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Annual Review of Environment and Resources

Indoor Air Pollution and
Health: Bridging Perspectives
from Developing and
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Developed Countries
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Ajay Pillarisetti,1 Wenlu Ye,1

and Sourangsu Chowdhury2
1
Division of Environmental Health Sciences, School of Public Health, University of California,
Berkeley, California, USA; email: [email protected], [email protected]
2
Center for International Climate Research (CICERO), Oslo, Norway;
email: [email protected]

Annu. Rev. Environ. Resour. 2022. 47:26.1–26.33 Keywords

The Annual Review of Environment and Resources is
household air pollution, biomass, exposure assessment, particulate matter,
online at environ.annualreviews.org
indoor air quality
https://doi.org/10.1146/annurev-environ-012220-
010602 Abstract
Copyright © 2022 by Annual Reviews.
Much of the global population spends most of their time indoors; however,
All rights reserved
air pollution measurement, a proxy of exposure, occurs primarily outdoors.
This fundamental disconnect between where the people are and where the
measurements are made likely leads to misestimation of the true burden of
air pollution on human health, which is already substantial, with exposure
leading to approximately 6.7 million deaths yearly. In this review, we de-
scribe the two disparate but linked fields commonly referred to as indoor
air pollution and household air pollution. Both fields focus on the measure-
ment and characterization of exposures and subsequent health effects that
occur primarily in the indoor environment. The former tends to focus on
issues in the developed world, whereas the latter focuses on issues in low-
and middle-income countries reliant on solid fuels, like wood, dung, coal,
and crop residues, for basic household energy needs. Both lead to substantial
exposures to air pollutants that are damaging to human health. We describe
and contrast both contexts and provide potential topics for conversation be-
tween the disciplines.

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Contents
INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.2
AIR POLLUTION AND THE GLOBAL BURDEN OF DISEASE . . . . . . . . . . . . . . . 26.4
Outcomes Associated With Air Pollution Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5
Exposure Estimation in the Global Burden of Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.5
Counterfactual Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.6
Concentration- and/or Exposure-Response Functions . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.6
Non–Household Air Pollution Indoor Air Pollution in the Global Burden
of Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.7
POLLUTANTS OF CONCERN . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.7
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INDOOR AIR POLLUTION IN THE DEVELOPED WORLD . . . . . . . . . . . . . . . . . 26.10

Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.10
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Assessing Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.10

Health Impacts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.12
Mitigating Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.13
HOUSEHOLD AIR POLLUTION PRIMARILY IN THE DEVELOPING
WORLD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.15
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.15
Inside Out . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.16
Reducing the Impact of Household Air Pollution Exposures: Shifting Paradigms . . 26.17
INDOOR AND HOUSEHOLD AIR POLLUTION: DISTINCTIONS
AND DISCOURSE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.20
Cooking With Gas: A Strong Source in High-Income Countries, A Strong
Solution for Solid Fuel–Using Households . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .26.20
Household Air Pollution in the Burden of Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.20
“Modern” Indoor Air Pollution Concerns in Countries With High Burdens
of Household Air Pollution . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.21
The Place’s the Thing! . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.21
Utilization of Low(er)-Cost Sensors for Air Pollution Assessment . . . . . . . . . . . . . . . . 26.21
CONCLUSION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26.21

Exposure:
the interface between INTRODUCTION
a pollutant
Exposure to air pollution is estimated by the Global Burden of Disease (GBD) effort1 to result
concentration in the
environment and an in approximately 6.67 million excess deaths per year (1) from a range of outcomes, including
individual; a function cardiovascular and respiratory diseases, diabetes, and cancers, among others. Much of this burden
of duration of contact is attributable to ambient exposure to particulate pollution (4.1 million annual deaths, ∼61% of
between people and the total burden) and ambient ozone (O3 ) exposure (0.37 million, 9% of the total). The levels
pollutants
of exposure to ambient air pollution (AAP) experienced by individuals and populations are often
Global Burden of
Disease (GBD):
quantifies morbidity 1 The Institute for Health Metrics and Evaluation at the University of Washington organizes the GBD effort.
and mortality from a
range of diseases and More than 7,000 researchers in over 156 countries and territories collect and analyze the data. The data
risk factors for estimate premature deaths and lost disability-adjust life years (DALYs) from 350 diseases and injuries in 195
ill-health countries, by age and sex, from 1990 to the present. For more details on the GBD effort, see https://www.

·.•�-
healthdata.org/gbd/about.

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estimated by combining ground monitoring data, satellite-based estimates of pollution levels, and
modeled concentrations from chemical transport models (2).
Disability-adjusted
For wealthy countries, however, these estimates rarely take into account the location in which life year (DALY):
many people spend most of their time—the indoor environment (3). They also tend to focus on a a combined metric of
narrow range of pollutants for which there is strong epidemiological evidence of health impacts— morbidity and
a justifiable approach, but one that presents perhaps an incomplete picture of the true burden of mortality; one DALY
represents the loss of
air pollution. In largely ignoring indoor environments, these estimates also ignore an arguably
one year of full,
fundamental tenant of exposure science: to measure where the people are (4). healthy life
Of the 6.67 million annual deaths attributable to air pollution, 2.3 million are estimated to arise
Ambient air
from direct exposure to household air pollution (HAP) generated during the combustion of solid
pollution (AAP):
fuels, typically for cooking, and largely in low- and middle-income countries (LMICs). Solid fuels contaminants in
are often burned indoors, but escape into the outdoor environment, thus contributing to AAP. outdoor air arising
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In some contexts, it is expected that individuals in LMICs are exposed to both solid fuel–related from a variety of
HAP and other sources of indoor air pollution (IAP)—in addition to their ambient exposures. sources—
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transportation,
On one hand, the location of exposure does not matter; reducing the combined or total expo-
industry, power
sure from all sources and locations is the overarching concern of policy and control measures. On generation, etc.
the other hand, and from a health and mitigation standpoint, it is vital to know what causes emis-
Concentration:
sions and exposures—and, critically, where these exposures occur—so that action can be taken to
the mass of a pollutant
protect health and the environment. per volume air,
Estimates of where people spend time—their so-called time-activity budgets—have been made typically measured in a
for the developed world over the past three decades (3, 5, 6). In these studies, individuals report microenvironment
spending the majority of their time—between 80 and 90% of a typical day—indoors, whether at Household air
home, at work, or in transit. Less data are readily available in LMICs (7–9), although they indicate pollution (HAP):
a similar trend, with the majority of time spent indoors. Regardless, given the substantial time arises from the
spent inside daily by a large fraction of the global population, investigation and characterization combustion of solid
fuels, like wood, dung,
of indoor air pollutants and environment are essential to (1) accurately understand and (2) mitigate
coal, and crop residues,
exposures. for cooking and other
In a 2016 review of indoor air quality (IAQ) and its impacts on humans, Kwok Wai Tham (10) end uses
suggested four explanations for the relative lack of focus on the indoor environment, which we
Solid fuels: wood,
expand upon here. First, large episodes—such as the Donora event in the US (11), the London dung, grass, coal,
Smog (12), and high air pollution occurrences in Delhi (13), Los Angeles, and Beijing (14)— crop-resides, etc.; also
received large attention and response due to the intensity of pollution levels and the magnitude referred to as biomass
of impacts on health. During some of these events, entire populations had elevated exposures. fuels
Such events are seemingly not as newsworthy for indoor pollutants, despite, at least for the case Emissions: the rate of
of solid fuel use, equally high concentrations being regularly experienced by a large fraction of release of pollutants
the global population. Second, data collection frequency and availability vary widely for outdoor into the environment,
typically per kilogram
and indoor environments; significantly more data are available for the former, especially at the
fuel or per unit time
population level. Recent advances in air pollution sensor technology, although useful in indoor
environments, have widely been applied to outdoor environments to date. The same data discrep-
ancy applies to health data; population-level associations between IAP and health are less well
characterized, in part because detailed exposure data are hard to obtain. Third, and primarily in
the developed world, there has been a reduction in magnitude and a change in the species emitted
and experienced indoors. Emerging concerns in these context are a result of new construction
materials and techniques, indoor use of chemicals, and the ways in which buildings are ventilated,
used, and maintained. Fourth, understanding IAQ as a substantial driver of total exposure is rela-
tively new (15, 16). Finally, we note that the issue of HAP from solid fuels has, until recently, been
under-recognized—a trend that shows signs of reversing, from the standpoint of both research

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and policies to mitigate exposure. This reversal has been slow, however, with the absolute number
of individuals exposed to HAP remaining relatively static over time, despite the substantial and
Indoor air
quality/indoor air disproportionate elevation in exposure and the substantial energy access and equity issues.
pollution (IAQ/IAP): In this review, we focus on describing IAP and its health impacts. We distinguish between
air quality within the HAP in developing countries and IAP in developed countries, a division mirrored in the scientific
built environment, literature on IAQ, science, pollution, and chemistry. The term household air pollution was coined
including in homes,
(17) to draw a distinction from the broader indoor air quality/indoor air pollution (IAQ/IAP)
businesses, workplaces,
vehicle cabins, and literature and as an acknowledgment that much household combustion of solid fuels happens
other places where in and around the home, not just indoors; that much of the byproducts of this combustion
people spend time ends up outdoors, impacting ambient air quality; and that chimneys alone—which may reduce
PM2.5 : particulate concentrations of indoor air pollutants—do not necessarily resolve the fundamental problem of
matter with an unclean, inefficient combustion.
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aerodynamic diameter The contrast between these contexts can be stark. The use of solid fuels as a source of house-
of 2.5 µm or less hold energy impacts approximately 3.8 billion people, primarily in LMICs, and results in high
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exposures to HAP, typically assessed by measurement of particulate matter with an aerodynamic

diameter of 2.5 µm or less (PM2.5 ) and/or carbon monoxide (CO). Exposure to HAP results in
between 2 and 4 million deaths per year. HAP is often experienced in the home, but exposure also
occurs outside of the home (from emissions that escape the indoor environment or from outdoor
cooking) and downwind of original emissions.
Non-HAP IAP arises from a variety of sources and likely impacts nearly everyone on the planet.
In many regions of the developed and developing world, indoor measurements of fine particulates
reveal high infiltration of ambient pollution (18–20). Within the built environment—an area often
perceived as clean—numerous factors contribute to degraded IAQ. Exposure sources in these
contexts are manifold and include, for example, cooking (with clean or unclean fuels); cleaning;
off-gassing from furniture, carpets, and electronic equipment; chemical product use and storage
indoors; and chemical reactions (21–23). The concentration of indoor species and exposure to
them is influenced by ventilation, other building characteristics, and occupant behaviors. The
study of the impacts of these indoor sources on human health and productivity is an ongoing area
of concern, with most work being performed in the United States and Europe.
This review summarizes IAP science, with a focus on pollution of indoor origin and its impacts
on health. It begins with an exploration and description of the current burden of disease from air
pollution exposure and continues with a discussion of measurement techniques and estimates of
emissions, exposures, and health effects. We discuss key measurement and mitigation strategies
for each context described above, noting areas of commonality and divergence. Additionally, we
attempt to identify areas of common interest to both types of IAP; research in each subfield has
diverged in recent years. We note that the difference in these types of pollution is not necessarily
easily reconcilable, but that the distinct disciplines likely could benefit from approaches taken by
the other and by continued dialogue between experts.

AIR POLLUTION AND THE GLOBAL BURDEN OF DISEASE

In the introduction, we stated the somewhat shockingly large numbers associated with exposure
to air pollution from both ambient and household sources. These burden of disease estimates,
which are generated yearly, have varied substantially in recent years and warrant description to
understand what they do and do not include and how they were derived (see the sidebar titled The
Global Burden of Disease and Comparative Risk Assessment). For the purposes of this discussion,
we focus primarily on particulate pollution, which dominates the air pollution–related burden of
disease.

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THE GLOBAL BURDEN OF DISEASE AND COMPARATIVE RISK ASSESSMENT

The GBD exercises, which seek to quantify the extent and impact of disease and injuries and associated risk fac-
tors for every country in the world, began in the 1990s. Risk factors, in this context, refer to particular activities,
behaviors, or exposures associated with disease and death and range from smoking cigarettes to unsafe sex to high
salt diets. Since the inception of GBD activities, the effort has evolved substantially, and now results in estimates of
disease burden yearly in terms of morbidity and mortality for 369 diseases and injuries and 87 risk factors, for two
sexes, and for 204 countries and territories (28, 29). The activity is housed at the Institute of Health Metrics and
Evaluation (IHME) at the University of Washington.
Since 2004, AAP burdens have been estimated for exposure to particulate air pollution and ozone and HAP
burdens have been estimated for exposure to particulates. Methods for estimating the burden have evolved sub-
stantially in the intervening years, leading to changes in burden estimates that may be attributable to changes in
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actual exposures, changes in GBD estimation methodology, addition of associated health endpoints, and/or better
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and more resolved exposure assessment.

There are five fundamental inputs to burden of disease calculations (24, 25): (a) the diseases or
outcomes for which there is sufficient and strong evidence to support association with a specific
risk factor or exposure; (b) background rates, typically at the country level, for each of these out-
comes; (c) time- and location-resolved exposures; (d) selection of a counterfactual level, that is, a
health-based “ideal” exposure; and (e) functions relating exposure and disease, known as exposure-
response or concentration-response functions.

Outcomes Associated With Air Pollution Exposure

In GBD, any relationships between exposure and disease that meet the criteria of convincing or
probable evidence, as defined by the World Cancer Research Fund grading system (26), are eligible
for inclusion. Convincing evidence includes multiple epidemiological studies [prospective studies
or randomized controlled trials (RCTs)] showing consistent, biologically plausible associations
and little or no contrary findings. Probable evidence is based on epidemiological studies that are
consistent and biologically plausible, but may be of insufficient duration, number, or sample size
and/or have issues with incomplete follow-up.
In the 2019 GBD, PM2.5 pollution exposure was associated with numerous health endpoints,
including lower respiratory infection in children and adults and five additional diseases in adults:
chronic obstructive pulmonary disease (COPD), ischemic heart disease, lung cancer, stroke, and
type 2 diabetes mellitus (T2DM). HAP is also associated with cataracts. All particulate air pol-
lution, regardless of source, is associated with low birthweight and gestational age (BWGA; a
substantial risk factor in its own right), which is in turn associated with 11 health endpoints: diar-
rheal diseases, lower respiratory infections, upper respiratory infections, otitis media, meningitis,
encephalitis, neonatal preterm birth, neonatal encephalopathy, neonatal sepsis, hemolytic disease
and other neonatal disorders. BWGA and T2DM were added to the burden of disease attributable
to particulate air pollution exposure in recent assessments, as evidence for these linkages improved.

Exposure Estimation in the Global Burden of Disease

Exposure estimation for household and AAP is a complex process involving fusing multiple scales
of data to derive global estimates that result in highly spatially and temporally resolved estimates
for nearly all populated points on the planet. For AAP, satellite-derived aerosol estimates,

·.•�-
ground-based measurements, chemical transport models, emissions inventories, and population

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and land-use data are utilized (2, 27). For HAP, the proportion of individuals using solid cooking
fuels is estimated; this is then mapped to actual exposures for men, women, and children based
Counterfactual
exposure: in the on existing ratios between measurements on respective groups and statistical models relating
context of GBD, an exposure levels with the type of fuel, socioeconomic indicators, and the like. Details on techniques
exposure that allows an used in GBD estimation of time- and location-resolved exposures and health impacts are available
ideal health state in the appendices to the recent GBD risk assessment papers (28, 29).
Exposure-response
functions: functions Counterfactual Exposures
that relate exposure
Counterfactual exposures to particulate air pollution in the GBD are based on theoretical min-
with disease; also
referred to as imum risk exposure levels (TMRELs). TMRELs are exposures that present a minimal risk to
exposure-response exposed populations; using these values allows estimation of a hypothetical population (nearly)
curves free of disease.
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For some exposures, like active smoking, a TMREL of 0 would be reasonable; for others, like
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air pollution, a minimum level is set that (a) acknowledges some background exposure and (b) rep-
resents current scientific understanding of risk at very low levels. For particulate air pollution, this
level is a uniform distribution between the minimum and fifth percentile of observed concentra-
tions (between 2.4 and 5.9 µg/m3 ). These values are the mean of the minimum and fifth percentiles
of exposure distributions from outdoor air pollution cohort studies conducted in North America.

Concentration- and/or Exposure-Response Functions

The risk of each disease at a given pollution exposure is estimated using exposure-response func-
tions. In the most recent version of the GBD, IHME transitioned from integrated exposure-
response (IER) curves (30) to meta regression-Bayesian, regularized, trimmed (MR-BRT) splines
(31). The IERs, which were used between 2010 and 2019, are referred to as integrated because
they included data from multiple sources of particulate air pollution, namely AAP, HAP, second-
hand smoke, and, anchoring the curves on the high end of the exposure range, active or mainline
tobacco smoke.
The MR-BRTs leverage recent measurements around the world, primarily from Chinese co-
hort epidemiological studies that provide sufficient range on the high end of exposures to drop
active tobacco smoking from the list of sources used to fit the curves. This process is also simplified;
it now uses shape-constrained splines with three knots instead of a power function. Finally, the
counterfactual used by GBD is not built into the model-fitting process and thus can be altered as
needed. Both the IERs and the MR-BRTs assume equitoxicity of particles across source categories.
Figure 1 depicts the MR-BRT curves for five outcomes (32). These curves are supralinear;
that is, the marginal benefit of an exposure reduction at higher levels is relatively small, as the
curves are flat. Incremental decreases in PM exposures at the low end of the curve provide the
most substantial risk reductions.
Relative risks derived from exposure-response functions are used to estimate the population
attributable fraction for each disease, which is the fraction of the background disease rate that is
attributable to PM2.5 pollution (rather than, say, high cholesterol). The difference between the
disease attributable to PM2.5 at measured versus counterfactual exposure levels is the modeled
estimate of the burden of disease.
To avoid double counting of disease burdens for individuals exposed to both AAP and HAP,
GBD estimates the burden of exposure to ambient PM2.5 and estimates the additional health bur-
den due to cooking with solid fuels. Put another way, the total exposure (ambient plus household)
is used to estimate burden; the total burden is then apportioned into ambient and household com-
ponents based on the fraction of the exposure coming from each source. Contributions of HAP

·.•�-
to AAP (discussed below) are attributed to the AAP burden.

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7.5 a
5.0
2.5

0 250 500 750 1,000

Relative risk

3.0
b
2.5

2.0
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1.5
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1.0
0 50 100 150
PM2.5 exposure (µg/m3)

COPD Lower respiratory infection Lung cancer Preterm birth Type 2 diabetes mellitus

Figure 1
MR-BRT curves for PM2.5 exposure. Panel a depicts the curves across an average annual exposure range spanning from 0 to
1,000 µg/m3 ; panel b zooms in on 0 to 150 µg/m3 . The colored lines represent individual diseases associated with PM2.5 exposure; the
corresponding shading represents 95% uncertainty bounds. Abbreviations: MR-BRT, meta regression-Bayesian, regularized, trimmed;
COPD, chronic obstructive pulmonary disease; PM2.5 , particulate matter with an aerodynamic diameter of 2.5 µm or less.

Non–Household Air Pollution Indoor Air Pollution in the Global Burden

of Disease
Given the elements required for inclusion of specific exposure-outcome pairs into the GBD, it is
perhaps not surprising that indoor air pollutants beyond PM2.5 exposures arising from HAP are
not currently included in burden estimates. A recent review of IAQ studies in the developed world
has pointed out that, even for these relatively well-studied countries, limited measurements exist
for a variety of species, with methodological inconsistencies between studies (33). Associations
with health effects are perhaps more robust, but without more comprehensive understanding of
emissions and exposures in indoor environments—and their spatial and temporal distribution—
estimates in the style of the burden of disease are likely to remain difficult.
This has not stopped some attempts at quantifying the burden of IAQ in the developed world
(34–36), however. These methodologies have not yet been applied globally to the best of our
knowledge and appear somewhat inconsistent with the methodologies employed by GBD. The
implication of this omission, given the paucity of global exposure data, is likely an underestimate of
the impact of the indoor environment on health globally above that of HAP. Given global trends
of rapid urbanization, changes in building practices, and availability of chemicals that may degrade
IAQ, it is possible that households whose exposure is dominated by smoke arising from solid fuel
use for cooking also experience a burden from these other, more modern indoor air concerns.

POLLUTANTS OF CONCERN
IAQ is complex and driven by numerous pollutants from a range of sources and pathways
(Figure 2), in which chemical, biological, and physical contaminants eventually become a portion

·.•�-
of the total indoor environment (10, 37). IAQ is influenced by three major factors: (a) outdoor

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RUR AL SET TINGS URBAN S ET TINGS

Power and industry

Crop burning

TR AFFIC
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Off-gassing and
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chemistry from
construction
materials, carpets,
cleaning supplies,
Indoor and outdoor cooking stored chemicals,
plants, mold and
mildew, others

OTHER INDOOR SOURCES

BIOMASS KEROSENE WASTE GAS INDOOR

SMOKING SMOKING
STOVE LAMP BURNING COOKING GAS APPLIANCES CHEMISTRY

Figure 2
Common sources of indoor air pollution in rural (left) and urban (right) settings (37, 111). Sources do not vary dramatically between
rural and urban contexts, but the magnitudes of emissions are different; for instance, cooking emissions in urban settings tend to be
much lower than in rural settings, where biomass combustion dominates. Similarly, the influence of traffic on exposure exists in both
settings, but the magnitude of exposure may vary due to individuals’ proximity to and frequency of contact with traffic and traffic-
related air pollution.

air quality, (b) indoor human activities (like cooking, cleaning, or smoking), and (c) building and
construction materials (38–40).
Important and frequently investigated indoor air pollutants include particulate matter (PM)
(including asbestos and fibers), volatile inorganic compounds (CO, CO2 , NOx , O3 ), volatile or-
ganic compounds (VOCs; benzene, toluene, ethylbenzene, xylenes, naphthalene, formaldehyde,
trichloroethylene, a-pinene, limonene), and biological pollutants (allergens, fungi, bacteria, and
viruses). We discuss each briefly below. References 23, 41–43 provide additional detail on the pol-
lutants, their interactions, and their levels.
PM is a complex mixture of solid particles and liquid droplets found in the air. These particles
come in many sizes and shapes and can be made up of hundreds of different chemicals (44). Two
size classes have been typically measured as part of indoor and outdoor monitoring campaigns:
PM10 (PM with an aerodynamic diameter of 10 µm or less) and PM2.5 . Indoor PM may come
from outdoor sources (e.g., construction sites, roads, fields, smokestacks, or fires), indoor combus-
tion activities (e.g., the use of stoves, fireplaces, ovens, heaters, and chimneys), and environmental
tobacco smoke (ETS). Indoor PM may also form indoors through the reaction between O3 and

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some VOCs (e.g., terpenes). PM can also undergo numerous transformations indoors, including

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coagulation, vapor deposition onto smaller aerosols, and evaporation of VOCs aerosols into the
gas phase. Similarly, PM can be removed from the indoor environment by deposition, intercep-
tion, settling, and exfiltration.
Fibers, such as fiberglass and asbestos, are sometimes included in this group (37). Asbestos
is a mineral fiber that occurs naturally in rock and soil and has been widely used in a variety of
materials and products (e.g., building material, friction products, heat-resistant fabrics, packaging,
insulation, gaskets, and coatings) and as a fire-retardant (45).
CO is an odorless, colorless, toxic gas emitted from incomplete combustion processes. Sources
of indoor CO emissions include ETS; unvented cooking and heating devices; leaking chimney
and furnaces; back drafting or incomplete combustion in furnaces, gas water heaters, wood stoves,
and fireplaces; generators and other gasoline-powered equipment; vehicle exhaust from attached
garages, nearby roads, or parking areas; poorly adjusted or maintained combustion devices; and
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improperly sized, blocked, disconnected, or leaky flues (22, 40, 46, 47).
Nitrogen oxides (NOx ) are a mixture of gases that are composed of nitrogen and oxygen. Two
Annu. Rev. Environ. Resour. 2022.47. Downloaded from www.annualreviews.org

of the major and most toxicologically significant NOx are nitrogen monoxide (NO) and nitrogen
dioxide (NO2 ); both are associated with combustion sources. Indoor NOx levels can be strongly
influenced by infiltration from outdoor air, in particular when indoor spaces are a short distance
from roadways or when high-density industrial areas are nearby. Combustion appliances (e.g.,
open-flame stoves, ovens, heaters), burning of tobacco, and fireplaces can also contribute to NOx
emissions (37, 40, 47).
O3 is a powerful oxidizing agent mainly produced by photochemical reactions of O2 , NOx , and
VOCs in the atmosphere. The main sources of indoor O3 come from infiltration of O3 -containing
outdoor air and the operation of some electrical devices (e.g., photocopiers), disinfecting devices,
air-purifying devices, and other office electronics (40, 48–51).
VOCs are organic chemical compounds with a low boiling point (ranging from 50/100°C to
240/260°C) that can evaporate under normal indoor temperatures and pressures (52, 53). Indoor
VOCs are often generated from building material; the number and types of VOCs identified in-
doors are growing as new materials are being used in construction and interior design (37, 40).
VOCs can also be identified from human activities (e.g., cooking, smoking, the use of cleaning
and personal care products, and the burning of scented candles and incense), indoor chemical re-
actions, and the penetration of outdoor air through infiltration and ventilation systems (54–58).
Typical VOCs found indoors include benzene, toluene, ethylbenzene, and xylenes, naphthalene,
formaldehyde, trichloroethylene, limonene, and alpha-pinene (37, 59), among others.
ETS or secondhand smoke is composed of a mixture of both sidestream smoke, the smoke re-
leased from burning the end of a cigarette, and exhaled mainstream smoke, the smoke exhaled by
the smoker (60). Burning a cigarette results in more than 4,000 measurable chemical compounds;
many are toxic and carcinogenic (61, 62). Sidestream smoke is many times more toxic than main-
stream smoke (60, 63). It has a similar chemical composition but tends to linger in the environment
for 1.5–2 hours. It thus may increase both exposure duration and potential penetration into lung
tissue and body cells (60, 63). Thirdhand smoke—smoke that remains in the environment long
after the cigarette has been extinguished—has also been identified as a source of potential expo-
sure (64, 65). ETS exposure is further complicated by the smoking habits and frequencies of active
smokers sharing the space.
Radon is a naturally occurring gas that originates from uranium ores in the ground. Radon
enters indoors primarily through the entry of radon-bearing soil gas, through basements and
floors and may build up to high concentrations in the air (42). Radon is radioactive and decays
in the air, resulting in other radioactive components that can attach to tiny dust particles, be

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inhaled, and adhere to the lining of lungs, eventually leading to lung cancer (42). Effects of radon

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exposure are cumulative, and radon is estimated to cause between 83,000 (29) and 92,000 (66)
deaths worldwide yearly.
Biological pollutants are or were living organisms. They promote poor IAQ and can travel
through the air and are often invisible (67). Common indoor biological pollutants include animal
dander (i.e., minute scales from hair, feathers, or skin), dust mite and cockroach parts, infectious
agents (i.e., bacteria or viruses), and pollen.

INDOOR AIR POLLUTION IN THE DEVELOPED WORLD

Exposure
Exposure to IAP has important health implications; in developed countries, adults spend 80%–
90% of their time indoors (5, 37, 68, 69); an additional 6% of daily time may be spent inside
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for transportation (38). Characterizing exposure to IAP is challenging due to the diversity and
variability of air pollutants in the indoor environment, as well as the complex physical, chemi-
Annu. Rev. Environ. Resour. 2022.47. Downloaded from www.annualreviews.org

cal, social, and behavioral factors and processes involved in determining IAQ. Table 1 provides
indoor concentrations and/or exposures to common pollutants in developed countries from se-
lected studies, as well as United States Environmental Protection Agency (US EPA) or World
Health Organization (WHO) standards.
The average exposure in an indoor space is directly related to room size and ventilation rate
(60), among other factors. Season and outdoor temperature impact physiochemical processes, ven-
tilation, and pollution sources (33). For example, during the winter, indoor concentrations of NO2
can be twice the outdoor levels due to the residential use of gas-fueled heating appliances and re-
duced natural ventilation (60).
IAP exposures vary across different socioeconomic groups. Women are at a higher risk of VOC
exposure than men because they generally perform more household cleaning tasks and have more
exposure to cleaning products (60). Building characteristics (i.e., building quality, airtightness,
volume, and ventilation) and occupant behavior (i.e., cooking and cleaning) are important deter-
minants of IAQ, and also differ across socioeconomic groups, leading to variations in exposure
(33). A scoping review of exposure to IAP across socioeconomic groups in high-income countries
found significantly higher concentrations of PM, NO2 , and VOCs in households of lower socioe-
conomic status (SES) (33). Conversely, elevated radon levels were observed in households with
higher SES (70, 71). Possible reasons include (a) higher SES households lived in large dwellings
with larger floor areas (72); (b) higher internal temperature increased the pressure gradient and
led to elevated rates of radon-bearing soil-gas entry into the homes (73); and (c) the energy effi-
ciency features (which lower the rates of background air exchange with the outdoors) in higher
SES homes may cause radon to accumulate (74) rather than be ventilated to the outdoors, either
intentionally or through leakage.

Assessing Exposures
Measurement within homes is the most common method to estimate indoor PM, NO2 , radon,
and VOC exposure. Although monitoring devices offer more reliable and objective results than
self-reported data, it can be challenging to determine actual exposure levels given the way that
occupants interact with monitoring instruments (75) and the single exposure route (i.e., inhalation)
being measured. Furthermore, stationary monitors in homes may not reflect the time-activity
patterns of residents and may thus misestimate exposure. In addition, sufficient and representative
sample sizes are hard to achieve when monitoring IAQ, especially for residential buildings, due to
the great variability in building characteristics and occupant behaviors, outdoor pollution levels,

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the high compliance requirement of residents, and associated costs (33, 72, 76, 77).

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Table 1 Indoor concentrations of common pollutants in developed countries

Pollutant Indoor concentration Standards
Particulate matter Kitchen: 25–1,526 µg/m3 Indoor particulate matter (PM) levels have the potential to
with an Bedroom: 13–27 µg/m3 exceed outdoor PM levels and the United States
aerodynamic Office: 10–44 µg/m3 Environmental Protection Agency (USEPA) National
diameter of School: 3–23 µg/m3 Ambient Air Quality Standards (NAAQS). However, less is
2.5 µm or less Shopping center: 74–164 µg/m3 known about the specific impacts of indoor PM on health.a
See References 106, 171–174
Carbon monoxide Average indoor level without gas stove: No standards for CO have been agreed upon for indoor air.
(CO) 0.5–5 ppm The NAAQS for outdoor air are 9 ppm (40,000 mg/m3 ) for
Levels near properly adjusted gas stoves: 8 h and 35 ppm for 1 h.a
5–15 ppm World Health Organization (WHO) guidelines relevant to
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Levels near poorly adjusted stoves: typical indoor exposure are recommended as follows:
>30 ppma 100 mg/m3 for 15 min, 35 mg/m3 for 1 h, 10 mg/m3 for 8 h,
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and 7 mg/m3 for 24 h.b

Nitrogen oxides Home: 5–7 µg/m3 No standards have been agreed upon for NOx in indoor air.
(NOx ) Office: 16–18 µg/m3 The American Society of Heating, Refrigerating and
Shopping center: <30 µg/m3 Air-Conditioning Engineers and the NAAQS list 0.053 ppm
See References 106, 173, and 175 as the average 24 h limit for NO2 in outdoor air.a
A 1 h indoor NO2 guideline of 200 µg/m3 and an annual
average indoor NO2 guideline of 40 µg/m3 are
recommended by WHO.b
Ozone Home: 0.9–21.4 ppb Health Canada recommends a residential maximum exposure
School: 0.9–31 ppb limit of 40 µg/m3 (20 ppb) ozone, based on an averaging
Office: 2.1–8.0 ppb time of 8 h.c
See Reference 176
Benzene Home: 0.7–4.4 µg/m3 No safe level of exposure is recommended.
Office: 1.4–5.5 µg/m3
Shopping center: 2.5–48 µg/m3
See References 106, 175, 177–181
Toluene Home: 3–20 µg/m3 Toluene is not a confirmed carcinogenic substance.
Office: 6–32 µg/m3
Shopping center: 15–164 µg/m3
School: 1.8 µg/m3
See References 106, 173, 175, 177–179, and
181
Ethylbenzene Home: 3–20 µg/m3 The National Institute of Occupational Safety and Health
Office: 6–32 µg/m3 recommended exposure limit is 435 mg/m3 (for an 8- to 10-h
Shopping center: 15–164 µg/m3 time-weighted-average exposure).
School: 1.8 µg/m3
See References 106, 177–179, and 181
Xylenes Home: 3.1 µg/m3 The National Institute of Occupational Safety and Health
Office: 2.2–16 µg/m3 recommended exposure limit is 435 mg/m3 (for an 8- to 10-h
Shopping center: 1.3–74 µg/m3 time-weighted-average exposure).
School: 0.3 µg/m3 Health Canada recommends an indoor environments
See References 106, 173, 175, 177–179 short-term (1 h) exposure limit of 7,000 µg/m3 (1,700 ppb)
and long-term (24 h) exposure limit of 150 µg/m3 (36 ppb).c

(Continued)

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Table 1 (Continued)
Pollutant Indoor concentration Standards
Formaldehyde Home: 7.7–30 µg/m3 No safe level of exposure is recommended by USEPA.a
Office: 8–17 µg/m3 WHO recommends a short-term (30 min) guideline of
School: 9–17 µg/m3 0.1 mg/m3 .b
See References 106, 171, 173, 175, 177, and
182
Naphthalene Home: 3–26 µg/m3 WHO recommends an annual average guideline of
See References 178, 182, 183 0.01 mg/m3 .b
Trichloroethylene Home: 0.3–0.6 µg/m3 No safe level of exposure is recommended.
Limonene Home: 32 µg/m3 No limits have been set.
Office: 19 µg/m3
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School: 11 µg/m3
See References 173, 175, 177–179, 181–183
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Alpha-pinene Homes: 11−32 µg/m3 No limits have been set.

Libraries: 10–30 µg/m3
Office: 6.3 µg/m3
School: 1.5 µg/m3
See References 173, 175, 177, 179, 181–183
Radon Home: 15–259 Bq/m3 WHO proposes a reference level of 100 Bq/m3 for 1 year to
School: 56–889 Bq/m3 minimize health hazards due to indoor redon exposure.b
Office: 54.9 Bq/m3
See References 184–187

a
See the United States Environmental Protection Agency Indoor Air Quality homepage: https://www.epa.gov/indoor-air-quality-iaq.
b
See WHO Guidelines for Indoor Air Quality: Selected Pollutants (188).
c
See Health Canada’s indoor air quality guidelines (https://www.canada.ca/en/services/health/publications/healthy-living.html).

Many studies estimate IAQ using models. Shrubsole et al. (78) and Liao et al. (18) used
building simulation software to predict IAP exposures from indoor and outdoor sources across
different building archetypes and scenarios. Rosofsky et al. (79) estimated infiltration using an air
exchange model and spatial data on building properties and metrological conditions. Despite the
uncertainties and assumptions associated with the inputs and outputs of the models, modeling
techniques allow for extensive estimates of exposure and predictions under future scenarios (33,
78, 80). Such models could be used, in theory, to estimate indoor air burdens for a county, region,
country, or the globe.

Health Impacts
Cumulative health impacts from inhalation in US residences of IAP are estimated at 400–
1,100 DALYs2 lost annually per 100,000 persons (34). In EU-26 countries, an annual loss of
2.1 million DALYs is associated with indoor and outdoor originating pollutants, with more than
half (1.28 million DALYs) caused by indoor exposure to outdoor air pollution and the remaining

2 A DALY is equivalent to one year of lost healthy life. DALYs thus occur when individuals die prematurely or

when they live with a disability or disease that impacts their life. DALYs are computed as the sum of years of
life lost, which estimate premature mortality, and years lost to disability, which quantify lost healthy life due
to suboptimal health. For a brief description of DALYs, see Salomon (81).

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0.74 million DALYs caused by indoor source pollutants (82). The pathogenesis of IAP exposure
results from a combination of effects at different levels (83). Gaseous air pollutants’ damage to
human tissue depends on solubility in water, concentration, ability to oxidize tissues, and suscep-
tibility of the exposed person (84). PM is usually classified by its sizes. Large particles (e.g., PM10 )
may affect mucous membranes and the upper airways, causing cough and lacrimation. Fine par-
ticles (e.g., PM2.5 and PM0.1 ) have greater systemic toxicity, as they easily enter the alveoli and
pass through the alveolar-capillary membrane and are carried through the bloodstream (83, 84).
In addition to particle sizes, their structure and composition [e.g., metals and polycyclic aromatic
hydrocarbons (PAHs)], may also be responsible for the tissue damage on contact (84).
In addition to causing direct damage, exposure to IAP can lead to inflammation with systemic
effects, trigger oxidative stress pathways, and activate oxidative stress response genes (83–85).
Moreover, epigenetics mediate genetic and physiologic responses to air pollution and are, there-
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fore, an important cause of susceptibility to pollution-related health effects (84, 86, 87).
Common indoor air pollutants and their effects on human health are summarized in Table 2.
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Illnesses caused by indoor environmental factors are commonly divided into two categories: sick
building syndrome (SBS) and building-related illness (BRI) (40). SBS refers to a group of symp-
toms that are linked to the physical environment of specific buildings (88). SBS symptoms caused
by IAP can be divided into four categories: (a) mucous-membrane irritation (e.g., eye, throat,
and nose irritations); (b) neurotoxic effects such as headaches, irritability, and fatigue; (c) asthma
and asthma-like symptoms including chest tightness and wheezing; and (d) issues such as skin and
gastrointestinal problems (3, 40). Common BRI illnesses include Legionnaire’s disease, hypersen-
sitivity pneumonitis, and humidifier fever (89). Indoor environmental pollutants can cause BRI
symptoms via four major mechanisms: (a) immunologic, (b) infectious, (c) toxic, and (d) irritant (90).
The respiratory system is the primary target of IAP exposure. Although findings are less robust
than those from research on the association between outdoor pollution and respiratory health,
IAP increases the risk of childhood acute lower respiratory infections (91). There is consistent
evidence suggesting that elevated indoor PM concentrations are associated with higher rates of
asthma attacks or asthma morbidity among populations with asthma. Indoor exposure to elevated
NO2 is also associated with greater asthma morbidity (92–95). The link between IAP exposure (i.e.,
PM2.5 , NO2 , and allergens) and COPD morbidity is also clear in populations living in developed
countries, even at relatively low pollution concentrations (96, 97).
Exposure to IAP may affect the natural defense of the body against airborne viruses, making
people more likely to contract viral diseases such as COVID-19 (98–100). It has been recognized
that short-range inhalation predominates the transmission of SARS-CoV-2 and the transmission
occurs mostly indoors in poorly ventilated spaces (101). This transmission pattern may be due
to the local climatic conditions with low temperature, mild daytime temperature range, and low
humidity that would favor the transmission of viruses, as a study demonstrated in China (102).
Exposure to IAP also increases the risk of specific cardiovascular diseases including ischemic
stroke, myocardial infarction, cardiac arrhythmia, heart failure, and atrial fibrillation due to in-
ducing oxidative stress, systemic inflammation, increased blood coagulability, and autonomic and
vascular imbalance (103, 104). Moreover, CO in the indoor air environment is likely to decrease
tissue oxygenation through carboxyhemoglobin production, which results in a high impact on
cardiovascular function (105).

Mitigating Exposures
Overall, improving ventilation is the easiest method to prevent accumulation of IAP. Poorer qual-
ity housing and/or occupant behavior may decrease dispersion via inefficient ventilation (33).

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Table 2 Health effects of selected indoor air pollutants

Pollutant Health effects Studies
Particulate matter with Respiratory symptoms and diseases including eye, nose, throat, and bronchial 189, 190
an aerodynamic irritation, asthma, fibrosis, anthracosis, and lung cancer; cardiovascular
diameter of 2.5 µm or diseases
less
Carbon monoxide Mortality; emergency department visit; cardiovascular diseases 190, 191
Nitrogen dioxide Exacerbate symptoms of respiratory illness; fatal pulmonary edema and 60, 92–95, 192
pneumonia at high concentration; bronchitis, bronchiolitis, and pneumonia
at lower concentrations
Ozone DNA damage: lung damage, asthma, decreased respiratory functions 49, 193
Environmental tobacco Contains many carcinogens: lung cancer, breast cancer, leukemia, lymphoma, 194–201
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smoke and brain tumors in children; nasal and sinus diseases; ischemic heart disease
Radon Lung cancer 202, 203
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Volatile organic compounds

Benzene Carcinogenic and genotoxic under chronic exposure, blood illness, 189, 190
neurological and reproductive problems
Toluene Long-term effect unclear; increased risk of developing asthma and other 37
respiratory conditions; impact on central nervous system
Ethylbenzene Ethylbenzene is a carcinogen. Acute effects include eye and throat irritation 37
and dizziness; long-term effects are unclear.
Xylenes Xylenes is a suspect carcinogen. Acute effects include eye and throat irritation, 204
headache, and nausea; long-term effects include issues in respiratory,
gastrointestinal, and central nervous systems, lungs, kidneys, heart, and the
reproductive system, and increased risks of leukemia, non-Hodgkin’s
lymphoma, and colon/rectum cancer.
Formaldehyde Formaldehyde is a carcinogen. Respiratory symptoms include cough, sputum 204–208
production, asthma, colds, chronic bronchitis, and respiratory cancer.
Naphthalene Acute intoxication can induce hemolytic anemia and cataracts; long-term 204
effects are unclear.
Trichloroethylene Trichloroethylene is a carcinogen. Acute effects include impacts on the 188, 204
nervous system at concentrations of ∼270 mg/m3 . Long-term exposure may
cause liver, kidney, and bile duct cancer and non-Hodgkin’s lymphoma.
Limonene Eye or skin irritation: Long-term effects are unclear; there is no evidence of 190, 204
carcinogenicity or genotoxicity.
Alpha-pinene Acute exposure to high concentrations can produce irritation and 204
inflammation; long-term effects are unclear.
Biological pollutants
Molds Allergic bronchopulmonary aspergillosis, hypersensitivity pneumonitis, and 60, 209–212
worsening of preexisting asthma; lower respiratory track disease
Animal dander Allergen, asthma 213–216
Dust mites Allergic diseases 217

Furthermore, new designs seeking to reduce energy consumption lead to airtight construction,
which can substantially reduce natural ventilation and may thus increase concentrations indoors
(37, 106, 107). Thus, the incorporation of adequate ventilation following energy-efficient building
modifications is necessary to reduce or prevent high IAP exposures, especially among lower SES

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households (33).

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Ventilation alone cannot prevent all IAP exposure and associated health effects in a cost-
effective or technically feasible manner. Current solutions for air purification include combina-
tions of air filtration, ionization, activated carbon absorption, ozonation, and photocatalysis (53,
108). These processes can be integrated into central ventilation systems (in ducts) or used in
portable air purifiers designed for limited spaces (108). Emerging air treatment methods include
membrane separation, enzymatic oxidation, botanical purification, and biofilters (37, 53, 108). In
developed countries, portable air cleaner devices may be effective for reducing IAP exposures (18,
109, 110). Community-level strategies [e.g., educational campaigns (111) and stove exchange pro-
grams (112, 113)], bolstered by policy [e.g., smoke-free legislation (114, 115)], have also been used
to reduce sources of pollution in developed countries.

HOUSEHOLD AIR POLLUTION PRIMARILY

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IN THE DEVELOPING WORLD

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Introduction
More than 20 years into the twenty-first century, one of the oldest sources of air pollution remains
the most dominant: Approximately 3.8 billion people (approximately the total world population
in 1970) lack access to clean energy for cooking, heating, and other basic needs. Despite national
policies and advocacy by global bodies, solid fuels remain by far the dominant energy source for
cooking in LMICs and for heating in much of East and Central Europe and Northern China
(116–118).
The use of wood as a fuel for fires is, in a way, as old as humanity: It has been described as
the distinguishing feature between the prehuman and human state (119, 120). Along with wood,
other biomass fuels—crop residues, which began to be used for heating and cooking during the
agricultural revolution; coal; and dung—form the major types of solid fuel still used today by just
shy of half of the global population (1).
The range of pollutants released from the combustion of these fuels, often in simple, unvented
stoves, is wide and varies with fuel and stove type and combustion conditions (Figure 3 pro-
vides an example). Species emitted include PAHs, VOCs, and hundreds of other health-damaging
compounds (121–123). In 2018, the WHO and others updated their HAP database, which col-
lects information on all available measurements made in solid fuel–using contexts. Although the
database focuses on PM2.5 and CO, two of the most commonly measured pollutants, it also in-
cludes numerous other pollutants, including PAHs and VOCs. The database contains more than
1,000 measurements from 196 studies performed in 53 countries. Kitchen levels of PM2.5 in house-
holds using solid fuels varied widely between regions, countries, and fuel types, ranging between
approximately 150 and 1,200 µg/m3 for wood and dung (124, 125). The burden of disease associ-
ated with cooking-related HAP is large—the ninth overall risk factor for mortality globally. HAP
exposure results in an estimated 2.3 million deaths yearly and 91 million DALYs—4.1% and 3.6%
of all deaths and DALYs, respectively. The distribution of this burden, not surprisingly, follows
the distribution of solid fuel use globally, and is most dominant in sub-Saharan Africa and South
and East Asia. Age-standardized mortality rates3 attributable to HAP in sub-Saharan Africa are
6–7 times higher than the global average (200/100,000 versus 30/100,000), and 200 times higher
than high-income countries (<1/100,000). This estimate of the burden of disease does not take
into account HAP’s contribution to AAP—a topic to which we turn our attention next.

3 Age-standardized rates adjust for population size and the age distribution of each country’s population. By

standardizing, mortality or morbidity rates can be compared between countries as though the countries had

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Figure 3
Cooking with wood fuel in a mud stove in Maharashtra, India. Note the kerosene lamp in the window and
the proximity of the cook to the fire and smoke. Picture by Ajay Pillarisetti, with permission.

Inside Out
HAP not only has an enormous health impact directly on those exposed to its emissions, but it also
escapes outdoors and likely accounts for a large fraction of AAP globally (126). The full impact of
HAP is thus composed of the exposures to HAP inside a given house and from its contribution to
AAP.
Until recently, the contribution of HAP to AAP was poorly characterized and quantified. This
contribution is generally quantified using either top-down or bottom-up source-apportionment
methodologies (127). These distinct approaches help in reconstructing the atmospheric concen-
tration of pollutants associated with the different emission sources. Whereas the former is based
on inferential methods, the latter is predictive of source contributions and, when operated in con-
junction, they may serve as an efficient tool for identifying major sources of PM2.5 and thus sup-
port air quality management decisions. These source-apportionment studies indicate that HAP
contributes to 12–31% of AAP globally (126, 128), with a larger footprint in LMICs. HAP is of-
ten a larger contributor than sources that are common indices of development, including road
transport, the industrial sector, coal-fired power plants, brick kilns, and construction dust. For in-
stance, in South Asia, studies estimate that more than half of AAP may come from use of solid
fuels in households (128), whereas in high-income countries of West Europe and North America,
this fraction is approximately 5−10%. Thus, the problem of HAP is confined not only to rural

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populations but also to all among the shared airshed.

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Regardless of the fairly large spread and uncertainty in the exact amount that HAP contributes
to AAP, it plays a nontrivial role in total air pollution exposure. These uncertainties arise from
differences in input variables, emission inventories, and the ways that different, complex air pol-
lution models account for chemistry and physics in the atmosphere. Furthermore, the definition
of residential emissions also differs between studies; emission inventories include varying combi-
nations of cooking, heating, and lighting emissions. Some also group commercial emissions with
residential emissions. These discrepancies can be improved by utilizing updated energy service
data—for instance, better data on primary and secondary fuel use for specific tasks (like boiling wa-
ter, cooking food, or space heating) acquired through nationally representative surveys. Detailed
characterization of emissions and comparisons of different emissions inventories enable regional
comparisons. By applying different emissions inventories in different geographies, the robustness
of findings can be evaluated. Such exercises are expected to increase the confidence of model-
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ing studies. Besides, consistent and coordinated efforts in assimilating top-down and bottom-up
approaches may be a significant step toward reducing the uncertainties in quantifying the con-
Annu. Rev. Environ. Resour. 2022.47. Downloaded from www.annualreviews.org

tribution of HAP to AAP. However, attributing the fraction of premature mortality burden to
contribution of HAP to AAP depends on additional factors including the shape of the exposure
response functions used to estimate the premature mortality burden, baseline mortality rates, and
the fraction of exposed population. Regardless of model or method, global source apportionment
studies indicate between 0.5 and 1 million deaths from AAP may be attributed to HAP annually,
in addition to the 2.3 million deaths from exposure to HAP indoors (29).

Reducing the Impact of Household Air Pollution Exposures: Shifting Paradigms

The late Professor Kirk R. Smith (129)—arguably the father of the field of HAP, the first to
measure exposures of women cooking in rural villages, and the principal investigator in the first
RCT of a HAP intervention—contextualized in recent years several paradigms for thinking about
household energy interventions, explicitly from a health perspective. We summarize and expand
upon those paradigms below.

With development comes wealth—and clean cooking. In some countries around the world—
including India and China—development trajectories and urbanization are leading to gradual im-
provements in clean fuel access and use. As households become wealthier, so the hypothesis goes,
they switch to clean fuels. Much of the information about solid fuel use—and trends in its preva-
lence over decadal or longer timespans—comes from national surveys administered at regular in-
tervals, including national censuses, Demographic and Health Surveys, and other energy-related
surveys. This type of transition may occur, but often occurs slowly; there is a need, given the large
burden of disease, to accelerate movement toward exclusive use of clean fuels. In some regions,
despite urbanization and increasing numbers of clean fuel users, rapid population growth has led
to a smaller overall fraction using clean fuels. Waiting for development to do its work thus may
be insufficient, especially when we have methods to reduce exposures now, rather than waiting on
development or waiting for a “silver bullet” solution that may not arrive or may arrive too late to
protect populations today.

Make the available clean. Decades of global programs have focused on replacing traditional
biomass stoves with more efficient and cleaner burning ones—hence making the available fuel
(more) clean. Among the most prominent of these many hundreds of programs were the Chi-
nese National Improved Stove Program and the Indian National Program on Improved Chulhas,
which installed approximately 130 million and 35 million stoves, respectively. Many of these early

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programs had the advantage of using the available fuel, being relatively inexpensive and made

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from locally available materials. The proliferation of these stoves led to many evaluations of their
effectiveness, with mixed results. Although many reduce air pollution concentrations and thus ex-
posures, they do not do so to a level thought to result in relatively safe pollution exposures (130).
In recent decades, the focus shifted from simple stoves to highly engineered devices, so-called
advanced biomass combustion stoves, that attempt to burn processed biomass more completely
through improved design and fan assistance. Although many of these devices show promise in the
lab (131, 132), their real-world performance has been less than ideal. A recent meta-analysis evalu-
ated the impact of various types of interventions, including cleaner cooking interventions, on pol-
lutant concentrations and exposures (130). None of the evaluated improved or advanced biomass
interventions reached the World Health Organizations Interim Target 1 annual average PM2.5
exposure guideline value of 35 µg/m3 . Reasons for this discrepancy between field and lab tests
are manifold and include, for example, differences in fuel preparation and fuel characteristics; the
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presence of other traditional stoves used concomitantly with intervention; poor performance and
maintainability of stoves over time; and design tradeoffs that optimize for emissions reductions,
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sometimes at the expense of usability for village cooks. Finally, these improved or advanced stoves
must burn biomass so cleanly as to not reduce pollution by half compared to the traditional stove,
but instead reduce it far more—to safer levels, such as the World Health Organization’s Interim
Target 1 Air Quality Guideline value of 35 µg/m3 and as evident in the exposure-response curves
depicted in Figure 1. To date, very few of these stoves have been able to consistently perform
at this level—unlike gas, electricity, and other clean fuels, which regularly achieve these exposure
reductions relative to traditional stoves.
RCTs of biomass cookstove interventions—in the mode of making the available clean—have
occurred in Guatemala (133), Malawi (134), Peru (135), Nepal (136), Rwanda (137), and Ghana
(138). These trials have mainly had null results or shown only small health benefits. One ex-
ception is the first trial of an improved cookstove, the RESPIRE project in the Western high-
lands of Guatemala. Although the measured exposure reductions were significant, they did not
result in a significant effect on physician-diagnosed pneumonia, but did significantly reduce se-
vere pneumonia. Numerous explanations exist for these findings, including insufficient or unmea-
sured reductions in exposure, mixed use of traditional and intervention stoves, and other sources of
exposure.

Make the clean available. This paradigm acknowledges the challenges of burning biomass ef-
ficiently in devices that are durable, reliable, and that cooks want to use. It also recognizes that,
for many cuisines and many cultures around the world, gas and electric cooking technologies
meet almost all regular needs. Under this mode of thinking, rather than trying to burn biomass
cleanly—a challenging task even under ideal circumstances—the focus is on taking clean options,
like liquefied petroleum gas (LPG), electricity, and piped natural gas, and making them more ac-
cessible, affordable, and available. This sort of transformation suggested by this paradigm is not
unprecedented. In the 1970s, Ecuador began heavily subsidizing LPG for household use, resulting
in widespread adoption, although some mixed use persists (139–141). Ecuador has further pursued
a transition from LPG to induction cooking, in part due to sufficient indigenous hydropower ca-
pacity and a desire to reduce the fiscal burden of LPG subsidies. A similar success story is noted
for Brazil, where LPG was promoted through a combination of market manipulations, subsidies,
and widespread urbanization (142).
Perhaps the most striking ongoing household energy transition—and one of the largest to
date—is occurring in India. The transition has been aided by several policy initiatives, beginning
in 2015 with Pahal, which sought to stop or slow leakage of subsidized LPG from the house-

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hold to commercial market. Pahal forced all consumers to purchase LPG at the market price;

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those eligible for a subsidy received it in their bank account. The second policy, known as “Give
it up,” encouraged middle- and upper-class households to voluntarily forego their LPG subsidy
in perpetuity. The recovered costs were used by the government to help offset connecting4 new,
poor households to the Indian LPG system. Approximately 10 million households gave up their
connection (142). The third policy—Pradhan Mantri Ujjwala Yojana (PMUY)—sought to sub-
sidize the cost of becoming connected to the LPG system by covering nearly all costs. PMUY-
eligible consumers were required to purchase a lower-cost two-burner stove, but this purchase
could be made via a no-interest loan with the LPG distributor. As of early 2022, the program
claims to have connected 90 million households to the LPG system. PMUY has been followed by
PMUY-2, which eased some eligibility criteria in order to ensure that all poor households were
eligible for the program.
Access and connection to the LPG system is a required step in ensuring a reduction in HAP
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emissions and exposures. It is, however, insufficient. At least two other parameters must be met:
near exclusive use of LPG or clean fuels (143) and cessation of biomass use. Audits and analysis
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of the PMUY program from India have shown that PMUY beneficiaries consume less fuel on
average than do non-PMUY beneficiaries, and likely not enough to cover all of their household
energy needs, indicating mixed use of clean and traditional fuels (144, 145). Among the many
reasons hypothesized for this incomplete transition, two that occur frequently in the literature are
difficulty in accessing refills and their unaffordability (145, 146). Nonetheless, the Indian program
has transformed the household energy landscape in India in less than a decade and appears to be
a prime example of making the clean available.
Randomized evaluations of LPG and other clean fuel interventions are fairly limited. The
largest to date—the multi-country Household Air Pollution Intervention Network (HAPIN) trial
(147)—is ongoing. HAPIN recruited 3,200 pregnant women in four LMICs (Guatemala, India,
Peru, and Rwanda) and randomized them to an LPG stove and fuel intervention arm or to a
control arm (continued traditional cooking). Preliminary results from HAPIN indicate signifi-
cant reductions between control and intervention groups and between baseline and postinterven-
tion measurements in the intervention arm, with approximately 70% of samples falling below the
WHO Interim Target 1 annual average PM2.5 guideline value of 35 µg/m3 (148). Health effects
have not yet been reported for the HAPIN trial. Three other trials of an LPG intervention—in
Ghana (138), Nepal (136), and Peru (149)—have null findings of the impact of the intervention
on health outcomes. The Ghana trial, however, has shown impacts in exposure-response analyses
on various health endpoints, including blood pressure (150), child growth (151), and birthweight
(152). An ethanol RCT in Nigeria showed no effect on birthweight in intention-to-treat analyses;
after controlling for covariates, there was a significant increase in birthweights in the intervention
group (153). The same trial reported a significant decrease in diastolic blood pressure (154) among
those with the intervention.

Cleaning up after clean cooking. In some contexts, as HAP from cooking decreases, identifying
the next most important sources of exposure—potentially from indoor emissions—becomes an
essential task. Additional uses of biomass stoves (often indoors, but also outdoors) include space
heating, water heating, animal fodder preparation, alcohol or other drink preparation, and com-
mercial cooking (155, 156). This focus—on end uses of energy, rather than on specific appli-
ances and/or fuels—is an emerging area of research, and one for which additional information is

4 In
India, a connection is required to access and become a formal part of the LPG distribution system. Be-
coming connected typically entails a deposit to a local distributor to cover the cost of the cylinder, regulator,

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hoses, and paperwork. Connection costs can be a substantial barrier to poor households.

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forthcoming, with the adoption of new, standardized household energy questions that specifically
focus on stoves, fuels, and end uses.

INDOOR AND HOUSEHOLD AIR POLLUTION: DISTINCTIONS

AND DISCOURSE
The distinctions between IAP in the developed world and HAP in the developing world may
appear vast. While conducting research for and writing this review, we identified areas where one
discipline can learn from the other, and some potential areas of overlapping future research that
would benefit both fields.

Cooking With Gas: A Strong Source in High-Income Countries, A Strong

Solution for Solid Fuel–Using Households
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In many developed countries, as part of a continued push toward electrification, cooking with
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gas—whether natural gas or LPG—is frowned upon for health, environmental, and climate-
related reasons (157, 158). This is in stark contrast with the role of LPG in LMICs, where it is
seen as a relatively affordable, transportable, and broadly usable fuel for households currently
using solid fuels (142, 159, 160). Even in the context of solid fuel–using homes, there is some
concern that levels of NO2 after intervention with an LPG stove may pose residual health threats
(161). Of note, these levels are lower than for cooking with biomass but above health-based
guidelines from WHO.
If we view this issue through an exposure apportionment lens, after identifying context-specific
strong sources, we could arrive at a transitory solution to the seeming contradiction of LPG pro-
motion. In the developed world, indoor combustion can be reasonably eliminated by replacing
gas with clean, low-cost, controllable, efficient electric devices—like induction cooking surfaces.
Indeed, such an approach likely makes some sense not only from a health perspective but also from
an energy savings and thus climate perspective. In LMICs—where electricity infrastructure is less
robust, less reliable, and unable to deliver sufficient energy for cooking—gas is an interim solution,
as it has been in the developed world for more than 100 years. There is strong motivation—from
health, environmental justice, and equity perspectives, among others—to provide clean fuels to
households using solid fuels now. The issue of gas cooking is one where scientists focused on
modern IAP and those focused on HAP would likely find fertile ground for discussion around
science and measurement, risk assessment and evaluation approaches, and overall mitigation and
intervention strategies.

Household Air Pollution in the Burden of Disease

The identification of HAP as a global risk factor for ill-health—and its inclusion in burden of dis-
ease estimates—was a long, multi-year process. Part of this process is outlined by Smith et al. (17)
and in the annexes to the WHO Indoor Air Quality Guidelines (162). Regardless, the process of
identifying the strongest evidence for exposure-outcome pairs and of identifying relatively precise
ways of quantifying specific exposures globally should be instructive for future attempts to quan-
tify the regional, national, or GBD associated with non-HAP indoor air pollutant exposure. We
note that some studies have already done this, but, to the best of our knowledge, no global effort
has been made. As with IAP, or with tobacco smoke, there are hundreds or thousands of species
that could be measured in biomass combustion smoke. Studies of HAP focused on measuring CO
and PM, pollutants for which there is (a) evidence of health effects; (b) relatively easy, inexpensive,
and validated measurement techniques; and (c) precedent for risk assessment. A similar, narrow

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selection of pollutants for “modern” IAP concerns may be appropriate.

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“Modern” Indoor Air Pollution Concerns in Countries With High Burdens

of Household Air Pollution
Given the large, global movement toward cities—and the identification of biomass use both within
and on the fringes of large mega-cities—there is clear risk overlap between the traditional HAP
risks and more modern IAP risks. Indeed, we speculate that there is likely a substantial population
experiencing both risks regularly. Furthermore, given the proliferation of commoditized goods,
like cleaning supplies and other household chemicals and construction materials, it is likely that the
burden of these “modern” exposures is experienced even by the rural poor. As above, identification
of the most important species—from an exposure, toxicity, or risk perspective—may help enable
global measurement databases using comparable techniques.

The Place’s the Thing!5

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Several papers reviewed in the course of writing this article cited Klepeis et al.’s (3) seminal Na-
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tional Human Activity Pattern Survey (NHAPS), from which the finding of time spent indoors
is derived. Although there have been follow-up studies—in California, Canada, and beyond—the
original NHAPS data are more than 25 years old. Personal devices that track location—including
smartwatches, cellular phones, and others—have widely proliferated and may provide a way for-
ward to more precisely—and with more spatial temporal granularity—identify where people spend
time. Understanding these activity patterns can help better understand where the potential for
exposure is largest and, concurrently, which sources in which microenvironments may be control-
lable. This type of technology likely has broad application for both HAP and IAP contexts and
could additionally contribute to better total air pollution exposure assessment.

Utilization of Low(er)-Cost Sensors for Air Pollution Assessment

HAP has a rich history of developing and using lower-cost air pollution sensors to measure expo-
sure, appliance usage, and time-activity patterns (163–167). Over the past decade, there has been
an explosion of low-cost particle and gas monitoring, leading to wide deployment of lower-cost
sensor networks for measurement of more finely spatiotemporally resolved air pollution, both in-
doors and outdoors (168–170). These sensors are often not purpose built for the environmental
conditions experienced in kitchens using solid fuels and may not be suitable for indoor or outdoor
measurements in contexts where continuous power and network access are not feasible (like, for
example, rural India or Kenya). Discussion of technologies, calibration techniques, placement, and
other issues between sectors would likely benefit both.

CONCLUSION
Likely every individual on the planet is exposed to some form of IAP, whether from electrical
devices, like printers; chemicals, like cleaning agents; or cooking-related aerosols, from either the
cooking itself or from the combustion of fuels like gas, wood, or dung to provide energy for food
preparation. In LMICs, a dominant form of indoor emissions is HAP arising from the inefficient
combustion of solid fuels for cooking, heating, lighting, and other energy end uses. These activities
contribute to a substantial burden of disease globally. Although much progress has been made on
reducing this burden, it remains persistent in many parts of the globe—and many of the same
individuals exposed to HAP may also be exposed to other forms of IAP. In developed countries,

5 With apologies to Shakespeare.

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cooking is a common and substantial source of exposure to indoor air pollutants; because of the
types of combustion occurring indoors, these emissions and exposures are much smaller than those
of households using solid fuels.
The global impact of “modern” IAP concerns—those not associated with household solid fuel
combustion—are not fully globally quantified to date in a way that enables easy comparison with
other risk factors. Given what is known about exposures based on where people spend time, how-
ever, it is likely that there is a substantial burden of disease associated with IAP. This likely means
that the strikingly large number of deaths and DALYs associated with air pollution exposure are
in fact underestimated.

SUMMARY POINTS
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1. Air pollution imposes a substantial burden on human health, but current estimates do
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not account for exposures indoors, other than for household air pollution (HAP) from
solid fuel use.
2. Exposure to air pollution occurs across a range of environments, including indoors at
home, indoors and outdoors at work, in transit, and outdoors; a total exposure approach
considers all environments.
3. Individuals that rely on solid fuels, like wood, dung, crop residues, and coal for household
energy, experience high exposures to harmful household air pollutants and substantial
ill-health, as a result of these exposures.
4. Hundreds, if not thousands, of harmful airborne pollutants have been measured in the
indoor environment; the magnitude of exposure to these pollutants depends on behavior,
the strength of the source, the duration of proximity to the source, and the underlying
health status of the exposed individual.
5. Particulate matter, carbon monoxide, and volatile organic compounds are among the
most commonly measured pollutants in both HAP and developed world indoor air pol-
lution (IAP) contexts.
6. It is likely that there is substantial risk overlap in developing countries with high solid
fuel use between HAP and “modern” IAP concerns; quantifying this overlap would help
more precisely estimate the total burden of disease.
7. In HAP contexts, liquefied petroleum gas interventions have, in some contexts, been
shown to reduce air pollution exposures substantially, to WHO Interim Target Guideline
values; improved and advanced biomass stoves have not been shown to do so, despite
promising laboratory findings
8. The fields of indoor air quality/indoor air pollution and HAP benefit from continued
dialogue between experts; areas of synergy may arise around low-cost sensors, around
prioritization of pollutants to measure and mitigate, and around better time-activity
estimation.

FUTURE ISSUES
1. The Global Burden of Disease currently estimates ill-health attributable to household
air pollution (HAP), ambient particulate air pollution, and ambient ozone. An additional

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risk factor—for indoor air pollution (IAP) in middle- and upper-income countries—may
be appropriate, although there would need to be consistent measurement of a subset of
measurable pollutants and related health effects.
2. The issue of gaseous fuels poses an interesting conundrum for indoor air scientists: They
are out of favor in the developed world, as they are fossil fuels that contribute to cli-
mate change, ill-health, and environmental degradation, whereas for many developing
economies, they represent a transitional fuel on the pathway to truly clean cooking with
renewably generated electricity. They offer a solution now to a pressing global health
threat, whereas other solutions—like cooking with electricity—may be years or decades
away.
3. Better time-activity estimates would benefit all: exposure scientists interested in improv-
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ing models of air pollution exposure; HAP scientists seeking more explanations for resid-
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ual exposure, after cooking is cleaned up; and burden of disease modelers, who seek the
best possible exposure estimate.
4. Low(er)-cost sensors, although not a panacea, can help fill gaps in knowledge about ex-
posure in both developed and developing world contexts, and should be applied more
broadly in indoor microenvironments, whether at home, in transit, or in occupational
settings, to name a few.
5. For HAP, beginning to consider what to clean up after cleaning up cooking is vital. In
many contexts, there is significant exposure even when using clean fuels; identifying the
next target for characterization and mitigation can help reduce exposures and health
effects.

DISCLOSURE STATEMENT
The authors are not aware of any affiliations, memberships, funding, or financial holdings that
might be perceived as affecting the objectivity of this review.

ACKNOWLEDGMENTS
This work is dedicated to the memory of Professor Kirk R. Smith, who helped plan early outlines
of this review and discussed its evolution with A.P. shortly before his unexpected death. His in-
sights, humor, dedication, and humanity are deeply missed; we acknowledge and honor his lifelong
commitment to decreasing exposure to all forms of air pollution.

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