research on their affects on the health of building occupants.
Molds
Fungi exist as single cells (yeasts), filaments, fruiting bodies, and spores.
They are composed of complex chemical compounds, including proteins,
glycoproteins, glucans, and proteases. They produce cellular toxins in their
competition for access to sources of nutrition in their environment, and
their metabolic byproducts include volatile organic compounds (Bush and
Portnoy, 2001; Storey et al., 2004).
Fungi are ubiquitous in nature and play a critical role in the natural
decomposition of organic materials. Indoor spaces without moisture prob-
lems generally have air concentrations of mold that are the same as or
lower than those outdoors, and the species are the same as those outdoors.
Many fungal taxa in the indoor environment are similar to those recovered
outdoors, but there are factors in the indoor environment (such as lack of
fungicidal ultraviolet radiation from the sun, stable temperature, stable
humidity, and shelter) that can allow some fungi to thrive better in the
indoor environment.
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142 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
Some structural components of mold can cause an immune response
in a person who is exposed mainly through inhalation. Such responses are
most commonly allergic and result in rhinitis or asthma. Other responses
can lead to hypersensitivity pneumonitis (Ikeda et al., 2002; Lee et al.,
2000; Patel et al., 2001; Seuri et al., 2000). The immunologic responses
are complex, inasmuch as mold components include antigens and adjuvants
that heighten the response to the antigens (Kheradmand et al., 2002; Reed,
2007).
Because the active agents that lead to those responses are macromol-
ecules on the cell wall, fungal fragments are at least as likely to cause the
reactions as are intact spores. Therefore, mold does not have to be living
to have an immunologic effect on building occupants. In addition, various
mold species share the macromolecules, so an allergy to one species results
in an allergy to many (Green et al., 2005a, 2009; Schmechel, 2007).
MVOCs include alcohols, esters, aldehydes, and aromatic compounds.
They cause the “musty” odor associated with moldy environments. They
can cause irritation of mucous membranes (Horner and Miler, 2003),
which can lead to irritation of the eyes, nose, throat, and respiratory
tract. Irritation of the trigeminal nerve can lead to headache and fatigue.
(1→3)-β-D-glucans, components of cell-wall fragments, alter reactions to
other agents (Rylander and Lin, 2000) and thus may add to the irritant
properties described here.
Molds produce mycotoxins under some growth conditions (Jarvis,
2002). There are hundreds of those compounds (Etzel, 2002; Norred et al.,
2001), and they include aflatoxins, fumonisins, ochratoxins, rubratoxins,
and trichothecenes (Jarvis et al., 1995; Wannemacher and Wiener, 1997).
Some have neurotoxic, cytotoxic, immunologic, reproductive, or carcino-
genic properties. Although the compounds can exhibit severe toxicity in
animals or humans when they are ingested or inhaled at high levels in, for
example, agricultural settings, it is less clear whether they have an effect at
the levels seen in occupied indoor spaces (IOM, 2004). Mycotoxins have
been identified in building materials and settled dust in water-damaged
buildings (Bloom et al., 2009). There is evidence that in these environments
they contribute to inflammatory responses (Miller et al., 2010). Other po-
tential effects are the subject of current investigation.
Not all dampness is the same for fungi. During Hurricane Katrina,
wind-driven saltwater inundated many homes in Mississippi. The result
was severe water damage, but the damage was different from that caused
by the sustained floods in New Orleans from Lake Pontchartrain. After the
water receded in Mississippi, the homes were dried, and mold growth was
easily initiated on building materials and furnishings. New Orleans had
homes that were essentially like sealed terrariums for several weeks at the
end of summer 2005. A common scene in such buildings was a high-water
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DAMPNESS, MOISTURE, AND FLOODING
mark on the drywall below which little mold growth was observed. There
are two possible explanations for that difference. First, almost all molds
need oxygen and cannot sporulate in liquid. That might explain why the
previously submerged drywall had less mold growth; the time it took for the
water to subside limited mold colonization. Second, flood waters contain
the chemicals found in homes themselves (for example, bleach, pesticides,
and other cleaning products), chemicals from the soil outside, and possibly
other toxicants from nearby industrial or agricultural sources. Some of
the chemicals can be fungus inhibitors or can be fungicidal. Perhaps some
combination of the two reasons explains the pattern in homes that have
endured long-term flooding.
The ramifications of long-term flooding could lead to differences in the
types of fungi that can proliferate, but research is lacking. One study found
that although Cladosporium spores and DNA were abundant and easily
collected in air samples from homes, culturable colonies were not as com-
mon in heavily damaged homes in New Orleans (Chew et al. 2006). Given
that Cladosporium is commonly recovered in home dust and air samples
(Chew et al., 2003; Li and Kendrick, 1995; Wouters et al., 2000) and can
easily compete with such species as Aspergillus and Penicillium, the lack of
growing colonies was perplexing to the researchers.
The Centers for Disease Control and Prevention (CDC) has published
detailed guidance on how to limit exposure to mold and how to identify
and prevent mold-related health effects in the wake of hurricanes and floods
(Brandt et al., 2006). It includes exposure-assessment instructions; reme-
diation advice (including cleaning of HVAC systems); personal protective
equipment recommendations for cleanup personnel; guidance on allergic,
infectious, and toxic effects of exposure to mold and other dampness-
related agents; adverse health-effects prevention strategies; and advice to
public health-authorities. The authors recommend surveillance of com-
munity health after hurricanes and floods to identify unrecognized hazards
and to gather information that will allow better responses in the future.
Few comprehensive epidemiologic studies have been conducted to as-
sess respiratory effects of residents who lived in homes after major flooding.
What is known is mainly from the Mississippi floods of 1993 and Hurri-
canes Katrina and Rita in 2005. Brown and colleagues (2006) estimate that
in the New Orleans area alone the latter two events caused at least 110,000
homes to have high levels of mold and bacteria and at least 40,000 to be
heavily contaminated.
Ross and colleagues assessed mold spores, lung function, and respi-
ratory symptoms in 57 asthmatic residents of 44 homes in East Moline,
Illinois, in April–October 1994 (Ross et al., 2000). The average mold-spore
concentration was 2,190 spores/m3. The researchers found that higher
Alternaria concentrations were associated with missing sleep because of
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144 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
asthma (odds ratio [OR], 4.8; 95% Confidence Interval [CI], 1.6–14.6). In
their second analysis of the data on the Mississippi floods, the researchers
had a slightly different sample size; they assessed mold spores, lung func-
tion, and respiratory symptoms in 59 asthmatic residents of 46 homes in
East Moline, Illinois, in April–October 1994 (Ross et al., 2002). Concentra-
tions in this study averaged 5,692 spores/m3. The researchers found that
higher mold-spore concentrations were associated with an improved peak
expiratory flow rate (PEFR) and respiratory symptom scores. They attri-
bute the paradoxical results partly to self-reported diary cards for PEFR
and symptoms.
Rabito et al. conducted two studies of mold exposure in post–Hurricane
Katrina New Orleans. In the first, the study site was a school that reopened
in January 2006, five months after the hurricane (Rabito et al., 2008).
Respiratory health questionnaire and spirometric data were collected on
children 7–14 years old, and air sampling for fungi in their homes was
conducted at baseline and again after two months. The 75th percentile for
mold concentration was 100 colony-forming units per cubic meter (cfu/m3)
and 70 cfu/m3 at the two times. The concentrations were several orders of
magnitude lower than those reported in unoccupied homes immediately
after the hurricane (Chew et al., 2006). Nonetheless, there was an overall
decrease in mold levels and respiratory symptoms over the study period,
and indoor mold levels were low despite reported hurricane damage. Al-
though many of the homes had sustained hurricane damage, the authors
stressed that their results might not be generalizable to the residents of other
homes who did not have the financial means to return to the city and to
repair their homes or relocate to a nonflooded area.
In the other study by Rabito and colleagues, 529 patients in an allergy
clinic were enrolled from December 1, 2005, to December 31, 2008. Mold
exposure was assessed with a questionnaire, and mold allergy with a skin-
prick test. Mold exposure (defined in terms of extent of home damage or
duration of exposure) was not associated with mold allergy. The authors
acknowledged that minorities and those without health insurance were un-
derrepresented in the study, and this limited generalizability of the results.
Overall, the studies did not observe a statistically significant association
between mold exposure and respiratory symptoms after flooding events.
That result may be influenced by such factors as selection bias, lack of gen-
eralizability of the study populations, the healthy-resident effect (whereby
healthy residents may be more able to conduct the necessary cleanup and
renovation efforts), and difficulties in discerning associations between mold
exposure and respiratory morbidity because of the presence of confounding
factors (Barbeau et al., 2010).
Separately, Dales and colleagues (1991) used questionnaires to gather
data on the health and home characteristics of more than 13,000 children
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DAMPNESS, MOISTURE, AND FLOODING
5–8 years old in 30 communities across Canada. Flooding, defined as “the
appearance of flooding, water damage, or leaks in basement in last year,”
was associated with statistically significant ORs for parent-reported cough,
wheeze, dyspnea, asthma, bronchitis, chest illness, upper respiratory symp-
toms, and eye irritation. The estimates were not adjusted for confounders,
but the authors stated that analyses that adjusted for age, sex, race, parental
education, presence of environmental tobacco smoke, presence of gas ap-
pliances, and hobbies that generate airborne contaminants yielded similar
results.
Recovery activities after hurricane and floods also present risks.
Cummings and colleagues (2008) found that people’s respirator use while
they were entering flooded areas and during cleanup and remediation de-
creased adverse exposures. They established that disposable-respirator use
in water-damaged homes was associated with lower odds of exacerbation of
moderate or severe upper respiratory symptoms (OR, 0.51; 95% CI, 0.24–
1.09) and lower respiratory symptoms (OR, 0.33; 95% CI, 0.13–0.83).
Methods used to assess exposure to mold and mold components are a
major area of research. For example, Ross et al. (2000) found that mold
spores reflect a small fraction of the antigen load in a mold-contaminated
space. Fungal fragments and conidia contribute allergens at concentrations
orders of magnitude greater than mold spores (Green et al., 2005b, 2006).
Airborne culturable fungi represent a yet smaller subset of the antigen load.
One study assessing asthma morbidity in inner-city children with docu-
mented allergy to fungi and focusing on four genera of fungi found that
elevated outdoor and indoor levels of culturable mold resulted in increased
asthma morbidity (Pongracic et al., 2010). Further studies of the health
impacts of post-flood events thus need to assess exposure using a number
of methods, including qualitative characterization of contaminated surfaces
and fungal fragments.
Bacteria
Bacteria also thrive in damp indoor environments and often coex-
ist with mold. As noted earlier, they can cause inflammatory responses
(Hirvonen et al., 2005). Endotoxin, a component of the cell wall of gram-
negative bacteria, has been particularly well studied and has been shown
either to have direct health effects or to augment the effects of other con-
taminants. Endotoxin in house dust has been associated with wheeze in
infants (Keman et al., 1998; Park et al., 2001) and with greater severity
of asthma in adults who are sensitive to dust mites (Michel, 1996; Michel
et al., 1991). In the workplace, endotoxin has been found at high levels
in association with hypersensitivity pneumonitis (Rose et al., 1998), and
levels in floor dust have been shown to be associated with lower and upper
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146 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
respiratory symptoms, fever and chills, and headache in a large office build-
ing and to interact with fungi in the floor dust and lead to higher rates of
lower respiratory symptoms in occupants who have increased fungal and
endotoxin levels (Park et al., 2006).
Emissions from Damaged Building Materials and Furnishings
Water damage can lead to decay of building materials and furnishings.
Polyvinyl chloride (PVC) floor coatings release phthalates when exposed
to water, and phthalates in house dust have been associated with allergic
symptoms, eczema, and asthma in children (Bornehag et al., 2004; Jaakkola
and Knight, 2008). Increased rates of asthma and allergy symptoms have
been associated with damp PVC floor coatings (Bornehag et al., 2005;
Tuomainen et al., 2004). Understanding of the complex chemical interac-
tions that occur indoors is growing. Research has shown that the indoor
chemistry of surfaces (vinyl tile, wall board, and carpet) and the gas phase
reactions that can occur when surfaces are disturbed can result in the rapid
formation of potential irritants (Forester and Wells, 2009; Ham and Wells,
2008; Harrison and Ham, 2009; Wells et al., 2008). Indoor surfaces can
also be important reservoirs of reactant chemicals—such as cleaning agents,
pesticides, and paints—that can undergo hydrolysis reactions because of
moisture. Characterization of those exposures and their associated health
effects is a subject of active research (Anderson et al., 2007, 2010).
SUMMARY COMMENTS
Dampness problems in buildings are pervasive, and strategies for avoid-
ing them well established, although not necessarily widely implemented.
There are several sources of guidance on design and retrofit strategies.
Lstiburek (2004, 2005a,b, 2006), for example, has produced a series of
books that offer design and construction advice specific to various housing
types and climatic conditions found in the United States, including advice
on avoiding water intrusion and excessive indoor dampness. Operational
advice—in particular, proper operation of HVAC systems—for avoiding
damp conditions indoors is also available (ASHRAE, 2009).
The 2004 IOM report Damp Indoor Spaces and Health summarizes
dampness and mold remediation guidelines issued by the New York City
Department of Health and Mental Hygiene (NYCDOH 1993, 2000), Health
Canada (1995), the American Conference of Governmental Industrial Hy-
gienists (ACGIH, 1999), the US Environmental Protection Agency (EPA,
2001), and the American Industrial Hygiene Association (AIHA, 2001). CDC
also offers advice based on the Occupational Safety and Health Administra-
tion, EPA, and New York City 2005 revised guidance (Brandt et al., 2006).
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147
DAMPNESS, MOISTURE, AND FLOODING
The summary advice of those authors and organizations is straightfor-
ward. Quoting from Damp Indoor Spaces and Health (IOM, 2004):
• omes and other buildings should be designed, operated, and main-
H
tained to prevent water intrusion and excessive moisture accumulation
when possible. When water intrusion or moisture accumulation is
discovered, the sources should be identified and eliminated as soon as
practicable to reduce the possibility of problematic microbial growth
and building material degradation.
• hen microbial contamination is found, it should be eliminated by
W
means that limit the possibility of recurrence and limit exposure of oc-
cupants and persons conducting the remediation.
Operationalizing the advice, however, is difficult. The 2004 IOM re-
port committee concluded that “the prevalence and nature of dampness
problems suggest that what is known about their causes and prevention
is not consistently applied in building design, construction, maintenance,
and use.” Buildings are a complex combination of foundation, structure
elements, and interior components, including insulation, plumbing, HVAC,
and ancillary systems. Changes in one may affect the function of others in
ways that are difficult to anticipate.
Climate change may complicate dampness prevention planning and re-
sponses. Buildings are—at least ideally—designed to operate in a particular
set of outdoor environmental conditions. Local building codes are predi-
cated on those conditions, specifying resistance against projected weather
extremes. Building-insurance interests base their premium calculations (and
their economic viability) on assumptions regarding the ability of the struc-
tures that they underwrite to survive such extremes. If climatic conditions
in a particular area change—for example, if there are more severe or more
frequent episodes of intense precipitation—buildings constructed under
existing codes and designed to operate under previously existing conditions
may fail to perform as designed under the new conditions. That suggests
that careful consideration must be given to revising building codes and
practices to anticipate future climatic conditions and to taking a coordi-
nated approach to addressing risks.
CONCLUSIONS
On the basis of its review of the papers, reports, and other information
presented in this chapter, the committee has reached the following conclu-
sions regarding the health effects of alterations in IEQ due to dampness
and flooding:
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148 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
• S
tudies reviewed in the 2004 IOM report Damp Indoor Spaces and
Health and confirmed by research indicate that
o Excessive indoor dampness is a determinant of the presence or
source strength of several potentially problematic exposures.
Damp indoor environments favor house-dust mites and the
growth of mold and other microbial agents, standing water
supports cockroach and rodent infestations, and excessive mois-
ture may initiate or enhance chemical emissions from building
materials and furnishings.
o Damp indoor environments are associated with the initiation or
exacerbation of a number of respiratory ailments.
• Extreme weather and flooding events that penetrate buildings—
which may become more frequent or severe in the future—increase
the number of people at risk for health conditions related to
standing water, wet building materials, and sustained high indoor
humidity.
• Dampness problems in buildings can be difficult to anticipate. The
information needed to minimize the risk of their occurrence or their
severity is available but is not being consistently applied.
• Current buildings and building design, construction, operation, and
maintenance practices may not be appropriate for managing indoor
dampness or flooding problems due to outdoor environmental
conditions that could result from climate change. New, flexible ap-
proaches that anticipate potential problems and take measures to
prevent them or minimize their adverse consequences are needed.
REFERENCES
ACGIH (American Conference of Governmental Industrial Hygienists). 1999. Bioaerosols—
Assessment and control. Cincinnati, Ohio.
AIHA (American Industrial Hygiene Association). 1996. Field guide for the determination of
biological contaminants in environmental samples. Fairfax, VA: AIHA Press.
AIHA. 2001. Report of the Microbial Task Force. Fairfax, VA: AIHA Press.
Akinbami L. 2011. Asthma prevalence, health care use, and mortality: United States, 2005-
2009. National Health Statistics Reports 32.
ASHRAE (American Society of Heating, Refrigerating and Air-Conditioning Engineers). 2009.
Indoor air quality guide: The best practices for design, construction and commissioning.
Atlanta, GA: ASHRAE.
Anderson SE, Wells JR, Fedorowicz A, Butterworth LF, Meade BJ, Munson AE. 2007. Evalu-
ation of the contact and respiratory sensitization potential of volatile organic compounds
generated by simulated indoor air chemistry. Toxicological Sciences 97:355-363.
Anderson SE, Jackson LG, Franko J, Wells JR. 2010. Evaluation of dicarbonyls generated
in a simulated indoor air environment using an in vitro exposure system. Toxicological
Sciences 115:453-461.
OCR for page 149
149
DAMPNESS, MOISTURE, AND FLOODING
Barbeau DN, Grimsley LF, White LE, El-Dahr JM, Lichtyeld M. 2010. Mold exposure and
health effects following hurricanes Katrina and Rita. Annual Review of Public Health
31:165-178.
Bloom E, Grimsley LF, Pehrson C, Lewis J, Larsson L. 2009. Molds and mycotoxins in
dust from water-damaged homes in New Orleans after Hurricane Katrina. Indoor Air
19(2):153-158.
Bornehag CG, Sundell J, Sigsgaard T. 2004. Dampness in buildings and health (DBH): Re-
port from an ongoing epidemiological investigation on the association between indoor
environmental factors and health effects among children in Sweden. Indoor Air 14(Suppl
7):59-66.
Bornehag CG, Sundell J, Hagerhed-Engman L, Sigsgaard T, Janson S, Aberg N, DBH Study
Group. 2005. “Dampness” at home and its association with airway, nose, and skin
symptoms among 10,851 preschool children in Sweden: A cross-sectional study. Indoor
Air 15(Suppl 10):48-55.
Brandt M, Brown C, Burkhart J, Burton N, Cox-Ganser J, Damon S, Falk H, Fridkin S, Garbe
P, McGeehin M, Morgan J, Page E, Rao C, Redd S, Sinks T, Trout D, Wallingford K,
Warnock D, Weissman D. 2006. Mold prevention strategies and possible health effects
in the aftermath of hurricanes and major floods. MMWR Recommendations and Reports
55(RR-8):1-27.
Brown C., Riggs M, Rao C, Cumming K. 2006. Health concerns associated with mold in
water-damaged homes after Hurricanes Katrina and Rita—New Orleans area, Louisiana,
October 2005. 38th Joint Meeting—Panel on Wind and Seismic Effects, 15-20 May
2006. http://www.pwri.go.jp/eng/ujnr/joint/38/paper/38-56brown.pdf (accessed Febru-
ary 13, 2011).
Bush RK, Portnoy JM. 2001. The role and abatement of fungal allergens in allergic diseases.
Journal of Allergy and Clinical Immunology 107(3):430-442.
CDC (Centers for Disease Control and Prevention). 2006. Behavioral Risk Factor Surveillance
System Survey data. Atlanta, GA: Centers for Disease Control and Prevention.
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):13-20.
Chew GL, Wilson J, Rabito FA, Grimsley F, Iqbal S, Reponen T, Muilenberg ML, Thorne
PS, Dearborn DG, Morely RL. 2006. Mold and endotoxin levels in the aftermath of
Hurricane Katrina: A pilot project of homes in New Orleans undergoing renovation.
Environmental Health Perspectives 114(12):1883-1889.
Cox-Ganser JM, White SK, Jones R, Hilsbos K, Storey E, Enright PL, Rao CY, Kreiss K. 2005.
Respiratory morbidity in office workers in a water-damaged building. Environmental
Health Perspectives 113(4):485-490.
Cummings, KJ, Cox-Ganzer JM, Riggs MA, Edwards N, Hobbs GR, Kreiss K. 2008. Health
effects of exposure to water-damaged New Orleans homes six months after Hurricanes
Katrina and Rita. American Journal of Public Health 98(5):869-875.
Dales R, Zwanenburg H, Burnett R, Franklin C. 1991. Respiratory health effects of home
dampness and molds among Canadian children. American Journal of Epidemiology
134(2):196-203.
Dangman KH, Bracker AL, Storey E. 2005. Work-related asthma in teachers in Connecticut:
Association with chronic water damage and fungal growth in schools. Connecticut
Medicine 69(1):9-17.
Dooley MA, Hogan SL. 2003. Environmental epidemiology and risk factors for autoimmune
disease. Current Opinion in Rheumatology 15(2):99-103.
Du Bois RM, Goh N, McGrath D, Cullinan P. 2003. Is there a role for microorganisms in the
pathogenesis of sarcoidosis? Journal of International Medicine 253(1):4-17.
OCR for page 150
150 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
EPA (US Environmental Protection Agency). 2001. Mold remediation in schools and com-
mercial buildings. Washington, DC: EPA Office of Air and Radiation.
Etzel RA. 2002. Mycotoxins. Journal of the American Medical Association 287(4):425-427.
Fairweather DL, Frisancho-Kiss S, Rose NR. 2008. Sex differences in autoimmune disease
from a pathological perspective. The American Journal of Pathology 173(3):600-609.
Fisk WJ, Lei-Gomez Q, Mendell MJ. 2007. Meta-analyses of the associations of respiratory
health effects with dampness and mold in homes. Indoor Air 17:284-296.
Forester CD, Wells JR. 2009. Yields of carbonyl products from gas-phase reactions of fra-
grance compounds with OH radical and ozone. Environmental Science and Technology
43(10):3561-3568.
Gleicher N, Barad DH. 2007. Gender as risk factor for autoimmune diseases. Journal of
Autoimmunity 28(1):1-6.
Gold LS, Ward MH, Dosemeci M, De Roos AJ. 2007. Systemic autoimmune disease mortality
and occupational exposures. Arthritis & Rheumatism 56(10):3189-3201.
Green BJ, Schmechel D, Sercombe JK, Tovey ER. 2005a. Enumeration and detection of
aerosolized Aspergillus fumigatus and Penicillium chrysogenum conidia and hyphae
using a novel double immunostaining technique. Journal of Immunological Methods
307(1-2):127-134.
Green BJ, Sercombe JK, Tovey ER. 2005b. Fungal fragments and undocumented conidia
function as new aeroallergen sources. Journal of Allergy and Clinical Immunology
115(5):1043-1048.
Green BJ, Tovey ER, Sercombe JK, Blachere FM, Beezhold DH, Schmechel D. 2006. Airborne
fungal fragments and allergenicity. Medical Mycology 44(Suppl 1):S245-S255.
Green BJ, Tovey ER, Beezhold DH, Perzanowski MS, Acosta LM, Divjan AI, Chew GL. 2009.
Surveillance of fungal allergic sensitization using the fluorescent halogen immunoassay.
Journal of Medical Mycology 19(4):253-261.
Ham JE, Wells JR. 2008. Surface chemistry reactions of α-terpineol [(R)-2-(4-methyl-3-
cyclohexenyl)isopropanol] with ozone and air on a glass and a vinyl tile. Indoor Air
18:394-407.
Harrison JC, Ham JE. 2009. β-Ionone reactions with the nitrate radical: Rate constant and
gas-phase products. International Journal of Chemical Kinetics 41(10):629-641.
Health Canada. 1995. Fungal contamination in buildings: A guide to recognition and man-
agement. http://individual.utoronto.ca/jscott/fpwgmaqpb001.pdf (accessed February 14,
2011).
Hirvonen MR, Huttunen K, Roponen M. 2005. Bacterial strains from moldy buildings are
highly potent inducers of inflammatory and cytotoxic effects. Indoor Air 15(Suppl
9):65-70.
Holme J, Hägerhed-Engman L, Mattsson J, Sundell J, Bornehag CG. 2010. Culturable mold
in indoor air and its association with moisture-related problems and asthma and allergy
among Swedish children. Indoor Air 20(4):329-340.
Horner WE, Miller JD. 2003. Microbial volatile organic compounds with emphasis on those
arising from filamentous fungal contaminants from buildings. ASHRAE Transactions:
Research 4621 (RP-1072).
Ikeda T, Kuroda M, Ueshima K. 2002. A case of hypersensitivity pneumonitis caused by Gy-
rodontium versicolor. Nihon Kokyuki Gakkai Zasshi 40(5):387-391.
IOM (Institute of Medicine). 2004. Damp indoor spaces and health. Washington, DC: The
National Academies Press.
Jaakkola JJ, Knight DL. 2008. The role of exposure to phthalates from polyvinyl chloride
products in the development of asthma and allergies: A systematic review and meta-
analysis. Environmental Health Perspectives 116(7):145-163.
OCR for page 151
151
DAMPNESS, MOISTURE, AND FLOODING
Jacobson DL, Gange SJ, Rose NR, Graham NM. 1997. Epidemiology and estimated popula-
tion burden of selected autoimmune diseases in the United States. Clinical Immunology
and Immunopathology 84(3):223-243.
Jarvis BB. 2002. Chemistry and toxicology of molds isolated from water-damaged buildings.
Advances in Experimental Medicine and Biology 504:43-52.
Jarvis BB, Salemme J, Morals A. 1995. Stachybotrys toxins. 1. Natural Toxins 3(1):10-16.
Jonkman SN, Maaskant B, Boyd E, Levitan ML. 2009. Loss of life caused by the flooding of
New Orleans after Hurricane Katrina: Analysis of the relationship between flood char-
acteristics and mortality. Risk Analysis 29(5):676-698.
Karvala K, Toskala E, Luukkonen R, Lappalainen S, Uitti J, Nordman H. 2010. New-onset
adult asthma in relation to damp and moldy workplaces. International Archives of Oc-
cupational and Environmental Health 83(8):855-865.
Keman S, Jetten M, Douwes J, Borm PJA. 1998. Longitudinal changes in inflammatory
markers in nasal lavage of cotton workers: Relation to endotoxin exposure and lung
function changes. International Archives of Occupational and Environmental Health
71(2):131-137.
Kheradmand F, Rishi K, Corry DB. 2002. Environmental contributions to the allergic asthma
epidemic. Environmental Health Perspectives 110(Suppl 4):553-556.
Kim JL, Elfman L, Wislander G, Ferm M, Torén K, Norbäck D. 2011. Respiratory health
among Korean pupils in relation to home, school and outdoor environment. Journal of
Korean Medical Science 26(2):166-173.
Laney AS, Cragin LA, Blevins LZ, Sumner AD, Cox-Ganser JM, Kreiss K, Moffatt SG, Lohff
CJ. 2009. Sarcoidosis, asthma, and asthma-like symptoms among occupants of a histori-
cally water-damaged office building. Indoor Air 19(1):83-90.
Lee SK, Kim SS, Nahm DH, Park HS, Oh YJ, Park KJ, Kim SO, Kim SJ. 2000. Hypersen-
sitivity pneumonitis caused by Fusarium napiforme in a home environment. Allergy
55(12):1190-1193.
Li DW, Kendrick B. 1995. A year-round study on functional relationships of airborne fungi
with meterological factors. International Journal of Biometeorology 39(2):74-80.
Lstiburek J. 2004. Builder’s guide to hot-dry/mixed-dry climates. Westford, MA: Building
Science Corporation.
Lstiburek J. 2005a. Builder’s guide to hot/humid climates. Westford, MA: Building Science
Corporation.
Lstiburek J. 2005b. Builder’s guide to mixed-humid climates. Westford, MA: Building Science
Corporation.
Lstiburek J. 2006. Builder’s guide to cold climates. Westford, MA: Building Science
Corporation.
Luosujärvi RA, Husman TM, Seuri M, Pietikäinen MA, Pollari P, Pelkonen J, Hujakka HT,
Kaipiainen-Seppänen OA, Aho K. 2003. Joint symptoms and diseases associated with
moisture damage in a health center. Clinical Rheumatology 22(6):381-385.
Mannino DM, Homa DM, Akinbami LJ, Moorman JE, Gwynn C, Redd SC. 2002. Surveil-
lance for asthma—United States, 1980-1999. MMWR Surveillance Summary 51(1):1-13.
Mendell MJ, Mirer AG, Cheung K, Tong M, Douwes J. 2011. Respiratory and allergic health
effects of dampness, mold, and dampness-related agents: A review of the epidemiologic
evidence. Environmental Health Perspectives 119(6): doi:10.1289/ehp.1002410.
Michel O, Ginanni R, Duchateau J, Vertongen F, le Bon B, Sergysels R. 1991. Domestic
endotoxin exposure and clinical severity of asthma. Clinical & Experimental Allergy
21(4):441-448.
Michel O. 1996. Endotoxin and asthma. Revue Française d’Allergologie et d’Immunologie
Clinique 36(8):942-945.
OCR for page 152
152 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
Miller JD, Sun M, Gilyan A, Roy J, Rand TG. 2010. Inflammation-associated gene transcrip-
tion and expression in mouse lungs induced by low molecular weight compounds from
fungi from the built environment. Chemico-Biological Interactions 183(1):113-124.
Mudarri D, Fisk JW. 2007. Public health and economic impact of dampness and mold. Indoor
Air 17(3):226-235.
Münz C, Lünemann JD, Teague Getts M, Miller SD. 2009. Antiviral immune responses: Trig-
gers of or triggered by autoimmunity? Nature Reviews Immunology 9:246-258.
National Oceanic and Atmospheric Administration (NOAA). 2011. Natural hazard statistics.
http://www.weather.gov/om/hazstats.shtml (accessed May 2, 2011).
Newman LS, Rose CS, Bresnitz EA, Rossman MD, Barnard J, Frederick M, Terrin ML,
Weinberger SE, Moller DR, McLennan G, Hunninghake G, DePalo L, Baughman RP,
Iannuzzi MC, Judson MA, Knatterud GL, Thompson BW, Teirstein AS, Yeager H Jr.,
Johns CJ, Rabin DL, Rybicki BA, Cherniack R, ACCESS Research Group. 2004. A case
control etiologic study of sarcoidosis: Environmental and occupational risk factors.
American Journal of Respiratory and Critical Care Medicine 170(12):1324-1330.
Nguyen T, Lurie M, Gomez M, Reddy A, Pandya K, Medvesky M. 2010. The National
Asthma Survey–New York State: Association of the home environment with current
asthma status. Public Health Reports 125(6):877-887.
Norred WP, Riley RT, Meredith FI, Poling SM, Plattner ID. 2001. Instability of N-acetylated
fumonisin B1 (FA1) and the impact on inhibition of ceramide synthase in rat liver slices.
Food and Chemical Toxicology 39(11):1071-1078.
NYCDOH (New York City Department of Health and Mental Hygiene). 1993. Assessment
and remediation of Stachybotrys atra in indoor environments. New York City: Depart-
ment of Health.
NYCDOH. 2000. Guidelines on assessment and remediation of fungi in indoor environments.
New York City: Department of Health.
Park JH, Spiegelman DL, Gold DR, Burge HA, Milton DK. 2001. Predictors of airborne en-
dotoxin in the home. Environmental Health Perspectives 109(8):859-864.
Park JH, Cox-Ganzer J, Rao C, Kreiss K. 2006. Fungal and endotoxin measurements in dust
associated with respiratory symptoms in a water-damaged office building. Indoor Air
16(3):192-203.
Park JH, Cox-Ganzer JM, Kreiss K, White SK, Rao CY. 2008. Hydrophilic fungi and ergos-
terol associated with respiratory illness in a water-damaged building. Environmental
Health Perspectives 116(1):45-50.
Patel AM, Ryu JH, Reed CE. 2001. Hypersensitivity pneumonitis: Current concepts and future
questions. Journal of Allergy and Clinical Immunology 108(5):661-670.
Pongracic JA, O’Connor GT, Muilenberg ML, Vaughn B, Gold DR, Kattan M, Morgan WJ,
Gruchalla RS, Smartt E, Mitchell HE. 2010. Differential effects of outdoor versus indoor
fungal spores on asthma morbidity in inner-city children. Journal of Allergy and Clinical
Immunology 125(3):593-599.
Rabito FA, Iqbal S, Kiernan MP, Holt E, Chew GL. 2008. Children’s respiratory health and
mold levels in New Orleans after Katrina: A preliminary look. Journal of Allergy and
Clinical Immunology 121(3):622-625.
Reed CE. 2007. Inflammatory effect of environmental proteases on airway mucosa. Current
Allergy and Asthma Reports 7(5):368-374.
Richie RC. 2005. Sarcoidosis: A review. Journal of Insurance Medicine 37(4):283-294.
Rose CS, Martyny JW, Newman LS, Milton DK, King TE Jr., Beebe JL, McCammon JB,
Hoffman RE, Kreiss K. 1998. “Lifeguard Lung”: Endemic granulomatous pneumonitis
in an indoor swimming pool. American Journal of Public Health 88(12):1795-1800.
OCR for page 153
153
DAMPNESS, MOISTURE, AND FLOODING
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(8):705-711.
Ross MA, Persky VW, Scheff PA, Chung J, Curtis L, Ramakrishnan V, Wadden RA, Hryhorczuk
DO. 2002. Effect of ozone and aeroallergens on the respiratory health of asthmatics. Ar-
chives of Environmental Health 57:568-578.
Rudd RA, Moorman JE. 2007. Asthma incidence: Data from the National Health Interview
Survey, 1980-1996. The Journal of Asthma 44(1):65-70.
Rylander R, Lin RH. 2000. (1→3)-β-D-glucan—Relationship to indoor air-related symptoms,
allergy and asthma. Toxicology 152(1-3):47-52.
Sahakian NM, White SK, Park JH, Cox-Ganzer JM, Kreiss K. 2008. Identification of mold and
dampness-associated respiratory morbidity in 2 schools: Comparison of questionnaire
survey responses to national data. Journal of School Health 78(1):32-37.
Schmechel D, Lindsley WG, Chen TB, Blachere FM, Green BJ, Brundage RA, Beezhold DH.
2007. A two-stage personal cyclone sampler for the collection of fungal aerosols and
direct ELISA and PCR sample analysis. Journal of Allergy and Clinical Immunology
119(1/Suppl 1):S188.
Seuri M, Husman K, Kinnunen H, Reiman M, Kreus R, Kuronen P, Lehtomäki K, Paananen
M. 2000. An outbreak of respiratory diseases among workers at a water-damaged
building—A case report. Indoor Air 10:138-145.
Storey E, Dangman K, Schenck P, DeBernardo R, Yang C, Bracker A, Hodgson M. 2004. The
recognition and management of health effects related to mold exposure and moisture
indoors. Storrs, CT: Center for Indoor Environments and Health at University of Con-
necticut Health Center.
Sun Y, Zhang Y, Bao L, Fan Z, Sundell J. 2010. Ventilation and dampness in dorms and their
associations with allergy among college students in China: A case-control study. Indoor
Air doi: 10.1111/j.1600-0668.2010.00699.x.
Swiss Re. 2011. Natural catastrophes and man-made disasters in 2010: A year of devastating
and costly events. Zurich: Swiss Reinsurance Company Ltd. Economic and Research
Counseling.
Tuomainen A, Seuri M, Sieppi A. 2004. Indoor air quality and health problems associated
with damp floor coverings. International Archives of Occupational and Environmental
Health 77(3):222-226.
USGCRP (US Global Change Research Program). 2009. Global climate change impacts in the
United States. New York: Cambridge University Press.
Wannemacher RW Jr., Wiener SL. 1997. Trichothecene mycotoxins. In medical aspects of
chemical and biological warfare (Textbook of military medicine. Part 1, Warfare, weap-
onry, and the casualty, V. 3.), edited by Sidell FR, Takafuji ET, Franz DR. Washington,
DC: Office of the Surgeon General, Borden Institute, Walter Reed Army Medical Center.
Wells JR, Morrison GC, Coleman BK. 2008. Kinetics and reaction products of ozone and
surface-bound squalene. Journal of ASTM International 5(7):JAI101629.
WHO (World Health Organization). 2009. WHO guidelines for indoor air quality: Dampness
and mould. Copenhagen: WHO Regional Office for Europe.
Wouters IM, Douwes J, Doekes G, Thorne PS, Brunekreef B, Heederik DJ. 2000. Increased
levels of markers of microbial exposure in homes with indoor storage of organic house-
hold waste. Applied and Environmental Microbiology 66(2):627-631.
OCR for page 154