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6
Infectious Agents and Pests
Many pathogens and allergens are profoundly affected by environmen-
tal conditions. Their survival may be directly influenced by temperature,
humidity, or moisture, or their availability may depend on the distribution,
abundance, or behavior of their hosts or vectors. A changing climate will
thus affect human exposure to these agents.
This chapter addresses indoor environmental quality concerns associ-
ated with the infectious agents and other pests that research suggests may
be influenced by climate-change–induced alterations in the indoor environ-
ment. The chapter also touches on exposure to chemicals used to control
pest infestations. Exposures that are directly related to dampness are the
subject of Chapter 5.
Two earlier National Academies reports have addressed issues relevant
to the material discussed in this chapter. The 2001 National Research
Council report Under the Weather: Climate, Ecosystems, and Infectious
Disease (NRC, 2001) and the 2008 Institute of Medicine workshop sum-
mary Global Climate Change and Extreme Weather Events (IOM, 2008a)
take on the larger question of the linkages among climate, ecosystems, and
infectious disease. A white paper commissioned by the US Environmental
Protection Agency (EPA) in conjunction with the present effort discusses
the potential effects of climate change on microbial air quality in the built
environment (Morey, 2010).
155
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156 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
INFECTIOUS AGENTS
Infectious diseases have been major drivers of evolution and of human
evolution in particular. The vast majority of infections are acquired from
the environment or transmitted from humans or other animals. Therefore,
factors that affect the physical environment, how we build in it, and how
we share it with other humans are critical determinants of the infections
to which we are exposed and how we perpetuate the exposures. Seasonal
variation—a complex summing of multiple influences ranging from sunlight
to moisture to wind speed and varying by region—has also been recognized
as a critical influence on infectious-disease epidemiology dating back to
Hippocrates (Naumova, 2006). Thus, climate change in general and indoor-
air exposure in particular are major elements in the spread or interruption
of infectious diseases in humans. Despite the extensive knowledge base on
the effects of climate change on environmental growth of microorganisms
and their vectors and hence infections, however, data on the effects of cli-
mate change on indoor air and infectious diseases are incomplete.
This section briefly reviews some of the most pertinent model systems
that highlight elements of the knowledge in direct effects of climate on in-
fectious disease. It explores them by category of infection, inasmuch as each
kingdom (for example, bacteria, fungi, and viruses) has distinct features
and is involved in different processes and exposures. One critical factor is
that air and moisture, and therefore water, are inextricably linked. Most
microorganisms are exquisitely sensitive to moisture, either requiring it or
avoiding it. Therefore, the study of indoor air is closely linked to the state
of indoor water, its aerosols, and the magnitude of humidity. Furthermore,
pipes and other water-delivery systems are prone to development of bio-
films, thin, removal-resistant layers of metabolically inaccessible bacteria
that are constantly available for release into water and indoor air through
taps, showers, humidifiers, and the like.
Respiratory Viruses
Experience dating back thousands of years has taught that infectious
diseases can be affected by seasonal changes; this suggests that environment
plays a critical role in the modulation of disease load, spread, and suscep-
tibility. Obvious and recurring examples are provided by the respiratory
viruses, most notably influenza viruses, respiratory syncytial virus (RSV),
and the rhinoviruses. Mechanisms of spread are varied and include aerosol,
fomite,1 and direct contact. Direct contact, such as hand-to-hand transfer, is
the most easily modified and is a major contributor to the spread of respira-
1 Fomites are inanimate objects or substances—a door knob, for example—that function to
transfer infectious organisms from one individual to another.
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INFECTIOUS AGENTS AND PESTS
tory viruses. Fomite spread is affected by ambient humidity, which can in
turn be affected by indoor air.
Influenza Viruses
Influenza viruses continue to account for substantial annual morbidity
and mortality interspersed with periods of increased activity. The 2009–
2010 H1N1 influenza epidemic is estimated to have involved around 61
million infections, 274,000 hospitalizations, and more than 12,000 deaths
in the United States (CDC, 2010b).
Although there has been prolonged controversy over the environmental
correlates of influenza epidemic spread, it appears that absolute humidity—
the amount of water vapor in a given volume of air—is a critical deter-
minant (Shaman and Kohn, 2009; Shaman et al., 2010a,b). In contrast,
relative humidity—the amount of water vapor in a given volume of air at a
given temperature expressed as the percentage of the maximum possible for
that temperature—is well regulated in the indoor environment and appears
not to be as important a determinant of influenza transmission and spread.
However, studies by Myatt et al. (2010) show that increased absolute hu-
midity and relative humidity, achieved by the use of indoor air humidifica-
tion, can lead to substantial reductions in viable influenza virus.2 Overall,
the effects of humidity on influenza virus outbreaks and peak epidemic peri-
ods are greater in temperate than in tropical environments. In some tropical
and subtropical settings, relative humidity has been more closely associated
with influenza epidemics (Tang et al., 2010a,b). Because periods of high
relative humidity corresponded to periods of increased indoor time and air
conditioning, the population-based correlations are confounded. However,
because indoor air conditioning affects indoor temperature and humidity,
these require more investigation to determine whether the critical aspects
of influenza spread are determined by the indoor or outdoor environmental
conditions. The different results in temperate and tropical zones may reflect
differences in viral and human biology in those regions. However, compara-
tive studies for tropical and subtropical regions for respiratory transmission
have not been completed in the United States.
Respiratory Syncytial Virus
RSV is the greatest cause of bronchiolitis and pneumonia in infants
worldwide and causes up to about 125,000 hospitalizations in US in-
2 As discussed later in this chapter, though, increased humidity may create a more hospitable
environment for mold growth and accelerate the degradation and subsequent off-gassing of
building materials and furnishings.
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158 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
fants each year. In the US elderly population, it accounts for an estimated
177,000 hospitalizations and 14,000 deaths (CDC, 2010). RSV appears to
contribute to invasive pneumococcal disease more than influenza viruses do
(Murdoch and Jennings, 2009; Talbot et al., 2005; Watson et al., 2006).
Like influenza virus activity, RSV activity is highest in temperate cli-
mates during fall and winter months and into spring. However, there can
be variability in the time of onset and duration, at least in more subtropical
regions (CDC, 2010a). Unlike influenza virus, RSV is stabilized by higher
humidity, and transmission in some studies correlates with relative humid-
ity, lower temperature, and increased cloud cover (Meerhoff et al., 2009).
Whether the mechanisms of these factors are due to direct effects on the
virus or to indirect effects in driving people indoors into crowded environ-
ments is an open question. In some settings, such as Indonesia, RSV activ-
ity correlated strongly with rainfall and temperature (Omer et al., 2008).
However, the apparently differing epidemiology in temperate and tropical
climates remains incompletely explained (Welliver, 2009). In Spain, RSV ad-
missions of infants with severe disease were strongly associated with lower
temperature and lower absolute humidity (Lapeña et al., 2005).
Rhinovirus
Human rhinovirus (HRV) is a common and relatively mild pathogen,
but one that by its very ubiquity and frequency has a major impact on
human health, especially in the setting of pre-existing airway disease like
asthma. Adults may have up to four bouts per year, typically in the fall
through spring, accounting for up to 62 million cases in the United States
annually (Sloan et al., 2011). In addition, because HRV is highly transmis-
sible, settings that favor human-to-human and fomite transmission tend to
result in relatively high rates of HRV during certain times of the year. Less
research has been conducted on HRV than on influenza and RSV, in part
because these latter organisms’ morbidity and mortality are much higher
and their etiologies somewhat less complex.
Human rhinoviruses are comprised of three main groups—A, B, and
C—which replicate in the epithelial cells of the upper and lower respiratory
tracts, leading to cough, wheeze, and rhinorrhea (Dulek and Peebles, 2011).
Allergic triggers act along with HRV to fuel the exacerbation of asthma.
Extensive work has shown that HRV is one of the most prevalent cofactors
in asthma exacerbations, making their role in overall medical care critical
to understand and interrupt.
A few studies address the determinants of HRV transmission and preva-
lence in indoor environments. Myatt et al. (2004) showed that the amount
of HRV recovered from building air handling filters varied with the amount
of outside air entrained, suggesting that HRV transmission might be influ-
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INFECTIOUS AGENTS AND PESTS
enced by the number of air exchanges in the work environment. Singleton
and colleagues (2010) found that HRV was recovered from 44% of Alaskan
native children hospitalized with a respiratory infection, but this rate was
quite close to that in control children who were not hospitalized. Tovey
and Rawlinson (2011) note that the rates of asthma rise precipitously two
to three weeks after the start of school, indicating that some new exposure
in the classroom is responsible. The authors hypothesize that these factors
include HRV as well as numerous other costimulators of asthma such as
endotoxin, proteins, and allergens. du Prel and colleagues (2009) found that
HRV rates are associated with higher humidity levels, which might become
more common as a result of climate change.
Gram-Negative Bacteria
The gram-negative bacteria present special issues in climate-associated
infectious-disease epidemiology. They are not dependent on human-to-
human spread, are not dependent on human inhabitation for survival, and
have the ability to form biofilms—slippery, poorly penetrable slimes that
cover the inside of water conduits. Given their close ties to the environment
and their access to humans through water consumption, aerosol generation,
heating, and cooling, the epidemiology of gram-negative rod infections is a
window into infectious diseases in the setting of climate change.
Legionella
From its initial recognition as a cause of human respiratory disease, Le-
gionella infection has been closely tied to water-droplet exposure in hotels
and hospitals (Stout and Yu, 1997). However, the modes of transmission
clearly can involve both aerosol spread (by water misters in grocery stores,
for example) and aspiration. Spread from potting soil has also been well
documented (de Jong and Zucs, 2010).
Regardless of the exposures or the modes of transmission, it is clear
that legionellae are relatively common in some water supplies and has
seasonal variation. In a case-crossover study in the greater Philadelphia
area, Fisman and colleagues identified summertime occurrence of reported
Legionella pneumonia to correlate with rainfall and increased relative hu-
midity in the preceding week or so, rather than temperature (Fisman et al.,
2005). Whether that reflects increased recruitment of legionellae into the
water supply through rainfall, increased survival in higher humidity, indoor
transmission, or outdoor transmission remains to be concretely determined.
However, it is clear that in many instances, such as in hospitals, Legionella
transmission is presaged by high levels of bacterial or bacterial DNA recov-
ery from ambient water sources, such as faucets (Feazel et al., 2009). This
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160 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
dynamic reservoir of organisms probably serves as the source of aerosol
generation, the source of bacteria that can be aspired by predisposed hosts,
or both. Thus, indoor water clearly influences Legionella transmission and
is itself influenced by regional environmental factors.
Pseudomonas aeruginosa
Stapleton et al. (2007) studied the incidence and causes of keratitis in
contact-lens wearers in Australia. They found that Pseudomonas aerugi-
nosa accounted for a plurality of cases and that it varied with higher mean
minimum temperature but not humidity. Conducting their study in a coun-
try with well-characterized tropical and more temperate zones, they found
that although P. aeruginosa was most common in the tropical regions,
gram-positive organisms, such as Staphylococcus aureus, predominated in
more temperate regions (Stapleton et al., 2007). Perencevich et al. (2008)
studied the effects of seasonal temperature on nosocomial infection rates at
the University of Maryland Medical Center. On review of almost 218,594
cases and 26,624 unique cultures, they found that rates of some gram-
negative bacillary infections, including P. aeruginosa infections, were higher
during warmer months and that rates of P. aeruginosa infection increased in
relation to temperature rise. Gram-negative organisms that showed similar
seasonal variation included Acinetobacter baumanii, Enterobacter cloacae,
and Escherichia coli. Rates of gram-positive bacteria, such as S. aureus and
Enterococcus spp., were not increased over the same periods and did not
show similar relationships to temperature. Those infections occurred in
hospitals, so they are reflections of effects of indoor environment, but they
presumably reflect some changes in the outdoor environment as well. That
other nosocomial pathogens, such as S. aureus, did not vary in the same
pattern excludes simple effects of climate on human practices and suggests
a more intrinsic effect of climate on gram-negative nosocomial pathogens.
As mentioned above, Perencevich et al. (2008) showed that gram-
negative nosocomial infections increased with increasing temperature in
Baltimore. In a national survey, McDonald et al. (1999) also found sea-
sonal variation in Acinetobacter baumanii nosocomial infections but not
in P. aeruginosa infections. They also noted marked differences in regional
rates of A. baumanii infections, with higher rates in the eastern than west-
ern parts of the United States.
Mycobacteria
The Mycobacteriaceae are typically environmentally hardy gram-
positive rods that include the high-grade primate pathogen Mycobacterium
tuberculosis, the more numerous environmental or nontuberculous myco-
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INFECTIOUS AGENTS AND PESTS
bacteria, and M. leprae, the agent of leprosy. Some of these organisms have
emerged as agents of lung infection in patients who have underlying lung
diseases that lead to impaired clearance of respiratory secretions. Those
diseases are best exemplified by cystic fibrosis, a genetic disease in which
impairment and dysfunction of the airway-lining cilia lead to the airway-
widening condition known as bronchiectasis. Bronchiectasis is a common
feature of the other syndromes in which nontuberculous mycobacterial
infections occur, including primary ciliary dyskinesia, alpha-1 antitryp-
sin deficiency, and hyper-IgE recurrent-infection syndrome (Zoumot and
Wilson, 2010).
The role of environmental exposure, including exposure to the indoor
environment, in nontuberculous mycobacterial infection has recently re-
ceived intense interest. The nontuberculous mycobacteria live in temperate
and tropical waters and soils throughout the world. Unlike M. tuberculo-
sis and M. leprae, which depend almost exclusively on human-to-human
spread for their propagation, the nontuberculous mycobacteria are environ-
mental opportunists that live in biofilms and can survive otherwise hostile
environments because of their waxy cell walls (Falkinham, 2010). Feazel et
al. (2009) showed recovery of M. avium complex genetic signatures from
biofilms collected from inside showerheads in homes. Other organisms
were also detected, including legionellae. Falkinham et al. (2008) reported
a case of pulmonary infection with a particular species of M. avium com-
plex that was recovered from the home water supply; this suggested spread
from the household water to the patient. That potential mechanism of
spread has been expanded on by Chan and Iseman (2010). The occurrence
of pulmonary nontuberculous mycobacterial infection is highest in cystic
fibrosis patients who have the mildest forms of disease, especially in women
(Rodman et al., 2005).
Fomites
Increasing relative humidity and temperature outdoors will probably
lead to increased indoor dampness and dampness-related health effects. As
is the case with many infectious-disease vectors, the effects of temperature
and relative humidity may increase or decrease the survival of viruses and
bacteria and facilitate the persistence of infectious fomites (Boone and
Gerba, 2007). Increases in environmental temperature decrease the survival
of many viruses. For example, the H5N1 avian influenza virus persisted on
duck feathers and on surfaces for long times but only at lower tempera-
tures (Wood et al., 2010; Yamamoto et al., 2010). The combination of a
stable indoor environment and increased dampness may actually decrease
the transmission of some respiratory viruses and increase the survival of
other pathogens on fomites, such as the ones that harbor bacteria and mold
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162 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
(Boone and Gerba, 2007; Gubler et al., 2001). Increased dampness indoors,
possibly exacerbated by building deterioration, may exacerbate or increase
the risk of developing select respiratory diseases caused by mold and bacte-
rial exposure (IOM, 2004; WHO, 2007).
Fungi
Fungi pose a special set of problems because they are ubiquitous,
grow easily in the environment, and cause human diseases. However, the
language surrounding fungal interactions with humans is fraught with im-
precision, which leads to confusion. In addition, there are several distinct
types of fungi, including yeasts, molds, and dimorphic yeasts (fungi that
live as yeasts under one set of circumstances but can act like molds in other
circumstances) (Holland and Vinh, 2009). The distinctions are important
because the dimorphic yeasts are able to live both in the environment and in
humans and cause some degree of invasive disease even in healthy humans.
Examples include Histoplasma capsulatum, Coccidioides immitis, Blasto-
myces dermatitidis, Sporothrix schenkii, and Paracoccidioides brasiliensis.
Those agents are relatively regional in their distribution and are therefore
often referred to as endemic fungi. In healthy hosts, they can cause usually
self-limited respiratory illnesses, such as valley fever due to C. immitis. They
are organisms that live in the upper layer of soil outdoors and are rarely
associated with indoor exposures and have rarely associated with indoor
exposures to date. However, a white paper commissioned by EPA (Morey,
2010) suggests a mechanism by which this could change. It indicates that
the upper layer of soil is prone to disturbance by dust storms, which may
become more common in geographic areas that experience drought because
of shifts in climatic conditions. This may in turn lead to greater indoor
penetration of pathogenic fungi contained in soil and to higher indoor ex-
posures in the absence of enhanced HVAC filtration or settled dust removal.
Invasive fungal infections are quite rare in humans and occur almost
exclusively in the setting of immunocompromise, either inborn, such as
some primary immunodeficiencies, or acquired, such as that acquired
through transplantation or chemotherapy. However, with the advent of
more drugs that affect immunity, such as tumor-necrosis factor alpha–
(TNF-α)-blocking agents used for rheumatoid arthritis and inflammatory
bowel disease, the number of people at risk for the development of fungal
infection is increasing (Tsiodras et al., 2008). In susceptible persons Asper-
gillus fumigatus, a thermotolerant filamentous mold, can cause invasive
disease that is usually spread by inhalation. Pneumonias that occur in the
setting of immunocompromise carry high morbidity and mortality.
In the nonimmunocompromised host, the most important fungal dis-
ease in the respiratory tract is allergic bronchopulmonary aspergillosis
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INFECTIOUS AGENTS AND PESTS
(ABPA), a syndrome of allergic response to fungi that is most common in
those who are atopic, those who have cystic fibrosis, and those who have
asthma (Patterson and Strek, 2010). Allergic fungal sinusitis is similar
in that eosinophil-rich secretions become dense and involved with fungi
without tissue invasion; in this case, the organisms involved include the
dematiaceous (dark-walled) molds Bipolaris spicifera and Curvularia lunata
or Aspergillus fumigatus, A. niger, and A. flavus (Schubert, 2009). The syn-
dromes of chronic fungal rhinosinusitis are regionally concentrated around
the South and Southwest of the United States. These allergic respiratory
syndromes straddle the lines between infection, colonization, and allergy.
Synthesis
Climate change has many effects on infectious diseases, some malign
and some ameliorative. How we adapt the indoor environment to the con-
tinuing changes in the outdoor environment will be critical determinants of
how we affect the occurrence and spread of infectious diseases. In particu-
lar, effects on moisture, temperature, and the organisms trafficked into our
homes, places of work, hospitals, and schools in water will determine the
rates of viral, bacterial, mycobacterial, fungal, and allergic diseases.
PESTS
Indoor environments contain a number of unwelcome insects, other
arthropods, and invasive animals. All of these are at some level sensitive to
environmental conditions, but some are more susceptible to the conditions
associated with climate change. This section summarizes the available lit-
erature on the characteristics of these pests; the health effects of exposure
to the allergens and microbial agents that they produce, host, or carry;
and how climate-change–induced alterations in the indoor environment—
including changes in occupant behavior—may affect adverse exposures
associated with them.
House Dust Mites
House dust mites are microscopic arthropods that are ubiquitous in
indoor environments. They are among the most important sources of aller-
gens in house dust and of allergic disease in the United States (IOM, 2000).
Exposure
Voorhorst and colleagues were the first to show that dust mites of
the genus Dermatophagoides were the source of “house dust” allergens
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164 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
(Voorhorst et al., 1969). Dermatophagoides pteronyssinus (de Boer and
Kuller, 1997; van Strien et al., 1994; Voorhorst et al., 1969) and D. farinae
(Antens et al., 2006) are commonly recovered in home settings. D. farinae is
the hardier of the two (Arlian, 1975; Arlian and Veselica, 1981). An inter-
vention study showed that the major allergen from D. pteronyssinus may
have been decreased by an extremely dry (and cold) winter during the study
period rather than by the home interventions themselves (Brunekreef et al.,
2005; Gehring et al., 2005).
Dust mite viability is highly influenced by environmental conditions.
There may be some inferences that as the climate warms, dust mites will
thrive (Ayres et al., 2009). That is not entirely true. As noted in Chapter
2, although some regions of the country will experience warmer climates,
they will not necessarily experience higher humidity. The critical factor for
dust mites is water activity (Aw), which is relative humidity at a surface.
Dust mites do not have lungs that can condition the air; rather, they conduct
transpiration through their exoskeletons. A decrease in ambient relative hu-
midity (which is paralleled by a drop in Aw) can affect dust mites not only
in laboratory settings (Arlian, 1975; Arlian and Veselica, 1981) but in the
home (Arlian et al., 2001; Cabrera et al., 1995; Harving et al., 1994) and
at a community level (Acosta et al., 2008; Chew et al., 1999).
New York and Boston are coastal cities, but many of their homes can
be dry in winter, and this factor eradicates the dust mite population. Studies
indicate that increased indoor temperature in those communities has not
been accompanied by an observed increase in the dust mite population;
rather, dust mites decreased (Acosta et al., 2008; Chew et al., 1999). The
homes where overheating was measured in these studies were multifamily
apartment buildings whose residents had little control over their heating.
The heating was turned on (building wide) early in fall and turned off
late in spring. Figures 6-1 and 6-2 illustrate how overheated apartments
compared with single-family homes whose residents had more control over
their heating.
A change in climate could also affect the ecologic niches of some types
of dust mites in such a way that the geographic patterns of endemic dust
mites could change. As discussed earlier, some dust mites are more sensitive
to humidity than others. The Dutch intervention study described earlier
(Brunekreef et al., 2005) showed not only that dust mite levels decreased
in this coastal country but that the profile of dust mite taxa had changed.
Although it was not highlighted in the study, careful examination of one of
the figures shows that between the beginning of the study (1996) and eight
years later, Der f 1 (the major allergen from D. farinae) apparently became
the most highly concentrated allergen in house dust (Antens et al., 2006).
Even if humidity does not change substantially, warmer climate patterns
are predicted, and this (in the absence of any adaptation measures, such as
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INFECTIOUS AGENTS AND PESTS
100 100
House temp
House RH
90 90
Apartment temp
Apartment RH
80 80
% Relative Humidity
Temperature (o F)
70 70
60 60
50 50
40 40
30 30
February
December
January
September
October
November
August
March
April
June
July
June
May
Month (June 1995–June 1996)
FIGURE 6-1 Variations in indoor temperature and relative humidity as functions of
housing type and time of year in a sample of urban residences. (Derived from data
presented in Chew et al., 1999.) Figure 6-1.eps
100
House (Bed)
House (Floor)
Apartment (Bed)
Der p 1 Geometric Means (ug/g)
Apartment (Floor)
10
1
0.1
0.01
September
November
December
February
January
October
August
March
April
June
July
June
May
Month (June 1995–June 1996)
FIGURE 6-2 Variations in Der p 1 allergen levels as a function of housing type
and location and time of year in a sample of urban residences. (Derived from data
presented in Chew et al., 1999.)
Figure 6-2.eps
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174 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
Synthesis
Generally speaking, alterations in outdoor environmental conditions
may affect indoor exposures to pests by changing the habitable range of
creatures known to invade indoor environments or by changing indoor
environmental conditions or behavior in ways that drive them indoors.
Buildings and building-maintenance practices that work well for one set of
environmental conditions may not protect against infestations under other
conditions. Termite infestations, for example, are less common in northern
parts of the United States, and buildings and building codes there do not
always require termite-prevention measures (Peterson, 2010). If termite
ranges move northward, it may lead both to increased property damage
and to occupant exposure to pesticides unless anticipatory maintenance and
regulatory changes are made.
CONCLUSIONS
Several of the key findings of the 2001 National Research Council
report Under the Weather: Climate, Ecosystems, and Infectious Diseases
remain pertinent and bear repeating. They are excerpted and quoted below;
additional explanatory detail is available in that report.
Key Findings Regarding Linkages Between Climate and
Infectious Diseases from the Report Under the Weather:
Climate, Ecosystems, and Infectious Diseases
• W
eather fluctuations and seasonal-to-interannual climate variabil-
ity influence many infectious diseases.
• O
bservational and modeling studies showing an association be-
tween climatic variations and disease incidence must be interpreted
cautiously.
• C
limate change may affect the evolution and emergence of infec-
tious diseases.
• T
he relationships between climate and infectious disease are often
highly dependent upon local-scale parameters and there are poten-
tial pitfalls in extrapolating climate and disease relationships from
one spatial/temporal scale to another.
• T
he potential disease impacts of global climate change remain
highly uncertain.
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INFECTIOUS AGENTS AND PESTS
Research Needs and Surveillance Regarding Climate and
Infectious Diseases from the Report Under the Weather:
Climate, Ecosystems, and Infectious Diseases
• R
esearch on the linkages between climate and infectious diseases
must be strengthened.
• F
urther development of disease transmission models is needed to
assess the risks posed by climatic and ecological changes.
• E
pidemiological surveillance programs should be strengthened.
• O
bservational, experimental, and modeling activities are all highly
interdependent and must progress in a coordinated fashion.
• R
esearch on climate and infectious disease linkages inherently re-
quires interdisciplinary collaboration.
Other Conclusions
In addition, on the basis of its review of the papers, reports, and other
information presented in this chapter, the present committee has reached
the following conclusions regarding infectious agents and pests:
• M
ore investigation is needed to determine the extent to which the
critical aspects of influenza spread are determined by indoor vs out-
door environmental conditions. It should consider air conditioning,
which affects indoor temperature and humidity, and geographic
location because there may be salient differences among regions in
viral and human biology.
• T
he ecologic niches for house dust mites will change in response to
climate change. Locations that are hotter and drier and that have
increased use of air conditioning will tend to have fewer dust mite
infestations. Decreased use of heating systems in winter because of
milder conditions may result in increased dust mite populations.
• D
ecreases in dust mite populations in some locations may lower
the incidence of allergic reactions to dust mites, but the overall
incidence of allergic disease may not go down, because those who
are predisposed to allergies may become sensitized to other air
contaminants.
• C
limate change may also lead to shifting patterns of indoor ex-
posure to pesticides as occupants and building owners respond to
infestations of pests whose ranges have changed.
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176 CLIMATE CHANGE, THE INDOOR ENVIRONMENT, AND HEALTH
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