Wood Smoke Particles Research Articles

Comparison of wood smoke PM2.5 obtained from the combustion of FIR and beech pellets on inflammation and DNA damage in A549 and THP-1 human cell lines

The aim of this study was to investigate the effect on the induction of interleukin-8 of particulate matter (PM) from fir and beech pellets burnt in domestic appliances on two human cells lines, namely the lung epithelial cell line A549 and the promyelocytic cell line THP-1. The effects of PM2.5 obtained from combustion of beech and fir pellets were compared to reference diesel exhaust particulates (DEP). In parallel, wood smoke PM-induced genotoxicity and oxidative stress were also investigated in A549 cells. Cells were treated for different times (3-72h) with increasing concentrations of PM2.5 obtained from sequential combustions of fir and beech pellets or reference DEP. Cell viability was assessed by lactate dehydrogenase leakage, and the release of interleukin-8 or CXCL8 (IL-8) was measured to evaluate the pro-inflammatory effect. Oxidative stress was evaluated by the 5(6)-carboxy-2',7'dichlorofluorescein diacetate (DCFH-DA) assay and DNA damage by the alkaline comet assay and micronucleus frequency by flow cytometry. Both A549 and THP-1 cells responded in a dose- and time-related manner to wood smoke PM2.5 with IL-8 release, particles obtained from late combustions being the most active. THP-1 cells were more sensitive than A549 cells. On a mass base, similar effects were observed for both fir and beech PM2.5. However, the combustion of beech pellets generated approximately three times more PM2.5 than fir pellets. Regarding the mechanism of PM2.5 uptake, in both THP-1 and A549 cells, cytochalasin D prevented PM2.5-induced IL-8 mRNA expression and cytokine release, indicating a key role for actin polymerization in particles uptake and that the production of IL-8 correlated with particle phagocytosis. As signal transduction pathway involvement, in both THP-1 and A549 cells, PM2.5-induced IL-8 release could be completely blocked by the selective inhibitor SB203580, indicating a role of p38 MAPK activation. PM2.5 from both fir and beech pellets also induced modest DNA lesions dose related, measured as strand breaks, whereas no increase in the number of micronucleus was observed. Similar effects were observed with DEP, arguing against less dangerous effects of wood smoke particles than other categories of combustion-derived particles in the same size range. Overall, results suggest that combustion conditions can significantly affect the characteristics of particles and the consequent toxicity, and that different woods can generate different amounts of PM2.5.

Activation of Transient Receptor Potential Ankyrin-1 (TRPA1) in Lung Cells by Wood Smoke Particulate Material

Cigarette smoke, diesel exhaust, and other combustion-derived particles activate the calcium channel transient receptor potential ankyrin-1 (TRPA1), causing irritation and inflammation in the respiratory tract. It was hypothesized that wood smoke particulate and select chemical constituents thereof would also activate TRPA1 in lung cells, potentially explaining the adverse effects of wood and other forms of biomass smoke on the respiratory system. TRPA1 activation was assessed using calcium imaging assays in TRPA1-overexpressing HEK-293 cells, mouse primary trigeminal neurons, and human adenocarcinoma (A549) lung cells. Particles from pine and mesquite smoke were less potent agonists of TRPA1 than an equivalent mass concentration of an ethanol extract of diesel exhaust particles; pine particles were comparable in potency to cigarette smoke condensate, and mesquite particles were the least potent. The fine particulate (PM < 2.5 μm) of wood smoke were the most potent TRPA1 agonists and several chemical constituents of wood smoke particulate, 3,5-ditert-butylphenol, coniferaldehyde, formaldehyde, perinaphthenone, agathic acid, and isocupressic acid, were TRPA1 agonists. Pine particulate activated TRPA1 in mouse trigeminal neurons and A549 cells in a concentration-dependent manner, which was inhibited by the TRPA1 antagonist HC-030031. TRPA1 activation by wood smoke particles occurred through the electrophile/oxidant-sensing domain (i.e., C621/C641/C665/K710), based on the inhibition of cellular responses when the particles were pretreated with glutathione; a role for the menthol-binding site of TRPA1 (S873/T874) was demonstrated for 3,5-ditert-butylphenol. This study demonstrated that TRPA1 is a molecular sensor for wood smoke particulate and several chemical constituents thereof, in sensory neurons and A549 cells, suggesting that TRPA1 may mediate some of the adverse effects of wood smoke in humans.

Emerging mechanistic targets in lung injury induced by combustion-generated particles.

The mechanism for biological effect following exposure to combustion-generated particles is incompletely defined. The identification of pathways regulating the acute toxicological effects of these particles provides specific targets for therapeutic manipulation in an attempt to impact disease following exposures. Transient receptor potential (TRP) cation channels were identified as "particle sensors" in that their activation was coupled with the initiation of protective responses limiting airway deposition and inflammatory responses, which promote degradation and clearance of the particles. TRPA1, V1, V4, and M8 have a capacity to mediate adverse effects after exposure to combustion-generated particulate matter (PM); relative contributions of each depend upon particle composition, dose, and deposition. Exposure of human bronchial epithelial cells to an organic extract of diesel exhaust particle was followed by TRPV4 mediating Ca(++) influx, increased RAS expression, mitogen-activated protein kinase signaling, and matrix metalloproteinase-1 activation. These novel pathways of biological effect can be targeted by compounds that specifically inhibit critical signaling reactions. In addition to TRPs and calcium biochemistry, humic-like substances (HLS) and cell/tissue iron equilibrium were identified as potential mechanistic targets in lung injury after particle exposure. In respiratory epithelial cells, iron sequestration by HLS in wood smoke particle (WSP) was associated with oxidant generation, cell signaling, transcription factor activation, and release of inflammatory mediators. Similar to WSP, cytotoxic insoluble nanosized spherical particles composed of HLS were isolated from cigarette smoke condensate. Therapies that promote bioelimination of HLS and prevent the disruption of iron homeostasis could function to reduce the harmful effects of combustion-generated PM exposure.

Effects of wood smoke particles from wood-burning stoves on the respiratory health of atopic humans

BackgroundThere is growing evidence that particulate air pollution derived from wood stoves causes acute inflammation in the respiratory system, increases the incidence of asthma and other allergic diseases, and increases respiratory morbidity and mortality. The objective of this study was to evaluate acute respiratory effects from short-term wood smoke exposure in humans. Twenty non-smoking atopic volunteers with normal lung function and without bronchial responsiveness were monitored during three different experimental exposure sessions, aiming at particle concentrations of about 200 μg/m3, 400 μg/m3, and clean air as control exposure. A balanced cross-over design was used and participants were randomly allocated to exposure orders. Particles were generated in a wood-burning facility and added to a full-scale climate chamber where the participants were exposed for 3 hours under controlled environmental conditions. Health effects were evaluated in relation to: peak expiratory flow (PEF), forced expiratory volume in the first second (FEV1), and forced vital capacity (FVC). Furthermore, the effects were assessed in relation to changes in nasal patency and from markers of airway inflammation: fractional exhaled nitric oxide (FENO), exhaled breath condensate (EBC) and nasal lavage (NAL) samples were collected before, and at various intervals after exposure.ResultsNo statistically significant effect of wood smoke exposure was found for lung function, for FENO, for NAL or for the nasal patency. Limited signs of airway inflammation were found in EBC.ConclusionIn conclusion, short term exposure with wood smoke at a concentration normally found in a residential area with a high density of burning wood stoves causes only mild inflammatory response.

Controlled human wood smoke exposure: oxidative stress, inflammation and microvascular function

BackgroundExposure to wood smoke is associated with respiratory symptoms, whereas knowledge on systemic effects is limited. We investigated effects on systemic inflammation, oxidative stress and microvascular function (MVF) after controlled wood smoke exposure.MethodsIn a randomised, double-blinded, cross-over study 20 non-smoking atopic subjects were exposed at rest to 14, 220, or 354 μg/m3 of particles from a well-burning modern wood stove for 3 h in a climate controlled chamber with 2 week intervals. We investigated the level of oxidatively damaged DNA, inflammatory markers and adhesion molecules before and 0, 6 and 20 h after exposure. Six h after exposure we measured MVF non-invasively by digital peripheral artery tonometry following arm ischemia.ResultsThe MVF score was unaltered after inhalation of clean air (1.58 ± 0.07; mean ± SEM), low (1.51 ± 0.07) or high (1.61 ± 0.09) concentrations of wood smoke particles in atopic subjects, whereas unexposed non-atopic subjects had higher score (1.91 ± 0.09). The level of oxidatively damaged DNA, mRNA of ITGAL, CCL2, TNF, IL6, IL8, HMOX1, and OGG1 and surface marker molecules ICAM1, ITGAL and L-selectin in peripheral blood mononuclear cells were not affected by inhalation of wood smoke particles.ConclusionsExposure to wood smoke had no effect on markers of oxidative stress, DNA damage, cell adhesion, cytokines or MVF in atopic subjects.

Wood smoke particles from different combustion phases induce similar pro-inflammatory effects in a co-culture of monocyte and pneumocyte cell lines.

BackgroundExposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles’ physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures.ResultsWSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved.ConclusionThe toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.

Restructuring of carbonaceous particles upon exposure to organic and water vapours

In this study, the change in mobility diameter (dm) was investigated for a range carbonaceous particle types (diesel exhaust, petrol exhaust, cigarette smoke, candle smoke, particles generated in a heptane/toluene flame, and wood smoke particles) exposed to different organic (heptane, ethanol, and dimethyl sulfoxide/water (1:1vol%) mixture) and water vapours. Particles were first size-selected and then bubbled through an impinger (bubbler) containing either an organic solvent or water, where particles trapped inside rising bubbles were exposed to saturated vapours of the solvent in the impinger. The size distribution of particles was simultaneously measured upstream and downstream from the impinger. A size-dependent reduction in dm was observed when bubbling fractal-like particles (diesel exhaust, particles generated in a heptane/toluene flame, and candle smoke particles) through heptane, ethanol and a dimethyl sulfoxide/water mixture. In addition, the size distributions of these particles after bubbling through an impinger were broader and thisincrease of the geometric standard deviation (σ) of the size distributions was also found to be size-dependent. Size-dependent reduction in dm and an increase of σ indicate that particles undergo restructuring to a more compact form, which was confirmed by TEM analysis. However, bubbling of these particles through water did not result in a size-dependent reduction in dm, nor in an increase of σ. Liquid particles or particles assumed to be spherical (cigarette smoke, petrol exhaust, and wood smoke particles) did not result in any substantial change in dm, or σ, when bubbled through organic solvents or water. Compaction of fractal-like particles was attributed to the ability of condensing vapours to efficiently wet the particles. Our results also show that the presence of an organic layer on the surface of fractal-like particles, or the surface tension of the condensed liquid do not influence the extent of compaction.

Expression of adhesion molecules, monocyte interactions and oxidative stress in human endothelial cells exposed to wood smoke and diesel exhaust particulate matter

Toxicological effects of wood smoke particles are less investigated than traffic-related combustion particles. We investigated the effect of wood smoke particles, generated by smouldering combustion conditions, on human umbilical endothelial cells (HUVECs) co-cultured with or without monocytic THP-1 cells. Standard reference material (SRM) 2975 diesel exhaust particles were used as benchmark particles. Wood smoke particles at 50μg/ml or 100μg/ml caused adhesion of THP-1 monocytes onto HUVECs in co-cultures, whereas SRM2975 had no such effect. Both types of particles from 1μg/ml increased VCAM-1 expression on HUVECs in mono-cultures. However, only the exposure to wood smoke particles was associated with increased expression of TNF and IL8 mRNA in THP-1 cells. We found no effect on the intracellular production of reactive oxygen species by the fluorescent probe DCFH-DA, whereas especially the wood smoke particles caused increased level of DNA strand breaks and oxidised guanines at concentrations with low cytotoxicity. In conclusion, our results indicate that the adherence of monocytes on endothelial cells in wood smoke particle exposed cultures depend on activation of both cell types.

Characterization of Residential Wood Combustion Particles Using the Two-Wavelength Aethalometer

In the United States, residential wood combustion (RWC) is responsible for 7.0% of the national primary PM(2.5) emissions. Exposure to RWC smoke represents a potential human health hazard. Organic components of wood smoke particles absorb light at 370 nm more effectively than 880 nm in two-wavelength aethalometer measurements. This enhanced absorption (Delta-C = BC(370 nm) - BC(880 nm)) can serve as an indicator of RWC particles. In this study, aethalometer Delta-C data along with measurements of molecular markers and potassium in PM(2.5) were used to identify the presence of airborne RWC particles in Rochester, NY. The aethalometer data were corrected for the loading effect. Delta-C was found to strongly correlate with wood smoke markers (levoglucosan and potassium) during the heating season. No statistically significant correlation was found between Delta-C and vehicle exhaust markers. The Delta-C values were substantially higher during winter compared to summer. The winter diurnal pattern showed an evening peak around 21:00 that was particularly enhanced on weekends. A relationship between Delta-C and PM(2.5) was found that permits the estimation of the contribution of RWC particles to the PM mass. RWC contributed 17.3% to the PM(2.5) concentration during the winter. Exponential decay was a good estimator for predicting Delta-C concentrations at different winter precipitation rates and different wind speeds. Delta-C was also sensitive to remote forest fire smoke.

Exposure to wood smoke particles produces inflammation in healthy volunteers

ObjectivesHuman exposure to wood smoke particles (WSP) impacts on human health through changes in indoor air quality, exposures from wild fires, burning of biomass and air pollution. This investigation tested...

Health effects of residential wood smoke particles: the importance of combustion conditions and physicochemical particle properties.

BackgroundResidential wood combustion is now recognized as a major particle source in many developed countries, and the number of studies investigating the negative health effects associated with wood smoke exposure is currently increasing. The combustion appliances in use today provide highly variable combustion conditions resulting in large variations in the physicochemical characteristics of the emitted particles. These differences in physicochemical properties are likely to influence the biological effects induced by the wood smoke particles.OutlineThe focus of this review is to discuss the present knowledge on physicochemical properties of wood smoke particles from different combustion conditions in relation to wood smoke-induced health effects. In addition, the human wood smoke exposure in developed countries is explored in order to identify the particle characteristics that are relevant for experimental studies of wood smoke-induced health effects. Finally, recent experimental studies regarding wood smoke exposure are discussed with respect to the applied combustion conditions and particle properties.ConclusionOverall, the reviewed literature regarding the physicochemical properties of wood smoke particles provides a relatively clear picture of how these properties vary with the combustion conditions, whereas particle emissions from specific classes of combustion appliances are less well characterised. The major gaps in knowledge concern; (i) characterisation of the atmospheric transformations of wood smoke particles, (ii) characterisation of the physicochemical properties of wood smoke particles in ambient and indoor environments, and (iii) identification of the physicochemical properties that influence the biological effects of wood smoke particles.

Particles from wood smoke and road traffic differently affect the innate immune system of the lung

The effect of particles from road traffic and wood smoke on the innate immune response in the lung was studied in a lung challenge model with the intracellular bacterium Listeria monocytogenes. Female Balb/cA mice were instilled intratracheally with wood smoke particles, particles from road traffic collected during winter (studded tires used; St+), and during autumn (no studded tires; St−), or diesel exhaust particles (DEP). Simultaneously with, and 1 or 7 days after particle instillation, 105 bacteria were inoculated intratracheally. Bacterial numbers in the lungs and spleen 1 day after Listeria challenge were determined, as an indicator of cellular activation. In separate experiments, bronchoalveolar lavage (BAL) fluid was collected 4 h and 24 h after particle instillation. All particles tested reduced the numbers of bacteria in the lung 24 h after bacterial inoculation. When particles were given simultaneously with Listeria, the reduction was greatest for DEP, followed by St+ and St−, and least for wood smoke particles. Particle effects were no longer apparent after 7 days. Neutrophil numbers in BAL fluid were increased for all particle exposed groups. St+ and St− induced the highest levels of IL-1β, MIP-2, MCP-1, and TNF-α, followed by DEP, which induced no TNF-α. In contrast, wood smoke particles only increased lactate dehydrogenase (LDH) activity, indicating a cytotoxic effect of these particles. In conclusion, all particles tested activated the innate immune system as determined with Listeria. However, differences in kinetics of anti-Listeria activity and levels of proinflammatory mediators point to cellular activation by different mechanisms.

The effect of a woodstove changeout on ambient levels of PM 2.5 and chemical tracers for woodsmoke in Libby, Montana

Residential woodstoves are the single largest source of PM 2.5 in Libby, MT, resulting in the community being designated as a nonattainment area for PM 2.5. Beginning in 2005, a community-wide woodstove changeout program was implemented that replaced nearly 1200 old stoves with EPA-certified units. In an effort to track the reduction of woodsmoke particles throughout the program, ambient PM 2.5 samples were collected before, during, and after the changeout. These samples were analyzed for seven selected woodsmoke tracers, including vanillin, acetovanillone, guaiacol, 4-ethylguaiacol (methoxyphenols), levoglucosan (sugar anhydride), abietic acid, and dehydroabietic acid (resin acids). Results of the changeout showed that PM 2.5 levels decreased by 20% during the changeout period, while levels of the seven chosen tracer compounds gave variable responses. Levoglucosan levels decreased by 50% while both resin acids increased after the changeout, suggesting a change in the chemistry of the particles. No trend was observed in the levels of methoxyphenols as a group over the changeout period. The results suggest that the concentrations of woodsmoke related PM 2.5 in the Libby airshed have decreased; however, the chemistry of the emitted particles also changed when old woodstoves were replaced with new EPA-certified stoves.

AIR POLLUTION: The Oxidative Punch of Wildfires

Thick smoke routinely cloaks Southern California hills, highways, and neighborhoods during this region’s autumn wildfire season, with drought contributing to worse fires than usual in the past two years. Wildfire emissions generate larger aerosols than those produced by vehicles—up to 0.4 micrometers (μm) in diameter compared with less than 0.15 μm—according to a new study led by Constantinos Sioutas, a professor of civil and environmental engineering at the University of Southern California, Los Angeles. In findings published online 6 January 2009 ahead of print in Environmental Science & Technology, the larger particles emitted by fires activated a standard assay of oxidative stress even more potently than traffic pollutants. The performance of different types of particulate matter in oxidative stress tests may provide clues as to how these pollutants cause damage such as proinflammatory or cytotoxic effects. Sioutas and colleagues took advantage of wildfires burning in Southern California in October 2007 to investigate their impact on urban air quality relative to traffic pollutants, with a special emphasis on particulate matter small than 2.5 μm in diameter (PM2.5). The researchers collected air samples on the University of Southern California campus, within 150 meters of a busy freeway near downtown Los Angeles. A series of wildfires had started on 20 October 2007, burning more than 500,000 acres of land and stretching from Santa Barbara County to the Mexican border. When air samples were collected on October 24, 25, and 27, fires were raging within 20 miles of the collection site. Measurements were taken from 4:30 p.m. until 10:30 a.m. the following day to capture pollution from evening and morning rush hour traffic as well as from the fires themselves. The fires in Los Angeles County were under control by October 30; post-fire samples collected on November 1 and 14 represented mostly traffic emissions. Compared with post-fire samples, samples collected on the three fire days in October contained a higher number of particles larger than 0.1 μm in diameter. Both carbon monoxide and nitrogen monoxide levels increased by threefold during fire days, while levels of other air pollutants—ozone, nitrogen dioxide, most polycyclic aromatic hydrocarbons, iron, copper, chromium, zinc, nickel, and vanadium—remained the same. In addition, during the fire period there was an approximate doubling in several indicators for biomass burning: levoglucosan, water-soluble organic carbon, and various minerals (magnesium, phosphorus, potassium, and manganese). Various chemical components of PM2.5 fuel oxidative stress and are toxic to human cells. Working in collaboration with James Schauer of the University of Wisconsin–Madison and Flemming Cassee of the National Institute of Health and the Environment of the Netherlands, the Sioutas team measured cellular toxicity with two standard tests of oxidative stress, the dithiothreitol (DTT) assay and the macrophage reactive oxygen species (ROS) assay. Particles collected during October showed nearly 5 times more DTT activity than those collected in November. In contrast, the macrophage ROS assay, a known indirect measure for combustion pollutants from vehicles that is more responsive to transition metals, peaked in November. “In this study we demonstrated that a substantial portion of the oxidative potential of air pollution during fires can be attributed to the wildfires,” says Sioutas. He attributes the difference to the increased water-soluble organic compounds that are abundant in wood smoke and show more activity in the DTT assay. According to Sioutas, the elevated levels of water-soluble organic carbon also mean wood smoke particles are more readily absorbed by the body than is PM from traffic sources. The DTT and macrophage ROS assays “appear to respond to different components of PM2.5,” notes Ted Russell, a professor of environmental engineering at the Georgia Institute of Technology in Atlanta. This observation suggests that environmental scientists need to further characterize the two redox assays. A detailed analysis of how these assays respond to specific PM2.5 components obtained from different environmental samples at different times “will lay a foundation for understanding the characteristics of ambient PM2.5 that have the greatest health impacts,” says Russell. Sioutas says that the larger particles from wildfires can persist longer in the atmosphere and infiltrate buildings about twice as effectively as traffic pollutants. He recommends that people living near wildfires try to remain inside, shut their doors and windows, and run an air conditioner with a good filter to recirculate the indoor air. “If you don’t have an air conditioner, go to an indoor mall or other public place that recirculates indoor air,” he says. Other practical suggestions are included in the State of California guidelines for wildfire smoke at http://www.arb.ca.gov/smp/progdev/pubeduc/wfgv8.pdf.

Oxidative damage to DNA and repair induced by Norwegian wood smoke particles in human A549 and THP-1 cell lines

Genotoxic effects of traffic-generated particulate matter (PM) are well described, whereas little data are available on PM from combustion of biomass and wood, which contributes substantially to air pollution world wide. The aim of this study was to compare the genotoxicity of wood smoke particulate matter (WSPM), authentic traffic-generated particles, mineral PM and standard reference material (SRM2975) of diesel exhaust particles in human A549 lung epithelial and THP-1 monocytic cell lines. DNA damage was measured as strand breaks (SB) and formamidopyrimidine DNA glycosylase (FPG) sites by the comet assay, whereas cell cytotoxicity was determined as lactate dehydrogenase release. The exposure to WSPM generated SB and FPG sites in both cell lines at concentrations from 2.5 or 25 μg/ml, which were not cytotoxic. Compared to all other studied particles, WSPM generated greater responses in terms of both SB and FPG sites. Organic extracts of WSPM and SRM2975 elicited higher levels of SB than native and washed PM at 25 and 100 μg/ml, whereas assay saturation precluded reliable assessment of FPG sites. During a 6 h post-exposure period, in which the medium with PM had been replaced by fresh medium, 60% of the DNA lesions generated by WSPM were removed. In conclusion, WSPM generated more DNA damage than traffic-generated PM per unit mass in human cell lines, possibly due to the high level of polycyclic aromatic hydrocarbons in WSPM. This suggests that exposure to WSPM might be more hazardous than PM collected from vehicle exhaust with respect to development of lung cancer.

Particles from wood smoke and traffic induce differential pro-inflammatory response patterns in co-cultures

The inflammatory potential of particles from wood smoke and traffic has not been well elucidated. In this study, a contact co-culture of monocytes and pneumocytes was exposed to 10–40 μg/cm 2 of particles from wood smoke and traffic for 12, 40 and 64 h to determine their influence on pro-inflammatory cytokine release (TNF-α, IL-1, IL-6, IL-8) and viability. To investigate the role of organic constituents in cytokine release the response to particles, their organic extracts and the washed particles were compared. Antagonists were used to investigate source-dependent differences in intercellular signalling (TNF-α, IL-1). The cytotoxicity was low after exposure to particles from both sources. However, wood smoke, and to a lesser degree traffic-derived particles, induced a reduction in cell number, which was associated with the organic fraction. The release of pro-inflammatory cytokines was similar for both sources after 12 h, but traffic induced a greater release than wood smoke particles with increasing exposure time. The organic fraction accounted for the majority of the cytokine release induced by wood smoke, whereas the washed traffic particles induced a stronger response than the corresponding organic extract. TNF-α and IL-1 antagonists reduced the release of IL-8 induced by particles from both sources. In contrast, the IL-6 release was only reduced by the IL-1 antagonist during exposure to traffic-derived particles. In summary, particles from wood smoke and traffic induced differential pro-inflammatory response patterns with respect to cytokine release and cell number. Moreover, the influence of the organic particle fraction and intercellular signalling on the pro-inflammatory response seemed to be source-dependent.

Pro-inflammatory potential of wood smoke and traffic-derived particles in a monocytic cell line

Lung inflammation is an important process in host defence to inhaled particulate matter. To what extent physicochemical properties of particles from different sources influence their inflammatory potential has not been fully clarified. The aim of this study was to investigate the potential of particles from wood smoke and traffic to induce a release of pro-inflammatory cytokines in the monocytic cell line THP-1. The influence of endotoxin on cytokine release was investigated using the inhibitor polymyxin B sulphate, whereas the responses to native particles, washed particles and their organic extracts were compared to determine the role of the organic fraction. Particles from the two sources showed a similar inflammatory potential, but the response was mediated by different particle characteristics. The organic fraction of wood smoke accounted for the majority of the cytokine release, whereas the response to the traffic-derived particles was in addition influenced by endotoxin and the particle core. The sum of the cytokine release induced by the organic extract and washed particles was lower than that induced by native particles, suggesting that the organic fraction must be adsorbed to the particles to exert biological activity. The results also indicated that different particle characteristics may activate different signalling pathways, since inhibition of endotoxin reduced release of TNF-α, IL-1β and IL-8, whereas organic extraction only affected release of TNF-α and IL-8. Together, these data illustrate that a similar inflammatory response may be mediated by different particle characteristics and possibly through different signalling pathways.

Allergy adjuvant effect of particles from wood smoke and road traffic

There is growing evidence that in addition to augmenting the severity of asthma and allergic diseases, particulate air pollution also increases the incidence of allergy and asthma. We studied the adjuvant effect of particles from wood smoke and road traffic on the immune response to the allergen ovalbumin (OVA). OVA with and without particles was injected into one hind footpad of Balb/cA mice. All particles together with OVA significantly increased the level of OVA-specific immunoglobulin E (IgE) in serum, compared to groups given OVA or particles alone. Reference diesel exhaust particles (DEP) with OVA induced the highest levels of IgE, whereas no clear difference was observed between particles from road traffic and wood smoke. Road traffic particles collected in the autumn induced higher IgE values with OVA than corresponding particles collected during the winter season when studded tires are used, suggesting that studded tire-generated road pavement particles have less allergy adjuvant activity than exhaust particles. Compared to OVA or particles alone, all particles with OVA increased popliteal lymph node cell numbers, cell proliferation, ex vivo secretion of IL-4 and IL-10 after ConA stimulation, and the expression of several cell surface molecules (CD19, MHC class II, CD86 and CD23). Wood smoke particles with OVA induced somewhat higher cellular responses than road traffic particles, but less than DEP with OVA which seemed to be the most potent particle in inducing cellular as well as antibody responses. Thus, wood smoke particles had about the same capacity to enhance allergic sensitization as road traffic particles, but less than diesel exhaust particles.

Woodsmoke Health Effects: A Review

The sentiment that woodsmoke, being a natural substance, must be benign to humans is still sometimes heard. It is now well established, however, that wood-burning stoves and fireplaces as well as wildland and agricultural fires emit significant quantities of known health-damaging pollutants, including several carcinogenic compounds. Two of the principal gaseous pollutants in woodsmoke, CO and NOx, add to the atmospheric levels of these regulated gases emitted by other combustion sources. Health impacts of exposures to these gases and some of the other woodsmoke constituents (e.g., benzene) are well characterized in thousands of publications. As these gases are indistinguishable no matter where they come from, there is no urgent need to examine their particular health implications in woodsmoke. With this as the backdrop, this review approaches the issue of why woodsmoke may be a special case requiring separate health evaluation through two questions. The first question we address is whether woodsmoke should be regulated and/or managed separately, even though some of its separate constituents are already regulated in many jurisdictions. The second question we address is whether woodsmoke particles pose different levels of risk than other ambient particles of similar size. To address these two key questions, we examine several topics: the chemical and physical nature of woodsmoke; the exposures and epidemiology of smoke from wildland fires and agricultural burning, and related controlled human laboratory exposures to biomass smoke; the epidemiology of outdoor and indoor woodsmoke exposures from residential woodburning in developed countries; and the toxicology of woodsmoke, based on animal exposures and laboratory tests. In addition, a short summary of the exposures and health effects of biomass smoke in developing countries is provided as an additional line of evidence. In the concluding section, we return to the two key issues above to summarize (1) what is currently known about the health effects of inhaled woodsmoke at exposure levels experienced in developed countries, and (2) whether there exists sufficient reason to believe that woodsmoke particles are sufficiently different to warrant separate treatment from other regulated particles. In addition, we provide recommendations for additional woodsmoke research.

Effects on Markers of Oxidative Stress After Exposure to Wood Smoke Particles

Effects on Markers of Oxidative Stress After Exposure to Wood Smoke Particles