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Cardiovascular and related health effects of wood smoke particles

Lykke Forchhammer


Over the last decade there has been an increased use of wood burning stoves in Denmark, which can result in a higher exposure of the general population to the pollutants associated with residential wood smoke. New results on particulate matter (PM) in ambient air have shown elevated PM levels in areas with many wood stoves, particularly during wintertime where wood burning is most common. A number of studies on ambient air particles have indicated associations between exposure and risk of cardiovascular and pulmonary disease and cancer. The effect of wood smoke particles (WPs) is less investigated compared to PM from e.g. traffic, although WPs are suspected to induce some of the same type of adverse health effects. In particular effects on the cardiovascular system, known from traffic-related particulates, have not been addressed for WPs. 

The toxicological mechanism of particles is thought to be related to inflammation and oxidative stress. This can result in the generation of oxidatively damaged DNA, leading to early events in the development of cancer. Furthermore particles are known to increase the risk of cardiovascular diseases by mechanisms of inflammation and endothelial dysfunction possibly through oxidative stress. These effects might be larger in individuals with risk factors of cardiovascular diseases such as asthma. The endothelium is a key regulator of vascular homeostasis, functioning as a barrier and an active signal transducer. This monolayer of cells responds to both physical and chemical signals by producing factors, which regulate vascular tone, cellular adhesion, and vessel wall inflammation. 

The aim of this thesis was to investigate the effects related to oxidative stress, inflammation, DNA damage and vascular function after exposure to WPs in I) atopic humans possibly susceptible to the development of atherosclerosis and II) in cultured Human Umbilical Vein Endothelial Cells (HUVECs) that served as a model for the direct cellular effects. Related DNA damage was used as a key marker of intracellular oxidative stress. The optimization and validation of the comet assay used to assess this was pursued in an international collaborative effort aiming at reducing the inter-laboratory variation by use of laboratory-specific calibration curves.  

In collaboration with the University of Aarhus we conducted a controlled human exposure study in which 20 atopic subjects were exposed to different concentrations of wood smoke; a clean air exposure, a low and a high dose of wood smoke, approximately 200 and 400 μg/m3. Endpoints in terms of oxidative stress, DNA damage, and inflammation measured as gene expression as well as surface marker expression were determined in mononuclear blood cells. Endothelial function was assessed as flow mediated changes in the digital artery tone. No statistically significant effect related to exposure was found on any of the markers. 

In the cell culture study we examined the effect of WPs from combustion with low oxygen supply and compared it with Standard Reference Material 2975 (SRM2975) which is a preparation of (carbon-based) diesel exhaust particles with well-characterized chemical and physical properties. We found no effect on the intracellular production of reactive oxygen species, whereas both particles induced this in acellular conditions. Nevertheless, the exposure at high concentrations induced DNA damage in term of both strand breaks and oxidized guanines. We found the particles to exert effect at relatively high concentration (50 and 100 μg/ml), at which the expression of cell adhesion molecules VCAM-1 were significantly upregulated. Monocytes adhered specifically to the endothelial cells after WP exposure already at relatively low concentrations, whereas SRM2975 had no such effect. This is consistent with increased VCAM-1 expression in endothelial cells and LFA-1 expression in monocytes caused by wood smoke exposure. In vitro WPs caused adverse reactions in terms of monocyte-endothelial cell interactions and DNA damage and these effects were stronger than the effects induced by the diesel exhaust particles. 

The result suggests that although wood smoke particles are capable of causing important adverse reaction at high concentrations in vitro they appear to show less effect per gram material than diesel exhaust particles in acute human exposure and that effect on the cardiovascular systems in particular are limited.