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6
INDOOR CHEMlcALExpos a res
~ oncern in recent years regarding the potential health ef-
fects of indoor air exposures, as well as the marked increase in the
prevalence of asthma in industrialized countries, has prompted a
burgeoning of scientific research on exposure to airborne agents
and asthma.
The committee was charged with the task of evaluating the
strength of the scientific evidence concerning the possible asso-
ciation between these agents and asthma prevalence and severity.
The committee was also tasked with examining possible means
of mitigating or preventing exposure to these agents. In this chap-
ter the committee evaluates indoor exposure to chemical agents,
addressing the following to the extent permitted by available re-
search:
1. which factors influence exposures to the agent;
2. whether a relationship exists between the agent and asthma
prevalence or severity, taking into account the strength of the sci-
entific evidence and the appropriateness of the methods used to
detect the relationship;
3. what type of relationship exists between the agent and
asthma;
4. whether there are special considerations regarding the
223
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224
CLEARING THE AIR
agent (for example, subpopulations at risk and interactions with
other exposures);
5. which strategies effectively mitigate or prevent exposure
to the agent;
6. whether these strategies only reduce exposures, or decrease
the occurrence or exacerbation of asthma; and
7. whether these strategies are reasonable for use by the tar-
get populations.
Each section begins by providing a definition of the agent and
a summary of the factors that influence exposure. The evidence
concerning the possible association between the agent and asthma
is discussed, followed by the committee's conclusions regarding
the health impacts. Where information is available, evidence re-
garding possible means of mitigating or preventing exposure to
the agent is addressed. Each section concludes with any commit-
tee recommendations for general or specific areas in which addi-
tional research is needed with respect to the agent. Because there
are great differences in the amount and type of information avail-
able on specific agents, the sections vary in their depth and focus.
NITROGEN DIOXIDE
Definition of Agent and Means of Exposure
Nitrogen dioxide (NO2) is a common indoor and outdoor pol-
lutant that is produced, along with other oxides of nitrogen,
whenever high-temperature combustion occurs. NO2 is one of six
"criteria" air pollutants for which National Ambient Air Quality
Standards are set by the U.S. Environmental Protection Agency
(EPA). The current standard is 50 parts per billion (ppb) averaged
over one year. Much higher indoor concentrations are sometimes
observed when indoor sources are present due to the limited di-
lution often observed in confined spaces. Indoor sources include
gas stoves and space heaters, kerosene space heaters, and poorly
vented furnaces and fireplaces. In homes with indoor combus-
tion sources, personal NO2 exposures are usually driven by in-
door concentration in the home, even in urban areas with elevated
outdoor levels.
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INDOOR CHEMICAL EXPOSURES
225
In addition to nitrogen oxides, indoor combustion appliances
may also emit CO, SO2, formaldehyde, volatile organic com-
pounds (VOCs), and submicron particulate matter (PM). Some of
these pollutants, including SO2 and PM, are known respiratory
irritants. Most epidemiologic studies reviewed in this section have
assessed NO2 exposure based on the presence or absence of gas
appliances in the home, rather than on the basis of NO2 measure-
ments. Few if any studies have simultaneously measured NO2
and associated co-pollutants such as PM. As a result, it is usually
not possible to attribute health effects associated with gas appli-
ance use to NO2 exposures per se.
Factors Influencing Exposure
Indoor exposure to NO2 resulting from the use of gas appli-
ances is common. On average, about half of U.S. homes have gas
stoves or ovens, and much higher percentages of gas appliances
exist in some urban areas (Samet et al., 1987~.
Considerable data exist on indoor NO2 exposures in U.S.
homes and the factors that influence them (Goldstein et al., 1988;
Leaderer et al., 1986; Quackenboss et al., 1986; Ryan et al., 1988;
Spengler et al., 1983, 1994, 1996~. Indoor NO2 concentrations de-
pend on the presence and emission strength of indoor sources,
the ventilation rate of the home, and the penetration of outdoor
NO2 (Drye et al., 1989; Spengler et al., 1996~. Important indoor
sources include unvented cooking and heating appliances that
burn gas or kerosene.
The use of a gas range results in an increase of about 25 ppb in
the background NO2 concentration in a home, with peaks as high
as 200 to 400 ppb in the kitchen during cooking (Samet et al.,
1987~. In a large study carried out in Albuquerque, New Mexico,
the highest two-week average indoor NO2 concentrations were
observed in homes with gas stoves that had continuous pilot
lights and in homes where the stove or unvented gas or kerosene
heaters were used for supplemental heating (Spengler et al., 1996~.
In the same study, higher indoor NO2 concentrations were ob-
served in gas cooking than in electric cooking homes, but this
difference was much less pronounced in the summer when home
ventilation rates were higher. Regardless of stove type, indoor
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226
CLEARING THE AIR
concentrations are generally higher in locations with high out-
door concentrations, such as large urban areas, due to the infiltra-
tion of outdoor air; however, indoor sources still explain most of
the variance in personal exposures in urban areas. There is some
evidence to suggest that homes with gas stoves in underprivi-
leged, inner city communities may have uniquely high NO2 lev-
els, possibly due to higher frequency and longer duration of cook-
ing, small home volume, and use of stoves for supplemental
winter heating (Goldstein et al., 1988~. Further research into this
question is warranted.
Data collected in multiple locations in homes with gas stoves
show that strong NO2 concentration gradients exist, with kitchen
levels higher than elsewhere (Matti et al., 1999~. Kitchen concen-
trations during cooking may exceed long-term average concen-
trations by an order of magnitude or more. These spatial and tem-
poral characteristics imply differential exposures for different
residents depending on time spent in the kitchen while cooking is
taking place.
Evidence Regarding Asthma
Exacerbation and Development
Numerous epidemiologic studies have examined whether
respiratory health effects are associated with exposures to typical
indoor NO2 concentrations. Most such studies have addressed
respiratory symptoms and/or Jung function variables as the pri-
mary outcomes, both of which include measures (i.e., wheeze or
decline in FEF25 75) that are usually associated with the clinical
diagnosis of asthma. However, few studies have focused on
asthma as an outcome or on respiratory effects among asthmatic
subjects specifically. This limits the utility of the existing litera-
ture for assessing the impact of NO2 on the development or exac-
erbation of asthma.
Epidemiologic study designs have included cross-sectional
surveys, case-control studies, longitudinal cohort studies, and
time-series pane] studies assessing acute impacts. Exposures in
most studies have been assigned based on answers to questions
regarding the presence of gas stoves or other indoor combustion
appliances. Some studies have included limited indoor or occa
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INDOOR CHEMICAL EXPOSURES
227
signally personal NO2 measurements using passive diffusion
samplers. As a group, epidemiologic studies have the advantage
of studying realistic levels and patterns of NO2 exposures. How-
ever, results can be difficult to interpret due to possible confound-
ing.
There have also been several clinical experiments involving
brief controlled exposures of humans in environmental chambers.
Such studies enable careful control of experimental conditions in-
cluding exposure level and duration. They also make it more fea-
sible to examine asthma-related respiratory outcomes other than
symptoms and lung function, such as airway hyperresponsive-
ness (AHR), pulmonary cells and cytokines obtained by bronchos-
copy, and effects on allergen responsiveness. A limitation of the
experimental chamber studies is that they usually employ NO2
concentrations much higher than those typically observed in the
indoor environment. Also, the study populations have typically
been small and, to some extent, unrepresentative of the more sen-
sitive members of the general population.
Very few epidemiologic studies have evaluated asthma diag-
nosis as an outcome in relation to NO2 exposure, and results from
these few studies have been mixed. A well-conducted case-con-
tro! study found no association between the presence of a gas
cooking appliance in the home and incident asthma (odds ratio
[OR]=1.33; 95°/O confidence interval [CI] 0.68-2.58) among chil-
dren 3-4 years old in Montreal (Infante-Rivard, 1993~. The main
study analyzed 457 cases (children with a first diagnosis of
asthma made by a pediatrician) and 457 controls (matched on age
and census tract), and found significant associations between in-
cident asthma and several factors other than gas appliances, in-
cluding heavy maternal smoking, childhood atopy, and others. A
subset of 140 subjects provided a 24-hour personal NO2 sample.
In an unmatched analysis of this subset, there was a significant
association with asthma for subjects in the highest category of
NO2 exposure (>15 ppb); however, the small size of the exposed
group and the post hoc nature of the analysis preclude any mean-
ingfu] inferences regarding the causality of this association.
Strachan and Carey (1995) analyzed environmental risk factors
for severe wheezing among school children aged 11-16 years in
Sheffield, England; 486 cases and 475 age- and school-matched
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228
CLEARING THE AIR
controls were analyzed, where cases were children whose parents
reported 12 or more wheezing episodes in the past 12 months or
an attack of wheezing that limited speech. Controls had no his-
tory of asthma or wheezing at any age. Non-feather bedding and
ownership of furry pets were both significantly associated with
case status; however, the use of gas for cooking was not.
In contrast, two large questionnaire-based cross-sectional sur-
veys, one in Canada and the other in Australia, reported signifi-
cant associations between asthma and gas stove use. The first
study analyzed data from a nationwide survey of Canadian par-
ents. It found a significant association between current, doctor-
diagnosed asthma and gas cooking in the homes of children be-
tween 5 and 8 years of age, controlling for age, race, sex, parental
education, environmental tobacco smoke (ETS), and other factors
(Dekker et al., 1991~. The adjusted odds ratio for gas cooking was
1.95 (95°/O CI 1.41-2.68) when 634 subjects with asthma were com-
pared to 9,207 with neither asthma, chest symptoms, nor other
respiratory diseases. However, the authors cautioned against
over-interpretation given the small number of asthma cases ex-
posed to gas cooking (N = 60 out of 634 total asthma cases). Asso-
ciations were also reported with ETS, living in a damp home, and
use of a humidifier. These factors, but not gas cooking, were also
associated with reports of wheezing. A second, similar study in
South Australia analyzed data from 14,124 families with a child
aged 4.25 to 5 years of age (Volkmer et al., 1995~. Gas versus elec-
tric stove use was associated with slightly increased prevalence
of asthma (OR = 1.24, 95°/O CI 1.07-1.42) and wheezing in the pre-
ceding 12 months (OR = 1.16, 95°/O CI 1.01-1.32~. The cross-sec-
tional associations found in these two surveys suggest the possi-
bility of small impacts of NO2 on asthma risk; however,
prospective cohort studies would be needed to rigorously test this
hypothesis.
Respiratory symptoms that are associated with asthma, such
as coughing, wheezing, and shortness of breath, have been stud-
ied in relation to gas stove usage and/or NO2 measurements in a
large number of cross-sectional surveys, longitudinal pane] stud-
ies, and a more limited number of prospective cohort studies.
Symptom outcomes have also been analyzed in one chamber ex-
posure study.
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INDOOR CHEMICAL EXPOSURES
229
Cross-sectional surveys assess association between symptoms
and measures of exposure collected simultaneously by question-
naires in general population samples, usually controlling for
covariates with known or suspected effects on symptoms, such as
ETS, home dampness, allergies, and so forth. Although results
have been mixed, the accumulating evidence supports the exist-
ence of small associations between respiratory symptoms and gas
appliance use. At least ten survey studies have reported signifi-
cant associations between symptoms and gas stove exposure in
adults and/or children (Dodge, 1982; Garrett et al., 1998; larvis et
al., 1996, 1998; ledrychowski et al., 1995; Koo et al., 1990; Melia et
al., 1977; Viegi et al., 1991, 1992; Volkmer et al., 1995~. For example,
in a survey of 1,159 men and women in England, larvis et al.
(1996) detected significant associations for women only between
symptoms in the past 12 months and the use of gas appliances,
adjusting for covariates. The adjusted odds ratios were 2.07 (95°/O
CI 1.41-3.05) for wheezing, 2.32 (95°/O CI 1.25-4.34) for waking
with shortness of breath, and 2.60 (95°/O CI 1.20-5.65) for asthma
attacks. Other cross-sectional survey studies have reported no as-
sociations between respiratory symptoms and gas appliances
(Braun-Fahriander et al., 1992; Dekker et al., 1991; Dijkstra et al.,
1990; Hosein et al., 1989~. There are no obvious differences be-
tween the two groups of studies that would explain the differ-
ences in results.
Several of the cross-sectional studies mentioned above have
assessed exposure using actual NO2 measurements, as well as the
more common questionnaire-based assessments of gas appliance
usage (Brunekreef et al., 1990; Garrett et al., 1998~. Interestingly,
such studies have generally found no analytical advantage to the
actual NO2 measurements. This counterintuitive finding may
have several explanations, including non-representativeness of
NO2 measurement times or locations, and/or that NO2 per se is
not the causal agent responsible for gas stove associations with
symptoms.
In a prospective cohort study, Neas et al. (1991) followed res-
piratory symptoms over a 12-month period in 1,567 white chil-
dren aged 7-11 living in six U.S. cities. Indoor home NO2 mea-
surements were collected over two weeks in the winter and in the
summer. Incident symptoms were analyzed in relation to mean
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230
CLEARING THE AIR
NO2 levels. A 15 ppb increase in average household NO2 concen-
trations was associated with increased cumulative incidence of
any of several lower respiratory symptoms (OR = 1.4,95% CI 1.1-
1.7~. The effect was larger for girls than boys. Two 1999 studies of
asthmatic children, available only in abstract form when this re-
port was completed, appear to generally support these findings
(Kattan, 1999; Smith et al., 1999~.
Longitudinal pane] studies and experimental chamber stud-
ies assess the acute relationship between brief (episodic) NO2 ex-
posures and respiratory symptoms. These studies have not pro-
vided strong evidence for acute effects on symptoms at relevant
indoor concentrations. Chamber studies involving one- to three-
hour exposures to 50-1,500 ppb NO2 did not detect effects on res-
piratory symptoms among normal or asthmatic subjects (Salome
et al., 1996; Utell et al., 1991~. In a pane! study involving daily
recording of symptoms and gas stove use among 164 asthmatic
adults over the winter months in Denver, Colorado, Ostro et al.
(1994) reported statistically significant associations between a va-
riety of respiratory symptoms and stove use. However, interpre-
tation of these results as a causal effect of gas stove emissions
(e.g., NO2) is hampered by questions of biologic plausibility as
well as concerns about potential reporting bias. One 1999 abstract
suggests acute effects of NO2 on the severity of symptoms associ-
ated with respiratory syncytial virus (RSV) infections (Chauhan
et al., 1999), and an environmental chamber study concluded that
NO2 exposure increases the susceptibility of airway epithelial cells
to injury from respiratory viruses (Boscia et al., 1999~.
Experimental chamber studies have noted increases in airway
responsiveness to carbocho! or methacholine following brief,
high-level (1,500 or 2,000 ppb) NO2 exposures in normal subjects
(Frampton et al., 1991; Mohsenin, 1988; Utell et al., 1991) expo-
sure levels that have not typically elicited direct effects on Jung
function. Studies in asthmatics report enhanced airway responses
to histamine or methacholine challenges at concentrations as low
as 500-600 ppb, suggesting that the airways of asthmatics, already
more responsive to nonspecific stimuli, are more sensitive to the
enhancing effects of NO2 (Mohsenin, 1987; Salome et al., 1996~.
While the mechanism for these effects remains uncertain,
proinflammatory effects of NO2 (Blomberg et al., 1999) may be
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INDOOR CHEMICAL EXPOSURES
231
involved. Although the relevance of these findings to typical in-
door NO2 concentrations encountered by the general public re-
mains unclear, they do raise concerns for persons, such as moth-
ers and infants, who may spend large amounts of time in kitchens
where gas stoves are being used, especially in conjunction with
low rates of home ventilation.
In addition to the enhancement of airway responses to non-
specific stimuli, NO2 exposure at 400 ppb has been shown in ex-
perimental chamber studies to enhance the lung response, mea-
sured by a drop in forced expiratory volume in one second (FIVE ),
to house dust mite aerosol inhalation by asthmatic adults
(Rusznak et al., 1996; Tunnicliffe et al., 1994~. Devalia and col-
leagues (1994) reported that exposure to a combination of SO2
and NO2 in concentrations that could be encountered in heavy
traffic areas produced a statistically significant decrease in the
concentration of allergen required to produce a 20% decrease in
FIVE (PD20FEV~) of adult asthmatics challenged with Dermato-
phagoides pteronyssinus dust mite allergen. Again, no direct effects
of NO2 on Jung function decline were noted in these studies.
Because of the importance of acute respiratory infections as
triggers of asthma symptoms, an effect of NO2 exposure on in-
creased risk of respiratory infections might represent an indirect
mechanism linking NO2 with asthma exacerbations. In the late
1970s, Melia and colleagues reported an increased risk of respira-
tory infections among children living in homes with gas stoves in
a large British cross-sectional survey (Melia et al., 1977, 1985~.
However, other studies have not confirmed this finding (Samet et
al., 1993; Ware et al., 1984~. In a prospective cohort study of in-
fants, no association was found between NO2 exposure or stove
type and the incidence rate or duration of respiratory infections
(Samet et al., 1993~. Samet and colleagues (1987) extensively re-
viewed the historical literature on NO2 and respiratory infections,
concluding that "the findings on NO2 exposure and respiratory
illnesses indicate that the magnitude of the NO2 effect at concen-
trations encountered in most U.S. homes is likely to be small."
Although there is insufficient new evidence to alter this conclu-
sion, it is worth noting that a 1999 longitudinal pane] study re-
ported enhanced severity of RSV infections in association with
high indoor NO2 concentrations (Chauhan et al., 1999~.
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CLEARING THE AIR
Inconsistent associations between gas appliance use or NO2
concentrations and declines in Jung function have been reported
in epidemiologic studies (Brunekreef et al., 1990; Dijkstra et al.,
1990; Dodge, 1982; Fischer et al., 1985; Garrett et al., 1998; Hack-
ney et al., 1992; Hasselblad et al., 1981; Hosein et al., 1989; larvis
et al., 1996, 1998; ledrychowski et al., 1995; Kattan, 1999; Speizer
et al., 1980; Viegi et al., 1991; Ware et al., 1984), with significant
associations reported in less than half of the studies. Where
present, the nature of the lung function associations has not been
consistent across studies, and the possibility of confounding ex
. .
fists In some cases.
As noted earlier, little evidence of acute Jung function impacts
of brief exposure to high concentrations of NO2 has been observed
in experimental chamber studies (Frampton et al., 1991; Hackney
et al., 1992; Mohsenin, 1987, 1988; Salome et al., 1996; Tunnicliffe
et al., 1994; Utell et al., 1991), except for four-hour exposures to
very high concentrations (i.e., 2,000 ppb) (Blomberg et al., 1999~.
The committee concludes that Jung function is not markedly af-
fected either acutely or chronically by NO2 at typical indoor con-
centrations.
Conclusions: Asthma Exacerbation and Development
· There is sufficient evidence of an association between brief
high-level exposures to NO2 and increased airway responses to
both nonspecific chemical irritants and inhaled allergens among
asthmatic subjects. These effects have been observed in human
chamber studies at concentrations (400-700 ppb) that may occur
only in poorly ventilated kitchens with gas appliances in use.
· There is limited or suggestive evidence of an association
between the use of gas appliances and increased risk of respira-
tory symptoms, increased risk of respiratory infections, and to a
lesser extent, decreased lung function. Data supporting this con-
clusion derive from epidemiologic studies.
· There is limited or suggestive evidence of no association
between brief NO2 exposures and acutely decreased Jung func-
tion. This evidence comes from chamber studies of human sub-
jects.
· There is inadequate or insufficient evidence to determine
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INDOOR CHEMICAL EXPOSURES
233
whether or not an association exists between emissions from gas
appliances and asthma development. However, the association
observed between the use of gas appliances and the diagnosis of
childhood asthma in two, large cross-sectional population sur-
veys indicates that this topic should be examined more carefully
in future research. As noted above, few studies have simulta-
neously measured NO2 and associated co-pollutants and it is thus
usually not possible to attribute health effects associated with gas
appliance usage to NO2 or other combustion by-product expo
sures per se.
Evidence and Conclusions:
Exposure Mitigation and Prevention
Indoor NO2 mitigation has received relatively little attention
in the published literature. Samet (1990) notes that general con-
tro! options for pollutants emitted by indoor combustion appli-
ances include source modification (removal, substitution, or emis-
sion reduction), ventilation (exhaust or dilution), or pollutant
removal (filtration or reactivity). Source modification is usually
the most effective approach. For example, that study recom-
mended that "unvented combustion space heaters should not be
used, particularly in cold climates where they may be on for pro-
longed periods." On the other hand, while removal of gas stoves
would in theory represent an effective exposure reduction strat-
egy, it may not be practical or economically feasible in most cases.
Continuous pilot lights add between 10 and 20 ppb of NO2 to
background indoor levels and should be turned off or eliminated
(Samet, 1990~. Kitchen ventilation has the potential to be effective
in reducing the impact of gas appliance emissions. However, ex-
haust hoods should be vented outdoors and must be used consis-
tently while the appliance is on to be effective. Evidence suggests
that only a small fraction of kitchens with gas stoves achieve these
objectives (Fuhibrigge and Weiss, 1997~. For NO2, pollutant re-
moval via air cleaning is not a feasible approach. The committee
did not identify any studies that addressed whether lowering in-
door NO2 levels had an effect on asthma outcomes.
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CLEARING THE AIR
primary indoor residential source of ozone is an appliance called
an ionizer or ozone generator, which is sold as an air freshening
or air cleaning device. The EPA report Ozone Generators That Are
Sold as Air Cleaners (U.S. EPA, 1999) details potential health prob-
lems from ozone exposure associated with the use of these de-
vices. Xerographic copying machines found in offices, schools,
and some other indoor environments also produce ozone.
Time-series epidemiologic studies have demonstrated signifi-
cant associations between daily asthma hospitalizations and/or
emergency room visits and daily outdoor ozone concentrations
(U.S. EPA, 1996~. Although outdoor ozone concentrations usually
exceed indoor levels, it is likely that relevant exposures in these
studies occurred predominantly indoors. Other studies indicate
that higher ozone levels cause coughing and shortness of breath
in asthmatics and nonasthmatics, and exacerbation of symptoms
in asthmatics (Bielory and Deener, 1998~. Peden and colleagues'
(19951 stub of 11 asthmatics who were allergic to dust mites
~ , ~
(Dermatophagoidesfarinae) found that ozone exposure had both a
priming effect on allergen-induced responses and an intrinsic in-
flammatory action in the nasal airways. A mixture of (+~-oc-pinene
and ozone yielded reaction products including formaldehyde and
induced strong airway irritation in male mice (Wolkoff et al.,
1999~. The authors determined that after accounting for sensitiv-
ity differences between mice and humans, the measured concen-
trations of formaldehyde and ozone in the reaction mixture were
"not unrealistic for indoor settings." There are no data suggesting
that ozone exposure is associated with the development of
asthma.
Chapter 10 contains an extended discussion of the impact of
ventilation on the indoor concentrations of gaseous pollutants.
As noted in that chapter, ozone is also removed from indoor air at
a significant rate by deposition on or reaction with indoor sur-
faces. Rates of removal depend on the intensity of indoor air mo-
tion and other factors.
Particulates {Nonbiologic Particles}
"Particulate matter" (PM) is the name given to solid and liq-
uid particles suspended in the air. Aside from outdoor infiltrate,
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INDOOR CHEMICAL EXPOSURES
253
the primary indoor sources of nonbiologic PM in indoor environ-
ments are combustion sources and tobacco smoke (which is ad-
dressed separately and in greater detail in Chapter 7~. Unvented
or poorly vented coal stoves and wood-burning stoves and fire-
places where present may be significant sources of indoor PM.
For spaces without significant sources, indoors is a protective en-
vironment.
Studies consistently report an association between exposure
to high outdoor levels of air pollutants, including PM, and ad-
verse respiratory health effects (Koren, 1995~. Evidence suggests
that for fine particles (i.e., those with aerodynamic diameters less
than 2.5 rim), outdoor PM often penetrates readily indoors. The
literature specifically addressing asthma suggests an association
between PM exposure and asthma exacerbation (e.g., Pope and
Dockery, 1992; Roemer et al., 1993; Sheppard et al., 1999~. Ostro
and colleagues (1998) list three classes of possible mechanisms
for this:
1. reflex bronchoconstriction via nonspecific irritant effects;
2. direct toxicity to the airway epithelium and resident im-
mune cells, augmenting preexisting inflammation and airway
hyperresponsiveness; and
3. induction of an inflammatory immune response, either be-
cause the particles themselves are allergenic or by permitting ac-
cess of other allergens to the underlying tissues.
Aside from studies of the health effects of environmental to-
bacco smoke, where PM is part of a more complex exposure, data
have not shown an association between PM and asthma develop-
ment. Ongoing research is addressing this topic, including stud-
ies using animal models.
Limiting or eliminating sources is clearly the most straight-
forward means of addressing indoor PM exposures. Chapter 10
includes a discussion of the use of high-efficiency particulate air
(HEPA) filters in lowering concentrations of indoor particulates.
Sulfur Dioxide
Sulfur dioxide (SO2) is one of a family of gases called sulfur
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254
CLEARING THE AIR
oxides (SOx) formed when fuel containing sulfur primarily coal
and of] is burned. Outdoor levels of SO2 have diminished sig-
nificantly since the 1960s in the United States due to the elimina-
tion of high-sulfur coal and of! as primary fuels for power genera-
tion and heating. Indoor sources include fossil fuel appliances and
furnaces. However, these are not significant in most indoor envi-
ronments, where outdoor infiltrate is the primary source.
Sensitive asthmatics breathing at elevated ventilation rates
(during exercise, for example) experience bronchoconstriction
and other airway responses in reaction to brief exposure to SO2.
These effects, which are relatively transitory, exhibit a dose-re-
sponse relationship. Sulfur dioxide may both have a direct irri-
tant effect and, possibly in combination with other air pollutants,
potentiate the effect of antigens (Bielory and Deener, 1998~. Expo-
sure to a combination of SO2 and NO2 in concentrations that could
be encountered in heavy-traffic areas produced a statistically sig-
nificant decrease in the concentration of dust mite allergen re-
quired to produce a 20% decrease in FEVER of adult asthmatics
(Devalia et al., 1994~. There is no established mechanism for the
effects of SO2 on airways, although candidate mechanisms have
been proposed (Peden, 1997~. The committee did not identify any
studies addressing indoor exposures to SO2 and asthma develop-
ment.
The exposure mitigation and prevention strategies discussed
above for indoor sources of NO2 are also relevant for SO2.
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Representative terms from entire chapter:
respiratory symptoms
