Indoor air pollution and the lung in low- and medium-income countries

Abstract

Over half the world's population, mostly from developing countries, use solid fuel for domestic purposes and are exposed to very high concentrations of harmful air pollutants with potential health effects such as respiratory problems, cardiovascular problems, infant mortality and ocular problems. The evidence also suggests that, although the total percentage of people using solid fuel is decreasing, the absolute number is currently increasing. Exposure to smoke from solid fuel burning increases the risk of chronic obstructive pulmonary disease (COPD) and lung cancer in adults, and acute lower respiratory tract infection/pneumonia in children. Despite the heterogeneity among studies, the association between COPD and exposure to smoke produced by burning different types of solid fuel is consistent. However, there is strong evidence that while coal burning is a risk factor for lung cancer, exposure to other biomass fuel smoke is less so. There is some evidence that reduction of smoke exposure using improved cooking stoves reduces the risk of COPD and, possibly, acute lower respiratory infection in children, so approaches to reduce biomass smoke exposure are likely to result in reductions in the global burden of respiratory disease.

Full text

SERIES ‘‘AIR POLLUTION AND LUNG DISEASE’’
Edited by I. Annesi-Maesano, J.G. Ayres, F. Forastiere and J. Heinrich
Number 1 in this Series
Indoor air pollution and the lung in low- and
medium-income countries
Om P. Kurmi, Kin Bong Hubert Lam and Jon G. Ayres
ABSTRACT: Over half the world’s population, mostly from developing countries, use solid fuel for
domestic purposes and are exposed to very high concentrations of harmful air pollutants with
potential health effects such as respiratory problems, cardiovascular problems, infant mortality
and ocular problems. The evidence also suggests that, although the total percentage of people
using solid fuel is decreasing, the absolute number is currently increasing. Exposure to smoke
from solid fuel burning increases the risk of chronic obstructive pulmonary disease (COPD) and
lung cancer in adults, and acute lower respiratory tract infection/pneumonia in children. Despite
the heterogeneity among studies, the association between COPD and exposure to smoke
produced by burning different types of solid fuel is consistent. However, there is strong evidence
that while coal burning is a risk factor for lung cancer, exposure to other biomass fuel smoke is
less so. There is some evidence that reduction of smoke exposure using improved cooking stoves
reduces the risk of COPD and, possibly, acute lower respiratory infection in children, so
approaches to reduce biomass smoke exposure are likely to result in reductions in the global
burden of respiratory disease.
KEYWORDS: Biomass fuel, indoor air pollution, lung diseases, solid fuel
The main activities that contribute signifi-
cantly to indoor air pollution in low- and
middle-income countries are the use of
solid fuels for residential energy, active and
passive smoking inside the house, oil mists and
fumes from cooking, smoke from burning mos-
quito coils during the summer and incense sticks
during religious rituals, and keeping pets and
animals in the same dwelling where the indivi-
duals live.
Globally, .3 billion people, approximately half
of the world’s population, rely on the use of
biomass (wood, crop residues, twigs, shrubs,
dried dung and charcoal) and coal, collectively
known as solid fuels, to meet their basic domestic
energy demands for cooking, lighting and heat-
ing [1, 2]. The proportion is even more staggering
in rural parts of Africa, Central and South
America, and Asia, being .90% [3]. The majority
of the solid fuels are burnt in inefficient tradi-
tional cooking stoves located in places without
adequate ventilation, although in sub-Saharan
Africa, burning in the open environment is not
uncommon [4, 5]. A large variety of harmful
substances are released during combustion of
solid fuels and remain in the indoor environment
at very high levels for a number of hours after
cooking and heating has stopped, because of the
lack of adequate room ventilation. Most people
spend ,90% of their time indoors, even more in
the case of females, children, elderly and those
with ill health. Cooking in developing countries
is often done by females; and mothers tend to
keep their young children, especially infants and
toddlers, close by during cooking, therefore
placing females and children at risk of both acute
and long-term ill health from emissions of solid
fuel combustion. The degree of risk is related to
the levels of exposure, which, in turn, are
determined by a number of factors. For instance,
kitchen type and the design of living areas in
dwellings in developing countries can increase
exposure to indoor air pollutants several-fold
through natural (but inadequate) ventilation and
lack of flues [6, 7]. Seasonality is also important,
as exposures to indoor air pollutants during the
winter are several times higher than the rest of
AFFILIATIONS
Institute of Occupational and
Environmental Medicine, School of
Population and Health Sciences,
University of Birmingham,
Birmingham, UK.
CORRESPONDENCE
O.P. Kurmi
Institute of Occupational and
Environmental Medicine, School of
Population and Health Sciences
University of Birmingham
Birmingham
B15 2TT
UK
E-mail: o.kurmi@bham.ac.uk
Received:
Nov 01 2011
Accepted after revision:
Feb 04 2012
First published online:
May 3 2012
European Respiratory Journal
Print ISSN 0903-1936
Online ISSN 1399-3003
For editorial comments see page 12.
EUROPEAN RESPIRATORY JOURNAL VOLUME 40 NUMBER 1 239
Eur Respir J 2012; 40: 239–254
DOI: 10.1183/09031936.00190211
CopyrightßERS 2012
c

the year, as people spend more time gathering around fires to
keep warm.
USE OF SOLID FUEL AS HOUSEHOLD ENERGY
Based on the classification by the United Nations Development
Programme, there are 140 developing countries, of which 50
are the least developed countries and 45 are sub-Saharan
Africa countries. 31 countries belong to both the least
developed countries and sub-Saharan Africa categories.
Access to clean energy (e.g. electricity and natural gas) is low
in developing countries, but the situation is even worse in the
least developed countries and in Sub-Saharan Africa (fig. 1),
where 82% and 89% of the populations, respectively, rely
primarily on solid fuels for domestic purposes, compared with
56% in developing countries [8]. Variation also exists within
these countries. In the least developed countries, as much as
97% of the rural population have access only to solid fuels,
compared with 73% among urban dwellers. The difference is
even more marked in sub-Saharan Africa (95% versus 58%) [8].
Most of the solid fuel users do not limit themselves to a single
type of fuel but rather combinations of different types
depending upon availability. Worldwide, wood is the most
common biomass used, although coal is predominantly used in
China while dried cow dung is used by a smaller fraction of
the rural South Asian populations.
Trends in biomass fuel use
Although the total population relying primarily on the use of
biomass as residential energy will increase from 2.68 billion in
2009 to ,2.77 billion in 2015, and probably remain at that level
until 2030 [9], the proportion of the total population from
developing countries will decrease from 54% in 2009 to 51% in
2015, with further reductions to 44% in 2030. In China, the
population relying on biomass fuel is readily on the decline
and is estimated to fall to 19% by 2030. It is anticipated that this
trend will be followed by India after 2020 [9] such that by 2030,
just 54% of the Indian population and 52% of other Asian
countries will be using traditional biomass fuels. Increase in
the price of kerosene and bottled gas in the developing
countries is one of the main reasons for this slower transition to
cleaner fuels. However, the pace of decline in sub-Saharan
Africa will be much lower compared with other developing
countries.
Factors preventing the use of clean fuel
The influence on the choice of fuel used is multifactorial, but
cost and socioeconomic status appear to be the main drivers
(fig. 2). Less well-off households spend most of their income
purchasing food and clothes and for medical expenses.
Depending upon the availability of biomass fuels and the
distance required to travel to acquire these fuels, those living in
the least developed countries can spend, on average, 2–3 h per
week collecting biomass, leaving little or insufficient time for
education [2] and work, thus making it very difficult for these
families to improve their socioeconomic status. In rural areas
of developing countries, poor families often receive subsidies
on clean fuels. However, many switch back to biomass when
they cannot afford even the subsidised fuel, making them
reliant on the cheaper but dirtier alternatives. The other
important factor is the inavailability of clean fuels in rural
areas, because of the lack of a sustainable supply-chain
mechanism and/or the necessary infrastructure to deliver
clean fuels. Consequently, clean fuel is not available at all or
Percentage
<5
5–50
51–80
81–95
>95
Data not available
Not applicable
FIGURE 1. Total population using solid fuels in percentage. Modified from [8] with permission from the World Health Organization (WHO). The boundaries used on this
map do not imply the expression of any opinion whatsoever on the part of WHO concerning the legal status of any country or territory, or concerning the delimitation of its
frontiers or boundaries.
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240 VOLUME 40 NUMBER 1 EUROPEAN RESPIRATORY JOURNAL

the demand for clean fuel cannot be met consistently, forcing
rural dwellers to continue their dependence on biomass fuels.
Characteristics and toxicity of solid fuel use
Traditional stoves burning solid fuels have a very low energy
conversion efficiency ranging from 12% to 25% depending
upon the types of fuels (fig. 2). Approximately 8–10% of
the solid fuels undergo partial combustion, often due to
inadequate oxygen supply [10]. As a result, one of the main
components of biomass smoke is carbon (5–20% of wood
smoke as particulate mass), which is found in the particulate
fraction of the smoke and is present across a range of particle
sizes. Biomass smoke also contains .250 organic compounds,
varying mainly by the type of fuel burnt and the combustion
conditions [11]. Partial oxidation of organic matter generates
high levels of carbon monoxide, as well as hydrogen cyanide,
ammonia and nitrogen oxides. In addition, a large number of
other toxic and carcinogenic compounds, such as polycyclic
aromatic hydrocarbons (PAHs) (e.g. benzo[a]pyrene (BaP)),
aldehydes and free radicals [11], have been demonstrated
in biomass smoke. While biomass fuels tend to have low
levels of halogenated compounds, they may be contaminated
by chemicals such as pesticides, or mixed with plastics.
Certain varieties of coal, particularly in China, have parti-
cularly high fluoride or silica content [12]. Consequently,
burning of these specific fuels may lead to production of toxic
halogen compounds, such as hydrogen chloride, phosgene,
dioxin, chloromethane, bromomethane and other halocarbons
[13–15].
The toxicity of biomass smoke has been studied extensively in
the laboratory. Rats exposed subchronically to wood smoke at
concentrations of 1–10 mg?m
-3
over a period of weeks showed
reduced carbon monoxide diffusing capacity and increased
airway resistance. There were also mild chronic inflammation
and squamous metaplasia in the larynx, alveolar macrophage
hyperplasia, and slight thickening of the alveolar septa [16].
Wood smoke can cause greater levels of DNA damage in
lymphocytes than exposure to liquefied petroleum gas com-
bustion products [17], andcan both impair macrophage function
and be mutagenic [11].
Wood smoke condensates may damage the lens in rats,
causing discolouration and opacities, probably through oxida-
tion by polycyclic aromatic compounds and metal ions [18],
while chemicals such as aldehydes and acrolein found in
biomass smoke can cause eye irritation.
Biomass smoke is pro-oxidant and burning of biomass fuel
may generate high levels of redox-active components. In one
study from India, the oxidative potential of particulate matter
(PM) from cow dung cake smoke was found to be increased
using an in vitro technique involving a synthetic model of the
respiratory tract lining fluid [19].
Inadequate combustion of biomass releases carbon monoxide
that binds haemoglobin, producing carboxyhaemoglobin, due
to the high affinity of haemoglobin for carbon monoxide (200–
250 times) compared with oxygen [2]. Potentially, this can
reduce oxygen transport to key organs and the developing fetus,
which may result in low birth weight and perinatal death [20].
Very low income Low income Middle income High income
Electricity
Natural gas
60% methane
Pressure
Wick
Bituminous coal
Efficient stoves
Traditional stoves
Traditional stoves
15% moisture
lncreasing prosperity and development
Crop residues,
dung
Wood
Charcoal
Non-solid fuels
(predominantly used by either urban or semi-
urban population)
Increasing use of cleaner fuels with higher efficiency and more
convenient for cooking
Solid fuels (predominantly used by rural
population)
15% moisture
Coal
Kerosene
Biogas (methane)
Ethanol, methanol
Liquefied petroleum gas (LPG)
(Straw, leaves and grass) 15% moisture
Efficient stoves
Energy content
MJ.kg-1
Conversion
efficiency
%
60
6045.5
60
55
35
25
30
20
25
15
12
1214.5
13.5
16
16
30
30
22.5
43
43
22 MJ.m-3
38 MJ.m-3
FIGURE 2. The energy ladder. Data from [2, 10].
O.P. KURMI ET AL. SERIES: AIR POLLUTION AND LUNG DISEASE
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EUROPEAN RESPIRATORY JOURNAL VOLUME 40 NUMBER 1 241

In humans, acute exposure to sulfur dioxide, which is often
released during biomass burning, can increase bronchial
reactivity in normal individuals and cause bronchoconstriction
in asthmatic individuals at levels of ,100 ppb. Longer term
exposure may increase susceptibility to viral infections of the
lung [21].
A few studies have looked at the toxicity of biomass smoke in
exposed populations in developing countries. In chronically
biomass smoke-exposed Indian females, activation of circulat-
ing platelets, neutrophils and monocytes has been reported
with high levels of leukocyte–platelet aggregates [22]. As a
number of studies on ambient air pollution suggest that
particulate pollutants increase fibrinogen levels, thus enhan-
cing blood coagulation [23], it is plausible that biomass smoke
exposure could be a risk factor for cardiovascular events. There
have been very few controlled biomass smoke-exposure
studies in humans, but there is a suggestion that exposure at
levels of ,250 mg?m
-3
are associated with an increase in
circulating factor VIII and serum amyloid A, both of which
confer an elevated cardiovascular risk [24].
The inherent toxicity of the smoke from biomass burning
differs by the type of fuel, implying differential health risks
conferred by different fuels. Airborne endotoxin concentra-
tions in homes burning different types of biomass fuels in
Nepal and Malawi [25] have been reported to be higher than
those found in occupational settings [26, 27] and in the indoor
environment in developed countries [28]. The median value of
endotoxin (in endotoxin units (EU) per cubic metre) was
greatest in households burning maize crop residue
(1,609 EU?m
-3
) followed by cow dung (365 EU?m
-3
) and wood
(113 EU?m
-3
), all values being much greater than 40 EU?m
-3
[29], a health-based guidance limit recommended in the
Netherlands for an 8-h time-weighted average occupational
exposure.
Improved cooking stoves
The most effective way of eliminating exposure to smoke from
solid fuels is to switch to cleaner fuels, such as electricity, but
this option is not always feasible. The most realistic alternative
would be to reduce the exposure levels by switching to more
efficient, improved cooking stoves. Major projects to produce
and disseminate improved cooking stoves in the developing
world have been initiated in the last decade. The aims were
two-fold. First, by reducing the levels of indoor air pollutants,
it was hoped that the health burden would be reduced.
Secondly, by improving burning efficiency, fuel use could be
economised to help slow down deforestation and desertifica-
tion. While there is no universal definition, generally speaking,
all improved cooking stoves are characterised by a higher
efficiency of thermal conversion, a higher heat transfer ratio
and a more complete combustion (and therefore a lower
emission of smoke and other pollutants) compared with their
‘‘traditional’’ counterparts. Tests (water boiling, kitchen
performance and controlled cooking) have been developed
and recommended to monitor the performance and efficiency
of the improved cooking stoves. Improved cooking stoves can
be classified on the basis of: 1) the types of fuel used (operable
on single or multiple fuel types), 2) construction materials
(made of a single or a combination of materials), 3) portability
(fixed or portable) and 4) end-use applications (monofunction
for cooking only, or multifunction for cooking, room heating,
etc.) [30]. The choice of stove should be customised for the
target users, taking into account local cooking requirements,
and affordability and availability of fuels. Local availability of
construction materials and maintenance are important criteria
to long-term self-sustainable projects. In areas where improved
cooking stoves are not available, certain modifications of the
cooking environment and practices, such as improving
ventilation, or even avoiding cooking indoors where possible,
could be helpful in reducing the smoke exposure.
At present, ,27% of the total population using solid fuels (or
38% of the population in developing countries) have access to
improved cooking stoves: more than two-thirds (70%) in China,
9% in India and 4% in other south Asian countries. However, in
sub-Saharan Africa and the least developed countries, the
figures are as low as 5.8% and 6.6%, respectively [3].
Exposure monitoring
Particulate matter
PM is classified on the basis of its aerodynamic diameter (AD),
which is a function of particle size, mass and shape. Most of
the studies where actual biomass smoke exposures have been
measured (as opposed to a simple exposed/unexposed
classification) have reported exposures as PM10 (PM with AD
,10 mm), although, more recently, PM2.5 (PM with AD
,2.5 mm) has been used as a PM metric, reflecting the
likelihood that greater toxicity resides in the smaller size
fraction. PM can be measured either by gravimetric techniques
or by photometric devices. Gravimetric techniques give an
aggregate of exposure concentrations over a period of time but
photometric techniques are gaining popularity as they mea-
sure real-time PM concentrations in a repeated manner, which
provides information on the variation of particle concentration
over time and in relation to different activities. The downside
of this technique is that measurements need to be calibrated
against gravimetric results in the environment, where expo-
sure monitoring needs to be performed, as the light scattering
method often tends to overestimate PM concentrations [31].
Previous work has shown 24-h indoor concentrations of PM10
generated from solid fuels in different settings to be in the
range of 300–3,000 mg?m
-3
, with peaks reaching as high as
20,000 mg?m
-3
during cooking [4, 32–35]. In a wood-using
community in Nepal, the 24-h average PM2.5 was found to be
680 mg?m
-3
(range 616–744 mg?m
-3
) [31], which is similar to
other studies from Guatemala (22-h average 520 mg?m
-3
) [4]
and China (24-h average 489 mg?m
-3
) [36]. All these reported
concentrations are several-fold higher than the World Health
Organization (WHO) global ambient air quality guidelines,
which recommend that the 24-h and annual mean PM10
concentration should not exceed 50 and 20 mg?m
-3
, respec-
tively, with PM2.5 not exceeding 25 and 10 mg?m
-3
, respectively
[37]. These results are several-fold higher than results from the
UK (12–34 mg?m
-3
for PM10) [38] and USA (f35 mg?m
-3
for
total suspended dust) [39].
Carbon monoxide
Carbon monoxide has been suggested as a cheaper but
surrogate measure of indoor air pollution caused by burning
biomass fuel. Carbon dioxide is measured by using either
colour-changing diffusion tubes or electrochemical monitors.
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242 VOLUME 40 NUMBER 1 EUROPEAN RESPIRATORY JOURNAL

Diffusion tubes can only measure total exposure over time and
the carbon monoxide concentration is indicated by the stain
inside the tubes when in contact with carbon monoxide. More
recently, small electrochemical devices (e.g. HOBO1Data
Logger (Onset1, Cape Cod, MA, USA) and EL-USB-CO Data
Logger (Lascar Electronics, Salisbury, UK)) have been used to
measure carbon monoxide concentrations. These devices are
cheaper, smaller and require less power to operate over
extended time periods than diffusion tubes.
BRUCE et al. [40] reported 24-h carbon monoxide concentration
in homes using an improved stove of just over 3 ppm,
compared with 12.4 ppm with open fires, while our own work
in Nepal found broadly similar levels (18 ppm) but with
substantial increases to around 200 ppm during cooking
(unpublished observations), while results from Guatemala
(average 5.9 ppm) were similar [4]. The concentration of
carbon monoxide will depend upon the efficiency of fuel
combustion and the moisture content of the fuel [41], wet
wood fuel generates more smoke, and thus more carbon
monoxide, due to incomplete oxidation of the carbon content.
WHO recommended time-weighted average guidelines for
carbon monoxide are 87 ppm (100 mg?m
-3
) for 15 min, 52 ppm
(60 mg?m
-3
) for 30 min, 26 ppm (30 mg?m
-3
) for 1 h and 9 ppm
(10 mg?m
-3
) for 8 h [42].
HEALTH EFFECTS FROM EXPOSURE TO SOLID FUEL
SMOKE
It is estimated that 1.9 million people die prematurely due to
exposure to smoke from solid fuel burning [43]. According to
WHO, exposure to smoke from solid fuel burning is ranked as
the top environmental risk factor worldwide, being responsible
for 3.3% of all mortality and 2.7% of all disability-adjusted life-
years per year [44]. Long-term exposure to solid fuel smoke is
clearly associated with chronic obstructive pulmonary disease
(COPD), increased risk of acute respiratory infections/pneu-
monia, lung cancer, tuberculosis (TB) and cataracts [45–51].
The evidence is weaker for end-points such as asthma, adverse
pregnancy outcomes, cancer of the upper aerodigestive tract,
interstitial lung disease and ischaemic heart disease. More
research, both from animal and human studies, is needed to
establish the causal association between these health effects
and exposure to biomass smoke. Some of the health effects
associated with solid-fuel smoke exposure are acute, and
include oxygen desaturation [52] and acute lower respiratory
infection (ALRI)/pneumonia [53].
Here we discuss in detail the respiratory health effects
associated with smoke from solid-fuel burning.
The epidemiological data on biomass use from Asia (most of
them from south Asia), sub-Saharan Africa, and central and
south America have provided substantial evidence to suggest
that there is an association between exposure to biomass
smoke and COPD in adults, and ALRI/pneumonia in children.
Chronic obstructive pulmonary disease
COPD, once regarded as a disease of developed countries, is
now recognised as a common disease in developing countries.
COPD is the fourth leading cause of all deaths: ,3 million
people died from the condition in 2004, of whom 90% were
from low- and middle-income countries [54]. While the main
contributing factors to COPD in developed countries are
cigarette smoke and occupational causes, exposure to solid
fuel smoke is a major contributing factor in developing
countries. According to WHO estimates, ,700,000 out of the
2.7 million global deaths due to COPD could be attributable to
indoor air pollution from solid fuels [55], particularly in
females. However, the purported link between exposure to
solid fuel smoke and COPD has often been based on surrogate
measures of exposure and no studies have shown a relationship
between direct measurement of biomass smoke exposure and
the incidence or prevalence of COPD. Lower socioeconomic
status increases the risk of developing COPD, although which
component factors (e.g. poor housing, poor nutrition, low
income and no/poor education) are the most important in
influencing COPD and to what extent is unclear. Nevertheless,
one indicator of low socioeconomic status, the use of solid fuel,
has been suggested as a key causal factor [56–58]. Although the
underlying mechanisms for the development of COPD among
nonsmokers exposed to biomass fuels are still unknown, some
human challenge [59] and toxicological studies [19, 60] have
reported that biomass burning produces chemicals with high
oxidative potential, and have implicated that oxidative stress
and DNA damage are underlying mechanisms responsible for
the pathogenesis of COPD [61, 62] in those exposed to biomass
smoke. RIVERA et al. [63] compared the lung morphology in
COPD secondary to cigarette and biomass smoke, and reported
that smokers with COPD had a larger extent of emphysema and
goblet cell metaplasia than females exposed to biomass smoke,
but the latter presented more local scarring and pigment
deposition in the lung parenchyma, and more fibrosis in the
small airways. In contrast, MORAN-MENDOZA et al. [64] found
that wood smoke-exposed, nonsmoking females had histo-
pathological findings (dyspnoea, airway obstruction, air trap-
ping, increased airway resistance, pathological evidence of
anthracosis, chronic bronchitis, centrilobular emphysema,
bronchial squamous metaplasia and pulmonary hypertension)
similar to smokers.
Studies on solid fuel use and COPD are often observational,
small in sample size with insufficient statistical power to show a
clear relationship, and have relevant confounding factors that
are often inadequately addressed. A further issue is the use of
nonstandard definitions of COPD or chronic bronchitis.
Therefore, the findings across studies should be viewed with
some caution, as the published estimates may be either under-
or overestimates of the true burden. A systematic review and
meta-analysis [45] identified 23 studies, 10 reporting COPD
based on both physician diagnosis and spirometric definitions,
11 reporting chronic bronchitis based on respiratory question-
naire data, and two reporting both COPD and chronic
bronchitis. The pooled effect estimate for lung function
diagnosed COPD (OR 2.96, 95% CI 2.01–4.37) was greater than
those diagnosed by a doctor in hospital (OR 2.29, 95% CI 0.70–
7.52), with a combined pooled effect estimate of 2.80 (95% CI
1.85–4.23) for COPD (fig. 3). Similarly, the pooled effect estimate
for chronic bronchitis (fig. 4) was 2.32 (95% CI 1.92–2.80). The
findings, published in 2010 [45], are similar to a recent meta-
analysis [87] published for both chronic bronchitis (OR 2.52, 95%
CI 1.88–3.38) and COPD (OR 2.40, 95% CI 1.47–3.93).
It is likely that exposure to biomass smoke from an early age
will be important in retarding lung growth. In a study from
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EUROPEAN RESPIRATORY JOURNAL VOLUME 40 NUMBER 1 243

Nepal where lung function was compared between a biomass
smoke-exposed population and an unexposed population [88],
the absolute values for various indices of lung function were
significantly lower in both males and females in the biomass
smoke-exposed group, the difference being evident even in the
youngest age group studied (16–25 yrs). This suggests an effect
of biomass smoke exposure on lung growth in addition to any
effect on rate of decline of lung function in later years. The
prevalence of airflow obstruction (defined as forced expiratory
volume in 1 s/forced vital capacity ratio ,0.70) in the biomass
smoke-exposed group was almost doubled compared with the
unexposed (20% versus 11%).
Overall, there is good evidence that exposure to biomass
smoke is associated with airflow obstruction and an at least
doubling of the risk of COPD, the effect being detected by
young adulthood.
Asthma
There is a wide variation in the prevalence of asthma
worldwide [89]. Asthma has been less widely studied in
developing countries compared with developed countries, and
understanding of the very different set of risk factors in these
countries associated with its development, notably indoor
environment and lifestyle, is limited. There is evidence that
growing up in an agricultural environment is associated with a
reduced risk of developing asthma, perhaps mediated by
exposure to endotoxin [90], so it might be expected that
exposure to biomass, which largely occurs in rural commu-
nities, might not be associated with development of asthma per
se, but could be associated with exacerbations of existing
asthma or with respiratory symptoms that might lead to a
mistaken diagnosis of asthma. Some studies in developing
countries have considered possible associations with biomass/
solid fuel pollutant exposures [91–93]. SAMUELSEN et al. [94]
studied allergy adjuvant effect of particles from wood smoke
and road traffic in laboratory animals, and found that particles
generated from wood burning had about the same capacity to
enhance allergic sensitisation as road traffic particles, but less
than diesel exhaust particles. Acute exposure to biomass
smoke causes bronchial irritation, inflammation and increases
bronchial reactivity that is possibly responsible for exacerba-
tion of asthma [20].
Published effect sizes for asthma in relation to biomass
exposure are presented in table 1. All these studies adopted
different techniques to determine asthma and none measured
actual biomass exposure levels. While this limits the ability to
compare the studies, all show positive associations between
indoor air pollution and asthma, at least in children.
Studies separated by diagnosis criteria OR (95%CI)
1.70 (1.20–2.40)
1.60 (0.80–3.20)
1.50 (0.52–4.30)
1.50 (0.49–4.60)
1.40 (1.31–1.50)
2.96 (2.01–4.37)
6.60 (2.16–20.20)
5.20 (4.74–5.70)
1.30 (0.77–2.20)
0.70 (0.45–1.10)
2.29 (0.70–7.52)
2.80 (1.85–4.23)
1 2 3 4 5 8 10 20 30
Log of odds ratio
6.52
5.73
4.73
4.55
6.81
76.18
4.55
6.80
6.15
6.31
23.82
100.00
Weight %
COPD: lung function
COPD: doctor diagnosed
OROZCO-LEVI et al. [67] 2006
2007
2004
2005
2007
2007
2006
LIU et al. [69]
LIU et al. [69]
REGALADO et al. [33]
ZHONG et al. [72]
SEZER et al. [73]
CHAPMAN et al. [74]
XU et al. [75]
XU et al. [75]
Subtotal (I2=91.8%; p<0.001)
Subtotal (I2=96.9%; p<0.001)
Overall (I2=97.3%; p<0.001)
2007
2007
Spain
Mexico
China
China
China
17.40 (10.55–28.70) 6.21DØSSING et al. [66] 1994 Saudi Arabia Wood
3.90 (1.67–9.10) 5.31DENNIS et al. [68] 1996 Columbia Wood
2.40 (1.99–2.90) 6.73CABALLERO et al. [71] 2008 Columbia Wood
1.80 (0.54–6.00) 4.33
OROZCO-LEVI et al. [67] 1996 Spain Wood
4.50 (1.43–14.20) 4.47OROZCO-LEVI et al. [67] 2006 Spain Wood and charcoal
28.90 (8.71–95.90) 4.34KIRAZ et al. [65] 2003 Turkey Biomass
Turkey Biomass
2.50 (1.56–4.00) 6.27EKICI et al. [70] 2005 Turkey Biomass
Biomass
Biomass
Biomass
3.10 (1.63–5.90) 5.86LIU et al. [69] 2007 China Biomass
2.80 (0.84–9.30) 4.33LIU et al. [69] 2007 China Coal
Coal
China Coal
China Coal
China Firewood/straw
Charcoal
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FIGURE 3. Forest plot showing risk of chronic obstructive pulmonary disease (COPD) in populations exposed to solid fuel smoke. Reproduced from [45] with
permission from the publisher.
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244 VOLUME 40 NUMBER 1 EUROPEAN RESPIRATORY JOURNAL

A case–control study in Nepal assessed the home environment
of schoolchildren in relation to asthma, using the International
Study of Asthma and Allergies in Childhood questionnaire,
and found that passive smoking and use of biomass fuels was
separately associated with an increased risk of asthma in males
only, but keeping animals in the home was associated with a
lower risk of asthma (OR 0.2, 95% CI 0.1–0.5) [97]. This finding
is supported by a similar case–control study from Kenya [95],
which found that dampness in the child’s sleeping area, indoor
air pollution and presence of rugs or carpets in the child’s
bedroom were strongly associated with asthma (OR 2.0–4.9),
and by a study from Guatemala in relation to asthma
symptoms in 4–6-yr-old children [89]. In contrast, a study
from Malaysia only found an association of asthma with
environmental tobacco smoke (ETS) and exposure to mosquito
coil smoke [96].
A meta-analysis of these four studies showed that exposure to
indoor air pollution approximately doubles the risk of
developing asthma in children (OR 1.96, 95% CI 1.29–2.99)
but some caution needs to be taken in interpretation, as the
methodology was imperfect in some way in all studies.
Only one study has considered biomass smoke exposure and
asthma in adults [89]. Using a simple approach to defining
asthma (a positive response by the head of household to the
question ‘‘Does anyone listed suffer from asthma?’’), the study
found that people living in houses using biomass as a domestic
fuel and who were active smokers had a significantly higher
risk of asthma. Although this study found that asthma in
elderly males and females (o60 yrs) is associated with use of
biomass fuel, the exposure was based on a crude yes/no
response and there is a high possibility of misclassifying
asthma.
In summary, the evidence possibly supports a role for biomass
exposure being causally related to asthma in children, but
formal, well-designed studies are needed to confirm this
possibility. In particular, methods should ensure as tight a
diagnosis of asthma as possible (perhaps including measures
of bronchial reactivity, e.g. using mannitol challenge or
exercise) to determine whether these findings simply reflect a
pattern of asthma-like symptoms or true asthma.
Acute respiratory infection
Acute respiratory infection (ARI) can be divided into two
types, upper respiratory tract infections (URTIs) and lower
respiratory tract infections (LRTIs), which can, in turn, be
categorised on clinical conditions, aetiology and markers of
severity [58]. Although there are clinical and epidemiological
criteria to separate URTI from LRTI worldwide, there are
no uniformly accepted definitions used in epidemiological
Studies Weight %OR (95% CI)
PANDEY [76]
DUTT et al. [77]
PÉREZ-PADILLA et al. [78]
UZUN et al. [79]
AKHTAR et al. [80]
1984
1996
1996
2003 Turkey
2007 Pakistan
GOLSHAN et al. [81] 2002 Iran
AKHTAR et al. [80] 2007 Pakistan
EKICI et al. [70] 2005 Turkey
ALBALAK et al. [82] 1999 Bolivia
AKHTAR et al. [80]
AKHTAR et al. [80]
2007 Pakistan
QURESHI [83] 1994 India
2007 Pakistan
CETINKAYA et al. [84] 2000 Turkey
KIRAZ et al. [65] 2003 Turkey
MENEZES et al. [85] 1994 Brazil
MENEZES et al. [85] 1994 Brazil
BEHERA and JINDAL [86] 1991 India
Overall (I2=68.9%; p<0.001)
12
Log of odds ratio
3 4 5 7 10 20 30 40
Mexico
Nepal 7.87 (4.67_13.26) 5.70
4.17 (0.46_38.02) 0.69
3.90 (2.00_7.60) 4.48
3.36 (1.80_6.26) 4.83
3.32 (1.12_9.88) 2.33
2.91 (1.92_4.40) 6.79
2.51 (1.64_3.83) 6.69
2.50 (1.56_4.00) 6.20
2.38 (1.88_3.01) 8.67
2.10 (1.50_2.94) 7.61
2.01 (1.67_2.42) 9.12
1.96 (1.36_2.82) 7.32
1.90 (1.20_3.01) 6.30
1.49 (0.92_2.41) 6.10
1.30 (0.74_2.27) 5.38
1.18 (0.83_1.67) 7.49
2.32 (1.92_2.80) 100.00
2.50 (1.25_5.00) 4.29
India
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FIGURE 4. Forest plot showing risk of chronic bronchitis in populations exposed to solid fuel smoke. Reproduced from [45] with permission from the publisher.
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EUROPEAN RESPIRATORY JOURNAL VOLUME 40 NUMBER 1 245

research. The lack of a uniformly accepted definition of ARI
may cause bias that would contribute to the heterogeneity in
reporting across different studies. The possible mechanism
related to respiratory infection from acute exposure to PM
from biomass burning might be due to reduced mucociliary
clearance, and long-term exposure increasing susceptibility to
bacterial and viral lung infections [20].
LRTIs are major causes of morbidity and mortality, leading to
.4 million deaths per year worldwide, ,69% of which occur
in developing countries [100, 101]. After neonatal deaths, ARI
(17%) is the second leading cause of deaths in children ,5 yrs
of age and the fourth leading cause of death in the world,
where 7.4% of females and 7.1% of males die annually due to
respiratory infections [101]. In low-income countries, respira-
tory infection is the leading cause of deaths (2.94 million,
11.2%) [101].
Mortality due to respiratory infection is higher in the ,5 and
o60 yrs age groups. Young children exposed to solid fuel
smoke have two to three times more risk of serious ARI than
unexposed children [58]. Deaths due to respiratory diseases are
highest in African countries followed by eastern Mediterranean
and then south-east Asian countries [101], where most of the
people are of low socioeconomic status. In these areas, .70% of
the population use solid fuels for domestic purposes and
respiratory deaths from respiratory tract infections could well
be attributed to the high exposure from the burning of biomass/
solid fuel. Exposure to air pollutants might increase the
incidence of ARI by adversely affecting specific and nonspecific
defences of the respiratory tract against pathogens [102]. It is
important to emphasise that death due to ARI is mainly
associated with LRTI rather than URTI.
A longitudinal study in rural Kenya studied ARI and acute LRTI
(ALRI) in children under the age of 5 yrs [5, 103]. The study
measured biomass exposure as PM10 and found a dose–response
relationship between PM10 and the increase in ARI and ALRI
frequency. The rates of ARI and ALRI were higher for exposures
of PM10 below 1,000–2,000 mg?m
-3
but the rate of increase
declined where exposure concentrations were .2,000 mg?m
-3
.
A longitudinal study (1984–1985) in Nepal of children ,2 yrs
of age showed a possible relationship between ARI and
average number of hours spent in the kitchen (OR 2.2)
reported by the mother [104]. A suggestion of a dose–response
relationship was found in this study but the exposure
assessment was not validated.
A case–control study from urban Nigeria did not find
significant associations between age, nutritional status, ETS
exposure, location of cooking and crowding with ALRI [105].
MISHRA [106] studied acute respiratory infection in preschool
children (,5 yrs of age) in Zimbabwe and found that ,16% of
the children had ARI at the time of their survey. The study
reported that, after adjusting for appropriate confounders,
children in households using biomass were more than twice
(OR 2.2) as likely to suffer from ARI as children from
households using clean fuel for domestic purposes. A 1-yr
cohort study carried out in 500 Gambian children ,5 yrs of age
reported that parental smoking appeared (nonsignificantly) to
increase the risk of ALRI [107]. However, the risk of ALRI was
six times higher in females than in males, perhaps due to the
fact that females are carried on their mother’s back more often
than boys during cooking and, hence, are exposed more to
biomass exposure.
A meta-analysis of 24 studies relating to pneumonia in
children ,5 yrs of age who were exposed to smoke from solid
fuels showed the exposure to solid fuel smoke approximately
doubles the risk of pneumonia (OR 1.78, 95% CI 1.45–2.18)
[108]. There is thus consistent evidence that biomass smoke
exposure is associated with an increased risk of ARI/
pneumonia in children.
Tuberculosis
There is inconsistent evidence that exposure to biomass smoke
increases the risk of TB [109, 110]. The proposed mechanism is
that biomass smoke compromises the respiratory system’s
ability to resist infection by Mycobacterium tuberculosis or to
resist development of active TB in already infected persons
[111]. There is enough evidence to support the belief that cur-
rent and/or former smoking is associated with TB [110, 112–
116] and some evidence to suggest that passive smoking is also
a risk factor [117, 118] acting via a range of potential immune
mechanisms. Similarly, biomass exposure interferes with mu-
cociliary clearance [119] and decreases several antibacterial
TABLE 1 Studies of the relationship between biomass exposure and asthma prevalence
First author
[ref.]
Country Fuel type Sample size Sample type Diagnosis criteria Effect size
OR (95% CI)
MOHAMED [95] Kenya Biomass and
clean fuel
77 cases and 77
controls
Children aged
9–11 yrs
Adapted from IUATLD 2.5 (2.0–6.4)
AZIZI [96] Malaysia Wood and kerosene 158 cases and
201 control
Children aged
1 month to 5 yrs
Hospital-based doctor
diagnosed
1.4 (0.60–3.60) wood and
0.9 (0.50–1.60) kerosene
MELSOM [97] Nepal Biomass and
clean fuel
121 cases and
126 control
Children aged
11–17 yrs
ISAAC criteria 2.2 (1.0–4.5)
MISHRA [98] India Biomass and
clean fuel
38595 subjects Adults aged
o60 yrs
Based on interviewee replying
yes to asthma questionnaire
1.59 (1.30–1.94)
SCHEI [99] Guatemala Wood 1058 subjects Children aged 4–6 yrs ISAAC criteria 1.8 (0.76–4.19)
IUALTD: International Union Against Tuberculosis and Lung Disease; ISAAC: International Study of Asthma and Allergies in Childhood.
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properties of lung macrophages, such as adherence and phago-
cytic rate [120, 121], providing theoretical mechanistic reasons
to support the possibility that biomass smoke might be a risk
factor for TB.
The available data suggest (table 2) that there might be a causal
link between exposure to biomass smoke and either an
increased risk of acquiring TB or progression of TB to clinical
disease. There are very few studies that have explored this link,
and there is heterogeneity in design, measurement of outcome
and the magnitude of risk estimates, which need to be explored
further to come to a firm conclusion. Most of the studies related
to biomass use and TB suggest that prevalence of TB is higher in
communities with poor sanitation and lower socioeconomic
status, and these communities primarily use solid fuel for
domestic purposes. A meta-analysis on the 10 studies men-
tioned in table 2 revealed a pooled effect estimate (OR 1.55, 95%
CI 1.11–2.18) suggesting that individuals exposed to solid fuel
smoke are 55% more likely to get TB than an unexposed group.
While there was significant heterogeneity among the studies
(I
2
70%, p,0.001), no significant publication bias was reported.
Lung cancer
Lung cancer is one of the leading causes of death, accounting
for 1.3 million deaths annually worldwide [129]. While
smoking is the major risk factor, as many as a quarter of cases
are not attributable to tobacco use [130]. Lung cancer in never-
smokers is more common in females than males, although
there is considerable regional variation in the proportions of
nonsmoking females with lung cancer; for instance, in east and
south Asia, up to 83% of female lung cancer cases are never-
smokers, compared with 15% in the USA [130]. Emissions from
combustion of solid fuels have been shown to have high
concentrations of PAHs, BaP and PM2.5, which in turn have
been associated with high lung cancer rates [130].
A meta-analysis of 28 studies relating to lung cancer in subjects
exposed to solid fuel smoke showed a greater effect of coal
smoke on lung cancer rates (OR 1.82, 95% CI 1.60–2.06) with
biomass smoke, predominantly wood (OR 1.50, 95% CI 1.17–
1.94) and mixed biomass fuel smoke (OR 1.13, 95% CI 0.52–
2.46), showing lesser effects. The higher risk of lung cancer in
coal users was not surprising as combustion products obtained
from in-home coal burning contain a range of PAHs classified
as group 1 carcinogens [131]. The general mechanism emer-
ging from the study of PAHs such as BaP is genotoxicity,
where BaP is metabolised to an electrophilic form that adducts
DNA. The International Agency for Research on Cancer
(IARC) has classified combustion products from biomass
(primarily wood) use as probably carcinogenic to humans
(group 2A) for lung cancer due to ‘‘limited evidence’’ in
humans and experimental animals [131].
TABLE 2 Studies of tuberculosis infections in relation to biomass exposure
Country Fuel type Sample size Sample type Effect size
OR (95% CI)
Case–control studies
GNINAFON et al. [122] Benin Solid fuel 200 cases and
400 controls
Age- and sex-matched,
community-based
controls
1.7 (1.1–2.8)
KAN et al. [123] China Solid fuel 202 cases and
404 controls
Age- and sex-matched,
community-based
controls
1.08 (0.62–1.87)
#
LAKSHMI et al. [124] India Biomass 126 cases and
252 controls
Age-matched, community-
based controls
3.14 (1.15–8.56)
"
KOLAPPAN et al. [125] India Biomass 255 cases and
1275 controls
Age- and sex-matched,
community-based
controls
1.7 (1.0–2.9)
+
POKHREL et al. [109] Nepal Biomass and
kerosene
125 cases and
250 controls
Age-matched, hospital-
based controls
1.21 (0.48–3.05) biomass and
3.36 (1.01–11.22) kerosene
SHETTY et al. [113] India Biomass 189 cases and
189 controls
Matched, hospital-
based controls
0.90 (0.46–1.76)
#
CRAMPIN et al. [110] Malawi Biomass 598 cases and
992 controls
Community-based
controls
0.60 (0.3–1.1)
#
PEREZ-PADILLA et al. [126] Mexico Biomass (present/
past)
288 cases and
545 controls
Hospital-based
controls
2.2 (1.1–4.2) present, 1.5
(1.0–2.40) present or past
and 1.1 (0.6–2.0) past
Cross-sectional studies
MISHRA et al. [127] India Biomass 260162 persons
screened
All aged o20 yrs in
the sampling location
2.58 (1.98–3.37)
GUPTA et al. [128] India Biomass 707 Adults 2.54 (1.07–6.04)
#
: nonsignificant;
"
:p50.02;
+
:p50.04.
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One methodological issue in such analyses is the use of
appropriate comparison populations. The pooled effect size
obtained from studies using population-based controls (carry-
ing 56% weight) (OR 1.83, 95% CI 1.51–2.21) were greater than
those using hospital-based controls (39% weight) (OR 1.63,
95% CI 1.34–1.97). This suggests the evidence of the carcino-
genicity of biomass smoke is still not conclusive, supporting
the IARC evaluation.
Cigarette smoking has been widely identified as the main
contributory factor for lung cancer worldwide [132, 133] but
no objective measurement of smoking was carried out in any
of the studies included here. However, all studies included in
this review either adjusted for smoking or studied a popu-
lation of nonsmokers. While it is accepted that self-reported
smoking history is the best that can be achieved when
considering life-long smoking details, objective measurement
of smoking, such as salivary cotinine, is becoming more easily
usable in field studies and, at least, provides information on
current smoking and will help reduce exposure misclassifica-
tion slightly.
Almost 75% of the studies included in this meta-analysis did
not adjust for ETS but studies dealing with coal smoke
exposure with ETS adjusted (OR 1.47, 95% CI 1.13–1.91) had
lower pooled effect sizes compared to those where ETS was not
adjusted for (OR 1.74, 95% CI 1.60–1.89). Only one study out of
eight related to biomass smoke exposure adjusted for ETS and
had an effect size higher than the others that were not adjusted
for ETS. Thus, ambiguity regarding the combined effect of
smoking, combustion products of solid fuel and ETS exposure
still prevails and future studies need to address this issue.
There is evidence from occupational studies that smoking and
some occupational exposures (e.g. asbestos and PAHs) have a
multiplicative, rather than simply an additive, effect on lung
cancer risk [134, 135], and it is therefore possible that such a
potentiating effect may be seen with respect to smoke from
solid fuel burning, especially that from coal.
Most of the cooking in developing countries is done by
females, who are therefore more likely to be exposed to indoor
air pollution than males. The pooled effect size shows that the
risk of lung cancer is greater in females (OR 1.81, 95% CI 1.54–
2.12) compared with males (OR 1.16, 95% CI 0.79–1.69), similar
to that reported in a limited earlier meta-analysis for females
only (OR 1.83, 95% CI 0.62–5.41) [136].
There may be an effect on cell type, as the pooled effect size for
squamous cell carcinoma was greatest (OR 3.58, 95% CI 1.58–
8.12) followed by adenocarcinoma (OR 2.33, 95% CI 1.72–3.17)
and unspecified lung cancer type (OR 1.57, 95% CI 1.38–1.80).
Squamous cell lung cancer is more commonly associated with
cigarette smoking [137], although reported series of lung
cancers have recently shown an increase in the proportion of
adenocarcinomas, which is thought not to be simply an issue of
changes in classification/grading [138].
INDOOR AIR POLLUTION FROM OTHER SOURCES AND
ASSOCIATED HEALTH EFFECTS
There are number of other sources that contribute to the
worsening of indoor air pollution in developing countries and
may thus contribute to ill health.
Cooking oil fumes
Cooking emissions
Cooking is the treatment of food with heat. High temperature
initiates volatilisation as well as a number of chemical
reactions in the food ingredients, generally involving decom-
position of lipids and amino acids [139]. The resulting
emissions have been found to contain PM [140], volatile
organic compounds (VOCs) [141] and other organic com-
pounds, including PAHs [142] and heterocyclic amines [143],
some of which are potent mutagens and carcinogens. The types
and levels of pollutants in cooking emissions are highly
heterogeneous and depend on food ingredients [144, 145]. For
example, beef steak fried with margarine generated signifi-
cantly higher levels of PM and aldehydes than when rapeseed
oil, olive oil or soybean oil was used under the same cooking
procedures [144]. However, CHIANG and co-workers [146, 147]
analysed emission samples in Taiwan and reported nonsigni-
ficant variations of levels of PAHs and aromatic amines using
different types of cooking oil. In a controlled environment,
FULLANA et al. [145] reported higher levels of acetaldehyde and
acrolein emissions from heated canola oil and olive oil, and
suggested this might be related to their difference in fatty acid
composition, where canola oil contains a higher proportion of
linolenic acid and a small proportion of oleic acid than that in
olive oil. The same report also provided evidence that the
levels of pollutants are positively correlated with heating time
and temperature [145]. Not surprisingly, different methods of
cooking, such as frying (pan, stir and deep frying), grilling and
baking, can affect the levels of emission. For instance, when stir
frying meat, the concentration of BaP (2.64 mg per 100 m
3
) can
be four times as high as that when it was boiled (0.65 mg per
100 m
3
) [148].
Chinese cooking appears to be of particular concern because
the techniques involved generally require high temperature
cooking with oil, such as in stir frying and deep frying. This is
supported by a study in Taiwan, which found the annual rate
of PAH emission was highest from Chinese restaurants
compared with Western, fast food and Japanese restaurants,
after taking into account a number of factors including cooking
oil consumption and cooking methods [149]. A study in
Singapore compared the concentrations of PM2.5 and PAHs in
three ethnic food stalls and found the levels of both pollutants
to be highest in Malay, followed by Chinese and Indian stalls.
The difference in the levels could be explained by the frying
processes predominantly used at the Malay (deep frying) and
the Chinese (stir frying) stalls, whereas simmering (at lower
temperature) was mostly used at the Indian stall [150].
Respiratory effects
Compared with the wealth of knowledge on the respiratory
effects of biomass and solid fuels, far fewer studies have been
dedicated to cooking-related emissions. Of those that did, the
majority focused on lung cancer. A recent monograph from the
IARC identified 17 case–control studies exploring the associa-
tion between exposure to cooking emissions and lung cancer,
and all were conducted exclusively in the Chinese population
[131]. Among these 17 studies, only four allowed the cooking-
related effects to be distinguished from those related to fuels
[151–154]. In a group of nonsmoking females in Hong Kong,
YUet al. [152] found an escalating dose–response relationship
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between cumulative exposure (frequency and duration, in
dish-years) and lung cancer risk, with a relative risk of ,3 for
101–150 and 150–200 dish-yrs exposure, and .8 for .200 dish-
yrs (referent exposure being f50 dish-yrs). In the two studies
from Shanghai, those females who stir fried most frequently
were 2.6 times [154] and 2.3 times [155] as likely to have lung
cancer compared with those who stir fried least often.
Similarly, a study in Gansu, China reported a relative risk of
2.2 [153]. These findings might explain the observed high
nonsmoking lung cancer incidence in Chinese females, which
could be attributed to their high cumulative exposure to
cooking emissions. However, confounding by cooking fuel
could not be ruled out because of the history of using biomass
or solid fuels in the study populations in the latter three
studies. In addition, recall and other forms of bias that are
found in case–control studies could be operating, and
contributing to the positive findings in some of these studies.
Therefore, the causal relationship has not yet been totally
confirmed.
There are few data on respiratory diseases other than lung
cancer and none was derived from developing countries. A
survey of 239 kitchen workers from 67 restaurants found a
four- and two-fold increase in risk of dyspnoea for females and
males, respectively, compared with controls [156]. However,
the results could have been confounded by combustion
products, although relatively clean fuel (gas) was used in
these restaurants. Assessing the possibility of acute responses,
the lung function of 12 healthy volunteers were monitored
over a 24-h period with and without exposure to cooking
fumes for 2 and 4 h but found no significant changes on
spirometry [156].
Burning of incense sticks
Incense is regularly burnt in homes and offices for religious or
ceremonial rituals and fragrance, particularly in developing
countries. Incense is available in various forms, including
sticks, joss sticks, cones, coils, powder, rope, rocks/charcoal
and smudge bundles. The substances widely used to produce
incense are resins (such as frankincense and myrrh), spices,
aromatic wood and bark, herb seeds, roots, flowers, essential
oils, and synthetic substitute chemicals used in the perfume
industry [157]. Burning of incense releases different air
pollutants, such as PM, VOCs, carbonyl compounds, carbon
monoxide, nitrogen oxides, methane, nonmethane hydro-
carbons, organic carbon, elemental carbon and inorganic ions
(chloride, nitrate, sulfate, sodium, ammonium and potassium
ions), depending on the types of incense sticks and aroma
TABLE 3 Research priorities on health effects of, exposure to and interventions for solid fuel smoke
Research priorities Types of studies
Health effects
Basic studies Genetic susceptibility to various health effects
Comparative studies on exposure to solid fuel smoke, tobacco smoke, passive smoking and traffic pollutions
Studies on different types of health outcomes associated with exposure to solid fuel smoke but with little evidence
Epidemiological studies Relationship between exposure and health outcomes
Different health outcomes, e.g. cervical cancer, visual impairment, lung growth in children, asthma in children
Studies on acute health effects of exposure to solid fuel smoke
Dose–response curve of health effects
Studies on toxicity of fuel types
Studies on health effects of other contributors to indoor air pollution (oil mist, deep frying, mosquito coil, etc.)
Clinical Mechanisms of health outcomes related to solid fuel smoke
Characterisation and early diagnosis of health outcomes
Histopathological differences between inhalation of biomass and tobacco smoke
Exposures
Measurements Standardisation of cross-sectional and longitudinal monitoring of exposure
Better data and more focus on personal monitoring of exposure
Modelling of personal exposure to better estimate the exposure data
Monitoring of intervention of improved cooking stoves in terms of exposure and their performance in the long term
Equipment Research and development on types of equipment, such as cost, size, weight, power supply and resistance to extreme conditions for
developing countries
Interventions
Improved cooking stoves Types of stoves (multiple stoves, multiple fuel scenarios, multiple types of food cooked and different cooking practices)
New biomass stove technology, better combustion and efficiency, and less pollutants emissions
Social intervention Impact of massive educational programmes on raising the awareness of health effects of exposure to biomass smoke
Acceptance of health interventions/health promotions
Resistance to stove/health intervention programmes
Fuel types Research on inexpensive but cleaner fuel types or source of heat such as production of briquettes and charcoal from agricultural wastes
Effects Impact of improved cooking stoves programmes on the health outcomes
Adapted from [20] with permission from the publisher.
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used, the concentration being much higher during the peak
burning time of incense sticks [157–159]. The types of
compounds present in the smoke released after burning incense
suggest that they can cause a number of acute and chronic health
effects. Although a number of studies has suggested that smoke
released from burning can cause respiratory health effects [160,
161], lung cancer [162–164] and dermatological allergic reactions,
and could be mutagenic and or genotoxic [165–167], the evidence
is inconsistent, with some studies finding inverse relationships
for lung cancer [168, 169] and COPD [66].
Burning of mosquito coils
Annually, 45–50 billion mosquito coils are used by ,2 billion
people worldwide [170], particularly in rural and semirural
communities of developing countries, to prevent mosquito
bites. LIU et al. [171] estimated that burning a mosquito coil can
release a mass concentration of PM2.5 equivalent to burning of
75–137 cigarettes, depending upon the types of base material
used to make the mosquito coil, and release formaldehyde
equivalent to 51 cigarettes. The smoke released from burning
mosquito coil contains some carcinogenic PAHs, including
BaP, benzo[a]anthracene, benzo[b]fluoranthene, benzo[k]fluor-
anthene, dibenzo[a,h]anthracene and indeno[1,2,3-cd]pyrene
[171, 172]. People in developing countries tend to burn
mosquito coils during the summer nights and are therefore
regularly exposed to the smokes released for about 6–8 h daily.
Inhalation of the smoke has been reported to cause breathing
difficulties, eye irritation, bronchial irritation, itching, cough
and asthma [171, 173, 174].
CONCLUSION
The available evidence suggests that, despite heterogeneity
among published studies, there is sufficient evidence and
consistency among published studies to conclude that expo-
sure to solid fuel smoke is a risk factor to COPD in adults and
pneumonia in children, particularly those ,5 yrs of age.
Although the field has been hampered by methodological
weaknesses, such as exposure not being measured directly and
inadequate accounting of possible confounding factors, the
overall data are sufficient to be sure that the effects size for
COPD is around a three-fold risk for those exposed and
around a two-fold risk for ALRI in children.
The available evidence also suggests that exposure to coal
smoke is a risk factor to lung cancer whereas the evidence from
biomass smoke exposure on lung cancer is not conclusive. As
for asthma, there remains uncertainty as to whether biomass
smoke does increase the risk of developing asthma in child-
hood and tighter methodological studies are needed to
determine any true causal association. While there is limited
information suggesting that deep frying, and using incense
and mosquito coils are risk factors for respiratory problems,
these risk factors should be regarded only as suggestive at this
stage and need to be explored further (table 3).
STATEMENT OF INTEREST
None declared.
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