Abstract
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.
Highlights
Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation
Wood combustion is a major source of particulate air pollution in many developed countries, and the adverse health effects associated with exposure to wood smoke do not seem to be weaker than for ambient particles from other sources [6,7]
Particle characteristics The chemical characterisation of the PM0.1–2.5 fractions from the different combustion phases is presented in Table 1, together with the data from the previous analyses of the reference samples
Summary
Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. Exposure to particulate matter (PM) in ambient air has been associated with effects on the pulmonary as well as the cardiovascular system. These effects include exacerbation of asthma and allergy, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, increased risk of lung cancer, atherosclerosis and acute cardiac effects [1,2,3,4]. Wood combustion is a major source of particulate air pollution in many developed countries, and the adverse health effects associated with exposure to wood smoke do not seem to be weaker than for ambient particles from other sources [6,7]. Controlled human exposure to wood smoke induced an increase of inflammatory markers in distal airways and increases in biomarkers that may be associated with systemic inflammation and cardiovascular diseases [10,11,12]
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