Published Literature on Woodsmoke and
Woodsmoke contains several
known human carcinogens, including benzene, benzo[a]pyrene and formaldehyde and has been nominated to the US National Toxicology Program Report on Carcinogens. It has been described as a "witch's brew of carcinogens" because of all the PAH and toxic chemicals it contains. Burning 10 kg of wood in a
modern Australian heater produces more benzo[a]pyrene than in the smoke from
270,000 cigarettes and more benzene and formaldehyde than in the smoke of 60,000
In human cell lines, woodsmoke
caused more DNA damage than traffic-generated PM per unit mass and was found to
induce lung cancer in mice. Oncogene mutations in human patients with advanced non-small
cell lung cancer were associated with exposure to wood smoke as well as tobacco
smoking. Organic extracts of ambient particulate matter containing substantial
quantities of woodsmoke were found to be 30- fold more potent than extracts of
cigarette smoke condensate in a mouse skin tumour induction assay.
Predominant wood (fuel) usersin North America and Europe had a 21% higher risk of lung cancer. Wood burning was reported to create top cancer risk in Oregon's air.
In developing countries,
exposure to woodsmoke is associated with lung, mouth and throat cancers, and
even cervical cancers in women who test positive for the HPV virus.
· In Launceston the increase in indoor PM2.5 levels from outdoor woodsmoke was similar to that from living with a 1-pack per day smoker.
· In Europe (where residential wood burning accounts for 45% of Black Carbon and PM2.5 emissions) an increase of just 5 ug/m3 of PM2.5 pollution was associated with and 18% increase in all lung cancers and a 55% increase in adenocarcinomas. See also: Air Pollution, Even at Low Levels, Tied to Lung Cancer.
In OECD countries, lung cancer
increases by 14% for every additional 10 ug/m3 of annual PM2.5
exposure. Woodsmoke seems to be as
dangerous as other PM2.5, e.g. causing more DNA damage in human cell lines than
traffic-generated particles. It is the
largest single-source of PM2.5 emissions in most Australian cities - 67% of
PM2.5 emissions in Canberra (where 3.9% of households have woodheaters) and 34%
in Sydney (where 4.3% use wood as the main form of heating). With 7626 lung-cancer deaths in 2007,
reducing wood heater use in major cities from 4% to 2% of households would
reduce PM2.5 emission by about 15%, leading to about 2.1% fewer lung cancer
deaths and eventually saving about 160 lives per year.
· Tumour initiation tests on mice. The review by Naeher notes: “Organic extracts of ambient particulate matter (PM) containing substantial quantities of woodsmoke are 30- fold more potent than extracts of cigarette smoke condensate in a mouse skin tumor induction assay (Cupitt et al., 1994).”
· Does household use of biomass fuel cause lung cancer? A systematic review and evaluation of the evidence ...
"What is the bottom line? ▸ The available evidence strongly supports a causal relationship, almost doubling the risk in women, somewhat less so for men, reflecting their generally lower exposures."
PM2.5 from woodsmoke in Australian Rural Towns is similar to living with a 1-pack
per day smoker, even in households without wood heating
Neas et al. (1994) reported
that living with a 1-pack per day smoker increases PM2.5 exposure by about 30
ug/m3. PM2.5 are so small
they behave like gases, infiltrating homes in similar way to the air we need to
breathe. CSIRO research (from the 2001 State of the Environment Report)
shows that indoor PM2.5 levels in winter track outdoor levels. Apart from the occasional spike from an
indoor source, a large proportion of the indoor woodsmoke pollution is from
In Launceston, where woodsmoke
accounts for the vast majority of PM2.5 pollution, indoor PM2.5 concentrations averaged
47.3 ug/m3 in winter, compared to 15.9 in summer (NHT 2004). The difference of 31.4 ug/m3 is
more than expected from living with a 1-pack per day smoker.
Tumour potency – wood vs tobacco
According to a recent review Naeher et al.
“Organic extracts of ambient particulate
matter (PM) containing substantial quantities of woodsmoke are 30- fold more
potent than extracts of cigarette smoke condensate in a mouse skin tumor
induction assay (Cupitt et al., 1994)”
Developed countries – 21%
increased risk of lung cancer from burning wood
Hosgood et al. (2010) concludes: “Predominant wood (fuel) users in North American and European countries
(OR = 1.21; 95% CI, 1.06–1.38) experienced higher risk of lung cancer.” This
increase in lung cancer for using wood fuel in North America and Europe was
similar to the estimated increase of 20-40% for environmental tobacco smoke.
Developing countries – 433%
increase in lung cancer from cooking with wood
In third world
countries, exposure to biomass smoke is associated with an even higher risk.
Delgado et al. (2005) reported that approximately 38.7% of lung cancer
patients had an association with wood smoke exposure. Adenocarcinoma was
present in 46.7% of these patients
Behera, D. and T. Balamugesh (2005) studied indoor air pollution as a risk
factor for lung cancer in women. Among non-smokers, out of all the cooking
fuels, the risk of development of lung cancer was highest for biomass fuel
exposure with an odds ratio of 5.33 (95% CI 1.7-16.7). Use of mixed fuels was
associated with a lesser risk (OR= 3.04, 95% CI 1.1-8.38 ). ). In multivariate
logistic regression analysis biomass fuel exposure was still significant with
OR of 3.59 (95% CI 1.07-11.97) even after adjusting for smoking and passive
Non-smoking Mexican women with
long periods of wood smoke exposure had about double the risk of lung
et al. 2004).
Mouth and Throat cancer
Pintos, J., E. L. Franco, et al. (1998) concluded: "The association of use of wood stoves with
cancers of the upper aero-digestive tract is genuine and unlikely to result
from insufficient control of confounding. Due to its high prevalence, use of
wood stoves may be linked to as many as 30% of all cancers occurring in the
Velema, J., A. Ferrera, et al. (2002) concluded that "Burning wood in the kitchen increases the
risk of cervical neoplasia in HPV-infected women in Honduras." The odds ratio was 2.3 for 25-34 years of
exposure, to wood smoke increasing to 9.5 for 35+ years compared with women who
had 1-14 years of exposure (p = 0.017). Two
recent studies have linked air pollution, and a third environmental tobacco
smoke, to breast cancer. The study that
linked PM2.5 exposure to breast cancer suggested that higher air pollution
exposure at birth may alter DNA methylation, which may increase levels of
E-cadherin, a protein important to the adhesion of cells, a function that plays
an essential role in maintaining a stable cellular environment and assuring
healthy tissues. More generally,
chemicals in both wood and tobacco smoke can pass into the bloodstream where
they can affect many different tissues.
Known human carcinogens in wood
Burning 1 kg firewood creates more benzene, benzo[a]pyrene &
formaldehyde than 6,000 cigarettes
Benzene, benzo[a]pyrene and formaldehyde
are listed by the International Agency for Research on Cancer as known human
carcinogens. Chemical analysis of the
smoke from Australian wood heaters shows that burning 1 kg of wood produces
more benzo[a]pyrene than in the smoke from 27,000 cigarettes and more benzene
and formaldehyde than in the smoke from 6,000 cigarettes – see http://woodsmoke.3sc.net/wood-vs-cigarette-smoke.
Group 2A (probably carcinogenic to humans)
chemicals includes dibenz[a,h]anthracene.
Burning 1 kg of wood in an Australian wood heater produces more
dibenz[a,h]anthracene than in the smoke from 225,000 cigarettes (http://woodsmoke.3sc.net/wood-vs-cigarette-smoke).
Although exposure to household combustion
of biomass fuel (mainly wood) is listed only as a probable human carcinogen, this
is probably due to a paucity of research.
As the evidence mounts, e.g. a recent conference paper “Wood Smoke
Stimulates Human Lung Cancer Cell Growth” (Tafur et al.
it seems likely that wood smoke will be listed as a known human carcinogen.
Damage to human DNA from woodsmoke
A Norwegian study (Danielsen et
compare the genotoxicity of wood smoke particulate matter, authentic
traffic-generated particles, and standard reference material (SRM2975) of
diesel exhaust particles in human A549 lung epithelial and THP-1 monocytic cell
lines. DNA damage was measured as strand breaks (SB) and formamidopyrimidine
DNA glycosylase (FPG) sites by the comet assay.
Wood smoke particulate matter generated
more DNA damage than traffic-generated PM per unit mass in human cell lines,
possibly due to the high level of polycyclic aromatic hydrocarbons in WSPM. The
authors suggested that “exposure to wood
smoke particles might be more hazardous than PM collected from vehicle exhaust
with respect to development of lung cancer”.
Another study Danielsen et
analyzed air samples from a Danish village where most homes used wood-burning
stoves, and compared them to background particles outside the smoke area. The
researchers concluded that wood smoke particulates were more powerful in
damaging DNA, activating genes linked to disease and weakening immune response
than were the background air pollution particles from a variety of sources.
"In this study, we found that wood
smoke ... has similar toxicity and effects on DNA as that of vehicle exhaust
particles," said University of Copenhagen researcher Steffen Loft, who
led the project.
Professor Loft also found that in rural
areas, wood smoke particles were
contaminating nearby fields of crops which, if eaten, caused DNA damage to
Woodsmoke induces lung cancer in
Mice were placed in an environment in which they inhaled coal smoke and
wood smoke in indoor air for 15 to 19 months (Liang et al.
The incidences of lung cancer in the control group and wood group were 17.0%
(29/171), 45.8% (81/177).
Human population exposure and
estimated number of cancers
Air pollution significantly increases the
risk of lung cancer. The most recent research shows from the Nurses Health Study found that, for non-smoking women, a 10 ug/m3 increase in PM2.5 exposure was associated with a 37% increase in lung cancer. Results were most elevated when restricted to the most prevalent subtype, adenocarcinomas, which are known to be associated with woodsmoke.
Previous research, e.g. able 2
of Pope et al. (2002) show that an
increase of 10 ug/m3 of PM2.5 pollution increases lung cancers by an
average of 14%.
PM2.5 in Australian cities averages about
10 ug/m3, compared to less than 3 ug/m3 in country areas
when no woodsmoke is present. A crude
estimate is therefore that at least 70% of PM2.5 air pollution is man-made, and
that the increase in lung cancer mortality from PM2.5 pollution is about 7*1.4
= 9.8%, i.e. about 740 deaths per year.
smoke represents a surprisingly large proportion of PM2.5 emissions. For example, the NSW DECC emissions inventory
for Sydney reports that domestic-commercial solid fuel combustion, virtually
all of which is emissions from wood heaters comprises 34.3% of all PM2.5
emissions. ABS data shows that burning
wood is the main form of heating in 4.3% of households, with another 2.2% using
wood as a secondary source.
In Canberra, 67% of PM2.5 pollution is from
wood heating, which is used by only 3.9% of households.
The average for all Australian capital
cities is 4.2% (and 19.1% in the rest of Australia). Thus, woodsmoke could account for up to a
third of all air-pollution related cancers per year.
Behera, D.,Balamugesh, T.,
2005. Indoor air pollution as a risk factor for lung cancer in women. JAPI 53.
O.L., Cantor, K.P., Hernández-Ramírez, R.U.,López-Carrillo., L., 2010. Passive
smoking increases the risk of breast cancer among pre- and postmenopausal
Mexican women Cancer Health Disparities Conference, Sept. 30-Oct.3,
American Association for Cancer Research, Abstract A99
Goldberg, M.S., Ross, N.A., Chen, H.,Labrèche, F., 2010. Postmenopausal Breast
Cancer Is Associated with Exposure to Traffic-Related Air Pollution in
Montreal, Canada: A Case–Control Study. Environ
Health Perspect 118.
Loft, S., Kocbach, A., Schwarze, P.,Møller, P., 2009. Oxidative damage to DNA
and repair induced by Norwegian wood smoke particles in human A549 and THP-1
cell lines. Mut. Res.-Genetic Toxicology
and Environmental Mutagenesis 674, 116-122.
Møller, P., Jensen, K.A., Sharma, A.K., Wallin, H.k., Bossi, R., Autrup, H.,
Mølhave, L., Ravanat, J.-L., Briedé, J.J., de Kok, T.M.,Loft, S., 2011.
Oxidative Stress, DNA Damage, and Inflammation Induced by Ambient Air and Wood
Smoke Particulate Matter in Human A549 and THP-1 Cell Lines. Chemical Research in Toxicology 24,
Delgado, J.,Martinez, L., Sanchez, T., Ramirez, A., Iturria, C.,Gonzalez-Avila, G., 2005.Lung Cancer Pathogenesis Associated With Wood Smoke Exposure*. Chest, AmColl Chest Phys. 128: 124-131.
Gras, J., 2002.
Emissions from Domestic Solid Fuel Burning Appliances., Environment Australia
Technical Report No. 5, March 2002.
Hernández-Garduño,E., Brauer, M., Pérez-Neria, J.,Vedal, S., 2004. Wood smoke exposure and lungadenocarcinoma in non-smoking Mexican women. The International Journal of Tuberculosis and Lung Disease 8,377-383.
III, Boffetta, P., Greenland, S., Lee, Y.-C.A., McLaughlin, J., Seow, A.,
Duell, E.J., Andrew, A.S., Zaridze, D., Szeszenia-Dabrowska, N., Rudnai, P.,
Lissowska, J., FabiÃ¡novÃ¡, E.r., Mates, D., Bencko, V., Foretova, L., Janout,
V., Morgenstern, H., Rothman, N., Hung, R.J., Brennan, P.,Lan, Q., 2010.
In-Home Coal and Wood Use and Lung Cancer Risk: A Pooled Analysis of the International
Lung Cancer Consortium. Environ Health
Liang, C., Quan, N., Cao, S., He, X.,Ma, F., 1988. Natural inhalation
exposure to coal smoke and wood smoke induces lung cancer in mice and rats. Biomed Environ Sci.
Naeher, L., Brauer, M., Lipsett, M., Zelikoff, J., Simpson, C., Koenig,
J.,Smith, K., 2007. Woodsmoke Health Effects: A Review. Inhalation Toxicology 19, 67-106.
Neas, L., Dockery, D., Ware, J., Spengler, J., Ferris, B., Jr,Speizer,
F., 1994. Concentration of indoor particulate matter as a determinant of
respiratory health in children. Am. J.
Epidemiol. 139, 1088-1099.
NHT, 2004. Technical Report No 8.
Personal Monitoring of Selected VOCs: The Contribution of Woodsmoke to
Exposure, CSIRO Atmospheric Research, for the Natural Heritage Trust.
(available at http://www.deh.gov.au/atmosphere/airquality/publications/pem/).
Pope, C.A., 3rd, Burnett, R.T., Thun, M.J., Calle, E.E., Krewski, D.,
Ito, K.,Thurston, G.D., 2002. Lung cancer, cardiopulmonary mortality, and
long-term exposure to fine particulate air pollution. JAMA 287, 1132-41.
Tafur, K.B., Ritzenthaler, J.D., Roman, J.,Accinelli, R.A., 2011. Wood
Smoke Stimulates Human Lung Cancer Cell Growth. Am. J. Respir. Crit. Care Med. 183, A3903-.
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
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 -
October 2013. Air pollution a leading cause of cancer
The International Agency for Research on Cancer
(IARC) cited data indicating that 223,000 deaths from lung
cancer worldwide resulted from air pollution in 2010, and said there was also
convincing evidence it increases the risk of bladder cancer.
"Our task was to evaluate the air everyone
breathes rather than focus on specific air pollutants," deputy head Dana
Loomis said in a statement. "The results from the reviewed studies
point in the same direction: the risk of developing lung cancer is
significantly increased in people exposed to air pollution."
Breast cancer. Five recent studies have linked air pollution and genetic damage from PAH exposure (the main toxins in woodsmoke) to breast cancer; a sixth linked environmental tobacco smoke to breast cancer.
1) Cancer Mortality Risks from Long-term Exposure to Ambient Fine Particle. a 10 ug/m3 increase in PM2.5 exposure was associated with a 22% increase in all cancers, a 42% increase in cancers of the upper digestive tract, a 35% increase in cancers of the digestive accessory organs, an 80% increase in breast cancer in women and a 36% increase in lung cancer in men.
2) Exposure to
air pollution early in life and when a woman gives birth to her first child may
alter her DNA and may be associated with premenopausal breast cancer later in
life. A study, by researchers at
the University at Buffalo, is based on data from the Western New York Exposures
and Breast Cancer (WEB) study, which collected information from 1,170 women
with recently diagnosed breast cancer and 2,116 healthy women who lived in New
York's Erie and Niagara counties between 1996 and 2001. "The
investigation looked for an association between exposure to pollution and
alterations to DNA that influence the presence or absence of key proteins. Such
genetic changes are thought to be major contributors to cancer development and
progression, including at very early stages," said lead investigator
Katharine Dobson, MPH –http://www.sciencedaily.com/releases/2011/04/110420125508.htm
3) The relationship between genetic damage from polycyclic aromatic hydrocarbons in breast tissue and breast cancer A number of polycyclic aromatic hydrocarbons (PAH) are widespread environmental contaminants that cause mammary cancer experimentally. We investigated whether exposure and susceptibility to PAH, as measured by PAH–DNA adducts in breast tissue, are associated with human breast cancer ....The odds ratio for elevated adducts in tumor tissue compared with control tissue was 2.56 (1.05–6.24), after controlling for potential confounders.
4) Exposure to multiple sources of polycyclic aromatic hydrocarbons and breast cancer incidence. "In multiple-PAH source models, breast cancer incidence was associated with residential ETS (environmental tobacco smoke) from a spouse (OR=1.20, 95%CrI=1.03, 1.40) and synthetic firelog burning (OR=1.29, 95%CrI=1.06, 1.57); these estimates are similar, but slightly attenuated, to those from single-source models. Additionally when we considered PAH exposure groups, the most pronounced significant associations included total indoor sources (active smoking, ETS from spouse, grilled/smoked meat intake, stove/fireplace use, OR=1.45, 95%CrI=1.02, 2.04).
CONCLUSIONS: Groups of PAH sources, particularly indoor sources, were associated with a 30-50% increase in breast cancer incidence. PAH exposure is ubiquitous and a potentially modifiable breast cancer risk factor.
5) The risk
of breast cancer - the second leading cause of death from cancer in women – was
linked to NO2 pollution by researchers from The Research
Institute of the MUHC (RI MUHC; Dr. Mark Goldberg), McGill University (Drs.
Goldberg, Dan Crouse and Nancy Ross), and Université de Montréal (Dr. France
Labrèche), (Crouse et al.
"We've been watching breast cancer rates go up for some time, "says
study co-author Dr. Mark Goldberg, a researcher at The RI MUHC. "Nobody
really knows why, and only about one third of cases are attributable to known
risk factors. Since no-one had studied the connection between air pollution and
breast cancer using detailed air pollution maps, we decided to investigate it."
The paper talks about emissions, including
"gases, particles, volatile organic
compounds, and polycyclic aromatic hydrocarbons (PAHs), many of which are
accepted or potential carcinogens.
Benzene … is an accepted human carcinogen
(International Agency for Research on Cancer 1987), and has been shown to cause
mammary carcinomas in rodents (Huff et al. 1989; Maltoni et al. 1988, 1989).
Exposure to other aromatic hydrocarbons including kerosene, toluene, and
xylenes, has also produced increased rates of mammary cancers in female rats
(Maltoni et al. 1997). Aromatic hydrocarbons are lipophilic and may therefore
reach elevated concentrations in breast tissue and promote carcinogenesis in
the cells of the breast (Morris and Seifter 1992)". Wood heaters emit
NO2 and most of the other toxic chemicals listed above. The best estimate is about 0.44 grams of NO,
0.18 grams of NO2 and 0.62 g of NOx are emitted for every kg of
firewood burned (Gras 2002) NOx mission
limits for petrol cars are 0.15 g/km (Euro-3), 0.08 g/km (Euro-4) and 0.07 g/km
banned the installation of new woodheaters because they account for 47% of
Montreal’s PM2.5 pollution, including 45 winter days from Nov 2008 to March
2009 with PM2.5 levels exceeding the standard - http://woodsmoke.3sc.net/policies-elsewhere
If NO2 is a proxy for benzene and
other aromatic hydrocarbons, it seems likely that woodsmoke
exposure as well as exposure to the same and similar chemicals from traffic
emissions is a contributory factor http://woodsmoke.3sc.net/woodheater-car-comparison.
6) Mexican women who do not smoke but
are exposed to smoking are at three times higher risk for breast cancer than
non-smoking women not exposed to passive smoking (Chilian-Herrera
et al. 2010)
Although this focussed on environmental tobacco smoke, research
suggests that the pollutants in wood smoke have a much greater biological
impact in the human body than cigarette smoke (http://woodsmoke.3sc.net/wood-vs-cigarette-smoke) or even automobile exhaust on a per unit weight basis (Danielsen, Loft et al. 2009;
Danielsen, Møller et al. 2011.)
Abstracts of Selected Papers
1) 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
Background: Domestic fuel combustion
from cooking and heating is an important public health issue because roughly 3
billion people are exposed worldwide. Recently, the International Agency for
Research on Cancer classified indoor emissions from household coal combustion
as a human carcinogen (group 1) and from biomass fuel (primarily wood) as a
probable human carcinogen (group 2A).
pooled seven studies from the International Lung Cancer Consortium (5,105 cases
and 6,535 controls) to provide further epidemiological evaluation of the
association between in-home solid-fuel use, particularly wood, and lung cancer
questionnaire data, we classified subjects as predominant solid-fuel users
(e.g., coal, wood) or nonsolid-fuel users (e.g., oil, gas, electricity).
Unconditional logistic regression was used to estimate the odds ratios (ORs)
and to compute 95% confidence intervals (CIs), adjusting for age, sex,
education, smoking status, race/ethnicity, and study center.
with nonsolid-fuel users, predominant coal users (OR = 1.64; 95% CI,
1.49–1.81), particularly coal users in Asia (OR = 4.93; 95% CI, 3.73–6.52), and
predominant wood users in North American and European countries (OR = 1.21; 95%
CI, 1.06–1.38) experienced higher risk of lung cancer. The results were
similar in never-smoking women and other subgroups.
results are consistent with previous observations pertaining to in-home coal
use and lung cancer risk, support the hypothesis of a carcinogenic potential of
in-home wood use, and point to the need for more detailed study of factors
affecting these associations.
J., L. Martinez, et al. (2005). Lung Cancer Pathogenesis Associated With WoodSmoke Exposure*. Chest, Am Coll Chest Phys. 128: 124-131.
Tobacco is considered the most important cause of lung cancer, but other
factors could also be involved in its pathogenesis. The aim of the present work
was to establish an association between wood smoke exposure and lung cancer
pathogenesis, and to analyze the effects of wood smoke on p53 and murine double
minute 2 (MDM2) protein expression.
Design: Blood samples were obtained
from 62 lung cancer patients, 9 COPD patients, and 9 control subjects. Of the
62 lung cancer patients, 23 were tobacco smokers (lung cancer associated with
tobacco [LCT] group), 24 were exposed to wood smoke (lung cancer associated
with wood smoke [LCW] group), and 15 could not be included in these groups.
Western blot assays were performed to identify the presence of p53,
phospho-p53, and murine double minute 2 (MDM2) isoforms in plasma samples.
Densitometric analysis was used to determine the intensity of p53, phospho-p53,
and MDM2 bands.
Results: Approximately 38.7% of the
lung cancer patients examined had an association with wood smoke exposure,
most of them women living in rural areas. Adenocarcinoma was present in
46.7% of these patients. The p53 and phospho-p53 proteins were
significantly increased in LCW samples (56,536.8 ± 4,629 densitometry units
[DU] and 58,244.8 ± 7,492 DU, respectively [± SD]), in comparison with the
other groups. The 57-kD MDM2 isoform plasma concentration was very high in LCW
and LCT samples (75,696.4 ± 11,979 DU and 78,551.7 ± 11,548 DU, respectively).
MDM2-p53 complexes were present in a high concentration in control and COPD
subjects. This allows p53 degradation and explains the low concentrations of
p53 found in these groups. MDM2-phospho-p53 complexes were observed in COPD but
not in the other samples. This correlates with the low concentration of p53
observed in the COPD group (13,657 ± 2,012 DU), and could explain the different
clinic evolution of this smoker population in comparison with the LCT subjects.
Conclusion: This study suggests that
there is a possible association of lung cancer with wood smoke exposure.
Likewise, our findings demonstrate that wood smoke could produce similar
effects on p53, phospho-p53, and MDM2 protein expression as tobacco.
3) Pintos, J., E. L. Franco, et al. (1998). "Use of wood stovesand risk of cancers of the upper aero-digestive tract: a case-controlstudy." Int J Epidemiol 27(6): 936-40.
BACKGROUND: Incidence rates for cancers
of the upper aero-digestive tract in Southern Brazil are among the highest in
the world. A case-control study was designed to identify the main risk factors
for carcinomas of mouth, pharynx, and larynx in the region. We tested the
hypothesis of whether use of wood stoves is associated with these cancers.
METHODS: Information on known and potential risk factors was obtained from
interviews with 784 cases and 1568 non-cancer controls. We estimated the effect
of use of wood stove by conditional logistic regression, with adjustment for
smoking, alcohol consumption and for other sociodemographic and dietary
variables chosen as empirical confounders based on a change-in-estimate
criterion. RESULTS: After extensive adjustment for all the empirical
confounders the odds ratio (OR) for all upper aero-digestive tract cancers was
2.68 (95% confidence interval [CI] : 2.2-3.3). Increased risks were also seen
in site-specific analyses for mouth (OR = 2.73; 95% CI: 1.8-4.2), pharyngeal
(OR = 3.82; 95% CI: 2.0-7.4), and laryngeal carcinomas (OR = 2.34; 95% CI:
1.2-4.7). Significant risk elevations remained for each of the three anatomic
sites and for all sites combined even after we purposefully biased the analyses
towards the null hypothesis by adjusting the effect of wood stove use only for
positive empirical confounders. CONCLUSIONS: The association of use of wood
stoves with cancers of the upper aero-digestive tract is genuine and unlikely
to result from insufficient control of confounding. Due to its high prevalence,
use of wood stoves may be linked to as many as 30% of all cancers occurring in
4) Behera, D.
and T. Balamugesh (2005). "Indoor air pollution as a risk factor for lungcancer in women." JAPI 53.
Objectives: Tobacco smoking is the most
common risk factor for lung cancer. But a significant proportion of lung cancer
occurs in non-smokers. Indoor pollution due to domestic fuels has been recently
implicated as a causative agent in lung cancer especially in women. We
conducted a case control study to find out the role of indoor air pollution due
to domestic cooking fuels in Indian women.
Methods: In a case control study 67 women with proven lung cancer were
recruited. Forty-six females having a non-malignant respiratory disease
constituted the control group. The patients and controls were asked about the
exposure in various cooking fuels using a questionnaire.
Result: There were 50(74.6%) non-smokers and 17(25.4%) smokers among the female
cancer cases (p=0.016). Adenocarcinoma was the commonest histological type of
malignancy (n=26, 38.8%) in the whole group and was the predominant form in the
nonsmoking females. Tobacco smoking was the most important risk factor for lung
cancer with OR of 4.87 (95% CI 1.34-17.76). Among non-smokers out of all the
cooking fuels the risk of development of lung cancer was highest for biomass
fuel exposure with an odds ratio of 5.33 (95% CI 1.7-16.7). Use of mixed fuels
was associated with a lesser risk (OR= 3.04, 95% CI 1.1-8.38 ). ). In
multivariate logistic regression analysis biomass fuel exposure was still
significant with OR of 3.59 (95% CI 1.07-11.97) even after adjusting for
smoking and passive smoking.
5) Wood smokeexposure and lung adenocarcinoma in non-smoking Mexican women. Hernández-Garduño E, Brauer M, Pérez-Neria J, Vedal S. Int J Tuberc Lung Dis. 2004 Mar;8(3):377-83. Department of
Tuberculosis Control, British Columbia Centre for Disease Control, Vancouver,
British Columbia, Canada. email@example.com
OBJECTIVE: To determine the association between long-term exposure to wood
smoke from cooking and lung adenocarcinoma in non-smoking Mexican women.
METHODS: We reviewed records of hospitalized patients at a chest referral
hospital in Mexico City and identified 113 histologically proven lung
adenocarcinoma cases in non-smoking women. Four control groups of non-smoking
women were also selected: 99 patients with pulmonary tuberculosis (PTB), 110
with interstitial lung disease (ILD), 64 with miscellaneous pulmonary
conditions (MISC), and the three control groups combined (COMB) (n = 273).
RESULTS: Exposure was assessed on the basis of questionnaire responses at the
time of hospital admission. Exposure to wood smoke for more than 50 years, but
not for shorter periods, was associated with lung cancer after adjusting for
age, education, socio-economic status and environmental tobacco smoke (ETS)
exposure. Adjusted odds ratios from the multivariable logistic regression
models were 1.4 (95%CI 0.6-2.0) for cases vs. TB controls, 1.9 (95%CI 0.9-4.0)
for cases vs. ILD controls, 2.6 (95%CI 1.0-6.3) for cases vs. MISC controls and
1.9 (95%CI 1.1-3.5) for cases vs. COMB controls.
CONCLUSION: These findings suggest that long-term exposure to wood smoke from
cooking may contribute to the development of lung cancer.
6) Velema, J., A. Ferrera, et al. (2002).
"Burning wood in the kitchen increases the risk of cervical neoplasia inHPV-infected women in Honduras." International Journal of Cancer 97(4).
suggestive evidence that the use of wood for cooking increases the risk of
invasive cervical cancer. We investigated this association in women with
cervical neoplasia in Honduras. Women aged 20-64 years with cervical
intraepithelial neoplasia (CIN) grade I (n = 44), CIN II (n = 36) or CIN III (n
= 45) were recruited from screening programs in Tegucigalpa City and each was
matched by age and clinic to 2 controls (241 total) without cervical
abnormalities. The clinics selected women of low socioeconomic status. Cervical
scrapes were tested for the presence of human papillomavirus (HPV) DNA using a
general primer set directed against the L1 open reading frame, and HPV
genotyping was performed. Odds ratios (ORs) were computed through conditional
logistic regression; p-values were from tests for linear trend of risk with
increasing exposure. HPV DNA was detected in 48% of women with CIN I, 67% with
CIN II and 89% with CIN III. The ORs were 1.5, 2.5 and 38.3 respectively. At
univariate analysis, age at first intercourse was consistently lower among
cases than controls. Risk was reduced by 50% or more in all 3 CIN classes when
initiation of sexual activity at age 20 years or older was compared with
initiation before age 16 years (p = 0.013 for CIN I). No effect was observed
for smoking, oral contraceptives or previous cytologic screening. Effects for
number of sexual partners, parity, age at first pregnancy and education were in
the expected directions but never persisted after adjustment for HPV. Chronic
exposure to wood smoke significantly increased the risk of CIN III (p = 0.022).
However, women who said No when asked if they ever used wood in the kitchen had
a higher risk than those with low or intermediate exposure. This was taken as
evidence that the initial screening question had either been misunderstood or
that answers were biased. Restricting the analysis to women who reported
exposure yielded positive associations in all CIN classes with for CIN III ORs
of 2.3 for 25-34 and 9.5 for 35+ years compared with women who had 1-14 years
of exposure (p = 0.017). A multivariate analysis of the complete dataset (n =
366) allowed for separate ORs for HPV in each CIN class. Inclusion of age at
first intercourse significantly improved this model (p = 0.021). Adding
exposure to wood smoke further improved the model only if an interaction
between woodsmoke and HPV was allowed for. If, as the data suggest, it was
assumed that wood smoke had its effect among HPV-positives only, there was a
significant linear dose-response relationship between exposure to woodsmoke and
risk of CIN (p = 0.026). This association was independent of other risk factors
including education, parity and number of sexual partners. ORs in the final
model were 0.37 for age at first intercourse 20 years or higher and 5.69 for
more than 35 years of exposure to wood burning in the kitchen. The present
study suggests that the use of wood for cooking is a risk factor for cervical
neoplasia that deserves further study, given its high prevalence in developing
7) K-RAS Oncogene Mutation in Patients with AdvancedNon-Small Cell Lung Cancer (NSCLC) Associated With Exposure to Wood Smoke andTobacco Smoking: Therapeutic Implications.
Wood smoke has been described as a
carcinogen and an important risk factor for the development of NSCLC.
frequency of exposure to wood smoke in patients with NSCLC is 28%.
indicates than lung cancer associated with tobacco smoking and the lung
with wood smoke exposure present different clinical characteristics,
that they might also have different genetic alterations, which are a
consequence of tumor etiology. Source:
8) CK, L., Q.
NY, et al. (1988). "Natural inhalation exposure to coal smoke and woodsmoke induces lung cancer in mice and rats." Biomed Environ Sci.
In a rural area with a high mortality
rate of lung cancer in humans, mice and rats were placed in an environment in
which they inhaled coal smoke and wood smoke in indoor air for 15 to 19 months.
The incidences of lung cancer in mice in the control group, wood group, and coal
group were 17.0% (29/171), 45.8% (81/177), and 89.5% (188/210), respectively:
in rats the incidences were 0.9% (1/110), 0 (0/110), and 67.2% (84/125),
respectively. In addition, the pollutants in the air were analyzed. The results
indicate that coal smoke is a highly significant risk factor for lung cancer in
humans in Xuan Wei County of Yun Nan Province in China.
9) Lung Cancer and Indoor Pollution from Heating and Cooking with Solid Fuels
The IARC International Multicentre Case-Control Study in Eastern/Central Europe and the United Kingdom.
odds ratio of lung cancer associated with solid
fuel use was 1.22 (95% confidence interval (CI): 1.04, 1.44) for cooking
heating, 1.37 (95% CI: 0.90, 2.09) for solid fuel
only for cooking, and 1.24 (95% CI: 1.05, 1.47) for solid fuels used for
both cooking and heating. ...The data suggest a modest increased
risk of lung cancer related to solid-fuel use for cooking rather than heating."
Text: " Among those who used only wood for cooking,the odds ratio of lung cancer was 1.23 (95 percent CI: 1.00,1.52). The odds ratio for exclusive use of wood for heating was 1.31 (95 percent CI: 1.06, 1.61)."
Comment: this suggests that exposure to wood and coal smoke increases the risk of lung cancer, but that exposure (and hence the overall risk) depends on the type of cooker or heater.
Does household use of biomass fuel cause lung cancer? A systematic review and evaluation of the evidence ... Other reportsWas Beau Biden’s Brain Cancer Caused by Burn Pit Exposure?
Bruce N, Dherani M, Liu R, Hosgood HD, Sapkota A, Smith KR, Straif K, Lan Q, Pope D (2015)
What is the bottom line? ▸ The available evidence strongly supports a causal relationship, almost doubling the risk in women, somewhat less so for men, reflecting their generally lower exposures.
Background Around 2.4 billion people use traditional biomass fuels for household cooking or heating. In 2006, the International Agency for Research on Cancer (IARC) concluded emissions from household coal combustion are a Group 1 carcinogen, while those from biomass were categorised as 2A due to epidemiologic limitations. This review updates the epidemiologic evidence and provides risk estimates for the 2010 Global Burden of Disease study.
Methods Searches were conducted of 10 databases to July 2012 for studies of clinically diagnosed or pathologically confirmed lung cancer associated with household biomass use for cooking and/or heating.
Findings Fourteen eligible studies of biomass cooking or heating were identified: 13 had independent estimates (12 cooking only), all were case-control designs and provided 8221 cases and 11 342 controls. The ORs for lung cancer risk with biomass for cooking and/or heating were OR 1.17 (95% CI 1.01 to 1.37) overall, and 1.15 (95% CI 0.97 to 1.37) for cooking only. Publication bias was not detected, but more than half the studies did not explicitly describe a clean reference category. Sensitivity analyses restricted to studies with adequate adjustment and a clean reference category found ORs of 1.21 (95% CI 1.05 to 1.39) for men (two reports, compiling five studies) and 1.95 (95% CI 1.16 to 3.27) for women (five reports, compiling eight studies). Exposure–response evidence was seen for men, and higher risk for women in developing compared with developed countries, consistent with higher exposures in the former.
Conclusions There is now stronger evidence for biomass fuel use causing lung cancer, but future studies need better exposure assessment to strengthen exposure–response evidence.