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Health effects assessment of exposure to particles from wood smoke

7 Risk assessment, wood smoke particles

• 7.1 Exposure assessment
• 7.2 Hazard assessment
  • 7.2.1 Hazard identification
  • 7.2.2 Hazard characterisation / dose-response relationship
• 7.3 Risk characterisation
  • 7.3.1 Estimated wood smoke PM exposure for risk characterisation
  • 7.3.2 Dose-response relationships for risk characterisation

Risk assessment for exposure to air pollutants, including wood smoke particles, generally follows the classical paradigm of chemical risk assessment and consists of an exposure assessment, a hazard assessment, and a risk characterisation.

The exposure to air pollutant(s) is assessed by determining the concentration of the pollutant(s) in the air and the volume of air inhaled over time, in order to define the intake dose.

The hazard assessment consists of a hazard identification, which is a qualitative description of the adverse health effects observed following exposure to the pollutant(s), and a subsequent hazard characterisation, which is a quantitative description of the dose-response relationships for the observed effects.

In the final step, the risk characterisation, the exposure and hazard assessments are integrated.

However, the risk assessment process for air pollutants varies from that for chemicals in general in two main aspects:

1. Toxicological information usually plays a confirmatory or explanatory role for air pollutants as most of the critical hazard information stems from epidemiology. This is in contrast to the situation with chemical substances in general where toxicological information plays a major role in the hazard assessment.
    
2. For air pollution, adverse health effects may be noted at or close to ambient exposure levels whereas for chemical substances in general, the margins between exposures and effects levels are often larger. Thus, for some air pollutants such as PM, it will only be possible to describe dose-response functions for the associated health outcomes.

Particulate matter (PM) in ambient air and in wood smoke is a complex mixture of multiple components ranging from a few nanometres in size to tens of micro-metres. The multiple components present in ambient air and wood smoke PM include many very toxic single constituents such as e.g. PAH, dioxin, heavy metals, and several volatile carcinogens such as formaldehyde, benzene and 1,3-butadiene. Hence, adverse health effects following inhalation of ambient air and wood smoke PM are unlikely to be related to a single PM component, but more likely related to a complex, eventually synergistic interaction of multiple components with the respiratory tract and subsequent target organs.

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. However, studies analysing different fractions of PM and studies analysing specific combustion related gaseous

pollutants in addition to PM have shown that especially PM from combustion sources are important in relation to the adverse health effects.

Therefore, this report mainly focuses on the adverse health effects related to PM from wood smoke.

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

1. To assess wood smoke PM as a part of ambient air PM and to benefit from the knowledge regarding adverse health effects from the PM in general. Especially important in this approach would be to identify epidemiological and toxicological studies in which wood smoke PM has been identified as an important source of the total PM fraction.
    
2. To separate the wood smoke PM into its different constituents and perform a risk characterisation for each constituent. Although a risk characterisation in theory may be performed for wood smoke PM by using this approach, it may be very difficult to evaluate the actual health risk of wood smoke PM as an evaluation also would require knowledge about the vast amount of possible physico-chemical and toxicological interactions between the several hundreds of different constituents in the wood smoke.

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.

7.1 Exposure assessment

Measurements of particulate matter (PM) levels in ambient air in areas with many wood-burning stoves have consistently shown elevated levels of PM emissions, particularly during wintertime when wood burning is common. Due to the size distribution of wood smoke particles essentially all will be contained in the PM_2.5 fraction.

There is only very limited information on population exposure to wood smoke particles in Denmark.

Measurements during a 6-week winter period (2002 and 2003-2004) in a Danish residential area with no district heating and many wood stoves showed that the contribution from wood combustion to ambient PM_2.5 was comparable to the contribution from a heavily trafficked road to PM_2.5 at the sidewalk. The average local PM_2.5 contribution from wood combustion was about 4 µg/m³ (Glasius et al. 2006).

In another residential area with natural gas combustion as the primary heating source and wood combustion as a secondary heating source, the average PM_2.5 concentration was elevated by about 1 µg/m³ compared to background measurements during four winter weeks (Glasius et al. 2007).

An increase in annual average PM_2.5 of 1 µg/m³ is a best maximum estimate of the whole population exposure based on the data from the measurements in these two residential areas.

Model calculations have been used to estimate the PM_2.5 levels resulting from wood combustion in Denmark. The results showed an increase in PM_2.5 of 0.4 µg/m³ during winter (October-March) corresponding to an increase in annual PM_2.5 of 0.2 µg/m³ (as a best minimum estimate) for the whole Danish population exposure (Palmgren et al. 2005).

In conclusion, the annual average PM_2.5 exposure from wood smoke is roughly estimated to be 0.2-1 µg/m³ for the whole Danish population with a best estimate of about 0.6 µg/m³. The best estimate of about 0.6 µg/m³ PM_2.5 will be taken forward to the risk characterisation.

7.2 Hazard assessment

7.2.1 Hazard identification

7.2.1.1 Non-cancer health effects, humans

The association of particulate air pollution with adverse health effects has long been recognised, especially in relation to respiratory and cardio-vascular diseases. 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.

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 also 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).

In conclusion, the available studies indicate that exposure to wood smoke PM is associated with the same kind of non-cancer health effects known from exposure to PM in general.

7.2.1.2 Carcinogenic effects, humans

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 suggest an excess risk of lung cancer with long-term exposure to air pollution. A cohort study from the Netherlands found lung cancer mortality associated with the yearly mean concentration of NO₂, and a Norwegian study found an association between lung cancer and increase in the yearly mean concentration of NO_x. In these studiees NO₂ and NO_x should be seen as indicators for combustion related pollutants including PM. A recent study 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 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 from open-fire domestic cooking. Two more recent case-control studies from Mexico and Southern Brazil 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 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 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.

In conclusion, 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. However, an excess risk of lung cancer associated with long-term exposure to particles in the general environment have been suggested and there are, for the time being, no indications that wood smoke PM should be different from ambient air PM in general regarding a carcinogenic potential. It should be noted that the International Agency for Research on Cancer (IARC 2008) has recently evaluated that indoor emissions from household combustion of biomass fuel (primarily wood) are probably carcinogenic to humans (Group 2A).

7.2.1.3 Data from studies in experimental animals

Toxicological studies in laboratory animals suggest that particulate matter (PM) in general can influence the functioning of the lung, the blood vessels and the heart. The relatively few inhalation studies available indicate that different types of PM may induce toxicity at relatively high exposure levels. Not only particles of a certain size or chemical composition are responsible for the adverse effects of PM. However, there are preliminary indications that primary, carbonaceous PM components may be more important for adverse health effects than secondary components like sulphates and nitrates. Both coarse and fine particles are capable of inducing toxicity; however, whether the ultrafine PM fraction, tested at environmentally relevant levels, is also toxic, remains more uncertain.

Various animal studies have been used to elucidate the carcinogenicity of diesel exhaust. In all valid inhalation studies in rats, diesel exhaust was found to be carcinogenic whereas no carcinogenic effects were seen in hamsters or mice. Diesel exhaust, without the particulate fraction, administered by inhalation to rats did not show a carcinogenic potential. Long-term inhalation of carbon black, virtually devoid of PAH, resulted in lung tumours in rats. In studies using intra-tracheal instillation, both diesel exhaust particles and carbon black induced tumours; the surface area of the carbonaceous particles appeared to be correlated with the carcinogenic potency. It is not clear whether the carcinogenicity of diesel exhaust involves DNA-reactive or non-DNA-reactive mechanisms (or a combination).

Although the adverse health effects associated with inhalation exposure of wood smoke in experimental animals are not as well studied as the effects of its individual components, a number of adverse health effects have been reported such as e.g. inflammation and damage to epithelial cells; inflammation has been seen both after single and repeated inhalation exposure of rats. One study in rats investigating the effects of wood smoke on pulmonary immunity has indicated that host defence and/or immune cell function, leading to impairment of lung clearance, is depressed in a manner similar to that produced by many of the individual wood smoke constituents. Similarly, another study has indicated that wood smoke may be immunosuppressive in mice. Recent studies have reported mild effects in mouse and rat models of asthma and mild effects on broncho-alveolar lavage parameters.

A very recent study in mice did not show any hardwood smoke exposure related lung carcinogenesis measured as either the percentage of young mice with tumours (incidence) or the number of tumours per tumour-bearing mouse (multiplicity).

A few in vitro studies with mammalian cells have shown that wood smoke may be associated with cytotoxicity, DNA and cellular damage, lipid peroxidation and cytokine release. Furthermore, wood smoke condensates have been shown to induce a dose-dependent increased mutagenicity in Salmonella typhimurium. The most recent study demonstrated that particles from wood combustion caused DNA damage in human lung cells (A549, Comet assay).

In conclusion, some of the available studies in experimental animals indicate that inhaled PM from wood smoke, similarly to PM in general, can cause adverse health effects in the respiratory tract and lungs such as inflammation, altered lung clearance, damage to epithelial cells, immuno-suppression, and hyperplastic lesions. Recent studies have demonstrated mild exposure effects on broncho-alveolar lavage parameters and in mouse and rats models of asthma.

7.2.2 Hazard characterisation / dose-response relationship

7.2.2.1 Non-cancer health effects, humans

The hazard characterisation of particulate matter (PM) in ambient air is mainly based on epidemiological studies (cohort studies and time-series studies). A limitation with both study designs is the exposure characterisation. The exposure estimates for ambient PM is generally based on the particle mass determined as PM₁, PM_2.5, and/or PM₁₀. Thus, the actual contribution from different PM sources is not known. A significant limitation in this approach is the lack of exposure data for individual persons as the exposure estimates 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 (< 0.1 µm in diameter) is limited.

Several time-series studies in USA and Europe are available showing a dose-response relationship for short-term changes in PM levels. 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; if the observation time was extended for 40 days, the increase in total mortality was 1%. 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. In a recently published update of this study, 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.

The available cohort studies show that a dose-response relationship in relation to long-term exposure to PM exists. The most recent American cohort study (Pope et al. 2002) revealed a clear and significant dose-response association between mortality and PM_2.5 as the mortality increased with 4% per 10 µg/m³ in PM_2.5 in 1979-83 and with 6% per 10 µg/m³ in PM_2.5 in 1999-2000; mortality caused by heart/lung disease was increased with 9% per 10 µg/m³ in PM_2.5. A very 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) 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 studies giving an indication of the dose-response relationship for wood smoke and non-cancer health effects in humans are summarised in Table 8. The relative risk (RR) between an increase in ambient PM₁₀ of 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 of 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 of 10 µg/m³.

Overall, an increased risk of experiencing adverse health effects in the respiratory tract from exposure to particles in wood smoke 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.

Table 8. Relation between exposure to wood smoke and non-cancer health effects

COPD: Chronic Obstructive Pulmonary Disease
PEF: Peak Expiratory Flow

Boman et al. (2003) have 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 in section 5.1.2.2.2). 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.

Forsberg et al. (2005) analysed the impact on human health from PM levels in Sweden. From the PM₁₀ levels, 5300 premature deaths per year were estimated. Of these, 3500 deaths could be attributed to the levels contributed from long range transported PM, while 1800 could be attributed to local sources in Sweden. The fraction of premature deaths due to local sources varied strongly geographically with about 29% in the far south, due to high concentrations of long-range transported particles, to about 84% in the far north. In the northern part, wood smoke PM is the predominant source of PM.

In conclusion, the uncertainties about the actual contribution of PM from wood smoke to ambient PM preclude, for the time being, precise characterisations of specific dose-response relationships for the adverse health effects associated with exposure to 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.

However, the available epidemiological studies indicate that wood smoke PM does not seem to be less harmful than ambient PM in general and it is worth noting that the results in the Boman et al. (2003) review indicated that the RR were even stronger in the studies in which residential wood combustion was considered a major PM source. None of the available epidemiological studies, on wood smoke PM as well as on ambient PM, have indicated a threshold concentration for effects.

7.2.2.2 Carcinogenic effects, humans

During the last decade, several cohort studies on cancer risk due to exposure to particles in the general environment have been published. One American study reported a rate ratio for lung cancer of 5.21 for PM₁₀ corresponding to an inter-quartile range of 24 µg/m³. In another American study, 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 found a 25% higher lung cancer mortality associated with a 30 µg/m³ difference in yearly mean concentration of NO₂, and a Norwegian study found an adjusted risk ratio for lung cancer of 1.08 for a 10 µg/m³ increase in yearly mean concentration of NO_x.

The only information available on the association between wood smoke exposure and lung cancer risk comes from a few Chinese studies. These studies 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.

In conclusion, based on the available epidemiological studies, it is not possible to evaluate the lung cancer risk due to exposure to particles from wood smoke, or to particles from other combustion sources.

7.2.2.3 Data from studies in experimental animals

Most studies on adverse health effects of wood smoke particles in experimental animals have used relatively high exposure levels compared to the levels generally measured in the environment.

In a recent study (Tesfaigzi et al. 2002), minor but significant changes in the airways of rats (mild chronic inflammation and squamous metaplasia in the larynx; alveolar macrophage hyperplasia and pigmentation, and slightly thickened alveolar septae) were observed following exposure (whole-body, 3 hours/day, 5 days/week for 4 or 12 weeks) to 1 or 10 mg/m³ wood smoke particles (size distribution of 63-74% in the < 1 µm fraction and 26-37% in the > 1 µm fraction).

A very recent study (Reed et al. 2006) has summarised health effects of subchronic exposure to environmental levels of hardwood smoke in rats and mice exposed (whole-body, 6 hours/day, 7 days/week) for 1 week or 6 months) to dilutions of whole emissions based on particulate (30-1000 µg/m³ total PM, mass median aerodynamic diameter of approximately 0.3 µm). Exposure to these concentrations presented little to small hazard with respect to clinical signs, lung inflammation and cytotoxicity, blood chemistry, haematology, cardiac effects, and bacterial clearance, and carcinogenic potential. However, parallel studies demonstrated mild exposure effects on broncho-alveolar lavage parameters and in mouse and rats models of asthma.

In the very recent study of exposure to environmental levels of hardwood smoke (Reed et al. 2006), lung carcinogenesis measured as either the percentage of young mice with tumours (incidence) or the number of tumours per tumour-bearing mouse (multiplicity) yielded no significant differences from the control group and there was no evidence of a progressive exposure-related trend.

Diesel exhaust has been found to be carcinogenic to rats at particle concentrations of > 2 mg/m³, corresponding to an equivalent continuous exposure of about 1 mg/m³.

7.3 Risk characterisation

In this section, the health impact of PM from wood smoke emissions will be assessed considering the impact on mortality and on hospital admissions for respiratory and cardio-vascular diseases as these health endpoints are the most well documented endpoints in quantitative terms in relation to ambient air PM exposure.

In order to assess the health impacts from the wood smoke PM, the dose-response relationship from the epidemiological studies on ambient PM in general (i.e., the relative risk RR) is used as the available epidemiological studies indicate that wood smoke PM does not seem to be less harmful than ambient PM in general. The increase in the RR for a health endpoint related to ambient PM in general is used to estimate the increase in RR for this specific health endpoint due to the contribution from wood smoke PM. Then this RR is used to estimate the number of cases for this specific health endpoint, which is associated to wood smoke PM.

7.3.1 Estimated wood smoke PM exposure for risk characterisation

At present, the population exposure to wood smoke PM in Denmark cannot be estimated precisely as only few measurements have been conducted in selected residential areas with different kinds of heating. An increase in annual average PM_2.5 of 1 µg/m³ is a best maximum estimate of the whole population exposure. This is based on the data from the two measurement campaigns in Denmark.

One campaign showed an increase in average PM_2.5 of 4 µg/m³ during winter in a residential area with no district heating and many wood stoves (Glasius et al. 2006, Palmgren et al. 2005).

The other campaign showed an increase in average PM_2.5 of 1 µg/m³ during winter in a residential area with natural gas combustion as the primary heating source and wood combustion as a secondary heating source (Glasius et al. 2007).

In addition to the measured PM_2.5 levels, model calculations have been used to estimate the PM_2.5 levels resulting from the total wood combustion in Denmark. If the total Danish PM_2.5 emissions from wood-combustion are assumed to be distributed evenly over the whole area of Denmark, this would result in a contribution to the annual average PM_2.5 of 0.2 µg/m³.

Based on the two measurement campaigns in Denmark as well as on the model calculations, the annual average PM_2.5 exposure from wood smoke can be set to 0.2-1 µg/m³ as a preliminary estimate for the whole Danish population with a best preliminary estimate of about 0.6 µg/m³. The best estimate of 0.6 µg/m³ will be used as the exposure estimate in the risk characterisation.

However, it should be remembered that in many residential areas people are concentrated near to the local wood burning sources and thus may be exposed to considerable higher PM levels. For individuals living in residential areas with many wood burning sources, the use of the best estimate of 0.6 µg/m³ will probably underestimate the exposure to wood smoke PM. However, the exposure estimated are based on measurements during the winter time and thus, the best estimate of 0.6 µg/m³ will probably overestimate the exposure to wood smoke PM.

7.3.2 Dose-response relationships for risk characterisation

7.3.2.1 Mortality

For mortality, an increase in the mortality rate of 6% (95% CI: 2-11%) per 10 µg/m³ increase in PM_2.5 for long-term exposure is used for the risk characterisation. This dose-response relationship was concluded by WHO (2005) by putting weight on the studies by Dockery et al. (1993), Pope et al. (1995, 2002) and Jerret et al. (2005). This dose-response relationship has also been used for health impact assessment in connection with the Clean Air for Europe Programme (CAFE), (European Commission, 2005). It should be noted, however, that the most recent studies by Jerret et al. (2005) and Laden et al. (2006) found a nearly 3 times higher increase in the mortality rate (17 and 16%, respectively) per 10 µg/m³ increase in PM_2.5 and thus, the use of the WHO estimate (6%) may result in an underestimation of the mortality rate.

From the WHO dose-response relationship, it can be estimated that the overall contribution of 0.6 µg/m³ of PM_2.5 from wood smoke to the annual population exposure is associated with an increase in the mortality rate of 0.36% (95% CI: 0.12-0.66%) as the dose-response relationship is linear.

According to Statistics Denmark (2007), the annual mortality is about 55,000 deaths. By using the increase in the mortality rate of 0.36% associated with an annual increase of 0.6 µg/m³ of PM_2.5 from wood smoke, the wood stove emissions would contribute to about 200 deaths each year (95% CI: 66-360). As mentioned before, this should be considered as a low estimate and the actual number of deaths due to exposure to wood smoke may be up to 2-3 times higher according to Jerret et al. (2005) and Laden et al. (2006).

7.3.2.2 Respiratory diseases, hospital admissions

7.3.2.2.1 Data from time-series studies

Five studies have found statistically significant associations between hospital admissions from respiratory diseases and ambient air short-term PM exposure predominantly from wood smoke (see Table 8, section 7.2.2.1).

When looking at the studies where all age groups were included, an increase of 10 g/m³ in PM₁₀ was associated with a 2-6% increase in hospital admissions (Lipsett et al. 1997, Schwartz et al. 1993, Sheppard et al. 1999). For PM_2.5, a 10 g/m³ increase was associated with a 3.3% increase in hospital admissions (Sheppard et al. 1999). Schreuder et al. (2006) found a 1.7% increase of emergency department visits per 10 g/m³ PM_2.5 (borderline significance) and a 7.7% increase per 10 g/m³ measured as total carbon, which was found to be a marker for vegetative burning.

One study that only included persons below the age of 18 (Norris et al. 1999) found a considerable higher increase in hospital admissions (12% for PM₁₀, 14% for PM_2.5). As this high increase has not been confirmed in other studies and as this study only included children, this study will not be taken into account for a quantitative health impact assessment for the overall general population as children are also included in the studies where all age groups were included. However, it should be noted that this study supports findings in other studies indicating that children are more susceptible to ambient air PM than the general population.

The estimated increase of 3.3% in respiratory hospital admissions for an increase of 10 g/m³ of PM_2.5 from the Sheppard et al. (1999) study will be used for the risk characterisation as this pertains to PM_2.5, which seems to be the most relevant measure for particle sizes from wood smoke. Furthermore, this seems also to be a plausible figure for a dose-response relationship when considering the ranges of the PM₁₀ dose-response relationships. Further studies are needed in order to confirm whether total carbon would be a better marker for wood burning as suggested by Schreuder et al. (2006), who found an increase in emergency department visits of 7.7% per 10 g/m³ total carbon in the PM_2.5 fraction.

Thus an annual increase of 0.6 g/m³ of PM_2.5 from wood smoke emissions would lead to an increase in respiratory hospital admissions of 0.2% as the dose-response relationship is linear.

It should be noted that using an estimate for increase in respiratory hospital admissions from short-term studies in relation to an annual increase in PM most probably will underestimate the actual health impact as it has been shown in general that effects observed in relation to short-term studies are often considerable less pronounced than effects observed in relation to long-term exposure. It should also be noted that the dose-response relationships considered from rather few studies on wood smoke PM show a steeper dose-response relationship (two to three times steeper) when compared to the dose-response relationships observed in numerous studies in which ambient PM in general have been assessed and in which no specific wood smoke contributions have been mentioned.

In Denmark, the annual rate of hospital admission for respiratory diseases has been reported to be approximately 78,000 cases (Raaschou-Nielsen et al. 2002). By using the increase in respiratory hospital admissions of 0.2% associated with an annual increase of 0.6 g/m³ of PM_2.5 from wood smoke, the wood stove emissions would contribute to about 156 cases each year.

7.3.2.2.2 Data from cohort studies (long-term exposure)

No data specifically addressing respiratory diseases and long-term exposure to wood smoke have been located; however, there are data pertaining to long term exposure to PM in general.

In the CAFE health impact assessment (European Commission 2005), the data from the cohort study conducted by Abbey et al. (1995a,b) are used for assessment of respiratory disease in relation to chronic PM exposure. An annual increase of 10 µg/m³ PM₁₀ was found to be associated to a 7% increase in new cases of chronic bronchitis among the adult population. For PM_2.5, the corresponding dose-response was a 14 % increase.

Using the dose-response relationship of 14% for new cases of chronic bronchitis for an annual increase of 10 µg/m³ of PM_2.5 and the base-line incidence of chronic bronchitis per year in Denmark, an annual contribution of 0.6 µg/m³ PM_2.5 from wood smoke is estimated to be associated with an increase of 0.84% for new cases of chronic bronchitis. This corresponds to about 60 new cases of chronic bronchitis each year. (Loft 2007).

7.3.2.3 Cardio-vascular effects

No epidemiological data on wood smoke exposure in relation to cardio-vascular diseases are available neither from time-series studies nor from cohort studies.

As data on cardiovascular effects from PM in general largely pertain to time series studies, estimations using these dose-response relationships would largely underestimate the impact in relation to chronic exposure. In a very recent study, however, Miller et al. (2007) found a 24% increase of cardiovascular events and a 76% increase of cardiovascular mortality per 10 µg/m³ PM_2.5 in a subgroup of women above the age of 50 years and without previous cardiovascular disease. The use of this dose-response relationship in relation to the general Danish population is difficult due to the rather specific selection of the study group for this study. However, although not specifically quantified, it could be concluded based on the high increased risks for cardiovascular events (coronary heart disease, cerebro-vascular disease, myocardial infarction, coronary re-vascularisation, stroke) and cardiovascular mortality found in the Miller et al. (2007) study that even an increase of 0.6 µg/m³ PM_2.5 would have a significant health impact for the Danish population with respect to cardiovascular events and mortality.

7.3.2.4 Conclusions

Based on an increase in the annual population exposure of 0.6 g/m³ PM_2.5 from wood smoke emissions and the dose-response relationships considered for specific health outcomes, about 200 premature deaths, about 156 respiratory hospital admissions and about 60 new cases of chronic bronchitis can be estimated for the Danish population.

It should be noted that this preliminary health impact assessment is limited by the poor exposure data available as well as by the absence of specific dose-response relationships for the health impacts due to long-term exposure to wood smoke PM. However, it should be noted that the approach taken to assess the health impacts for wood smoke PM is in general considered to underestimate the health impacts as recently published dose-response relationships for mortality indicate a 2-3 times higher dose-response relationship compared to the WHO (2005) dose-response relationship used in our assessments.

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Version 1.0 May 2008, © Danish Environmental Protection Agency