A SUMMARY OF THE EMISSIONS CHARACTERIZATION AND
NONCANCER RESPIRATORY EFFECTS OF WOOD SMOKE
TIMOTHY V. LARSON AND JANE Q. KOENIG
Departments of Civil Engineering and Environmental Health University of Washington
Seattle, WA
Prepared for:
Air Risk Information Support Center (Air RISC)
US Environmental Protection Agency
Co-sponsored by:
Office of Air Quality Planning and Standards
Office of Air and Radiation
Research Triangle Park, NC 27712
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
Office of Research and Development
Research Triangle Park, NC 27712
U.S. Fr-v'rcrv • ' P'-v^tion Agency
Region 5,! ?j)
77 West J-. .::-vard, 12th Floor
Chicago, IL -.,„-;-o590
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DISCLAIMER
This document has been reviewed by the Air Risk Information Support Center (Air RISC)
of the Office of Air Quality Planning and Standards and the Environmental Criteria and
Assessment Office, and approved for publication. Approval does not signify that the
contents necessarily reflect the views and policies of the US Environmental Protection
Agency, nor does mention of trade names or commercial products constitute an
endorsement or recommendation for use. This project was funded in part by Contract No.
1D3253NAEX from the Environmental Protection Agency.
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EXECUTIVE SUMMARY
During the past twenty years, the use of wood has become popular as an alternative
to conventional home heating fuels. This report summarizes the current state of knowledge
concerning chemical composition of wood smoke, emission rates from different wood
burning devices, impacts from wood burning on airborne particle levels, and the human
respiratory responses to inhaled wood smoke.
Wood consists of approximately 50 to 70 weight percent cellulose and
hemicellulose, which are polysaccharides, and about 30 weight percent lignin, which is a
skeletal network of branch-chain polymers that provide structural integrity. Cordwood
heaters bum wood with a deficit of oxygen and readily generate products of incomplete
combustion, including carbon monoxide and numerous organic compounds. If these
vapors are not immediately oxidized, they cool as they are exhausted to the atmosphere
with subsequent formation of fine particles rich in relatively high molecular weight organic
compounds.
Exposure to wood smoke can occur via a number of pathways. In addition to
outdoor exposure, indoor exposure to elevated levels of wood smoke can occur either from
the use of a wood burning appliance or by infiltration of outdoor air. In the past ten years,
there have been a number of studies documenting the outdoor levels of airborne particles
resulting from wood burning. The average night time levels of fine particle wood smoke
vary from location to location. As expected, levels are higher in residential areas than in
downtown urban or industrial areas and generally higher at night than during the day. The
agreement between different source apportionment methods, when compared, is good.
Although smoke levels in outdoor air are important, most people spend a majority of their
time indoors, especially at night in residential areas.
Epidemiological investigations of adverse respiratory effects of wood smoke
emissions in the US have centered on either symptomatology or pulmonary function. The
symptoms measured have been the traditional respiratory disease outcomes; that is, cough,
wheeze, and upper or lower respiratory infection. Pulmonary functions measured have
been FEVj, a measure of air flow limitation caused by obstruction in the airways, or FVC,
a measure of the total amount of air that can be forcibly exhaled from the lungs. There are
eight published reports of associations between residential wood smoke and lung function
in children studied in the field and one study of responses in adult subjects. All but one of
the studies found adverse respiratory outcomes associated with exposure to wood smoke.
The adverse respiratory effects noted were increased respiratory symptoms, increased
lower respiratory infection and decreased pulmonary function . These different endpoints
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show a coherence of the data which is all the more remarkable when one considers that
only one of the eight studies targeted a susceptible population of children (asthmatics).
This coherence supports the plausibility of a case-effect relationship. However, a
biological gradient (dose response) has not been shown, most likely due to the lack of
exposure assessment data in most of the available studies.
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INTRODUCTION
During the past twenty years, the use of wood has become popular as an alternative
to conventional home heating fuels. Part of this movement has been due to uncertainty
about the availability of fossil fuels. About ten percent of space heating in urbanized areas
of the northern U.S. is from wood burning, with up to fifty percent in some smaller, rural
towns (Skog and Wattersen, 1983; Lipfert and Dungan, 1983; Hough, 1988; Pierson et al,
1989). Wood is obviously a renewable resource. This attraction is offset, however, by the
increased air pollution emissions from wood heating devices compared with devices fueled
with oil or gas. As noted initially by Cooper (1981), particle and organic carbon emission
rates can be as much as one to two orders of magnitude larger in wood heating devices than
in oil or gas heating units. Not surprisingly, legislation restricting the sale of conventional
wood stoves first appeared in Oregon in 1984, followed by nationwide restrictions in
1988. Although rapid progress has reduced emissions in some types of modern wood
heaters, older "conventional" wood stoves and fireplace inserts are still the predominant
appliance in use today. As discussed later in this document, a number of communities
continue to experience elevated levels of wood smoke during the winter heating season. In
addition, elevated indoor air pollution levels have been observed in homes with non-airtight
or improperly operated wood stoves. As a result, there has been an ongoing interest in the
potential health effects of exposure to wood smoke. Several reviews of the health effects of
wood smoke have been prepared (Ammann, 1986; Koenig et al, 1988; Anderson, 1989;
Pierson et al, 1989; Marbury, 1991; Dost, 1991). The present review will attempt to
summarize the available information on the chemical and physical properties of wood
smoke, levels of wood smoke in both indoor and outdoor environments, emission data and
the adverse respiratory responses in animal toxicity studies and epidemiologic studies of
human populations.
WOOD COMBUSTION AND WOOD SMOKE
Most wood burned for heat is cordwood with some increasing use of wood pellets.
Cordwood heaters burn wood with a deficit of oxygen and readily generate products of
incomplete combustion, including carbon monoxide and numerous organic compounds. If
these vapors are not immediately oxidized, they cool as they are exhausted to the
atmosphere with subsequent formation of fine particles rich in relatively high molecular
weight organic compounds. A "conventional" wood stove fits this description. In order to
reduce emissions from cordwood heaters, these vapors are oxidized directly downstream of
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the combustion zone either by using a noble metal catalyst to more completely combust
vapors at the lower exhaust temperatures, or by using an insulated secondary combustion
chamber in order to maintain a high exhaust temperature while mixing the gases with a
separate stream of additional combustion air. The former method is employed in "catalytic"
stoves, the latter in "non-catalytic" or "high technology" stoves. In contrast to cordwood
heaters, pellet stoves take advantage of the larger wood surface area per unit mass of wood.
Consequently, the higher heat transfer rates from the combustion gases to adjacent,
uncombusted wood results in efficient vaporization of the wood prior to combustion.
Mixing these vapors with excess combustion air at the top of a pellet bed results in much
more complete combustion than that in conventional stoves.
Table 1 compares the emission rates from each of these wood heating devices. Values are
summarized from both controlled, laboratory tests and also from actual in-home, field tests. As
expected, conventional stoves emit greater amounts of paniculate matter and carbon monoxide per
kilogram of wood than do catalytic, non-catalytic and pellet stoves. The pellet stove appears to be
the consistently lowest emitter in both laboratory and field tests. Notice, however, that both the
non-catalytic and pellet stoves, which bum wood at relatively high temperatures, emit greater
amounts of nitrogen oxides than do the conventional or catalytic stoves, which burn wood at
relatively lower temperatures. Higher temperatures favor formation of nitrogen oxides and
oxidation of organic vapors, including both condensible organic compounds as well as volatile
organic compounds (VOCs).
The large variability in emission rates for a given appliance is due to a number of factors
including stove design, wood moisture content, and burn rate. High wood moisture content
reduces combustion temperatures and efficiency. In conventional stoves, increasing burn rate
increases combustion temperatures and efficiencies, but in catalytic and non-catalytic devices the
higher burn rates actually decrease combustion efficiency by decreasing the times in the secondary
combustion zone. Increased burn rates also increase PAH emissions independent of stove type
(McCrillis and Burnet, 1990). Pellet stoves operate at a fixed burn rate and are not as susceptible
to operator variability.
Compared to wood stoves, we know little about fireplace emissions. Here we distinguish
fireplaces from conventional fireplace inserts. Inserts are a home heating device with emissions
similar to conventional wood stoves. Standard, open fireplaces can be a net home cooling device
because of the large amounts of air they draw from outside during maximal burn rates. In general,
conventional fireplaces emit comparable amounts of paniculate matter and less carbon monoxide
per kg wood burned compared to conventional wood stoves. However, fireplaces usually operate
at higher wood burn rates and for shorter time periods than most wood heating devices.
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It is clear from Table 1 that we know relatively little about the chemical composition
of wood stove exhaust as a function of stove type. Most studies of the chemical
composition of wood smoke have been conducted using conventional wood stoves.
Despite this, we can make a number of general conclusions based upon our knowledge of
the wood combustion process and the measurements of exhaust from conventional stoves.
Table 2 summarizes the reported constituents in wood smoke and provides quantitative
information on their emission rates.
Wood consists of approximately 50 to 70 weight percent cellulose and
hemicellulose, which are polysaccharides, and about 30 weight percent lignin, which is a
skeletal network of branch-chain polymers that provide structural integrity. In addition,
there are small amounts of resinous materials and inorganic salts. The lignin polymer
consists of two main monomers, a guaiacyclopropane structure and a syringylpropane
structure. Upon heating, these structures break apart producing a large variety of smaller
molecules, many of which are part of the general class of oxygenated monoaromatics
(Steiber et al, 1992). Included in this class are methoxy phenols and methoxy benzenes, as
well as phenols and catechols. This decomposition also produces benzene and alkyl
benzenes. The presence of guaiacol, syringol and their derivatives as a group are unique to
the burning of wood because they are a direct consequence of the destruction of the unique
lignin structure. In contrast, phenols, catechols, benzene and alkyl benzenes are not unique
to wood combustion and have been found in the exhaust gases of other combustion
sources.
Hawthorne (1988, 1989) has identified approximately 30 guaiacol and syringol
derivatives in wood smoke. Guaiacol was found in the vapor phase, substituted guaiacols
in both vapor and paniculate phases, and syringol and derivatives predominately in the
particulate phase. These two classes of compounds comprised as much as twenty percent
of the particulate carbon in the wood smoke. These structures can also be transformed at
higher temperatures to napthalene and substituted napthalenes, the predominant PAHs
found in wood smoke. The thermal destruction of polysaccharides are thought to be
responsible for the formation of furan and its derivatives, including benzofuran and furfural
(Edye and Richards, 1991). These same researchers point to the acetyl ester groups found
in the hemicelluloses as the source of acetic acid in wood smoke.
Retene has also been proposed as a unique marker of wood smoke (Ramdahl,
1983). Retene is produced from the decomposition of abietic acid (a polar cyclic
terpenoid), a resinous component of wood. However, other aromatic rich fuels will also
produce concensed ring aromatics. Therefore retene may not be unique to wood burning.
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Abietic acid and dehydroabietic acid as well as other cyclic di- and tri-terpenoids have also
been identified in wood smoke. Woody plants also contain terpenes (Cio cycle and
bicyclo-alkanes and alkenes). These compounds can boil off a low temperature wood fire
and are found in wood smoke (Steiber and Dorsey, 1988). Because they are relatively
volatile, they are also emitted directly into the air by trees and thus are not necessarily only
produced by the combustion of wood.
The size distribution of wood smoke particles has been measured by several
investigators (Dasch, 1982; Kamens et al, 1984; Kleindeinst et al, 1986). The particle
volume peaks at between 0.15 and 0.4 micrometers, with essentially no particles greater
than one micrometer. This is consistent with the fact that the majority of the mass is
formed by condensation processes in the exhaust. Owing to their relatively small size, they
are very efficient at reducing visibility and are not readily removed by inertial and
gravitational processes.
PAHs and oxy-PAHs are formed during the combustion of a variety of fuels
including wood. As mentioned previously, PAH emission rates increase with increasing
burn rate, implying that the combustion conditions in the wood burner determine their
formation and emission rates. However, it has also been observed that PAH emissions are
higher in conventional stoves burning pine than in similar stoves burning hard wood,
implying that fuel type is also a factor (Steiber et al, 1992; McCrillis and Bumet, 1990).
Of the trace elements, potassium is found at relatively high levels in wood smoke.
Combustion of hardwoods produces more ash (and thus higher levels of trace elements )
than does combustion of softwoods. The paniculate elemental carbon levels reported in
wood smoke are somewhat controversial. Some researchers claim that up to 95 weight
percent of the total particle mass is extractable in dichloromethane and/or methanol (Steiber
and Dorsey, 1988), while others claim that up to 50 percent of the total paniculate carbon is
elemental carbon as measured by optical and thermal methods (Rau, 1989). It seems
reasonable to conclude that 5 to 20 percent of the total particulate mass is unextractable and
that this unextractable fraction contains elemental carbon.
Upon release to the environment, many of the compounds in wood smoke are
expected to undergo some degree of chemical transformation in the atmosphere. The
relatively few studies of these transformations are summarized in Table 3. In fact, the only
laboratory study of actual wood stove exhaust that was designed to observe the
transformation of selected organic compounds was done under simulated daytime
conditions in the presence of intentionally added nitrogen oxides (Kleindeinst et al, 1986).
Under these photochemically active conditions, there was rapid destruction of the alkenes
and furans as well as production of aldehydes including formaldehyde.
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The nature and extent of these transformations in the dark without added nitrogen
oxides has not been reported. We have only indirect evidence largely obtained from field
measurements of selected compounds. These field studies compare the levels of a given
compound or compounds in both the stack and the ambient air relative to each other and/or
to a reasonably conservative tracer such as fine particle mass. If the relative amounts are
similar in both the stack and the environment, then this constitutes evidence that the
chemical transformations are relatively minor over the time of the measurement. If order-
of-magnitude changes occur, then this implies chemical transformation has also occurred.
The night time field studies listed in Table 3 found that the methoxy phenols and the total
levels of one, two and three oxygen atom monoaromatics remain relatively constant relative
to particle mass and to each other respectively. These observations imply that these
compounds undergo relatively little atmospheric transformation during the night in winter.
This result is interesting in light of the potential for substituted phenols to undergo
relatively rapid reaction with nitrate radicals (Carter et al, 1981). In contrast to the stability
of these selected compounds, the acidity of wood smoke particles appears to degrade upon
release to the night time environment (Lindell, 1991). The specific acids that contribute to
particle acidity are unknown. We do know, however, that some of the constituents of
wood smoke are found in fogwater (Muir, 1991) and rainwater (Luenberger et al, 1985).
This may be an important scavenging route for these compounds in the atmosphere.
EXPOSURE TO WOOD SMOKE
Exposure to wood smoke can occur via a number of pathways. In addition to
outdoor exposure, indoor exposure to elevated levels of wood smoke can occur either from
the use of a wood burning appliance or by infiltration of outdoor air. In the past ten years,
there have been a number of studies documenting the outdoor levels of airborne particles
resulting from wood burning. These studies are summarized in Table 4. We have included
only those studies in this table that quantified the levels of airborne particles using one of
several chemical tracer methods. There have also been a large number of studies that have
documented elevated levels of paniculate matter in residential communities where wood
burning is prevalent, but have not employed receptor models to estimate the wood burning
fraction. Perhaps the most notable of these are the measurements taken in Klamath Falls,
Oregon that have exceeded 600 |ig/m3 on a 24 hour basis during the winter (Hough,
1988). Based upon inventories of fuel use, wood smoke may account for as much as 80
percent of the airborne particle concentrations during the winter (Heumann et al, 1991).
The Klamath Falls studies emphasize another important point- the location of the air
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monitoring device. There is up to a four fold difference between various parts of town,
with the highest readings in the residential area (Heumann et al, 1991). This same spatial
variability was observed by Larson et al (1990) using a mobile nephelometer. They found
that the nighttime drainage flow tended to concentrate the wood smoke at valley floors,
with a consistent factor of two to three difference between ridge line and valley flow smoke
levels. With this caveat in mind, we can see from Table 4 that the average night time levels
of fine particle wood smoke vary from location to location. As expected, levels are higher
in residential areas than in downtown urban or industrial areas and generally higher at night
than during the day. The agreement between different source apportionment methods,
when compared, is good.
Several studies are of interest to later discussions of the health effects of wood
smoke. In addition to the Klamath Falls studies discussed above, the limited measurements
by Carlson (1982) in Missoula, Montana indicated that the majority of the fine particle mass
was due to wood burning. The measurements taken in Boise, Idaho also found that the
majority of the extractable organic material found in fine particles was from wood burning,
with the remainder due to mobile sources (Klouda et al, 1991; Lewis et al, 1991). Finally,
the measurements taken in Seattle, Washington (Larson et al, 1990; Larson et al, 1992)
indicate not only that there are elevated levels of wood smoke particles during winter
evening periods at a residential location, but also that the majority of the fine particle mass
at this location is due to wood burning all weeks of the year. The fine particle mass
concentrations at this site are low in the summer, and therefore the absolute concetrations
due to wood burning are about an order of magnitude less in summer than in winter. Open
burning restrictions went into effect in this area in September, 1992. Thus wood burning
is not expected in the summer from yard waste burning and land clearing fires.
Although smoke levels in outdoor air are important, most people spend a majority
of their time indoors, especially at night in residential areas. Indoor exposure can occur not
only from infiltration of outdoor air, but also from emissions into the home from a wood
burning appliance. Table 5 summarizes our current knowledge of indoor wood smoke
levels. Emissions occur into the home during fueling of the stove and may also occur
during stove operation. More modern, airtight stoves generate less emissions directly into
the home than older non-airtight stoves or improperly operated and/or maintained stoves.
To put the emission rates listed in Table 5 into perspective, consider a 100 cubic meter
room. If seven tenths of the volume of air in the room is exchanged with outside air every
hour, and if 70 percent of the fine particles from the outside air penetrate into the home,
then for a typical outdoor level of 20 (ig/m^ of wood smoke particles there is an effective
infiltration rate of 20x0.7x0.7x100 = 1 milligram per hour of fine particle mass. Higher
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outdoor levels or more rapid air exchange rates would give larger infiltration rates. For a
majority of the studies of fine particle mass in homes with airtight stoves, the indoor
outdoor ratios are at or below 1.0, implying that infiltration is important even in homes
with stoves. Recently unpublished work in nine homes in Seattle, Washington without
stoves and without smokers also found a median indoor/outdoor ratio less than 1.0 for over
3000 hours of continuous nephelometer data, with elevated indoor levels in wood burning
neighborhoods (J.Anusewski, M.S.E. thesis, Univ. of Washington, 1992). As also
shown in Table 5, the indoor/outdoor ratios are much higher for carbon monoxide and
formaldehyde, two species that have a number of indoor sources in addition to wood
stoves. The data for formaldehyde are particularly striking, implying that although wood
stoves emit formaldehyde, their emissions are not a major determinant of overall exposure
to this specie.
HEALTH EFFECTS
Many of the constituents of wood smoke described earlier are known to aggravate
respiratory disease and irritate mucous membranes. Knowledge of the toxicity of a
compound usually depends on data from three sources, animal toxicology, controlled
human studies, and epidemiology. In this section, we review the available information on
wood smoke exposures, with emphasis on studies of human subjects.
Animal toxicology:
We restrict our discussion of animal toxicology to those studies employing whole
wood smoke; we do not discuss data on individual compounds found in wood smoke.
Unfortunately there is a paucity of data on acute effects and no data on chronic effects of
inhalation of wood smoke in animals. One study investigated the pulmonary toxicity of
respirable combustion products from residential wood and coal stoves in guinea pigs (Beck
and Brain, 1982). Suspensions of the respirable fraction of particles from wood and coal
smoke were instilled in the lungs of guinea pigs who were then sacrificed. The lungs were
lavaged and assayed for biochemical or cellular indicators of pulmonary damage. The
response to wood smoke products was less than that from coal-derived products; however
adverse effects were seen. There was an overall depression in macrophage activity,
increases in albumin and lactose dehydrogenase (LDH) levels (both indicating damage to
cellular membranes), and a large increase in red blood cell numbers.
A morphological study of injury from inhalation of white pine wood smoke in
rabbits showed a reproducible, necrotizing tracheobroncial epithelial cell injury (Thoming
et al, 1982). The exposure was achieved by combusting a 30.4 cm by 1.9 cm square piece
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of white pine wood. Air pumped through the combustion chamber was delivered to the
exposure chamber for head-only exposure of the rabbit Carbon monoxide and aldehydes
were chosen as the indicator species in this study; the concentration of particulate matter
was not measured. Aldehyde levels ranged from 285 to 1707 ppm total aldehyde. The
pattern of injury first appeared six hours after exposure and, at 24 hours after the exposure,
ciliated and secretory cells were mostly destroyed. By 72 hours, cells began to recover their
normal structural appearance. Another pathological result from wood smoke exposure
comes from an investigation of smoke from burning pine wood delivered to the lungs of
dogs (Brizio-Molteni et al, 1984). Significant increases in angiotensin-1 -converting
enzyme, a substance which regulates vasomotor activity in endothelial cells, was measured
immediately after exposure and was even higher 30 minutes post exposure. This
pathological change could be an initial step toward pulmonary hypertension which is a
suggested risk factor for a myocardial infarction.
Two animal studies of toxicity of wood smoke were reviewed by Marbury
(Marbury, 1991). She cited a study by Pick and co-workers (Pick et al, 1984) who studied
the effects of wood smoke from Douglas fir on pulmonary macrophages in rabbits. In this
study, young adult New Zealand white rabbits were exposed to smoke from pyrolysis of
Douglas fir using a smoke combustion chamber. Three rabbits were exposed
simultaneously; their heads were held in a plexiglass restraint which directed their noses
into the smoke stream. These researchers reported significant changes in the numbers and
functions of the macrophages after smoke exposure compared with control. There were a
greater number of cells but their adherence and antibacterial activity was depressed. The
other study, carried out by Wong and co-workers (Wong et al, 1984), demonstrated a
blunted respiratory response to CO2 in wood smoke exposed guinea pigs which may
indicate disruption of respiratory neural control.
Clark and co-workers (Clark et al, 1990) studied the distribution of extra vascular
lung water after acute smoke inhalation in mongrel dogs. The exposures were for 2 hours.
Extravascular lung water, determined using Evans dye which binds quickly to plasma
albumin, was increased in the smoke exposed dogs compared with controls. Wood smoke
was generated by burning a standard mixture of fir plywood sawdust and kerosene.
Whether the plywood contained epoxys and the contribution of toxicity from kerosene were
not discussed.
Extrapolation of the results of these animal studies to human populations living in
areas with elevated wood smoke concentrations is very difficult. Instillation of material
directly into the lung certainly is different from inhalation. Also inhalation from a smoke
stream would result in breathing considerably higher concentrations of smoke than seen in
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neighborhoods in the human breathing zone. None of the animal studies evaluated
pulmonary function or symptoms of respiratory illness, the end points assessed in
epidemiological studies.
Controlled laboratory studies:
No controlled laboratory studies of human subjects exposed to wood smoke per se
have been reported. There are some related studies with formaldehyde and environmental
tobacco smoke but these are not discussed here.
Studies of wildfire and prescribed burn fire-fighters:
Municipal fire-fighters are exposed primarily to smoke from synthetic products and
these studies are not discussed in this report. Forest fire-fighters of wildfires or prescribed
burns are exposed to very high concentrations of carbon monoxide, aldehydes, volatile
organic compounds and paniculate matter (Reinhardt, 1991). There are very few data
describing the health effects of this level of exposure. Rothman and co-workers (Rothman
et al, 1991) studied cross seasonal changes in pulmonary function and respiratory
symptoms in 52 wildfire fighters in California. Both the forced expiratory volume in one
second (FEVi) and the forced vital capacity (FVC) were significantly decreased at the end
of the season compared to values before the season began. Individual functional decreases
appeared to be related to the duration of exposure. Significant changes in eye irritation and
phlegm were also seen from beginning to end of the fire fighting season. No air
monitoring data were given.
Studies in Developing Countries:
The health effects of inhalation of wood smoke has been documented in third world
countries where women spend many hours close to an open unvented indoor fine used for
cooking (Ammann, 1986; Marbury, 1991). Increased respiratory symptoms, decreased
pulmonary function and large increases in the prevalence of chronic bronchitis have been
reported in New Guinea, India and Nepal. However, measurements of paniculate matter
have not been reported in most of these studies. Other studies, such as one in Nepal,
compared indoor paniculate matter concentrations in huts using traditional cooking methods
to those using an improved cookstove (Reid et al, 1986). Concentrations of total
suspended paniculate matter in the huts using the traditional method averaged 2.7 mg/m3; a
similar average concentration associated with the improved cook stove was 1.0 mg/m3, still
much higher than concentrations of paniculate matter to which US populations currently are
exposed. A recent report of indoor air pollution in a similar situation in China (indoor use
of an open cooking fires) measured concentrations up to 25 mg/m3 PMio (Harris et al,
1992).
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A recent clinical report describes a group of 30 nonsmoking patients whose lung
disease may be due to wood smoke exposure(Sandoval et al, 1992). These individuals
were seen in Mexico City and all had a history of living in the countryside away from urban
air pollution. The smoke exposure was the result of the use of wood and biomass for
home cooking. These patients had abnormal chest X-ray scans showing a diffuse,
bilateral, reticulonodular pattern and evidence of pulmonary arterial hypertension. Their
pulmonary function tests were consistent with a mixed restrictive-obstructive disease
diagnosis. The authors suggest that this group of patients was suffering from wood-smoke
inhalation-associated lung disease (WSIALD) (Sandoval et al, 1992).
Epidemiology:
Epidemiological investigations of adverse respiratory effects of wood smoke
emissions in the US have centered on either symptomatology or pulmonary function. The
symptoms measured have been the traditional respiratory disease outcomes; that is, cough,
wheeze, upper or lower respiratory infection. Pulmonary functions measured have been
FEVi, a measure of air flow limitation caused by obstruction in the airways, or FVC, a
measure of the total amount of air that can be forcibly exhaled from the lungs. All but one
of the available studies have been carried out in children, most likely on the assumption that
children are most at risk for adverse effects from inhaled irritants due to the small size of
their lungs and also due to the immature nature of their immune system. Other advantages
of children as subjects in studies of respiratory effects of air pollution are the relative lack
of confounders such as years of cigarette smoking or occupational exposure. There is
good precedence for suspecting that young children are vulnerable to inhaled agents from
the numerous studies of the effects of environmental tobacco smoke on childrens'
respiratory health. There are eight published reports of associations between lung function
and wood smoke in children studied in the field and one study of responses in adult
subjects. The results of these studies are summarized in Table 4. An additional study of
the association between visits to emergency departments for asthma and fine particulate
matter (Schwartz et al, 1993) is included since this study was conducted in Seattle where a
considerable percentage of fine particles are produced by residential wood burning.
The earliest report of adverse health effects from exposure to wood smoke in the
US came from Michigan. Honicky and co-workers studied 31 young children who lived in
homes with wood stoves and compared them to 31 children who lived in homes with other
sources of home heating (Honicky et al, 1985). They recorded respiratory symptoms over
the telephone using a modified Epidemiology Standardization Project Children's
Questionnaire (Ferris, 1978). The occurrence of cough and wheeze was much greater in
children from the homes with stoves and in general, both moderate and especially severe
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symptoms of respiratory diseases were significantly greater in the wood smoke exposed
children (p < 0.001). No measurements of wood smoke were reported.
Previously Tuthill reported the results of an investigation of symptoms of
respiratory illness and respiratory disease prevalence associated with wood smoke and
formaldehyde exposure (Tuthill, 1984). Symptoms were collected using a questionnaire;
chronic respiratory illness was defined as physician-diagnosed chronic bronchitis, asthma
or allergies. The subjects were 399 children from kindergarten through the sixth grade.
Two hundred fifty eight lived in homes with wood stoves and 141 lived in homes without
stoves. Although he found increased risk ratio = 2.4 (confidence intervals 1.7-3.4) for
exposure to formaldehyde (from off-gassing of building materials after new construction or
remodeling, from foam insulation, or from wood burning), the risk ratio for exposure to
wood smoke of 1.1 (0.76-1.7) was not significant. The difficulty assigning formaldehyde
exposure to sources other than wood burning was not discussed, althought it is consistent
with data from studies reviewed in Table 3.
The effects of wood stoves on general respiratory health in preschool age children
was studied by Butterfield and others (Butterfield et al, 1989). Ten symptoms of
respiratory disease were tracked in 59 children during the 1985-86 winter heating season in
the Boise, ED area. The ages of the children ranged from 1 to 5 1/2 years. The symptoms
which were significantly associated with living in a home with a wood stove in use were
frequency of wheeze, severity of wheeze, frequency of cough, and waking up at night with
cough. An independent study of sources of extractable organic material in ambient particles
in Boise during the 1986-87 heating season showed an average of 67% due to wood
burning (Lewis et al, 1991).
Another study compared the incidence of lower respiratory tract infection in
American Indian children with presence of a wood stove in the home (Morris et al, 1990).
The children lived on the Navajo reservation in Arizona. Cases were children less than 24
months of age with lower respiratory tract infection (bronchiolitis or pneumonia) who were
matched with a control case visiting the clinic as part of a well-child program. Fifty-eight
age and gender matched pairs participated in the study. Forty-nine percent of the cases lived
in home using wood-burning for heat, whereas only 33 percent of the control children lived
in such home. In this study, living in a home with a wood burning source of heat was a
risk factor for lower respiratory tract infection (odds ratio = 4.2, p < 0.001).
Heumann and co-workers (Heumann et al, 1991) studied pulmonary function in a
group of elementary school children in Klamath Falls, Oregon using standard spirometnc
values . Pulmonary function test data were collected on 410 children in grades 3 through 6
at three time periods during the 1990 heating season. There was a significant decrease in
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average FEVi and FVC among children who had the highest exposure to wood smoke. A
preliminary report of this study was presented (Heumann et al, 1991); analysis is still on-
going.
The 1977 Montana legislature funded an extensive Montana Air Pollution Study
(Johnson et al, 1990) which was designed to evaluate whether air pollution was associated
with adverse health effects in urban centers. The study involved third, fourth, and fifth
grade children in five Montana cities. It measured lung function both within and between
communities. Thus lung function of school children living in communities with different
levels of air pollution was ascertained. Also comparisons of lung function changes of
school children and air quality within a single community were evaluated. Each child
served as his or her own control and analysis of co-variance was used to test for statistical
significance in the acute study within a single community. In the multi-city study, linear
regressions and principal components techniques were used and appropriate adjustments
were made for factors such as altitude which varied from city to city. Three-day averages
of the pollutants were used. Both studies detected significant lung function effects
associated with total suspended particulate matter (TSP) and both fine and coarse respirable
particulate matter. Pulmonary function decrements ranged from 1% to 10%, 24-hour
average TSP ranged from 24 to 128 (ig/m3 during the study period. Sources of the
particulate matter were not identified, however the authors state that the particulate matter
essentially was from wood burning and entrained dust. Measurements of fine particles
(PM3.s) during this period found 68% by weight attributable to wood smoke in Missoula,
Montana (Carlson, 1982).
One study in Denver, CO of a panel of adult subjects with asthma was conducted
evaluating the presence of a wood stove or fireplace in the home and symptoms of
respiratory disease and shortness of breath (Lipsett et al, 1991). Using logistic regression
analysis, the presence of a wood stove in the home was associated with shortness of breath
in females and both shortness of breath and moderate or severe cough in males (p < 0.01 in
all cases).
Two studies of the health effects of wood smoke have been conducted at the
University of Washington. The first was a questionnaire study of respiratory health in areas
of high and low ambient wood smoke pollution (Browning et al, 1990). The communities
were chosen based on extensive air monitoring of wood smoke distributions in the greater
Seattle area (Larson et al, 1990). Six hundred residences in each community were sent
questionnaires and asked to answer for one adult and one children at each address. The
initial questionnaire asked about chronic symptoms of respiratory disease, in mild,
moderate and severe categories (Ferris, 1978). Two follow-up mailings asked about acute
16
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symptoms over the past two weeks. During the study period, PMio concentrations in the
low wood smoke area averaged 33 |ig/m3; in the high wood smoke area, the average for
the three months of the study was 55 |u,g/m3. Questionnaire responses were stratified by
age; 1-5; 6-14; 14-44; 45-64; and >65. There were no statistically significant differences
between residents of the high and low wood smoke communities, however there was a
pattern of increased symptoms and chronic illness in children aged 1-5 in the area with high
wood smoke.
These suggestive data stimulated another study in the same air shed. In this second
study, pulmonary function was measured in third through sixth grade children in two
elementary schools in the area characterized as being impacted by wood smoke (Koenig et
al, in press). FEVi and FVC were measured before, during, and after the heating season
in 326 children during 1988-89 and in just 26 children with asthma in 1989-90. Wood
smoke was assessed using an integrating nephelometer, a light scattering device. In this
airshed there is a high correlation between light scattering coefficient and PMio Analyses
show that greater than 80% of particles in residential neighborhoods are from wood
burning during winter months (Larson et al, 1992). Random and mixed effects models of
statistical association were used to evaluate the relationships between lung function and
wood smoke concentrations. Lung function measurements were compared with wood
smoke concentrations for the previous 12 hour period from 7 PM to 7 AM. Statistically
significant decrements in both FEVi and FVC were seen in young children with asthma,
both at the p < 0.05 level. FEVi and FVC dropped an average of 34 ml and 37 ml
respectively for each unit of light scattering coefficient (1 X 10'4 nv1). During the study
period the PMio levels were over 90 |ig/m3 on four nights in 1988-89 but not above 110;
the highest value during 1989-90 was 103 |ig/m3. Thus the National Ambient Air Quality
Standard for PMio was not violated during either heating season. It was concluded that
wood smoke is significantly associated with respiratory function decrements in young
children with asthma.
A study of the relationship between fine paniculate matter and emergency room
visits for asthma in the metropolitan Seattle area was designed to help confirm whether air
pollution was a risk factor for asthma (Schwartz et al, 1993). Using Poisson regressions
controlling for weather, season, time trends, age, hospital, and day of the week, a
significant association (p < 0.005) was found between fine particles measured at the
residential monitoring station used in the studies described above and visits to emergency
departments in eight participating hospitals. Analyses show that between 60 and 90% of
particles in residential neighborhoods measured either gravimetrically or by nephelometers
are from wood burning year round (Larson et al, 1992).
17
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Suspended paniculate air pollution is associated with decreased lung function and
increased prevalence of respiratory disease symptoms in young children under 12 years of
age (Dockery et al, 1989). In this two-year study of the relationship between pulmonary
function changes in third and fourth grade children and air pollutant alerts in Steubenville,
Ohio, researchers found a decline in pulmonary function tests associated with increasing
24-hour concentrations of total suspended paniculate matter (TSP). Peak values of TSP
ranged from 27 {ig/m3 to 422 jig/m3. The pulmonary function declines were small but
persisted for up to two weeks. The elimination of children with reported prevalence of
coughs, colds and other respiratory symptoms did not change the estimated mean effect.
Similar findings were reported from the Netherlands (Dassen et al, 1986) in a study of
children aged 6-11 years before and during an air stagnation episode, although the effects
of allergy and chronic respiratory disease were not evaluated. More recently, Dockery and
co-workers (Dockery et al, 1982) have reported increased rates of cough, bronchitis and
chest illness in children exposed to inhaled paniculate pollution.
It certainly is biologically plausible that wood smoke could cause adverse
respiratory effects. The average size of the particles (< 1 Jim) is such that these will travel
deep into the lower respiratory tract (Ammann, 1986). Some of the chemical species in
wood smoke are chemically reactive and thus present a risk to respiratory tissues. The
complex mixture of wood smoke allows deposition of reactive chemical onto particles
which then can be carried into the alveolar region of the lung. As stated by Ammann
(Ammann, 1986), "irritants such as phenols, aldehydes, and quinones, as well as nitrogen
oxides and sulfur oxides, in smoke may also contribute to both acute and chronic health
problems. Generally irritants interfere with ciliary activity... and hence the flow of the
particle-trapping mucous stream. Inflammation, with all of its sequelae, also results."
In the earlier Six City Study report of children in Steubenville (Dockery et al,
1989), a group median estimate of the slope between FVC and total suspended paniculate
was -0.081 mL/|ig/m3 for all children. When the estimate of a similar relationship
(FVC/measure of fine particle concentration) is made using the Seattle data (Koenig et al, in
press), the estimated mean FVC decrease per unit increase of PM2.5 is -1.8 mL/ng/m3 and
+0.34 mL/jig/m^ for asthmatic and nonasthmatic children respectively. The FVC change
per unit increase in PM2.5 for the asthmatic children in our study is sufficiently pronounced
as to suggest that fine paniculate matter measured with a nephelometer may be more
irritating than general industrial TSP. However, the difference between the two studies
may be due solely to a increased sensitivity to airborne irritants in children with asthma.
Based on prior work by Larson (Larson et al, 1990), the fine paniculate matter measured
18
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on winter nights in this Seattle residential area is almost exclusively the result of residential
wood-burning.
SUMMARY
In conclusion, this review summarizes extensive information about the constituents
and fate of wood smoke but, due to limited data, less information about the health effects.
Animal toxicological studies show that wood smoke exposure can disrupt cellular
membranes, depress macrophage activity, destroy ciliated and secretory respiratory
epithelial cells and cause aberrations in biochemical enzyme levels. With respect to the
human epidemiological data, the literature summarized in Table 4 show a coherence of the
data from young children, with seven of eight studies reporting increased respiratory
symptoms, lower respiratory infection and decreased pulmonary function as a result of
exposure to wood smoke. The findings were especially pronounced in the study of
children with asthma. As Bates (1992) has discussed the coherence of the data, although
not amenable to statistical tests, carries the weight of linkage and plausibility. These
adverse respiratory effects associated with wood smoke exposure also comply with many
of Brandon Hill's aspects of association necessary to establish causation (Hill, 1965).
There is strength of association, consistency (seven of eight studies showing positive
associations), temporality, plausibility, coherence, and analogy (using ETS exposure; Nat.
Res. Council, 1986; US EPA, 1992). A biological gradient (or dose response) has not
been shown, although one is suggested in the study of pulmonary function in wildfire
fighters. We conclude that the preponderance of the data suggest a causal relationship
between elevated wood smoke levels and adverse respiratory health outcomes in young
children.
19
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Rau JA. 1989. Composition and size distribution of residential wood smoke particles Aerosol
Sci. Technol. 10:181-92
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30
-------
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•
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32
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domestic stoves burning wood and coal. J. Aerosol Sci. 17: 635-38
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and aldehyde distribution for the IACP Boise, ID, Residential Study. Proc. EPA/ Air
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Publication VIP-10 (EPA 600/9-88-015)
33
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Table 2. Chemical Composition of Wood Smoke
Species1
g/kg wood2 Physical State3 Reference
Carbon Monoxide
Methane
VOCs (C2-C7)
Aldehydes
Formaldehyde
Acrolein
Propionaldehyde
Butry aldehyde
Acetaldehyde
Furfural
Substituted Furans
Benzene
A Iky I Benzenes
Toluene
Acetic Acid
Formic Acid
Nitrogen Oxides (NO.NOj)
Sulfur Dioxide
Methyl chloride
Napthalene
Substituted Napthalenes
Oxygenated Monoaromatics
Guaiacol (and derivatives)
Phenol (and derivatives)
Syringol (and derivatives)
Catechol (and derivatives)
Total Particle Mass
Particulate Organic Carbon
Oxygenated PAHs
PAHs
Fluorene
Phenanthrene
Anthracene
80-370
14-25
7-27
0.6-5.4
0.1-0.7
0.02-0.1
0.1-0.3
0.01-1.7
0.03-0.6
0.2-1.6
0.15-1.7
0.6-4.0
1-6
0.15-1.0
1.8-2.4
0.06-0.08
0.2-0.9
0.16-0.24
0.01-0.04
0.24-1.6
0.3-2.1
1-7
0.4-1.6
0.2-0.8
0.7-2.7
0.2-0.8
7-30
2-20
0.15-1
4xlO'5 - 1.7xlO-2
2xlO'5 - 3.4xlO-2
5xlO-5 - 2.1xlO-2
V
V
V
V
V
V
V
V
V
V
V
V
V
V
V
V
V
V
V
V/P
V/P
V/P
V/P
V/P
V/P
p
p
V/P
V/P
V/P
V/P
4,5
5
5
4,6
4,6
6
4,6
4,6
4,6
7,8
7,8
5
9
9
7
7
4,5
4
10
9
9
9
11
11
11
11
5
12
9
13
13
13
-------
Species1
g/kg wood2 Physical State3 Reference
Methylanthracenes
Fluoranthene
Pyrene
Benzo(a)anthracene
Chrysene
Benzofluoranthenes
Benzo(e)pyrene
Benzo(a)pyrene
Perylene
Ideno( 1 ,2 ,3-cd)pyrene
Benz(ghi)perylene
Coronene
Dibenzo(a,h)pyrene
Retene
Dibenz(a,h)anthracene
Trace Elements
Na
Mg
Al
Si
S
Cl
K
Ca
Ti
V
Cr
Mn
Fe
Ni
Cu
Zn
Br
Pb
7xlO'5 - SxlO"3
7X10-4- 4.2x10-2
SxlO-4 - 3.1xlO-2
4X10-4 - 2xlO'3
SxlO"4 - IxlO-2
6X10-4 - SxlO-3
2x10^ - 4xlO-3
3x10^ - 5xlO-3
5xlO'5 - 3xlO-3
2xlO'4 - 1.3xlO-2
3xlO*5 - 1.1x10-2
SxlO-4 - 3x10-3
3x10^ - IxlO-3
7xlO-3 - 3xlO-2
ZxlO'5 - 2x10-3
3x10-3 - 1.8x10-2
2x10^ - 3x10-3
IxlO-4 - 2.4x10-2
SxlO-4 -3.1x10-2
IxlO-3 - 2.9x10-2
7xlO'4 - 2.1xlO'1
3x10-3-8.6x10-2
9xlO'4- l.SxIO-2
4xlO'5 - 3xlO-3
2xlO'5 - 4x10-3
2xlO'5 - 3xlO-3
7xlO'5 - 4xlO-3
3x10^ - SxlO-3
IxlO-6 - IxlO-3
2X10-4 - QxlO-4
7X10-4 - SxlO-3
7xlO-5-9xlO-4
IxlO-4 - 3x10-3
V/P
V/P
V/P
V/P
V/P
V/P
V/P
V/P
V/P
V/P
V/P
V/P
V/P
V/P
V/P
p
p
p
p
p
p
p
p
p
p
p
p
p
p
p
p
p
p
13
13
13
13
13
13
13
13
13
13
13
13
13
14
13
15
15
15
15
15
15
15
15
15
15
15
15
15
15
15
15
15
15
-------
Species1 g/kg wood2 Physical State3 Reference
Paniculate Elemental 0.3-5 P 16
Carbon
Normal alkanes (C24-Cso) IxlO'3 - 6xlO'3 P 17
Cyclic di-and triterpenoids
Dehydroabietic acid 0.01 - 0.05 P 18
Isopimaric acid 0.02-0.10 P 18
Lupenone 2xlO"3 - 8xW3 P 18
Friedelin 4x10-* - 2xlO'5 P 18
Chlorinated dioxins IxlO'5 - 4xlO'5 P l9
Paniculate Acidity . 7xlO'3 - 7xlO'2 P 20
1 Some species are grouped into general classes as indicated by italics
2 To estimate the weight percentage in the exhaust, divide the g/kg value by 80. This assumes that there are 7.3 kg
combustion air per kg of wood. Major species not listed here include carbon dioxide and water vapor (about 12 and
7 weight percent respectively under the assumed conditions).
3 At ambient conditions; V = vapor, P = paniculate, and V/P = vapor and/or paniculate (i.e., semi-volatile).
4DeAngelis (1980)
5 OMNI (1988)
6Lipari (1984), values for fireplaces
7 Edye et al (1991). smoldering conditions; other substituted furans include 2-furanmethanol, 2 acetylfuran, 5-
methyl-2furaldehyde, and benzofuran
8 Value estimated for pine from Edye et al (1991) from reported yield relative to guaiacol, from guaiacol values of
Hawthorne (1989) and assuming paniculate organic carbon is 50% of total particle mass
9 Steiber et al (1992), values computed assuming a range of 3-20 g of total extractable, speciated mass per kg wood
10 Khalil (1983)
11 Hawthorne (1989), values for syringol for hardwood fuel; see also Hawthorne (1988)
12 Core (1989), DeAngelis (1980), Kalman and Larson (1987)
13 From one or more of the following studies: Cooke (1981), Truesdale (1984), Alfheim et al (1984), Zeedijk
(1986), Core (1989), Kalman and Larson (1987); assuming a range of 7 to 30 grams of paniculate mass per kg wood
when values were reported in grams per gram of paniculate mass. Similar assumptions apply to references 14,15 and
references 17-19
14 Core (1989), Kalman and Larson (1987)
15 Watson (1979), Core (1989), Kalman and Larson (1987)
16 Rau (1989), Core (1989)
17 Core (1989)
18 Standley and Simoneit (1990); Dehydroabietic acid values for pine smoke, lupenone and isopimaric acid values
for alder smoke, and friedelin values for oak soot
19 Nestrick and Lamparski (1982), from paniculate condensed on flue pipes; includes TCDDs, HCDDs, H7CDDs
andOCDDS
20 Bumet et al (1986); one gram of acid = one equivalent of acid needed to reach a pH of 5.6 in extract solution
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Table 6. Summary of studies of respiratory effects of exposure to wood smoke.
Referene Age of Subjects Number of Subjects Endpoints Results
Measured
Honicky
Tuthill
Browning
1-7 JO-
S' 11 *yr
lyr and
older
34 w/stoves
34 without
258 w/stoves
141 without
455,high smoke**
368 low smoke
Symptoms
Symptoms
Symptoms
Disease
prevalence
More symptoms in
children with
stoves p <0.001.
Risk ratio = 1.1,
showing no sign.
effect
No significant effects.
Trend in children
aged 1-5.
Koenig
(In Press)
Butterfield
Morris
Heumann
Johnson
Lipsett
Schwartz
8-1 lyr
296 healthy***
30 asthmatic
Spirometry
1-5 1/2 yr 59
Symptoms
< 24 mo 58 pairs
8-11
410***
8-11
495
Respiratory
Disease
Spirometry
Spirometry
Significant assoc
between fine particles
and lung function in
asthmatics in an area
heavily impacted by
wood smoke, p =0.05.
Significant corr
between woodstove
use and wheeze and
cough frequency
p = 0.01.
Woodstove
significant risk
factor for lower
resp infection.
Significant
decrease in PFTs
with elevated
wood smoke
Significant relation
of function decrease
with increasing TSP
Xage,46yr 182
Symptoms Significant assoc
2955 cases
3810 controls
Emergency room visits for asthma or gastroenteritis.Significant
association (p < 0.005) with particle concentrations at a site
heavily impacted by wood smoke year round.
* Described as kindergarten through grade 6.
** Geographical areas chosen as having high or low wood smoke pollution.
*** Grades 3 through 6.
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TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing)
1. REPORT NO. 2.
EP.A-453/R-93-036
4. TITLE AND SUBTITLE
A Summary of the Emissions Characterization and
Noncancer Respiratory Effects of Wood Smoke
7. AUTHOR(S)
Timothy V. Larson and Jane Q. Koenig
University of Washington, Seattle, WA
9. PERFORMING ORGANIZATION NAME AND ADDRESS
USEPA, Air Risk Information Support Center
Office of Air Quality Planning and Standards
Emission Standards Division
Research Triangle Park, N.C. 27711
12. SPONSORING AGENCY NAME AND ADDRESS
3. RECIPIENT'S ACCESSION NO.
5. REPORT DATE
December 1993 (Date of Aoprova
6. PERFORMING ORGANIZATION CODE
8. PERFORMING ORGANIZATION REPORT NO.
10. PROGRAM ELEMENT NO.
11. CONTRACT/GRANT NO.
1D3253NAEX
13. TYPE OF REPORT AND PERIOD COVERED
Final
14. SPONSORING AGENCY CODE
N
15. SUPPLEMENTARY NOTES
*—
16. ABSTRACT
This report summarizes the available literature on constituents and fate of wood
smoke and the health effects of wood smoke. The emission characterization of wood
smoke focuses on the chemical composition, 'emission rates from different wood burning
devices, and impacts from wood burning' on airborne particle levels. The epidemio-
logical data focus on human respiratory responses to inhaled wood smoke such as
increased respiratory symptoms, lower respiratory infection and decreased pulmonary
function in children, especially those with asthma. The report concludes that the
data demonstrate a causal relationship between elevated wood smoke concentrations
and adverse respiratory effects in children.
•17. KEY WORDS AND DOCUMENT ANALYSIS
a. DESCRIPTORS b.lDENTIFI
Wood Smoke
Respiratory Effects
Emissions Characterization
Exposure Assessment
Lung Function
18. DISTRIBUTION STATEMENT 19- SECURI
Uncla
20. SECURI
Uncla
ERS/OPEN ENDED TERMS C. COSATI Field/Group
TY CLASS (Tins Report! 21. NO. OF PAGES
ssified 47
TY CLASS (This page) 22. PRICE
ssified
EPA Form 2220-1 (Rev. 4-77) PREVIOUS EDITION is OBSOLETE
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