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Health effects assessment of exposure to particles from wood smoke

5 Human health effects

• 5.1 Epidemiological studies, non-cancer health effects
  • 5.1.1 Particles in the general environment
  • 5.1.2 Particles from residential wood burning
  • 5.1.3 Other settings with wood smoke exposure
  • 5.1.4 Summary, non-cancer health effects
• 5.2 Epidemiological studies, carcinogenic effects
  • 5.2.1 Particles in the general environment
  • 5.2.2 Particles from wood burning
  • 5.2.3 Summary, carcinogenic effects

From the latest 10-15 years of toxicological and epidemiological research an extensive body of evidence has been generated documenting the adverse health effects resulting from ambient air PM. The numerous epidemiological studies show a very consistent and uniform pattern with regard to different types of health outcomes and dose-response relationships.

Associations between adverse health effects and ambient air PM have typically been identified in relation to PM levels measured in the background urban air in general and these PM levels have been taken as a surrogate for the population exposure in the area. From such data it is generally very difficult to assess the health impacts of different sources of PM, as all PM sources are included in the PM levels in the background urban air. However, studies in which different fractions of PM have been analysed (e.g. elemental or organic carbon) and studies in which specific combustion related gaseous pollutants in addition to PM have been measured have shown that especially PM from combustion sources are important in relation to the adverse health effects.

Epidemiological studies have identified a variety of adverse health effects following acute (episodic increased) PM exposure as well as following long-term exposure. From an overall evaluation of these studies it is generally concluded that the adverse health effects are not solely linked to acute exposure from episodic increases. In contrary, the average level of long-term exposure over a year or more has a much stronger influence on public health compared to the effects calculated from them sum of episodes with increased PM levels within the same period.

Another important finding is that it has not been possible to identify a lower threshold for adverse health effects, neither in connection with acute nor with long-term exposure. (WHO 2003, WHO 2004).

When assessing the adverse health effects of wood smoke and wood smoke PM, there are at least two different methodological approaches that can be used.

One approach would be to assess wood smoke PM as a part of PM in general and to benefit from the knowledge regarding adverse health effects from the PM area in general. Especially important in this approach would be to identify toxicological studies and epidemiological studies in which wood smoke PM has been identified as an important source of the total PM fraction.

Another, more classical toxicological, approach would be to separate the wood smoke into its different constituents and to evaluate the hazard and risk profile of each constituent. As shown in section 2, a variety of very toxic single constituents have been identified in wood smoke, e.g. benzo[a]pyrene and other carcinogenic PAHs, dioxins, a variety of heavy metals, and several volatile carcinogens such as formaldehyde, benzene and 1,3 butadiene. Although a hazard profile may be created by using this approach, it may be very difficult to evaluate the actual health risk of wood smoke as an evaluation also would require knowledge concerning the vast amount of possible physico-chemical and toxicological interactions between the several hundreds of different constituents in the wood smoke as well as of the toxicokinetic properties of the different constituents.

For ambient PM, Valberg & Long (2003) has attempted to compare the levels of the individual constituents in ambient air and the toxicologically based human health reference concentration of the individual constituents. For none of the constituents, an unacceptable risk could be identified, as the human health reference concentration for a specific constituent generally was far below the actual level in ambient air. This indicates that data on a single constituent is not sufficient in order to assess the risk and that the adverse health effects from PM can not at present be properly characterised by using this approach.

Consequently, the approach chosen in this report is to assess the adverse health effects of wood smoke PM based on the current knowledge on PM in general with focus on the epidemiological studies where wood smoke PM has been identified as an important source of the total PM fraction.

5.1 Epidemiological studies, non-cancer health effects

The association of particulate air pollution with adverse health effects has long been known, especially in relation to respiratory and cardiovascular disease. The fraction of very small particles probably constitutes one of the most important health problems in relation to air pollution (Brunekreef & Holgate 2002). WHO has estimated that 1% of all heart- and lung diseases and 3% of respiratory cancer cases in the whole world is caused by particulate air pollution. This leads to 600,000 (1.2%) early deaths and loss of 7.4 million (0.5%) DALYs (Disease Adjusted Life Years). The most significant air pollution problems are seen in the developing countries and in Central- and East Europe. It has recently been estimated that air pollution is responsible for 288,000 early deaths in the EU (CAFE CBA 2005).

Our knowledge about quantitative associations between health effects and particulate air pollution is mainly based on epidemiological studies performed as cohort studies or time-series studies.

In cohort studies, population groups living in different areas with different levels of air pollution are studied, and cohort studies generally reflect effects following long-term exposure.

In time-series studies, one population group is studied and their health is related to changes in air pollution levels; time-series studies generally reflect effects following acute exposure episodes or short-term exposure.

The dose-response relationship, i.e., the relative risk for the various health outcomes studied, is substantially higher following long-term exposure when compared to acute or short-term exposure. This indicates that long-term effects from air pollution is not just adding up the effects from acute short-term episodes, but rather that long-term exposure raises the general level of mortality and morbidity in the population.

A limitation in both study designs is the exposure characterisation, which is usually based on data from a single monitoring site in the area, and assumed to be representative for all individuals in the area. Another limitation is that most of the knowledge is based on fine particles (PM_2.5) and the sum of fine and coarse particles (PM₁₀), whereas knowledge on ultrafine particles is limited.

5.1.1 Particles in the general environment

5.1.1.1 Effects from short-term exposure, time series studies

Early air pollution episodes, such as in 1952 in London, were dramatic examples of the impact of air pollution on mortality and other health effects (Logan 1953). During this episode the daily levels of particles, measured as soot, increased 10-fold compared to the “normal” levels at that time of 300-500 µg/m³ (which is more than 10-fold the levels seen today). These air pollution episodes were the motivation for regulations and consequent air quality improvements in the past 30-40 years. The effect of air pollution control was clearly observed in Dublin in the 1990s when coal sales were banned and residential heating with coal was stopped (Clancy et al. 2002). About 116 fewer respiratory deaths and 243 fewer cardiovascular deaths were seen per year in Dublin after the ban.

Several time-series studies in USA and Europe have demonstrated that days with increased concentrations of particulate air pollution are associated with an increase in hospital admissions and death due to lung and cardiovascular disease, for example demonstrated in 10 European cities (Zanobetti et al. 2003).

A meta-analysis showed that an increase of 10 µg/m³ PM₁₀ is associated with 0.6% increased total mortality, 1.3% increased respiratory related deaths and 0.9% cardiovascular deaths in a city area in the first days after the PM₁₀ increase (Anderson et al. 2004). If the observation time is extended for 40 days, the effect on total mortality is as high as 1% (Zanobetti et al. 2003).

Especially patients with pre-existing respiratory or cardiovascular disease are at risk of these air pollution effects.

The time-series design has also been used in a study where ultrafine particles were measured in the German city Ehrfuhrt with about 300 000 inhabitants (Wichmann et al. 2000). In this study, the effect of ultrafine particles on death due to cardiac and respiratory disease was comparable to the effect of PM_2.5 and PM₁₀. This study has recently been updated using data on PM number and mass concentrations and death certificates during 1995-2001 (Stölzel et al. 2006). A significant association between total mortality and cardio-respiratory mortality and the number concentrations of ultrafine particles was found whereas the increased mortality in relation to particle mass (PM₁₀) did not reach a significant response.

In another European study of Amsterdam, Ehrfuhrt and Helsinki, it was found that effects on cardiac and respiratory disease correlated better with PM_2.5 than with the ultrafine particles (de Hartog et al. 2003, Pekkanen et al. 2002).

5.1.1.2 Effects from long-term exposure, cohort studies

Only a few cohort studies are available at present.

Dockery et al. (1993) studied about 8000 persons in six cities, while Pope et al. (1995) studied about 550,000 persons in 151 city areas. Both studies showed a significant association between mortality and particle level (PM_2.5). The increased mortality was most pronounced among persons with pre-existing respiratory and cardiovascular disease. The results of the studies were based on the general particle level in background areas and no estimation was made of the contribution from the traffic or other sources.

Laden et al. (2006) conducted a follow-up of the Dockery et al. (1993) six cities study from 1990 to 1998. They found an increase of 16% in overall mortality associated with each 10 µg/m³ PM_2.5 as an overall mean during the period or an increase of 14% in relation to the annual mean of PM_2.5 in the year of death. Particulate air pollution had decreased from the first to the second period (1974-1989 and 1990-1998). Overall, between the two periods a decrease in mortality of 27% was found for each 10 µg/m³ reduction in the PM_2.5 level.

Pope et al. (2002) have made an update of their study population of 550,000 persons. Health effects were now registered until 1999 and the result of the new study was in accordance with the result from 1995. A clear and significant association between mortality and PM_2.5 level was observed. There was a considerable reduction of about 1/3 in PM_2.5 level in the period from 1979-83 to 1999-2000 in all areas. In 1979-83, a difference in the annual mean of 10 µg/m³ PM_2.5 between the areas was associated with a difference in annual mortality of 4% while in the period of 1999-2000, a difference of 10 µg/m³ PM_2.5 was associated with a difference in annual mortality of 6%.

Jerret et al. (2005) studied 23,000 persons in the Los Angeles area for the period 1982-2000. The population was a subset of the Pope et al. study; however, the exposure could be assessed more accurately as the exposure was determined using model extrapolations of PM-data from 23 measurement stations. After controlling for covariates, a 10 µg/m³ increase in the annual PM_2.5 level was associated with an increase in mortality of 17%. The corresponding increase in ischaemic heart disease was 38% and for lung cancer 46%. Thus, this study found an association in relation to mortality that was three times higher than that of Pope et al. (2002). The increase was judged to be due to a more accurate exposure assessment than in the prior studies. Furthermore, the authors suggested that a higher contribution of traffic PM in the Los Angeles area might have increased the adverse health outcome.

Miller et al. (2007) studied a cohort of 66,000 women (older than 50 years and without previous cardiovascular disease) from 36 U.S. metropolitan areas and analysed the association between PM_2.5 and first appearance of cardiovascular events (coronary heart disease, cerebro-vascular disease, myocardial infarction, coronary re-vascularisation, stroke), and cardiovascular mortality. Each increase of 10 µg/m³ PM_2.5 was associated with a 24% (95% interval: 9-41%) increase in risk of cardiovascular event and a 76% (95% interval: 25-147%) increase of death from cardiovascular disease. When differences in PM_2.5 and cardiovascular mortality within cities (between 4 and 78 PM monitors per city) were studied this resulted in a considerable higher increased risk of cardiovascular mortality (128% increase per 10 µg/m³ PM_2.5) compared to intercity comparisons (58% increase per 10 µg/m³ PM_2.5). These findings show an even higher increased risk for cardiovascular mortality than described in the recent cohort studies where the whole adult population, i.e., both men and women were studied (Laden et al. (2006) – study of intercity comparisons; Jerret et al. (2005) – study of intra-city comparisons).

In a study from the Netherlands, a cohort of 5000 persons was studied from 1986 to 1994 (Hoek et al. 2002). Exposure was assessed using background levels of soot and NO₂. Mortality caused by cardiopulmonary disease was 2-fold increased for persons living less than 100 m from a highway or less than 50 m from a larger city road. Five percent of the Dutch cohort lived near roads with heavy traffic, and the effect on mortality was 1.5-fold higher in this group compared to the remaining 95%.

In a recent Norwegian cohort study, 16,209 men in Oslo aged 40-49 years in 1972-73 were studied until 1998 (Nafstad et al. 2004). Their exposure to air pollution was assessed by estimating NO_x at the home address in 1974-1978. The study showed an increase in total mortality with a relative risk of 1.08 (95% CI 1.06-1.11). The relative risk for death caused by respiratory disease was 1.16 (95% CI, 1.06-1.26), for heart disease 1.08 (95% CI, 1.03-1.12). These results support the results from the earlier cohort studies and since NO_x was used as exposure parameter, the results indicate that traffic is the most important particle source.

5.1.1.3 Air quality standards

Air quality standards have been set for particulate matter by different organisations and by federal and national institutions. The basis for the air quality standards has been the adverse health effects and the dose-response associations observed in connection with ambient air PM levels in epidemiological studies. The standard values are the maximum concentrations allowed when averaged over time, typically 24-hour concentrations and annual concentrations.

In the US, the US-EPA standards for 24 hours are 150 µg/m³ for PM₁₀ and 35 µg/m³ for PM_2.5. The annual standard for PM_2.5 is 15 µg/m³ while the former annual standard of 50 µg/m³ for PM₁₀ has been revoked. (US-EPA 2006).

The EU Commission has recently proposed a 24-hour standard for PM₁₀ of 50 µg/m³ and an annual standard of 40 µg/m³. For PM_2.5, no 24-hour standard has been set but an annual standard of 25 µg/m³ was set as a concentration cap. Furthermore, the existing annual ambient air PM_2.5 levels (monitored in the period of 2008-2010) in the EU have to be reduced by 20% in 2020. (EU 2005).

The WHO has recently set 24-hour air quality guidelines of 50 µg/m³ for PM₁₀ and of 25 µg/m³ for PM_2.5. The annual air quality guidelines were set to 20 µg/m³ and 10 µg/m³ for PM₁₀ and PM_2.5, respectively (WHO 2006). The WHO states that combustion of wood and other biomass fuels are important sources contributing to the PM_2.5 fraction. Based on the available data. it is further assumed that the health effects of PM_2.5 from fossil and biomass combustion are broadly the same. With respect to dose-response associations, the WHO concludes that an increase in the annual level of 10 µg/m³ PM_2.5 is associated with an increase in the annual mortality of 6% in the population whereas an increase of 10 µg/m³ in the 24-hour PM_2.5 level is associated with an increase in short-term mortality of 1%.

5.1.2 Particles from residential wood burning

The particle emission from wood burning stoves has received much attention lately. Since these particles are combustion products, they are expected to have effects similar to other combustion particles, e.g. from traffic. The studies described in the following are summarised in Table 5 (indoor air) and Table 6 (ambient air).

Table 5. Studies with indoor exposure to wood smoke (low level)

No measurements were made of wood smoke exposure.

5.1.2.1 Indoor air

Several early studies focused on the presence of a wood stove in the home as a risk factor. Several studies indicate that wood stoves, especially older varieties can emit smoke directly into the home (Larson & Koenig 1994). While these earlier studies strongly suggest that there are adverse health impacts associated with wood smoke exposure, their crude exposure assessments preclude more specific conclusions.

Honicky et al. (1985) studied 34 preschool children living in homes with wood stoves compared to 34 children in homes with other heating sources, mainly gas. Occurrence of wheeze and cough was greater in the group of children living in homes with wood stoves. No measurements were made of the wood smoke.

Levesqu et al. (2001) examined the frequency of respiratory symptoms and illnesses among occupants of wood-heated homes. Out of the 89 houses included in the study, 59 had wood burning appliances. There was no consistent relationship between the presence of a wood burning appliance and respiratory morbidity in residents. However, residents exposed to emissions from wood burning reported more respiratory illnesses and symptoms.

In a prospective cohort study of adults with asthma residing in Denver, Colorado, metropolitan area, a panel of 164 asthmatics recorded in a daily diary the occurrence of several respiratory symptoms as well as the use of wood stoves and fireplaces (Ostro et al. 1994). It was found that that the use of wood stoves or fireplaces was related to more respiratory symptoms.

In contrast, another study of 349 adults with asthma living in Northern California showed no evidence of a negative influence of indoor wood smoke exposure on adult asthma (Eisner et al. 2002). In that study based on telephone interviews, exposure to environmental tobacco smoke was clearly associated with worse severity of asthma symptoms.

5.1.2.2 Ambient air

Most of the studies described in the following were also included in a review by Boman et al. (203) concerning adverse health effects from ambient air pollution in relation to residential wood combustion. The results of the studies included in this review are described below and summarised in Table 6, and the review is further addressed in sections 5.1.2.2.1 and 5.1.2.2.2.

Several studies have evaluated adverse health effects in communities where wood smoke was a major, although not the only, source of ambient air particulate. A questionnaire study of respiratory symptoms compared residents of 600 homes in a high wood smoke pollution area of Seattle with 600 homes (questionnaires completed for one parent and two children in each residence) of a low wood smoke pollution area (Browning et al. 1990). PM₁₀ concentrations averaged 55 and 33 µg/m³ in the high and low exposure areas, respectively. When all age groups were combined, no significant differences were observed between the high and low exposure areas. However, there were statistically significant higher levels of congestion and wheezing in 1-5 year old children between the two areas for all three questionnaires (one baseline questionnaire and two follow-up questionnaires which asked about acute symptoms).

A more comprehensive study in the same high exposure Seattle area was initiated in 1988 (Koenig et al. 1993). During the heating season 80% of the particles is from wood smoke in these residential areas in Seattle (Larson & Koenig 1994). Lung function was measured in 326 (including 24 asthmatics) elementary school children before, during and after two wood burning seasons. Fine particulates were measured continuously with an integrating nephelometer. Significant lung function decrements were observed in the asthmatic subjects, in association with increased wood smoke exposure. The highest (night-time 12-hour average) PM_2.5 level measured during the study period was approximately 195 µg/m³ and PM₁₀ levels were below the US National Ambient Air Quality Standard of 150 µg/m³ during the entire study period. For the asthmatic children FEV1 and FVC decreased by 17 and 18.5 ml for each 10 µg/m³ increase in PM_2.5, while no significant decreases in lung function were observed in the non-asthmatic children.

A companion study evaluated the impact of particulate matter on emergency room visits for asthma in Seattle during the period September 1989 through September 1990 (Schwartz et al. 1993). In this study a significant association was observed between PM₁₀ particle levels and emergency room visits for asthma for persons under age 65. The mean PM₁₀ level during the 1-year study period was 30 µg/m³ (range 6-103 µg/m³). The daily risk for a 30 µg/m³ increase on PM₁₀ was 1.12 (95% CI 1.20-1.04). The study showed clear evidence of a dose-response relationship, but did not identify a threshold below which effect were not observed.

Yu et al. (2000) observed a panel of 133 children (5-13 years of age) with asthma residing in Seattle, Washington, for an average of 58 days (range 28-112 days) in the period November 1993 through August 1995. The daily average levels of PM₁₀ and PM_1.0 were 25 µg/m³ (range 8-86) and 10.4 (range 2-62), respectively. Increased exposure to air pollutants, specifically CO and PM, was associated with increased odds of at least one mild asthma symptom, like use of medication and night awakening for asthma. Data for CO, PM and SO₂ was measured at 6, 3 and 1 monitoring sites, respectively. PM was measured both as PM₁₀ and PM_1.0 by gravimetric and/or nephelometric methods.

Sheppard et al. (1999) investigated the relation between ambient air pollutants in Seattle, Washington and hospital admissions for asthma in the period 1987 through 1994. All persons were <65 years of age and 23 hospitals were included in the study. Data on PM₁₀ and PM_2.5 were available from three and two monitoring sites, respectively. Four monitoring sites provided data for CO, while SO₂ and O₃ were measured at one site each. The daily average levels of PM₁₀ and PM_2.5 were 31.5 µg/m³ and 16.7 µg/m³, respectively. An estimated 4-5% increase in the rate of asthma hospital admissions was found to be associated with an interquartile range change in PM₁₀ or PM_2.5 after a lag of one day. Positive associations were also found for O₃ and CO after a lag of two and three days, respectively.

In a study by Norris et al. (1999), they found a significant association between fine particles (PM₁₀ and PM_2.5) and daily hospital admissions for asthma in Seattle during September 1995 to December 1996. Six hospitals were included in the study and only data for persons <18 years of age was used. Data on PM₁₀ and PM_2.5 were available from three monitoring sites. CO data was obtained from four sites, and SO2, NO2 and O3 from one site each. The daily average level of PM₁₀ was 22 µg/m³ (range 8-70 µg/m³). A change of 11 µg/m³ in fine PM (< 2.5 µm) was associated with a relative rate of 1.15 (95% CI 1.07-1.23). An increase in CO was also associated with hospital visits for asthma. The majority of the hospital admissions were for children younger than 5 years of age.

Table 6. Epidemiological studies with residential wood smoke as a major exposure source.

* The nine studies included in the review of Boman et al. (2003) discussed below.
COPD: Chronic Obstructive Pulmonary Disease
PEF: Peak Expiratory Flow

Schreuder et al. (2006) used source appointment techniques in order to separate different sources of PM in the state of Washington during the period 1995-2001. Total carbon and arsenic had high correlations with vegetative burning (arsenic due to burning af arsenic treated wood) while other markers were correlated to motor vehicles (Zn) and airborne soil (Si). Vegetative burning contributed to about half of the total PM_2.5 level. The association between the different markers and hospital admissions for cardiac diseases and emergency departments visits for respiratory diseases were analysed. The rate of respiratory emergency department visits increased 2% for a 3.0 µg/m³ interquartile range change in total carbon (1.023, 95% CI 1.009-1.038) at a lag of one day. For total PM_2.5, an interquartile increase of 7.7 PM_2.5 was associated with an increase in respiratory department visits of 1.3% (RR = 1.013, 95% CI 0.999-1.025). The results suggest that vegetative burning is associated with acute respiratory events.

Vedal et al. (1998) have studied the acute effects of ambient particles in 206 asthmatic and non-asthmatic children living on the west coast of Vancouver Island. The children, aged 6-13 years, were followed for up to 18 months with twice daily measurements of peak expiratory flow (PEF) and daily recording of symptoms. Data on PM₁₀ were available from two monitoring sites, and the daily mean PM₁₀ concentration was 27 µg/m³ (range 0- 159 µg/m³). Increases in PM₁₀ concentrations were associated with reductions in PEF and increased reporting of cough, phlegm production, and sore throat. For asthmatics, an increase of 10 µg/m³ in PM₁₀ was associated with a reduction of PEF by 0.55 l/min (95% CI, 0.06-1.05) and increased odds of reported cough by 8% (95% CI, 0-16%). The authors concluded that children with asthma are more susceptible to these effects than other children.

Two time series studies have been conducted in Santa Clara County, California, an area in which wood smoke is the single largest contributor to winter PM₁₀, accounting for approximately 45% of winter PM₁₀ (Fairley 1990, Lipsett et al. 1997). Particulate levels are highest during the winter in this area.

The first study was one of the initial mortality time series studies, which indicated an association between relatively low PM₁₀ levels and increased daily mortality (Fairley 1990).

In the second study, Lipsett et al. (1997) found a consistent relationship of asthma emergency room visits in Santa Clara County and winter PM₁₀ during the winter seasons (November-January) 1988-89 through 1991-92. The mean PM₁₀ concentration during the study was 61 µg/m³ (9-165 µg/m³). Specifically, a 10 µg/m³ increase in PM₁₀ was associated with a 2-6 % increase in asthma emergency room visits. These results demonstrate an association between ambient wintertime PM₁₀ and increased daily mortality and exacerbations of asthma in an area where one of the principal sources of PM₁₀ is residential wood smoke.

Particulate air pollution was found to be associated with increased daily mortality in Christchurch, New Zealand (Hales et al. 2000). Due to the local topography, Christchurch experiences temperature inversion conditions in winter. Pollutants, especially from household fires, then accumulate over most of the city. In summer, temperatures rise rapidly during north westerly wind conditions and can exceed 35°C, leading to heat stress. Hourly SO₂, NO_x, CO and PM₁₀ data were available from a representative, centrally located site for June 1988 - December 1993. An increase in PM₁₀ of 10 ug/m³ was associated (after a lag of one day) with a 1% (0.5-2.2%) increase in all-cause mortality and a 4% (1.5-5.9%) increase in respiratory mortality. There were no statistically significant associations between mortality from cardiovascular causes and PM₁₀. Furthermore, there were no statistically significant associations between mortality and other air pollution variables.

Harré et al. (1997) investigated respiratory symptoms and peak expiratory flow (PEF) in subjects with chronic obstructive pulmonary disease (COPD) living in Christchurch, New Zealand. Forty subjects aged over 55 years were studied for three months during the winter 1994. Data on PM₁₀, NO₂, SO₂ and CO were measured at one monitoring site. The mean daily PM₁₀ level was generally below the NZ air quality guideline of 120 µg/m³ (the guideline was exceeded five times). An increase in PM₁₀ concentration of 35 µg/m³ was associated with an increase in relative risk of 1.38 (95% CI 1.13- 1.79) in night-time chest symptoms. A rise in NO₂ concentration of 10 µg/m³ was associated with increased use of reliever inhaler (RR 1.42, 95% CI 1.13-1.79). No association was found between PEF and any of the pollution variables.

A Swedish research programme “Biobränsle-Hälsa-Miljö” (“Biomass burning-Health-Environment”) consisting of more than 25 different projects during the period 2000-2003 has been reported in a summary report, BHM (2003).

One of the BHM studies examined the association between hospital admissions due to respiratory diseases and levels of soot and PM_2.5 in Lycksele – a town with a high concentration of residential wood burning. During five winter periods a significant association was found between 24-hour soot levels and asthma hospital admissions on the same day. For daily PM_2.5 levels (a parameter less associated with wood burning compared to soot), a positive and significant association was found for hospital admissions from chronic obstructive pulmonary diseases on the same and the following day. (BHM 2003).

In a panel study in Lycksele, 26 persons with asthma kept a dairy concerning respiratory symptoms for 10 weeks. An association was found between the increase in asthma symptoms and increases in soot as well as in PM_2.5-levels.

In another panel study in Lycksele, 46 persons were followed during January to March 2001. Blood samples were taken on days with expected high air pollution and analysed for fibrinogen and C-reactive protein, i.e., inflammatory markers in relation to cardiovascular diseases. No association could be found for the various air pollution measures and the levels of the inflammatory markers. However, an effect of the pollution could not be ruled out as it was concluded that the power of the study was too low due to small variation in air pollution in combination with the small size of the study group. (BHM 2003).

Johanson et al. (2004) sent out questionnaires to 1250 people in four small towns with a high concentration of residential wood burning. The response rate was 74% and of these, 28% used wood / pellets as the dominant heating source. The average heating time for the respondents was 25 hours per week during winter. In total, 19% found that air pollution from wood burning was the greatest disadvantage by living in the area. Fifteen percent reported discomfort due to smell especially in winter and 22% reported nuisance due to soot/dust. Among the 10% who had asthma, there was an increased rate of discomfort from smell, nuisance from soot/dust, and difficulties in breathing.

5.1.2.2.1 Review by Boman et al. (2003)

Boman et al. (2003) have reviewed the scientific literature concerning adverse health effects from ambient air pollution in relation to residential wood combustion in modern society and attempted to extract quantifications for the associations. Based on a literature search, references that fulfilled the following inclusion criteria were included for further analysis: (1) an epidemiological study, (2) concerning adverse health effects from ambient air pollution concentrations (not indoor or occupational exposure), (3) from settings in which residential wood combustion was mentioned as an important air pollution source, (4) full scientific paper published in English. These selection criteria resulted in nine papers, which were either population studies (N=5) or panel studies (N=4). The studies, marked with an asterix, are summarised in Table 6.

Four different geographic areas have been studied: Seattle, Washington, and Santa Clara County, California in the United States; Port Alberni, British Columbia, in Canada; and Christchurch in New Zealand. Five of the studies were conducted in the Seattle metropolitan area and two in Christchurch.

Only a few studies were found in which residential wood combustion was identified as a (or the) major source of ambient air pollution. One reason can be that wood smoke emissions are often the dominating air pollution only in rural areas and small towns and that there are difficulties associated with studying sparsely populated areas using epidemiological methods. However, of the four studied areas, only Port Alberni can be considered a small rural town, while the other three are large cities. Of the few existing studies, only in studies from two areas (Seattle and Santa Clara County), does there seem to exist some published material that confirms that residential wood combustion was a major source of ambient PM in the areas.

Different exposure assessment parameters were used in the included papers. The most common indicators were PM₁₀ (8 studies), SO₂ (5 studies), CO (5 studies), and NOx/NO₂ (4 studies). PM_2.5, PM₁, and ozone were only occasionally used.

The nine included studies focused on the effects of short-term exposure on asthma, respiratory symptoms, mortality, and lung function. All of the studies reported positive significant associations between variations in air pollution levels and adverse health outcomes. PM was the parameter that showed the most frequent and most obvious associations with the addressed health effects: in all the studies, significant positive associations were found when PM₁₀, PM_2.5, and PM₁ were used as an indicator of air pollution.

Overall, the relative risk (RR) between an increase in ambient PM₁₀ with 10 µg/m³ and different health outcomes varied between 1.018 and 1.117. CO showed significant positive associations with the addressed effects in 3 of the four studies, and NO₂ in one of the four studies. Associations with SO₂ or O₃ were not found in any study. No relevant long-term exposure studies with health outcomes like cardiopulmonary mortality, lung cancer, or chronic bronchitis were found.

5.1.2.2.2 Comparison of PM from wood smoke and PM in the general environment (Boman et al. 2003)

Boman et al. (2003) also compared the results from the studies in which residential wood combustion was mentioned as an important air pollution source with the estimations for the association between PM and health effects in the general environment. For these comparisons, they used a dose-response relationship from WHO (2000), a “state of the art” review (Pope et al. 1999), and a recent European study (Atkinson et al. 2001). They compared the results from the five wood smoke studies with associations between increases in ambient PM₁₀ and asthma symptoms, hospital admissions, and emergency room visits, together with one study with associations for cough. Although recognising the difficulties in comparing the results from different studies due to differences in the statistical analyses and presentation of the results, the comparison gives some indications of the relations, see Figure 3. All the included studies showed significant positive associations, and, in comparison with the estimations of WHO and other “state of the art” estimations concerning ambient PM and health, the effects (RR) are even stronger in the studies in which residential wood combustion is considered a major PM source, especially for children. Thus there seems to be no reason to assume that the health effects associated with PM in areas polluted with wood smoke are weaker than elsewhere.

There are not enough data to allow for a comparison of different PM indicators, e.g., if PM₁₀ is better than PM_2.5 as an indicator.

Figure 3. Relative risks for different morbidity outcomes in association with a 10 µg/m³ increase in PM₁₀ with 95% confidence intervals as error bars. The studies in which wood smoke was considered a major air pollution source are shown by closed columns, and the comparison estimates are represented by open columns (APHEA2: European study by Atkinson et al. 2001). Reproduced from Boman et al. (2003).

In most of the studied areas, residential wood combustion was expected to be an important source of ambient PM mainly during the winter season. Several of the studies used observation periods of years, including months in which wood smoke pollution was not a major factor. Two of the studies reported seasonal effect estimations. One study (Vedal et al. 1998) reported that the effect estimates for the autumn-winter period were essentially identical with those for the spring period. The other study (Sheppard et al. 1999) reported season-specific estimates, which were negative for summer, but were higher for spring and fall than for the winter season. The authors suggested that their results indicate a persistent effect of pollution from automobiles on health. In the study by Schwartz et al. (1993), the effect estimations were based on the whole study period (1 year), and they suggested that the high PM concentrations in association with asthma visits during the winter reflect, in large part, the toxicity of wood smoke. However, they also commented on the fact that these associations continue even at relatively low PM concentrations, and, therefore, wood smoke is probably not the only contributing factor.

5.1.2.2.3 Review by Naeher et al. (2007)

Naeher et al. (2007) conducted recently a detailed overall review regarding wood smoke and health effects. This review, which is based on an extended list of references, confirms the overall picture presented by Bomann et al. (2003) as well as the present report. The authors concluded that there is a large a growing body of evidence that wood smoke cause acute and chronic illness. Although the health effects should be considered to be linked to the whole complex mixture of components in the wood smoke there is insufficient data to regulate otherwise than on single components. In that respect fine particulate matter is considered the most relevant parameter. Further data is needed in order to clarify whether toxicity and risk associated to wood smoke particles should be considered otherwise than ambient particulate matter in general.

5.1.3 Other settings with wood smoke exposure

Around 50% of people, almost all in developing countries rely on coal and biomass in the form of wood, dung and crop residues for domestic energy (Bruce et al. 2000). These materials are typically burned in simple stoves with very incomplete combustion. Consequently, women and young children are exposed to high levels of indoor air pollution every day. There is consistent evidence that indoor air pollution increases the risk of chronic obstructive pulmonary disease and of acute respiratory infections (ARI) in childhood, the most important cause of death among children less than 5 years of age in developing countries. Evidence also exists of associations with low birth weight, increased infant and peri-natal mortality, pulmonary tuberculosis, and nasopharyngeal and laryngeal cancer. Conflicting evidence exists with regard to asthma. All studies are observational and very few have measured exposure directly, while a substantial proportion have not dealt with confounding. As a result, risk estimates are poorly quantified and may be biased.

A number of studies have reported associations of adverse health impacts with use of biomass fuels, although few have directly measured exposure. The studies are described below and summarised in Table 7.

A case-control study conducted in Zimbabwe found a significant association between lower respiratory disease and exposure to atmospheric wood smoke pollution in young children. Data from 244 cases was compared with information from 500 children seen at the local well baby clinic. Air sampling within the kitchens of 40 children indicated very high concentrations (546-1998 ug/m³) of respirable particulates. Blood COHb was determined for 170 out of 244 children confirming that they did experience smoke inhalation. (Collings et al. 1990).

A case-control study of Mexican women reported an increased risk of chronic bronchitis and chronic airway obstruction (CAO) associated with cooking with traditional wood stoves (Perez-Padilla et al. 1996). Crude odds ratios for wood smoke exposure were 3.9 (95% CI, 2.0-7.6) for chronic bronchitis only, 9.7 (95% CI, 3.7-27) for chronic bronchitis plus CAO, and 1.8 (95% CI, 0.7-4.7) for CAO only. The risk of chronic bronchitis alone and chronic bronchitis with CAO increased linearly with hour-years (years of exposure multiplied by average hours of exposure per day) of cooking with a wood stove. The median duration of wood smoke exposure were 25 and 28 years for the chronic bronchitis and chronic bronchitis/CAO disease groups, respectively. The median time of wood smoke exposure was 3 hours per day in the case groups.

Table 7. Studies with indoor exposure to wood smoke from cooking (high level)

COPD: Chronic Obstructive Pulmonary Disease
Nd: not determined

The association between exposure to air pollution from cooking fuels and health aspects was studied in Maputo, Mozambique (Ellegard 1996). Personal air samples for particulate (roughly equivalent to PM₁₀) were collected when four types of fuels (wood, charcoal, electricity, and liquefied petroleum gas) were used for cooking. Wood users were exposed to significantly higher levels of particulate pollution during cooking time (1200 µg/m³) than charcoal users (540 µg/m³) and users of modern fuels (petroleum gas and electricity) (200-380 µg/m³). 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. There was no difference in cough symptoms between charcoal users and users of modern fuels. Other respiratory symptoms such as dyspnoea, wheezing, and inhalation and exhalation difficulties were not associated with wood use.

A case-control study conducted in Colombia identified a similar risk of obstructive airways disease (OAD) in women who cooked with biomass (Dennis et al. 1996). Univariate analysis showed that tobacco use (OR = 2.22; p < 0.01); wood use for cooking (OR = 3.43; p < 0.001) and passive smoking (OR = 2.05; p = 0.01) was associated with OAD. The adjusted odds ratio for obstructive airways disease and wood use (adjusted for smoking, gasoline and passive smoke exposure, age and hospital) was 3.92. The mean number of years of wood smoke exposure was 33 in the cases. The authors suggested that wood smoke exposure in these elderly women was associated with the development of OAD and may help explain around 50% of all OAD cases.

Schei et al. (2004) studied the prevalence and severity of asthma in relation to indoor cooking on open wood fires in Western Guatemalan Highlands. The mothers of 1058 children aged 4-6 years were interviewed using a standardised questionnaire. The authors found that the asthma prevalence among children in Guatemala is low compared to other populations in Latin America. The prevalence of all the symptoms of asthma was higher in children from households that used open fires compared to improved stoves with chimneys. In a logistic regression model, use of open fire for cooking was a significant risk factor for a number of asthma symptoms, with odds ratios varying from 2.0 to 3.5.

Pneumonia was found to be associated with the use of solid fuel for cooking (e.g. coal, wood, dung) in a case-control study of children in Calcutta (Mahalanabis et al. 2002). Cases were 127 children aged 2-35 months. Solid fuel use was associated with risk of pneumonia in a logistic regression model after adjusting for confounding (OR = 3.97, CI = 2.00-7.88).

Bruce et al. (2000) reviewed the epidemiological evidence for the health effects of indoor smoke from solid fuels and concluded that, despite some methodological limitations, the epidemiological studies together with experimental evidence and pathogenesis provide compelling evidence of causality for acute respiratory infections and chronic obstructive pulmonary disease.

Smith et al. (2000) reviewed the details of biologic mechanisms and epidemiological studies on indoor air pollution and childhood acute respiratory infections (ARI). The authors concluded that the association of smoke from biomass fuels with ARI should be considered as causal, although the quantitative risk has not been fully characterised. Risk estimates from individual studies are imprecise because of relatively small sample sizes and misclassification of exposure and outcome. Given the imprecision and uncertainty in characterising the risk of biomass smoke exposure, quantitative risk assessments cannot be offered with great confidence.

Orozco-Levi et al. (2006) found a strong association between years of wood or charcoal smoke exposure from cooking or heating and increased risk for hospitalisation for chronic obstructive pulmonary disease (COPD) among 120 Spanish women during the period 2001-2003. Wood or charcoal alone independently increased the risk of COPD with odds ratios (OR) of 1.8 (95% interval: 0.6-6.0) and 1.5 (95% interval: 0.5-4.6), respectively, but only the combination of wood and charcoal was statistically significant (OR 4.5, 95% interval: 1.4-14.2).

5.1.4 Summary, non-cancer health effects

The association of particulate air pollution (PM) with adverse health effects has long been recognised, especially in relation to respiratory and cardio-vascular diseases. The experience is mainly based on epidemiological studies (cohort studies and time-series studies). A limitation with both study designs is the exposure characterisation, which is usually based on data from a single monitoring site in the area, and assumed to be representative for all individuals in the area. Another limitation is that most of the exposure information is on fine particles (PM_2.5), or the sum of fine and coarse particles (PM₁₀), whereas the information on ultrafine particles is limited.

Numerous studies have demonstrated that urban particulate air pollution is associated with increased mortality, primarily in the elderly and in individuals with pre-existing respiratory and/or cardiac diseases.

Several time-series studies in USA and Europe are available. A meta-analysis showed that an increase of 10 µg/m³ PM₁₀ was associated with a 0.6% increase in total mortality, a 1.3% increase in respiratory related deaths, and a 0.9% increase in cardiovascular deaths in a city area in the first days after the PM₁₀ increase (Anderson et al. 2004); if the observation time was extended for 40 days, the increase in total mortality was 1% (Zanobetti et al. 2003). A study in the German city Ehrfuhrt indicated that the effect of ultrafine particles on death due to cardiac and respiratory disease was comparable to the effect of PM_2.5 and PM₁₀ (Wichmann et al. 2000). In a recently published update of this study (Stölzel et al. 2006), a significant association between total mortality and cardio-respiratory mortality and the number concentrations of ultrafine particles was found whereas the increased mortality in relation to particle mass (PM₁₀) did not reach a significant response. Another European study (in Amsterdam, Ehrfuhrt and Helsinki) reported that effects on cardiac and respiratory disease correlated better with PM_2.5 than with the ultrafine particles (de Hartog et al. 2003, Pekkanen et al. 2002).

A few cohort studies are available at present. The most recent American cohort study (Pope et al. 2002) revealed a clear and significant association between mortality and the PM_2.5 level as the mortality increased with 4% per 10 µg/m³ PM_2.5 in 1979-83 and with 6% per 10 µg/m³ PM_2.5 in 1999-2000; mortality caused by heart/lung disease was increased with 9% per 10 µg/m³ PM_2.5. A recent study (Jerret et al. 2005) on a subset (Los Angeles area) of the American cohort has reported a 10 µg/m³ increase in the annual PM_2.5 level to be associated with an increase in mortality of 17%. The corresponding increase in ischaemic heart disease was 38% and for lung cancer 46%. Thus, the study on the subset of the American cohort found an increase in mortality that was three times higher than that reported for the entire American cohort in the period 1999-2000. The increase in the subset study was considered to be due to a more accurate exposure assessment than in the prior studies. The authors also suggested that a higher contribution of traffic PM in the Los Angeles area might have resulted in the higher increased mortality.

A recently published follow-up of the Dockery et al. (1993) six cities study found an increase of 16% in the overall mortality to be associated with each 10 µg/m³ PM_2.5 as an overall mean during the period, or an increase of 14% in relation to the annual mean of PM_2.5 in the year of death (Laden et al. 2006). The particulate air pollution had decreased from the first to the second period (1974-1989 and 1990-1998). When compared with the Dockery et al. (1993) study, a decrease in mortality of 27% was found for each 10 µg/m³ reduction in the PM_2.5 level between the two periods.

The most recent cohort study (Miller et al. 2007) of 66,000 women from 36 U.S. metropolitan areas showed a higher increased risk for cardiovascular mortality than described in the cohort studies by Laden et al. (2006 – study of intercity comparisons) and Jerret et al. (2005 – study of intra-city comparisons). In the Miller et al. (2007) study, each increase of 10 µg/m³ PM_2.5 was associated with a 24% increase in risk of cardiovascular event and a 76% increase of death from cardiovascular disease. A considerable higher increased risk of cardiovascular mortality (128% increase per 10 µg/m³ PM_2.5) was observed within cities compared to intercity comparisons (58% increase per 10 µg/m³ PM_2.5).

The emission of particles from residential wood burning and their impact on human health has received much attention lately.

Several early studies (Table 5) have focused on the presence of a wood stove in the home as a risk factor. While these studies strongly suggest that there are adverse health impacts in form of more respiratory symptoms and diseases associated with wood smoke exposure, their crude exposure assessments preclude more specific conclusions.

In addition, a number of studies (Table 7) have reported associations of adverse health impacts in the airways with use of biomass fuels. All these studies are observational and very few have measured exposure directly, while a substantial proportion have not dealt with confounding. As a result, risk estimates are poorly quantified and may be biased.

A number of studies (Table 6) have evaluated adverse health effects from ambient air pollution in relation to residential wood combustion in communities where wood smoke was a major, although not the only, source of ambient air particulate. The studies indicate a consistent relationship between PM₁, PM_2.5 and/or PM₁₀ and increased respiratory and asthmatic symptoms, and decreased lung function. The studies have mainly focused on children, but the few studies focusing on adults as well have shown similar results. There are also indications from several of the studies that asthmatics are a particularly sensitive group. The studies giving an indication of the dose-response relationship are summarised in Table 8 (section 7.2.2.1).

Boman et al. (2003) have reviewed nine selected studies (marked with an asterix in Table 6) concerning adverse health effects from ambient air pollution in relation to residential wood combustion and attempted to extract quantifications for the associations. Only a few studies were found in which residential wood combustion was identified as a (or the) major source of ambient air pollution. In all the studies using PM₁₀, PM_2.5, and PM₁ as an indicator of ambient air pollution, significant positive associations between variations in air pollution level(s) and adverse health outcome(s) were found. The relative risks (RR) between an increase in ambient PM₁₀ with 10 µg/m³ and different health outcomes varied between 1.01 and 1.12. An RR for increased asthma hospital admissions of 1.15 and 1.04 has been reported for an increase in ambient PM_2.5 with 11 and 12 µg/m³, respectively. An RR for increased asthma symptoms in children of 1.17 has been reported for an increase in ambient PM₁ with 10 µg/m³.

Overall, these studies showed that an increased risk of experiencing adverse health effects in the respiratory tract from exposure to particles in wood smoke (RR 1.04-1.17) is associated with an increase in ambient PM (PM₁, PM_2.5 and PM₁₀) of about 10 µg/m³. None of the available studies have indicated a threshold concentration for effects. However, it should be noted that due to differences in the statistical analyses and presentation of the results in the various studies, it is difficult to compare the results from different studies.

Boman et al. (2003) also compared the results from the five wood smoke studies in which residential wood combustion was mentioned as an important air pollution source with estimations for the association between PM and health effects in the general environment (Figure 3). All the included studies showed significant positive associations for respiratory symptoms evaluated. In comparison with the estimations concerning ambient PM and health effects in the general environment, the RR were even stronger in the studies in which residential wood combustion was considered a major PM source. Based on this comparison, the authors concluded that there seems to be no reason to assume that the health effects associated with PM in areas polluted with wood smoke are weaker than elsewhere.

A very recently published review (Naeher et al. 2007), which is based on an extended list of references, confirms the overall picture presented by Bomann et al. (2003) as well as the present report.

Overall, the available studies indicate that exposure to wood smoke PM is associated with the same kind of health effects known from exposure to PM in general and that the health effects associated with PM in areas polluted with wood smoke are not weaker than elsewhere. However, the uncertainties about the actual contribution from wood smoke to ambient concentrations of PM preclude, for the time being, precise characterisations of specific dose-response relationships for wood smoke PM and whether differences exist compared to the known dose-response relationships from PM in general. Therefore, a more precise evaluation of the impact on human health of air pollution related to residential wood combustion is not possible for the time being.

5.2 Epidemiological studies, carcinogenic effects

5.2.1 Particles in the general environment

During the last decade, several cohort studies have been published. Three studies were performed on cohorts in the United States.

The Harvard Six Cities study was based on 8111 adults in six U.S. cities followed from 1976 to 1989 (Dockery et al. 1993). Exposure was estimated by assessment of long-term average levels of pollution from background air-monitoring stations. There was a 37% (95% CI 0.81-2.31) higher lung cancer risk in the most polluted city compared with the least polluted city after adjustment for age, sex, smoking, education and body-mass index.

A study by Beeson et al. (1998) was based on 6338 California Seventh Day Adventists (non-smoking) followed from 1977 to 1992. Exposure to air pollution was estimated by monthly ambient concentrations of NO₂, SO₂ and PM₁₀ using fixed-site monitoring stations, which were interpolated to zip codes of individual home and working addresses. The study reported rate ratios for lung cancer of 5.21 (95% CI 1.94-13.99) for PM₁₀ corresponding to an inter-quartile range of 24 µg/m³, and of 1.45 (95% CI 0.67-3.14) for NO₂ corresponding to an inter-quartile range of 1.98 ppb.

The largest US investigation analysed cause-specific mortality among approximately 550 000 adults followed from 1982 to 1998 (Pope et al. 1995, 2002). Participants were assigned to metropolitan areas of residence, for which mean PM_2.5 concentrations were compiled from urban background monitoring stations in 1979-83 and 1999-2000. In this study an increase in yearly mean concentration of 10 µg/m³ of PM_2.5 was associated with increased lung cancer mortality (RR=1.14; 95% CI 1.04-1.23) (Pope et al. 2002).

These three U.S. cohort studies suggest an excess risk of lung cancer with long-term exposure to air pollution. However, it is unknown whether these results can be transferred to European settings as the European populations may experience different exposures and living habits (smoking, diet etc.), which could modify the results (Vineis et al. 2004).

A cohort study from the Netherlands found an insignificant 25% higher lung cancer mortality associated with a 30 µg/m³ difference in yearly mean concentration of NO₂ level among 5000 subjects between 1984 and 1994, for which the exposure was estimated for the home address (Hoek et al. 2002).

Nafstad et al. (2004) investigated the lung cancer incidence among 16 209 men living in Oslo between 1974 to 1998, and found an adjusted risk ratio for lung cancer of 1.08 (95% CI 1.02-1.15) for a 10 µg/m³ increase in yearly mean concentration of NO_x, but no associations with SO₂.

Harrison et al. (2004) investigated whether exposure to known chemical carcinogens, e.g. PAHs, can explain the observed association between PM_2.5 and lung cancer mortality by calculating lung cancer rates. They concluded that it appears plausible that known chemical carcinogens are responsible for the lung cancers attributed to PM_2.5 exposure. However, they also stated that the possibility should not be ruled out that PM is capable of causing lung cancer independent of the presence of known carcinogens.

5.2.2 Particles from wood burning

There is little direct information regarding the human cancer risks associated with biomass air pollution. The findings of relatively low mutagenicity for wood smoke, have, to some extent, been validated in a study of indoor environmental exposure risks and lung cancer in China. Cross-sectional comparisons of population subgroups in Xuan Wei, China, an area noted for high mortality from respiratory disease and lung cancer, suggested that the high lung cancer rates could not be attributed to smoking or occupational exposure (Mumford et al. 1990a). Since residents of Xuan Wei, especially women, are exposed to high concentrations of coal and wood combustion products indoors, a study was undertaken to evaluate the lung cancer risks of these exposures. On average women and men in Xuan Wei spend 7 and 4 hours per day, respectively, near a household fire. A 1983 survey indicated that the lung cancer rate in Xuan Wei was strongly associated with the proportion of homes using smoky coal in 1958. No relationship was observed between lung cancer and the percentage of homes using wood.

A follow-up study compared exposures in two otherwise similar Xuan Wei communes, one with high lung cancer mortality (152/100,000) where smoky coal was the major fuel, and another with low lung cancer mortality (2/100,000) where wood (67%) and smokeless coal (33%) were used. Lung cancer mortality was strongly associated with indoor burning of smoky coal and not with wood burning. This association was especially strong in women who had low smoking and were more highly exposed to cooking fuel emissions than men (Chapman et al. 1988). Indoor PM₁₀ concentrations measured during cooking were extremely high (24, 22 and 1.8 mg/m³ for smoky coal, wood and smokeless coal, respectively). In contrast to other studies of wood smoke particle size distribution, measurements in Xuan Wei indicated that only 6% of the particles emitted during wood combustion were smaller than 1µm in size, whereas 51% of the smoky coal particles were sub-micron. This study suggests that there was little association between open-fire wood smoke exposure and lung cancer, despite very high exposures with long duration (women generally start cooking at age 12). One possible explanation is the relatively low biological activity of wood smoke particulate combined with less efficient deposition of the larger particles.

In a recent study, Mustapha et al. (2004) evaluated the DNA damage in 179 Indian women cooking with biofuels, including wood. They found a significant increase in both micronucleus (MN) and chromosomal aberrations (CA) in peripheral lymphocytes from users of biomass fuel compared to lymphocytes from users of liquefied petroleum gas (LPG). The relative MN and CA frequencies for the users of the various fuels decreased in the order cow dung > cow dung / wood ³ wood > kerosene ³ LPG. Further, the results indicated an effect of subject age, and the duration of exposure on the MN and CA frequencies in biomass fuel users.

The frequency of sister chromatid exchange (SCE) after acute overexposure to combustion products originating from coal or wood stoves was investigated in 20 patients with acute carbon monoxide intoxication (Ozturk et al. 2002). All cases were domestic accidents due to dysfunctioning coal or wood stoves. The mean SCE frequency per metaphase was significantly higher in the study group compared to the control group: 8.11 (± 2.39) vs. 6.33 (± 1.60). There was no positive correlation between the blood carboxyhaemoglobin concentration and SCE frequency. The results suggest that acute exposure to combustion products of wood or coal is genotoxic.

Long-term exposure to wood smoke from cooking was found to contribute to the development of lung cancer in a case-control study of Mexican non-smoking women (Hernandez-Garduno et al. 2004). Exposure information was obtained from 113 lung cancer cases and 273 controls. Controls were patients with miscellaneous pulmonary conditions (e.g. pulmonary tuberculosis, interstitial lung disease). 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 exposure, odds ratio 1.9 (95% confidence interval 1.1-3.5).

A case-control study has shown that the use of wood stoves for cooking or heating may be linked to as many as 30% of all cancers in mouth, pharynx and larynx in Southern Brazil (Pintos et al. 1998). Information on known and potential risk factors was obtained from 784 cases and 1568 non-cancer controls. After adjustment for all empirical confounders (e.g. smoking, alcohol consumption), the odds ratio for all upper aero-digestive tract cancers was 2.68 (95% confidence interval: 2.2-3.3). Increased risks associated with use of wood stoves were also seen in site-specific analyses for mouth, pharynx and larynx. An important limitation of this study was the lack of exposure assessment; there was no information on lifetime or average daily exposure, house ventilation, or the presence of a kitchen separated from the rest of the house.

Recently, Ramanakumar et al. (2006) performed a case-control study among 1205 persons diagnosed with lung cancer during the period 1996-2001 in Montreal and 1541 controls using questionnaire information about heating and cooking facilities. Among women using traditional heating facilities (stove or fireplace) and traditional cooking facilities (gas or wood stove) they found an increased odds ratio of 2.5 (95% CI 1.5-3.6) after adjusting for smoking and a number of other covariates. The authors speculated that the lack of a significant correlation for men may be due to less exposure from the heating and cooking sources because of less time spent in the home and less time spent in the kitchen.

5.2.3 Summary, carcinogenic effects

During the last decade, several cohort studies on cancer risk due to exposure to particles in the general environment have been published. Three U.S. cohort studies (Dockery et al. 1993, Beeson et al. 1998, Pope et al. 2002) suggest an excess risk of lung cancer with long-term exposure to air pollution. One study (Beeson et al. 1998) reported a rate ratio for lung cancer of 5.21 for PM₁₀ corresponding to an inter-quartile range of 24 µg/m³. In another study (Pope et al. 2002), the largest one, an increase in the yearly mean concentration of 10 µg/m³ of PM_2.5 was associated with increased lung cancer mortality (RR=1.14). A cohort study from the Netherlands (Hoek et al. 2002) found a 25% higher lung cancer mortality associated with a 30 µg/m³ difference in yearly mean concentration of NO₂, and a Norwegian study (Nafstad et al. 2004) found an adjusted risk ratio for lung cancer of 1.08 for a 10 µg/m³ increase in yearly mean concentration of NO_x. A recent study (Harrison et al. 2004) found it plausible that known chemical carcinogens, e.g. PAHs, associated with the PM are responsible for the lung cancer risk attributable to PM_2.5 exposure; however, it was also stated that it should not be excluded that PM in itself is capable of causing lung cancer independent of the presence of known carcinogens.

There is limited information regarding the human cancer risks associated with biomass air pollution. The Chinese studies (Mumford et al. 1990a, Chapman et al. 1988) on an association between wood smoke exposure and lung cancer risk do not indicate an increased risk even after long-term exposure to very high levels of biomass smoke (PM₁₀ 22 mg/m³) from open-fire domestic cooking. Two more recent case-control studies from Mexico (Hernandez-Garduno et al. 2004) and Southern Brazil (Pintos et al. 1998) are suggestive of a small increased risk of lung cancer due to long-term exposure to wood smoke from cooking; however, these studies are limited by the lack of exposure assessments. The most recent case-control study (Ramanakumar et al. 2006) found an increased risk for lung cancer among Canadian women in homes with wood stove or fireplace heating and with gas or wood stove cooking facilities.

One study (Mustapha et al. 2004) has reported a significant increase in the occurrence of both micronuclei and chromosomal aberrations in peripheral lymphocytes from Indian women cooking with bio-fuels, including wood.

Overall, there is limited information regarding the human cancer risk associated with biomass air pollution, including wood smoke. The available studies do not provide a sufficient basis in order to evaluate whether there is an association between wood smoke exposure and increased risk of lung cancer.

Cohort studies on cancer risk associated with particles in the general environment have suggested an excess risk of lung cancer associated with long-term exposure to PM. Known chemical carcinogens, e.g. PAHs, associated with the PM might be responsible for the excess risk of lung cancer; however, it can not be excluded that PM in itself is capable of causing lung cancer.

It should be noted that the International Agency for Research on Cancer (IARC 2008) has evaluated that indoor emissions from household combustion of biomass fuel (primarily wood) are probably carcinogenic to humans (Group 2A). In reaching this evaluation, the IARC Working Group considered mechanistic and other relevant data including the presence of PAHs and other carcinogenic compounds in wood smoke, evidence of mutagenicity of wood smoke and multiple studies that show cytogenetic damage in humans who are exposed to wood smoke.

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