Some recent studies linking woodsmoke and cancer Childhood brain tumours linked with using a closed wood heater. An AUSTRALIA-wide case-control study found men who use a closed wood heater before their
child's birth or refuel their cars
more than four times per month or may increase the risk of their offspring developing brain
tumours. Wood stove use increased the risk of acute lymphoblastic leukaemia in childhood. A study published in 2011 by researchers at the Telethon Institute for
Child Health Research found that wood stove use increased the risk of
acute lymphoblastic leukaemia in childhood -
www.ncbi.nlm.nih.gov/pubmed/21980942 In-Home Coal and Wood Use and Lung Cancer Risk: A Pooled Analysis
of the International Lung Cancer Consortium, H. Dean Hosgood, III et
al. Environ Health Perspect 118(12) Dec 2010 Delgado,
J., L. Martinez, et al. (2005). Lung Cancer Pathogenesis Associated With WoodSmoke Exposure*. Pintos, J., E. L. Franco, et al. (1998). "Use of wood stovesand risk of cancers of the upper aero-digestive tract: a case-control study." Behera, D.
and T. Balamugesh (2005). "Indoor air pollution as a risk factor for lung cancer in women." Wood smoke exposure and lung adenocarcinoma in non-smoking Mexican women.Velema, J., A. Ferrera, et al. (2002).
"Burning wood in the kitchen increases the risk of cervical neoplasia inHPV-infected women in Honduras." K-RAS
Oncogene Mutation in Patients with Advanced Non-Small Cell Lung Cancer
(NSCLC) Associated With Exposure to Wood Smoke and Tobacco Smoking:
Therapeutic Implications. CK, L., Q.
NY, et al. (1988). "Natural inhalation exposure to coal smoke and woodsmoke induces lung cancer in mice and rats.Lung Cancer and Indoor Pollution from Heating and Cooking with Solid Fuels
AAQG's bibliography - air pollution and health
Energy Justice Network's compilation of scientific reports & papers
Peer-reviewed paper: Published Studies on the Health
Effects of Woodsmoke.
UNE Air Quality Research
Group
This research was published as a refereed paper in
Clean Air, V32, No 3, August 1998. Download the pdf file
Contents
Developing
Countries
Developed
Countries
City-Wide
Detrimental Health Effects
Laboratory
evidence
Summary
References
Developing
Countries
Exposure to woodsmoke can have serious consequences for health. In developing
countries, some stoves may emit smoke to indoor air. Several studies have shown
that exposure to woodsmoke reduces lung function, especially in children, and
increases coughs and other respiratory diseases. In Bogota, woodsmoke exposure
may explain about half of all cases of obstructive airways disease. In Mexico
City, famous for its traffic pollution, women exposed to woodsmoke had 3.9 times
the risk of chronic bronchitis and 9.7 times the risk of chronic bronchitis plus
chronic airway obstruction. If exposed for an average of 33 mins or more a day
(200 or more hours/year), risks were 15 and 75 times higher than in women not
exposed to woodsmoke. In Arfica, cooking with wood increased the risk of
stillbirth by 50%. Homes with woodstoves were found to have greater
concentration of mutagenic material in the air, resulting in increased risk of
cancer. There results are summarised in Table
1.
Table 1. Symptoms from woodstove use,
developing countries. Text in italics constitutes direct quotes from the
paper.
Reference
|
Symptoms in households using wood heat or
cooking in developing countries
|
Dennis et al., 1996. |
Conclusions: "This study showed
that among elderly women of low socioeconomic status in Bogota, woodsmoke
exposure is associated with the development of Obstructive Airways Disease
(OAD) and may help explain around 50% of all OAD cases." |
Ellgard, 1996 |
"The association between
exposure to air pollution from cooking fuels and health aspects was
studied in Maputo, Mozambique. Almost 1200 randomly selected women
residing in the suburbs of Maputo were interviewed … Wood users were found
to have significantly more cough symptoms than other groups. This
association remained significant when controlling for a large number of
environmental variables." |
Gharaibeh, 1996 |
A significant negative impact was
found with regard to environmental exposure to both passive smoking and
wood and kerosene unvented cooking stoves. Reduction in lung function for
wood and kerosene were FVC (L): 1.02-1.32; FEV(1) (L): 0.91-1.25;
FEF(25-75) (L/S): 1.24-1.86; PEFR (L/S): 1.67-2.64. Primary school
children in Jordan. |
Guneser et al., 1994 |
"Pulmonary function levels were
diminished in passive smokers and in children whose houses were heated by
a wood-burning stove As a result, passive smoking, using a wood-burning
stove for heating, and family history of respiratory diseases are to be
considered risk factors for the respiratory system." 617 primary
school children, aged 9-12 studied in Turkey. |
Hamada et al., 1992 |
"Strikingly higher (p <
0.01) levels of Polycyclic Aromatic Hydrocarbons, and much higher (p =
0.07) levels of Suspended Particulate Matter were found in the kitchens
with wood stoves. These findings appear to support the hypothesis that
domestic wood burning stoves are risk factors for some upper digestive and
respiratory tract cancers in Brazil." |
Perez-Padilla et al., 1996 |
"A case-control study was
performed in women older than 40 yr of age in Mexico City to evaluate the
risk of cooking with traditional wood stoves for chronic bronchitis and
chronic airway obstruction (CAO). Crude odds ratios for wood smoke
exposure were 3.9 (95% CI, 2.0 to 7.6) for chronic bronchitis only, 9.7
(95% CI, 3.7 to 27) for CAO plus chronic bronchitis, and 1.8 (95% CI, 0.7
to 4.7) for CAO … The findings support a causal role of domestic wood
smoke exposure in chronic bronchitis and chronic airflow
obstruction." |
Sandoval et al., 1993 |
Describes " the clinical,
radiologic, functional, and pulmonary hemodynamic characteristics of a
group of 30 nonsmoking patients with a lung disease that may be related to
intense, long-standing indoor wood-smoke exposure. ... Fibrous and
inflammatory focal thickening of the alveolar septa as well as diffuse
parenchymal anthracotic deposits are the most prominent pathologic
findings. Pulmonary arterial hypertension in wood-smoke
inhalation-associated lung disease appears to be more severe than in other
forms of interstitial lung disease and tobacco-related COPD." Authors'
address: Mexico City. |
Zhang et al., 1996 |
"Among the 6 fuel/stove
combinations, wood stove generated the highest cancer risk and LPG
generated the least risk … The cancer risk of benzene or that of styrene
from use of biomass cookstoves might exceed the risk from all sources of
airborne benzene or styrene in the US." |
Ardayfio Schandorf E, 1993 |
"cooking over an open fuel wood stove resulted in an
almost 50% greater chance of stillbirth among pregnant
women." |
Developed
Countries
Many recent studies have also found significant effects in woodstove users in
developed countries such as the US. Children living in such homes tend to have
increased respiratory symptoms, acute lower respiratory infection, increased
frequency and severity of wheeze, increased frequency of cough and waking up at
night with a cough. Measured lung function has also been found to decline (See
Table
2). Forest firefighters in the US had decreased lung function after fighting
fires. Use of wood for indoor heat by these firefighters was also associated
with decreased lung function. Van Houdt
et al. (1986) found increased indoor mutagenicity in 8 out of 12 homes using
woodstoves. In New York, woodstove use was found to be significantly associated
(P<.05) with increased otitis (an inflammation of the middle ear marked by
pain, fever, dizziness, and abnormalities of hearing.) Studies detecting adverse
health effects in families using wood heating are listed in Table 2. Three
studies, also listed in Table 2 show increased mutagenicity or genotoxity of the
air inside, or in the vicinity of, homes using wood heating. Three case studies,
from North Carolina, Pennsylvania and Canada, describe illnesses attributed
specifically to fumes from woodstoves.
Very few studies have found little or no effect of exposure to woodsmoke or
woodstove use. Exceptions are one study, in Bavaria, (Von
Mutius et al., 1996) which found that woodstove use was associated with a
reduced incidence of allergies to pollen. The authors postulated that this may
have been due to wood heating being associated with farming or country areas,
where children were more likely to be exposed to pollens eg from haymaking. A
study in South Australia (Volkmer et
al. 1995) found parental smoking was associated with decreased eczema and
use of evaporative cooling was associated with increased dry cough. Woodstove
use was also associated with many factors. However, when the data for Adelaide
where considered by themselves, most of these apparent effects were no longer
significant. Some of the associations could therefore be explained by
differences in woodstove use or other factors between city and country areas.
The study was not adjusted for socio-economic factors except on an area-wide
basis. Some of the methodological problems which led to the apparent
associations in the State-wide analysis may well remain in the data for
Adelaide, explaining the unusual associations.
It is also possible that, as woodstoves become more air tight, neighbours
downwind of the stove receive at least as much of the noxious pollution as the
family using the stove, making such effects easier to detect on an area-wide
basis, rather than by heating methods for individual families. Alfheim et
al. (1984) found the effect on the mutangenicity of the air of burning wood
in an airtight stove was in the vicinity of the house, rather than in the room
with the stove. Table 3
shows how use of woodstoves increases health risk for entire cities or areas.
Table 2. Studies in
the US and other developed countries of symptoms associated with households
using wood heat.
Reference
|
Respiratory and other symptoms in
households using wood heat
|
Honicky et al., 1985 |
Moderate and severe respiratory
symptoms were significantly greater ( P<.001) in 34 children, aged 1-7
years in houses with woodstoves than in 34 children houses without.
Conclusion: "Present findings suggest that indoor heating with
wood-burning stoves may be a significant etiologic factor in the
occurrence of symptoms of respiratory illness in young children."
Michigan, US. |
Butterfield, et al., 1989 |
Significant correlation
(P<.01), between woodstove use and frequency of wheeze, severity of
wheeze, frequency of cough and waking up at night with cough , based on 59
subjects aged 1 to 5.5 years. |
Lipsett et al., 1991 |
Presence of woodstove or fireplace
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 for
all cases). 182 asthmatics living in Denver, Colorado. |
Betchley et al., 1997 |
Forest firefighters had
significant declines in lung function (FEV(1)). Average declines,
pre-shift to midshift of 0.089 L, 0.190 L, and 0.439 L/sec in TVC, FEV(1)
and FEF (25-75). The use of wood for indoor heat also was associated with
the declines in FEV(1). |
Morris et al., 1990 |
58 Navajo children under 2 years
with diagnosed pneumonia or bronchiolitis were compared with matched
control children. Use of a wood burning stove was associated with a 4
times higher risk of lower respiratory tract infection
(P<.001). |
Robin et al., 1996 |
Matched pair analysis revealed an
increased risk of Acute Lower Respiratory Infection (ALRI) for children
living in households that cooked with any wood (odds ratio 5.0; 95%
confidence interval 0.6 to 42.8. Cooking with wood-burning stoves was
associated with higher indoor air concentrations of respirable particles
and with an increased risk of ALRI in Navajo children. Studied 45 children
under 2 years. |
Tuthill, 1984. |
Risk of respiratory symptoms
increased by 10%, but this was not statistically significant. Study of
children aged 5-11, 258 with woodstoves, 141 without. Exposure to
formaldehyde from any source, including wood burning, significantly
increased risk. |
Daigler et al., 1991 |
A comparison of patients in New
York with physician-diagnosed otitis media (n = 125, 74% response), and
controls (n = 237, 72% response) showed exposure to a woodburning stove
was significantly associated (P<.05 with increased otitis (an
inflammation of the middle ear marked by pain, fever, dizziness, and
abnormalities of hearing.) |
Hogg, 1997 |
The author comments on the case
report by Dr. David T. Janigan and colleagues of classic bronchiolitis
obliterans in a man who used a wood-burning stove to dispose of
construction materials in Candada. |
Dean et al., 1992 |
Case of methemoglobinemia, sudden
onset of cyanosis, irritability, metabolic acidosis, and a lethal
methemoglobin level of 71.4% in a 10 week old infant. Family history
revealed a wood-burning stove which emitted pine tar fumes as the
potential environmental methemoglobin-producing source. The infant's
cradle was situated five feet from the stove. The baby was treated and
recovered. |
Ramage et al., 1996 |
Case study of 61-yr-old woman
suffering shortness of breath on exertion and interstitial lung disease.
Bronchoalveolar lavage revealed numerous carbonaceous particulates and
fibers, as well as cellular and immunoglobulin abnormalities. Inflammation
and fibrosis were found surrounding them on open biopsy. The particle
source was traced to a malfunctioning wood-burning heater in the patient's
home. |
Von Mutius et al., 1996 |
Children in Bavarian homes heated
with wood had less hayfever and were less sensitive to pollen, cold air or
other irritatants. Postulated that wood heating may be more common in
farming or country areas where children are more likely to be exposed, and
hence desensitised, to pollens eg from haymaking. |
Volkmer et al., 1995 |
"The use of a wood fire/heater
compared to other forms of heating was significantly associated with a
reduced prevalence rate for dry cough (OR 0.84) and ever having wheezed
(OR 0.82)." Findings contradict most other studies. Data not adjusted
for confounders such as socio-economic status, except by area code.
|
van Houdt et al., 1986 |
"The use of wood stoves caused
an increase of indoor mutagenicity in 8 out of 12 homes."
|
Boone et al., 1989 |
"Woodsmoke prove to be a major
source of indirect genotoxins in homes. The increase is probably due to
higher concentrations of polycyclic aromatic hydrocarbons in the wood
smoke aerosol …" USA. |
Alfheim et al, 1984 |
"Whereas wood heating in an
"airtight" stove was found to cause only minor changes in the
concentration of PAH and no measurable increase of mutagenic activity of
the indoor air, both these parameters increased considerably when wood was
burned in an open fireplace, yielding PAH concentrations comparable to
those of ambient urban air. Woodburning in the closed stove did, however,
result in increased concentrations of mutagenic compounds and PAH on
particles sampled in the vicinity of the
house." |
City-Wide Detrimental
Health Effects When a Proportion of the Population uses Wood
Stoves
In areas with airtight stoves, the smoke is vented to the
outside air. Neighbours living downwind probably suffer greater exposure. The
whole neighbourhood has been found to suffer as a result. For example, in
Seattle, where 90% of particulate air pollution was found to originate from
woodsmoke, hospital admissions for asthma were found to increase on days with
high pollution. Similar effects have been observed in Santa Clara County, where
residential wood burning is also a principal source of particulate air
pollution. Separate studies in Klamath Falls, Oregon and in Montana found
declines in measured lung function in children when ambient levels of woodsmoke
were high. Declines in lung function with woodsmoke exposure were also found
found for asthmatic children in Seattle. In Sydney, the majority of particle
pollution in winter arises from a less than 13% of of households using wood
heaters (EPA NSW,
1996). Particle pollution on a daily basis has found to be associated with
increased death rates (Morgan,
1996). In Boise, Idaho, US, air containing smoke emitted from woodheaters
was tested for mutagenicity using the Ames test on salmonella and tumor
initiation assays in mice. Woodsmoke was estimated to be 12 times more
carcinogenic than an equal concentration of cigarette smoke ( Lewtas et
al., 1991).
Table 3. Studies relating outdoor
concentrations of woodsmoke to adverse health effects in the whole
population.
Reference
|
Adverse effects of Outdoor Woodsmoke
|
Schwartz, 1993 |
Significant association between
visits to 8 hospital emergency departments in Seattle for asthma and PM10
pollution. In 1993, wood burning was found to be the dominant source of
PM10 pollution in Seattle in all seasons of the year, ranging from 60% in
summer to 90% in winter. |
Koenig et al., 1993 |
Significant association in Seattle
(where the majority of particulate air pollution originates from
woodsmoke) between outdoor fine particle pollution and decreased lung
function (measured by spirometry) in asthmatic children aged
8-11. |
Heumann et al., 1991 |
Children with the highest exposure
to wood smoke had a significant decrease in lung function, measured by
FEV1 and FVC. 410 children aged 8-11 in Klamath Falls,
Oregon. |
Johnson, 1990 |
Particle pollution from woodsmoke
in the air was associated with significant decreases in lung function in
children aged 8-11. 495 subjects in Montana. |
Browning, et al., 1990 |
No statistically significant
differences, but a pattern of increased symptoms and chronic illness in
children aged 1-5 in the area with high wood smoke. |
Lipsett et al., 1997 |
Conclusion from abstract:
"These results demonstrate an association between ambient wintertime
PM10 and exacerbations of asthma in an area where one of the principal
sources of PM10 is Residential Wood Combustion." Santa Clara County,
California. |
Betchley, et al., 1997 |
Forest firefighters had
significant declines in lung function (FEV(1)). Average declines,
pre-shift to midshift of 0.089 L, 0.190 L, and 0.439 L/sec in TVC, FEV(1)
and FEF (25-75). ). The use of wood for indoor heat also was associated
with the declines in FEV(1). |
Morgan, 1996
EPA NSW, 1996 for % from wood
|
In Sydney, Australia, death rates
are generally higher in winter and increase on days of, or days following
high particle pollution. Particle concentrations are generally higher in
winter. Carbon dating of air samples at Rozelle, near the CBD in July and
August 1993, found that two-thirds of particles originated from wood, not
coal, oil or diesel. At Winmalee in the Blue Mountains, the proportion was
81%. Samples were taken when the air was essentially free of smoke from
bushfires or hazard reduction burns. Solid fuel use in Sydney increased
from 7% of households in 1988 to 13% in 1995. The majority of winter
particle pollution in Sydney is thus caused by a small minority of
households using wood heaters. |
Lewtas et al., 1991 |
Mutagenicity testing of air
containing smoke emitted from woodheaters in Boise, Idaho, US, using the
Ames test on salmonella and tumor initiation assays in mice found that
woodsmoke was 12 times more carcinogenic than an equal concentration of
cigarette smoke. |
Larson & Koenig, 1994. |
"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." |
Laboratory
evidence
Mounting laboratory evidence is now available to explain many of these
adverse effects. Lal et al.
(1993) describe in detail some of the nasty effects seen in lungs of rats
exposed to woodsmoke. Other researchers have found deleterious effects after
only 1 hour's exposure to 800ug/m3 of woodsmoke. Following exposure, bacteria in
rats' lungs were found to be more virulent Stone,
1995). In Australia, woodsmoke concentrations can approach this level and
remain high for serveral hours. For example, in Armidale, NSW, measured hourly
woodsmoke concentrations have peaked at 467 ug/m3 and remained over 200 ug/m3
for several hours (for more details see Monitoring Armidale's
Air Quality.) Another experiment (Stone,
1995), subjected mice either to woodsmoke, oil furnace fumes, or clean air
for 6 hours. Mice were then challenged by a respiratory bug. 21% of the mice
exposed to wood smoke were dead two weeks later, compared with only 5% mice
exposed to fumes from the oil furnace or to clean air. The article comments:
"Part of the problem is that wood smoke is a witch's brew of carcinogens,
including aldehydes and polycyclic aromatic hydrocarbons, carbon monoxide, and
organic particles less than 10 microns in diameter, called PM10. PM10s have been
implicated in increased morbidity and mortality on days of heavy air pollution."
Very recent research has found that only the smaller particles less than 2.5
microns are linked with mortality and morbidity. Schwartz
et al. (1996) analysed daily mortality in six Eastern US Cities over 8
years. Particles between 2.5 and 10 microns had no association with daily
mortality. The strongest association was with PM2.5s, particles less than 2.5
microns in diameter, which arise mainly from combustion. Woodsmoke is almost
entirely PM2.5s. (Larson and
Koenig, 1994). Autopsies have shown that particles less than 2.5 microns in
diameter are retained in human lungs, but not larger particles (Churg et al.,
1997). Godleski
et al. (1996) exposed rats with bronchitis for 6 hours per day to 272ug/m3
PM2.5 (ie daily average of 68 ug/m3 - similar or lower to PM2.5 concentrations
measured in a residential area of Armidale on 32% of nights in June-August 1995
and 1996). 37% of rats exposed to particles died, compared to none exposed to
filtered air.
Reference |
Physiological measurements of effects of
exposure to woodsmoke
|
Stone, 1995 |
Mice were exposed for 6 hours to
wood smoke, emissions from an oil furnace or no pollution (control) and
then an aerosol of the bacterium Streptococcus zooepidemicus, which causes
severe respiratory infections. After 2 weeks, 5% of the mice in the
control group exposed to air and bacteria had died, along with a similar
percentage of the mice breathing the oil fumes. But 21% of the wood-smoked
mice were felled. |
Stone, 1995 |
Rats were exposed to no pollution
or 800 ug/m3 wood smoke for 1 hour, then to golden staph bacteria. The
bacteria were more virulent in animals which breathed the woodsmoke. This
was attributed to a suppression in activity of the rats' macrophages,
immune cells that roam the body, looking to engulf and destroy foreign
particles. |
Kou et al. , 1997 |
"These results suggest that an
increase in OH. burden following smoke inhalation is actively involved in
evoking the acute irritant effects of wood smoke on breathing in
rats." |
Rao et al., 1995 |
Metabolites of woodsmoke
condensate accumulate in cultured rat eye lenses, compromising ability to
accumulate rubidium-86 (mimic of K) and choline. Says may explain
implication of smoke in cataract. |
Lal et al., 1993 |
Rats exposed to woodsmoke suffered
"bronchiolitis, hyperplasia and hypertrophy of bronchiolar epithelial
lining cells, some necrosed lining cells desquamated into lumens,
congestion of parenchymatous blood vessels, oedema, hyperplasia of
lymphoid follicles, peribronchiolar and perivascular infiltration of
polymorphonuclear cells, and mild emphysema" Conditioned worsened with
accumulated exposure ."The results indicate progressive
pathomorphological pulmonary lesions with subsequent exposure to wood
smoke in controlled conditions." |
Churg et al., 1997. |
Autopsies were carried out of lung
tissue from 10 never-smoking long-term residents of Vancouver. Retained
particles in human lung parenchyma were counted, sized, and identified by
analytical electron microscopy. 96% of particles had aerodynamic diameter
less than 2.5microns. |
Godleski et al., 1996 |
Rats with bronchitis were exposed
for 6 hours per day to 272ug/m3 PM2.5 (ie daily average of 68 ug/m3 -
similar or lower to PM2.5 concentrations in parts of Armidale). 37% of
rats exposed to particles died, compared to none exposed to filtered air.
|
Summary
More than 40 studies relating woodsmoke to health are referenced here. They
cover all aspects, from use of wood for cooking or heating in developing
countries, to use of modern heaters in developed countries, to detrimental
health effects found in whole towns or cities when woodsmoke is allowed to build
up. The epidemiological evidence is supported by tests on laboratory animals,
which show exposure to woodsmoke reduces the ability of the lungs to fight
infection. After exposure to a pathogen, 21% of mice exposed to woodsmoke became
sick and died within 2 weeks, compared with 5% exposed to oil furnace fumes.
It would be totally dishonest and misrepresentative of the wealth of
scientific evidence presented here to selectively quote only the two studies
cited here that do not show adverse effects of woodsmoke.
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