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Abstract

In addition to developing nations relying almost exclusively upon biomass fuels, such as wood for cooking and home heating, North Americans, particularly in Canada and the northwestern and northeastern sections of the United States, have increasingly turned to woodburning as an alternate method for domestic heating because of increasing energy costs. As a result, the number of households using woodburning devices has increased dramatically. This has resulted in an increase in public exposure to indoor and outdoor woodsmoke-associated pollutants, which has prompted widespread concern about the adverse human health consequences that may be associated with prolonged woodsmoke exposure. This mini-review article brings together many of the human and animal studies performed over the last three decades in an attempt to better define the toxicological impact of inhaled woodsmoke on exposed children and adults; particular attention is given to effects upon the immune system. General information regarding occurrence and woodsmoke chemistry is provided so as to set the stage for a better understanding of the toxicological impact. It can be concluded from this review that exposure to woodsmoke, particularly for children, represents a potential health hazard. However, despite its widespread occurrence and apparent human health risks, relatively few studies have focused upon this particular area of research. More laboratory studies aimed at understanding the effects and underlying mechanisms of woodsmoke exposure, particularly on those individuals deemed to be at greatest risk, are badly needed, so that precise human health risks can be defined, appropriate regulatory standards can be set, and accurate decisions can be made concerning the use of current and new woodburning devices.
THE TOXICOLOGY OF INHALED WOODSMOKE
Judith T. Zelikoff, Lung Chi Chen, Mitchell D. Cohen,
Richard B. Schlesinger
New York University School of Medicine, Nelson Institute
of Environmental Medicine, Tuxedo, New York, USA
In addition to developing nations relying almost exclusively upon biomass fuels, such as
wood for cooking and home heating, North Americans, particularly in Canada and the
northwestern and northeastern sections of the United States, have increasingly turned to
woodburning as an alternate method for domestic heating because of increasing energy
costs. As a result, the number of households using woodburning devices has increased
dramatically. This has resulted in an increase in public exposure to indoor and outdoor
woodsmoke-associated pollutants, which has prompted widespread concern about the
adverse human health consequences that may be associated with prolonged woodsmoke
exposure. This mini-review article brings together many of the human and animal studies
performed over the last three decades in an attempt to better define the toxicological
impact of inhaled woodsmoke on exposed children and adults; particular attention is
given to effects upon the immune system. General information regarding occurrence and
woodsmoke chemistry is provided so as to set the stage for a better understanding of the
toxicological impact. It can be concluded from this review that exposure to woodsmoke,
particularly for children, represents a potential health hazard. However, despite its wide-
spread occurrence and apparent human health risks, relatively few studies have focused
upon this particular area of research. More laboratory studies aimed at understanding the
effects and underlying mechanisms of woodsmoke exposure, particularly on those individ-
uals deemed to be at greatest risk, are badly needed, so that precise human health risks
can be defined, appropriate regulatory standards can be set, and accurate decisions can
be made concerning the use of current and new woodburning devices.
BACKGROUND AND OCCURRENCE
In developing nations, biomass fuels such as wood, animal dung, and
crop residues are used extensively for home heating and cooking (Inter-
national Institute for Population Science
[
IIPS
]
, 1995; Smith, 2000). For
example, three-quarters of all households in India use unprocessed biomass
as their primary fuel for cooking, and among those homes, more than 90%
use either wood or animal dung (IIPS, 1995). In countries such as India,
daily air pollution exposures from cooking with biomass fuels typically
exceed relevant health-based guidelines by at least 20-fold (Smith & Liu,
1994; Smith, 2000). It has been estimated that indoor air pollution in
developing countries accounts for 2.2–2.5 million deaths annually (WHO,
1997). While biomass fuels are at the high end of the fuel ladder in terms of
269
Journal of Toxicology and Environmental Health, Part B, 5:269–282, 2002
Copyright© 2002 Taylor & Francis
1093-7404 /02 $12.00 + .00
DOI: 10.1080/1093740029007006 2
Support for studies performed in this laboratory was provided by the Center for Indoor Air
Research, contract 94-03C.
Address correspondence to Judith T. Zelikoff, New York University School of Medicine, 57 Old
Forge Road, Tuxedo, NY 10987, USA. E-mail: judyz@env.med.nyu.edu
pollution emissions, they score low for combustion efficiency. Thus, efflu-
ents from these sources contain numerous toxic/carcinogenic components,
such as formaldehyde and polyaromatic hydrocarbons (PAH), which at high
exposure concentrations can cause serious health problems (Smith, 1987,
1993; Larson & Koenig, 1994; Nolte et al., 2001). Among the major respi-
ratory illnesses, cooking smoke appears to increase the risk of chronic ob-
structive lung disease (Pandey, 1984; Malik, 1985; Perez-Padilla et al.,
1996), lung cancer (Sobue, 1990; Franco, 1998), and respiratory infections
(Pandey et al., 1989; Mishra & Retherferd, 1997; Kammen et al., 1998). In
fact, a recent study in northern India noted an association between the use
of wood and/or cow-dung cakes and an increased incidence of pulmonary
tuberculosis in children (Gupta et al., 1997).
In addition to domestic woodburning in developing countries, over the
past two decades, due to rising energy costs and the uncertain availability of
petroleum and natural gas, homeowners in the United States and Canada
have increasingly turned to the use of wood as an alternate heating fuel.
Interestingly, most of the residential woodburning in the United States is
done by people in the middle to upper-middle socioeconomic class. In-
creased usage of wood for home heating has been especially striking in the
northeastern and northwestern United States (National Research Council,
1981). For example, the Washington State Department of Ecology estimated
that during the 1980s wood was burned in 60% of all Washington house-
holds, with about 2.2 million cords consumed annually (Pierson et al.,
1989). In Massachusetts, studies during this same time frame showed that
65% of all households surveyed used woodburning devices, and of those,
68% were in use all day (Tuthill, 1984). Between 1972 and 1989, sales of
woodstoves increased 10-fold (by the late 1980s, the number of operating
woodstoves was thought to exceed 11 million), and it is estimated that
approximately 10% of the total space-heating input for the United States is
from firewood (Lipfert & Dungan, 1983; Samet et al., 1987). While usage of
wood for home heating and sales of woodburning devices declined after
1989, woodburning has resurged in the new millennium, again as a result of
increasing energy costs.
In Canada, it is estimated that about 400,000 homes use wood as the
primary heating fuel, and many others use fireplaces and woodstoves as sup-
plementary sources of heat or for aesthetics. While the Atlantic provinces
are more dependent upon wood for home heating than other locations, it
is in British Columbia that smoke from residential woodburning poses the
greatest threat to health (British Columbia Ministry of Environment, 1995).
Here, inversions in weather patterns frequently warm the air on mountain-
sides, trapping cooler air and smoke at ground level in valleys and allowing
the buildup of pollutants to high concentrations.
Increased usage of woodburning devices has resulted in greater public
exposure to smoke-associated pollutants generated during combustion and
an increased concern by local residents regarding the health effects associ-
270 J. T. ZELIKOFF ET AL.
ated with such exposure. Although legislative action mandating the reduc-
tion of residential woodsmoke levels is moving forward (Koenig et al.,
1988), only a few states are currently affected by regulations (i.e., Colo-
rado, Washington, Oregon), and legislation in other states will take several
years to enact. Meanwhile, those most vulnerable to health impairment due
to air pollutants, such as very young children, individuals with preexisting
cardiopulmonary disease, asthmatics, and the elderly, will continue to be
exposed both indoors and outdoors for prolonged periods of time to high
concentrations of woodsmoke-generated pollutants (Koenig & Pierson, 1991).
CHEMICAL CHARACTERIZATION AND POLLUTANT DISTRIBUTION
Woodsmoke is a complex mixture of numerous gases and respirable fine/
ultrafine particles of varying inorganic/organic composition and diameter
(Pierson et al., 1989; U.S. EPA, 1993; Nolte et al., 2001). Smoke generated
from burning wood is thought to consist of over 200 chemicals and com-
pound groups, which are contained in an effluent that is almost entirely in
the inhalable size range (Cooper, 1980; U.S. EPA, 1993). Woodburning
stoves, furnaces, and fireplaces emit significant quantities of toxic com-
pounds, including respirable particulate matter (PM) with diameters <10
µm (PM
10
), carbon monoxide (CO), nitrogen and sulfur oxides (NO
X
and
SO
X
), aldehydes, PAHs, volatile organic compounds (VOCs), chlorinated di-
oxins, and free radicals (Cooper, 1980; Dasch, 1982; Lao, 1983; Tuthill,
1984; Sexton et al., 1986; Traynor et al., 1987; Lachocki et al., 1989; Koenig
& Pierson, 1991; Hildemann et al., 1991; Koenig et al., 1993; U.S. EPA,
1993; Larson & Koenig, 1994; Nolte et al., 2001).
Under normal usage conditions, woodburning devices create indoor
pollution (Lao, 1983; Sexton et al., 1986; Traynor et al., 1987; Samet et al.,
1987, 1988). It has been reported that both airtight and non-airtight stoves
release fine/ultrafine-sized PM, CO, and PAHs directly within the indoor
environment (Traynor et al., 1987). Concentrations of PM as great as 820
µg/m
3
(U.S. EPA standard for PM
10
is 150 µg/m
3
for a 24-h period, not to be
exceeded >2% of the time) have been measured indoors from non-airtight
stoves over a 24-h period (Traynor et al., 1987). In addition to that amount
released directly inside the home, a large percentage (i.e., 70%) of outdoor
woodsmoke from chimneys actually reenters the house and permeates
neighboring dwellings (Pierson et al., 1989). Many circumstances, including
improper installation, negative indoor air pressure, and downdrafts, facilitate
entry of incomplete combustion products back into the home (Pierson et al.,
1989; U.S. EPA, 1994). Since individuals typically spend 60–70% of their
out-of-work time at home (Szalar, 1972; Chapin, 1974; Sexton et al., 1986),
indoor woodsmoke potentially represents a major source for human expo-
sure.
In addition to pollution created indoors, woodburning devices also con-
tribute to outdoor air pollution (Butcher & Sorenson, 1979; Cooper, 1980;
TOXICOLOGY OF WOODSMOKE 271
Koenig et al., 1988, 1993; Koenig & Pierson, 1991). For example, alde-
hydes released into the ambient environment from woodburning have been
measured at levels comparable to those emitted from power plants and
automobiles (Lipari et al., 1984). Moreover, studies have demonstrated that,
on a moderately cold winter day, 51% of the respirable air particulates in
the Portland, OR, area were from residential wood combustion sources
(Cooper, 1980). Investigations examining other parts of the northwest re-
ported that residential woodsmoke in the Olympia, WA, area accounted for
50% (on clear days) to 85% (on polluted days) of airborne PM (Koenig et
al., 1988). Additional studies in the same geographic area have demon-
strated that 80–90% of the PM measured in the ambient air was due to use
of woodburning devices during nighttime hours (Larson et al., 1992). Such
studies have led to the conclusion that woodsmoke represents a more sig-
nificant source of ambient PM, VOCs, and CO, than the sum total of all
industrial point sources in the state of Washington (Koenig et al., 1988).
While most residential woodburning is currently associated with wood-
stoves, burning in fireplaces also contribute to elevated concentrations (both
indoors and outdoors) of woodsmoke-associated pollutants. For example,
studies have demonstrated that the levels of PAH and PM in homes with
open fireplaces were approximately equal to those with non-airtight stoves,
and substantially greater than those with airtight woodstoves (Maschandreas
& Zabransky, 1980). Moreover, it has been reported that wood burned in an
open fireplace yielded indoor PAH concentrations comparable to those of
ambient urban air (Alfheim & Ramdahl, 1984). These same studies also
reported that the mutagenicity of air samples collected from burning fire-
places exceeded the activity from samples emitted from airtight stoves. On
the other hand, because airtight stoves burn wood in an oxygen-starved
environment, organic chemicals are produced in greater variety in a wood-
burning stove than in a fireplace.
HEALTH EFFECTS
Individually, many woodsmoke constituents have been shown to pro-
duce acute and chronic biologic effects and/or cause deleterious physiologic
responses in exposed humans (Anderson et al., 1973; Speizer et al., 1980;
Ramage et al., 1988; Koenig et al., 1988; Pierson et al., 1989; Koenig &
Pierson, 1991; Schwartz, 1993). For example, CO at levels measured in
homes using woodstoves (in the range of 1.2–43 ppm, compared to the
indoor level of 5 ppm recommended by the American Society for Heating,
Refrigeration, and Air Conditioning Engineers
[
ASHRAE
]
and the current
outdoor standard of 9 ppm for an 8-h period) has been shown to produce
carboxyhemoglobin and increase the incidence of angina among persons
with cardiac disease (Anderson et al., 1973). Nitrogen oxides (primarily
nitrogen dioxide and nitric oxide) bind to hemoglobin to produce methemo-
globin and hematologic aberrations, affect the activity of several enzyme
272 J. T. ZELIKOFF ET AL.
systems, cause vascular membrane injury and leakage leading to edema,
and may produce bronchoconstriction in asthmatics at low levels. The PAHs
that are released into the environment adsorbed onto emitted PM are im-
munosuppressive in laboratory animals (White et al., 1994), as well as car-
cinogenic in animals and possibly humans (Koenig et al., 1988; Pierson et
al., 1989). Aldehydes, mostly as formaldehyde and acrolein, measured
indoors during operation of a woodburning device at concentrations rang-
ing from 0.3 to 1 ppm (compared to ASHRAE recommended indoor levels
of 0.1 ppm), are associated with upper airway irritation, headaches and
other neurophysiologic dysfunctions, exacerbation of bronchial asthma, and
possibly cancer (Kerns et al., 1983). In addition to the effects previously
cited, other chronic health ailments have also been associated with expo-
sure of humans to individual woodsmoke constituents. These include in-
creased airway resistance, decreased vital capacity, increased respiratory
symptoms (i.e., cough, wheeze, dyspnea), and infections in children (Koenig
et al., 1988; Butterfield et al., 1989).
One of the most interesting components of woodsmoke pollution is PM
(Butcher & Sorenson, 1979; Hytönen et al., 1983; Sexton et al., 1986; Tray-
nor et al., 1987; Pierson et al., 1989; Hildemann et al., 1991; U.S. EPA,
2001). Woodsmoke-emitted respirable particulates (<3.5 µm), composed of
a relatively equal mixture of ultrafine/fine (0.02–2.5 µm) and coarse (2.5–3.5
µm) particles (Sexton et al., 1986; Traynor et al., 1987; Hildemann et al.,
1991) can penetrate into the deep lung, producing a variety of morphologi-
cal and biochemical changes. A considerable body of epidemiologic evi-
dence has associated short-term exposure to PM from a variety of sources
with respiratory symptoms, increased use of asthmatic medication, hospital
admissions, early mortality, exacerbation of preexisting medical conditions
including a reduced likelihood of recovering from infectious diseases such
as pneumonia, and an increased incidence and rate of infectious respiratory
diseases in children (Schwartz, 1991, 1993; Pope, 1991; Kammen et al.,
1998).
Although health effects associated with exposure to whole woodsmoke
emissions are not as well studied as its individual components, a number of
adverse health effects have been demonstrated. For example, exposure of
laboratory animals to woodsmoke effluents decreased ventilatory frequency
and ventilatory response to CO
2
(Wong et al., 1984), increased microvascu-
lar permeability and produced pulmonary edema (Nieman et al., 1988),
caused necrotizing tracheobronchial epithelial cell injury (Thorning et al.,
1982), possibly increased the lung cancer incidence in mice (Liang et al.,
1988), increased levels of angiotensin-1-converting enzyme in the lungs
(Brizio-Molteni et al., 1984), and compromised pulmonary macrophage-
mediated immune mechanisms important in antimicrobial defense (Zelikoff
et al., 1995a, 1995b), most likely via alterations in the integrity of the
macrophage surface membrane or cytoskeletal components (Fick et al.,
1984; Loke et al., 1984).
TOXICOLOGY OF WOODSMOKE 273
In humans, health effects seem to be related to host age at the time of
woodsmoke exposure. In adults, effects include prolonged inhalation of
woodsmoke contributed to chronic bronchitis (Rajpandey, 1984), chronic
interstitial pneumonitis and fibrosis (Ramage et al., 1988), cor pulmonale,
interstitial lung disease, pulmonary arterial hypertension (Sandoval et al.,
1993), and altered pulmonary immune defense mechanisms (Demarest et
al., 1979; Ramage et al., 1988).
While adverse effects of prolonged woodsmoke exposures on adults are
notable, children appear to be at greatest risk. Exposure of preschool chil-
dren living in homes heated with woodburning stoves or in houses with
open fireplaces yielded these effects: decreased pulmonary lung function in
young asthmatics (Koenig et al., 1993); increased incidence of acute bron-
chitis and severity/frequency of wheezing and coughing (Butterfield et al.,
1989); and increased incidence, duration, and possibly severity of acute
respiratory infections (Honicky et al., 1983, 1985; Rajpandey, 1984; Morris
et al., 1990; Collings et al., 1990; Honicky & Osborne, 1991; Kammen et
al., 1998). Even in those few epidemiological studies that failed to correlate
woodsmoke exposure with respiratory disease/symptoms (Anderson, 1978;
Tuthill, 1985; Browning et al., 1990), the authors concluded that wood-
smoke pollution may have aggravated symptoms of respiratory disease and
should not be disregarded as a possible contributing factor to increased res-
piratory infections in young children.
THE IMMUNE SYSTEM AS A TARGET OF WOODSMOKE TOXICITY
In addition to the aforementioned health effects associated with inhaled
woodsmoke and/or its components, many of the constituents have also been
shown to alter pulmonary immune defense mechanisms in a persistent and
often progressive manner (Jakab, 1977, 1992, 1993; Speizer et al., 1980;
Hatch et al., 1981; Aranyi et al., 1983; Samet et al., 1987; Pierson et al.,
1989; Burrell et al., 1992; Jakab & Hemenway, 1993; Zelikoff et al., 1999;
Thomas & Zelikoff, 1999; Zelikoff, 2000). For example, studies have shown
that in the absence of an inflammatory response, inhalation exposure of
mice for 4 d to 15 ppm formaldehyde following bacterial challenge im-
paired intrapulmonary killing of
Staphylococcus aureus
24 h after expo-
sure; the same effect on lung antibacterial defenses was produced by
formaldehyde at 1 ppm when exposure preceded, and was then continued
after, bacterial challenge (Jakab, 1992). In the same study, F
cg
receptor-
mediated phagocytosis by alveolar macrophages recovered from mice
exposed to 10 mg/m
3
carbon black and 5 ppm formaldehyde (4 h/d, 4 d)
was progressively suppressed up to 25 d following exposure. In a later
study by the same investigator (Jakab, 1993), coexposure of mice to carbon
black (10 mg/m
3
, 4 h/d, 4 d) and acrolein (2.5 ppm) suppressed intrapul-
monary killing of
S. aureus,
impaired elimination of
Listeria monocytogenes
and influenza A virus, and enhanced intrapulmonary killing of
Proteus mira-
274 J. T. ZELIKOFF ET AL.
bilis;
it was suggested that the observed biologic effect was due to carbon
particles acting as vehicles to carry acrolein into the deep lung. In addition,
the same coexposure regime persistently suppressed alveolar macrophage-
mediated tumor necrosis factor-
a
(TNF
a
) production and phagocytosis;
phagocytic activity was significantly reduced at 1 through 11 d following
exposure, while TNF
a
production was depressed after 4 d and reached
control levels by d 20. Studies by this laboratory investigating the immuno-
toxicity of inhaled ambient PM (which could include particles generated
from woodburning) demonstrated the ability of particulates <2.5 µm con-
centrated from New York City air to exacerbate an ongoing
Streptococcus
pneumoniae
infection in PM-exposed rats (Zelikoff et al., 1999, in press).
Thus, many respirable pollutants found in woodsmoke can offset the bal-
ance necessary for immunoregulation of the lung. This disruption in home-
ostasis may produce a cascade of detrimental secondary events, including
pathogenesis and compromised host resistance which may lead to increased
respiratory infections.
While only a limited number of studies have investigated the effects of
whole woodsmoke emissions on pulmonary immunity, it appears that host
defense and/or immune cell function is depressed in a manner similar to that
produced by many of the individual woodsmoke constituents (Demarest et
al., 1979; Fick et al., 1984; Loke et al., 1984; Zelikoff et al., 1995a, 1995b).
For example, a single inhalation exposure of rabbits to smoke from the py-
rolysis of Douglas fir wood produced an increase in the total number of
recovered pulmonary macrophages and a transitory decrease in macrophage
adherence to glass (Fick et al., 1984). Moreover, this same exposure regime
decreased macrophage uptake of the gram-negative bacterial pathogen
Pseudomonas aeruginosa
in the absence of an inflammatory response or
changes in macrophage viability. In another study, a single inhalation expo-
sure of Douglas fir-generated woodsmoke altered macrophage morphology
and membrane ultrastructure (Loke et al., 1984). Inhaled woodsmoke has
also been reported to alter the chemotactic migration of bronchopulmonary
lavaged human macrophages (Demarest et al., 1979).
The aforementioned studies have provided some evidence that inhala-
tion of woodsmoke effluents can alter pulmonary immune defense mecha-
nisms, and that the macrophage, a primary defense of the deep lung that
provides a link between the nonspecific and specific defense systems of the
respiratory tract, is the likely target for woodsmoke-induced immunotoxicity.
However, some of the most compelling evidence demonstrating the ability
of woodsmoke to modulate pulmonary immunocompetence comes from
animal toxicology studies performed in this laboratory (Zelikoff et al.,
1995a, 1995b). For these laboratory studies, 3-mo-old Sprague-Dawley rats
were exposed repeatedly (1 h/d, 4 d) to a single concentration of wood-
smoke (i.e., 750 µg PM
2.5
/m
3
) generated from red oak burned in a combus-
tion furnace, originally developed for generating coal fly ash (Chen et al.,
1990) and later adapted for woodburning (Figure 1).
TOXICOLOGY OF WOODSMOKE 275
Narrowly size-classified wood dusts (i.e., 53–63 µm) produced through
mechanical grinding, were used for all experiments. The effluent concentra-
tions of CO, PAH (measured as benzo
[
a
]
pyrene), PM
2.5
, and NO
X
used in
these studies were within the range of those measured indoors during non-
airtight/airtight stove operation (Traynor et al., 1987). Mass median diame-
ter of the emitted particles was 0.16 µm (
s
g
= 2.23), which is within the
same particle size range shown to be released during the burning of oak
wood in a residential fireplace (Hildemann et al., 1991).
At 3, 24, 72, and 120 h following the final woodsmoke exposure, rats
were intratracheally instilled with the pneumonia-producing bacteria
Staphy-
276 J. T. ZELIKOFF ET AL.
FIGURE 1. Combustion furnace for generating woodsmoke. The generation system consists of a feeder,
laboratory-scale laminar-flow drop-tube furnace, and a collection probe. Wood dust is carried in a
nitrogen gas stream and injected axially downward into the furnace, where the particles are ignited and
burned in a narrow zone along the furnace axis. The temperature of combustion, as well as the bulk gas
temperature, is controlled by the partial pressure of oxygen in the O
2
/N
2
bulk gas mixture. At the exit of
the collection probe, a three-stage virtual impactor was used to remove particles larger than 10 µm and
the remaining particles and gas mixture then entered the exposure chamber.
lococcus aureus
to assess effects upon pulmonary clearance, or were sacri-
ficed and their lungs either lavaged for recovery of pulmonary macrophages
or fixed for histopathological examination (Zelikoff et al., 1995a, 1995b).
Inhalation of woodsmoke emissions for 4 d (1 h/d) progressively reduced
(compared to control) the in vivo clearance/killing of
S. aureus.
Effects of
inhaled woodsmoke on intrapulmonary clearance appeared as early as 3 h
following the final woodsmoke exposure and persisted for up to 5 d; killing/
clearance was reduced to 60% of control values after 3 h and then progres-
sively declined to 2% after 5 d. While the mechanisms by which wood-
smoke may have acted to persistently suppress bacterial clearance are not
yet clear, results from this part of the study demonstrated that short-term
repeated inhalation of woodsmoke generated from the burning of a com-
mon hardwood used for home heating compromised pulmonary host resis-
tance against an infectious, pneumonia-producing lung pathogen well after
exposures ceased.
In this same study, both phagocytic activity and superoxide production
by macrophages recovered from smoke-exposed animals were decreased
(compared to control values) in a time-dependent manner. The persistent
effects of short-term exposure to woodsmoke on F
c
-dependent opsonized
particle uptake were similar to previous studies that demonstrated a pro-
gressive decrease in F
c
-receptor-mediated phagocytosis that began after 4 d
and was persistent for up to 25 d following repeated coexposure to carbon
black and the woodsmoke constituent formaldehyde (Jakab, 1992). It was
concluded from this latter study that the observed onset delay and persis-
tence of effects were due to formaldehyde desorption from the particle over
an extended period of time, resulting in a slow accumulation of an internal
dose, which, in turn, produced a continuous progressive effect. Given that
woodsmoke is a mixture of gases and respirable particulates, a similar ex-
planation could apply to the study with red oak effluents. Effects upon
macrophage function along with those observed on bacterial clearance
may help explain the increased incidence of respiratory infections observed
in woodsmoke-exposed children, particularly those under 5 yr of age living
in developing nations.
Even though information concerning the immunomodulating potential
of inhaled woodsmoke is rather sparse (Demarest et al., 1979; Loke et al.,
1984; Fick et al., 1984; Zelikoff et al., 1995a, 1995b), it appears that only a
brief exposure to woodsmoke can alter intrapulmonary bacterial clearance
and macrophage-mediated immunity. However, whether similar effects
occur following long-term exposure, a scenario more reflective of the
human situation, remains to be seen.
SUMMARY
This mini-review has provided an overview of the health effects associ-
ated with exposure to woodsmoke and its individual constituents. In gen-
TOXICOLOGY OF WOODSMOKE 277
eral, combustion effluents from woodburning devices are increasing world-
wide, and this has resulted in greater public exposure and increased con-
cern by exposed individuals. While more studies are needed to determine
the effects of long-term exposure, and the particular woodsmoke con-
stituent(s) that may be responsible for the observed toxicities, it appears
clear that inhalation of combustion products from wood can have a signifi-
cant impact upon pulmonary homeostasis and/or exacerbation of ongoing
disease processes, especially for those members of the population deemed
most susceptible (i.e., young children, asthmatics, elderly, and individuals
with ongoing cardiopulmonary disease).
Because of public outcry, a number of health-related agencies have
offered some recommendations to individuals using woodburning devices,
including consideration for your neighbors—that is, the smoke you gener-
ate also affects your neighbors “lungs”; burn cleanly and use only dry
wood; avoid burning wood during hazy windless days and nights when
temperature inversions might trap woodsmoke and other pollutants close to
the ground; if possible, convert your woodburning fireplace to use natural
gas or propane; and if your woodstove was manufactured before July 1988,
replace it with one that is certified by the U.S. Environmental Protection
Agency (British Columbia Ministry of the Environment, 1995; American
Lung Association of Washington State, 1998; American Lung Association,
2000). Regarding the use of U.S. EPA-certified stoves, while it is true that
these stoves generate only about half as much PM as uncertified ones (i.e.,
4.0 vs. 10 µg PM/h, respectively), they still create as much particulate pol-
lution as 12,000 houses heating with propane or natural gas.
Overall, more resources need to be devoted to woodsmoke research,
particularly in the areas of air pollution measurements and adverse health
effects, so as to better understand this continuing dilemma (American Lung
Association, 2000).
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Around 41% of the world’s population continue using solid fuels, including wood and other types of biomass, for cooking or heating their homes. Long-term indoor exposure to wood smoke, and biomass smoke in general, is a risk factor for developing chronic obstructive pulmonary disease (COPD). In some regions of the world, biomass exposure is a more frequent cause of COPD than exposure to cigarette smoke. Recently it has been described notable differences between COPD associated with wood smoke (WS-COPD) and that caused by tobacco smoking (TS-COPD): significantly less emphysema and more airway inflammation in WS-COPD. Recognizing these differences, some authors have suggested that WS-COPD should be considered a new COPD phenotype. This chapter summarizes the differences between WS-COPD and TS-COPD. The information about the characteristics of COPD caused by other types of biomass fuels, different from wood, is very scarce. Accepting that the smoke derived from wood burning and tobacco smoking have some differences (etiology), the inhalation patterns are different (pathogenesis) and the physiopathological mechanisms they induce may also differ, we analyze if the disease caused by indoor chronic exposure to wood smoke should be considered as another COPD phenotype or a distinct nosological entity.
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Introduction: Pulmonary hypertension (PH) is a common and well-established complication of chronic obstructive pulmonary disease (COPD). Its presence is associated with decreased survival. This study was designed to investigate the PH frequency and its relations in hospitalized tobacco and biomass related COPD patients. Methodology: The study population in this retrospective study of 320 patients was conducted in COPD patients who had history of smoking or biomass fuel exposure and who had undergone echo-cardiography for evaluation of pulmonary hypertension. The duration of study was over a period of two year. Result: The result of this study, patients exposed with biomass smoke for more than 10 years had increased incidence of pulmonary hypertension when compared to patients exposed to tobacco smoke for more than 10 years. Conclusion: This study concludes that, suggest implementing strategies like medication of stove design, switching over to
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Wood smoke results in general air pollution similar to that caused by cigarette smoke. Therefore, the increased use of wood stoves has caused additional concern for the health effects of wood smoke on the affected population. The resultant legislation and its implementation are discussed for Northwest states, focusing on the 1988 Washington State law which is written to decrease air pollution and its deleterious health effects. -from Journal summary
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The very young and elderly are most vulnerable to health impairments 'secondary' to air pollution. A study was conducted in the winter of 1985-1986 to analyze the impact of woodstove burning on the general respiratory health of pre-school children living in homes where wood was burned. There was no attempt to separate out the potential impacts from the various types of woodstoves, for example, airtight or catalytic filters. The frequency and severity of 10 respiratory symptoms in 59 children were recorded by parents over a six-week period. The study focused on eliciting symptoms of upper respiratory tract irritations and upper respiratory illness. Data analysis yielded a significant correlation between hours of woodstove use and wheeze frequency, wheeze severity, cough frequency and waking up with cough (P = 0.01). The correlation between woodstove use and cough severity was significant at the P = 0.05 level. No evidence was found suggesting an association between hours of woodstove use and the symptoms of fever, shortness of breath or runny nose.
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Over the past two decades, due to rising energy costs and the uncertain availability of petroleum and natural gas, homeowners in the United States have increasingly turned to the use of wood as an alternate heating fuel. This trend has been especially striking in the northeastern and northwestern United States (National Research Council, 1981). For example, the Washington State Department of Ecology estimated that wood was burned in 60% of all Washington households, with about 2.2 million cords of wood consumed annually (Pierson et al., 1989). In Massachusetts, studies showed that 65% of all households surveyed used wood-burning devices, and of those, 68% were in use 24 hr a day (Tuthill, 1984). While sales of woodstoves have been recently declining, the current numbers of woodstoves in the United States is thought to exceed 11 million. It is estimated that approximately 10% of the total space-heating input for the United States is from firewood (Lipfert and Dungan, 1983).
Evaluation of the gas exchange responses to steady state treadmill exercise of 176 patients with chronic disorders of the lower respiratory tract demonstrated that alveolar disease significantly affects O2 transfer with little effect on CO2 transfer. At exercise levels requiring oxygen delivery 2- to 3-fold above resting levels, patients with interstitial lung disease [idiopathic pulmonary fibrosis (IPF), sarcoidosis, histiocytosis-X (HX)] and “pure” destructive lung disease [αl-antitrypsin (αlAT) deficiency] demonstrated no ventilation or cardiac limitation, but all exhibited marked reductions in O2 transfer. Strikingly, although resting values of PaO2 were normal or mildly reduced, the average estimated PaO2 at a of 1 L/min was 47 mmHg in IPF, 65 mmHg in sarcoid, 54 mmHg in HX, and 41 mmHg in αlAT deficiency. Comparison of resting and exercise parameters revealed that: (1) exercise studies can uncover alveolar dysfunction in the presence of normal resting parameters, and (2) resting parameters cannot predict the magnitude of O2 related abnormalities induced by exercise. These observations suggest that exercise testing is a useful clinical tool in detecting alveolar disease and gauging the magnitude of abnormalities of O2 transfer.
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• The cellular responses in the lungs of rabbits and the morphologic features of the tracheobronchial tree by scanning electron microscopy were examined 24 hours following acute Inhalation of Douglas fir wood smoke. Thermal Injury to the upper airway was excluded. Injury to proximal tracheal lining cells was severe and consisted of loss of the epithelium. The changes of the epithelial barrier in the proximal major bronchi were less severe in nature. However, the alterations observed by scanning electron microscopy suggested dysfunction of the mucociliary blanket. Both cell counts of bronchoalveolar lavage fluid and morphologic findings reflected an increase in alveolar macrophage response. Smoke-exposed alveolar macrophages showed significant changes In the surface features. These findings may explain the tracheobronchitis seen clinically, and the propensity of patients to lung infection following smoke inhalation. (Arch Surg 1984;119:956-959)
Article
Ten volunteers with ischemic heart disease (stable angina) were exposed in a double-blind experiment to 0, 50, or 100 ppM CO for 4 hr prior to treadmill exercise. COHb averaged 1.3, 2.9, and 4.5% just after exposure. CO decreased exercise time to anginal pain and prolonged duration of pain after stopping exercise. 5 of 10 had deeper ST-segment depression.