Elsevier

Toxicology Letters

Volume 165, Issue 3, 10 September 2006, Pages 203-211
Toxicology Letters

Comparison of genotoxic and inflammatory effects of particles generated by wood combustion, a road simulator and collected from street and subway

https://doi.org/10.1016/j.toxlet.2006.04.003Get rights and content

Abstract

The health effects of exposure to airborne particles are of increasing concern in society. In order to protect public health, a clarification of the toxic properties of particles from different sources is of importance. The aim of this study was to investigate and compare the genotoxicity and the ability to induce inflammatory mediators of nine different particle types from wood and pellets combustion, from tire–road wear and collected from an urban street and a subway station. The comet assay was used to assess genotoxicity after exposure of the human lung cell line A549. Inflammatory effects were measured as induction of IL-6, IL-8 and TNF-α after exposure of human macrophages. We found that all particles tested caused DNA damage and those from the subway caused more damage than the other particles (p < 0.001) likely due to redox-active iron. In contrast, particles collected from an urban street were most potent to induce inflammatory cytokines. Particles from tire–road wear collected using a road simulator were genotoxic and able to induce cytokines. Finally, more effective combustion of wood led to less emission of particles, but those emitted did not show less toxicity in this study.

Introduction

Airborne particles are a recognized health risk in the society. Epidemiological studies show a wide range of health effects associated with particles including increased rates of hospital admissions for respiratory diseases (Atkinson et al., 2001), increased use of asthma medication (von Klot et al., 2002) and death in cancer and cardiopulmonary diseases (Dockery et al., 1993, Pope et al., 2002). Recently, an association between particles and adverse effects on lung development in children was presented (Gauderman et al., 2004). The underlying mechanisms for these health effects are under investigation with oxidative stress and inflammation considered to be of importance (Donaldson and Tran, 2002, Li et al., 2003). Particles can lead to up-regulation of cytokines including interleukins 6 and 8 (IL-6, IL-8) and tumor necrosis factor alpha (TNF-α), which have been seen after exposure to particles of both macrophages (Becker et al., 1996) and epithelial cells (Carter et al., 1997) in vitro, and in the lungs of mice (Shukla et al., 2000) as well as humans (Schaumann et al., 2004). Both IL-6 and TNF-α are regarded as proinflammatory cytokines, which among other properties can induce hepatic secretion of proinflammatory proteins, while IL-8 acts as a chemokine by attracting and activating inflammatory promoting cells. IL-6 in particular has been associated with hepatic secretion of C-reactive protein (CRP) and fibrinogen that are considered to be of importance in development of cardiac diseases (Castell et al., 1989, Harris et al., 1999) Together with IL-1 and TNF-α, IL-6 has been suggested to play a role in the development of atherosclerosis (Yudkin et al., 2000). It is possible that particles that induce secretion of these cytokines have a link with the epidemiological results connecting particles to cardiovascular disease, and the levels of such particles should therefore be limited. Further, since there is a link between DNA damage, mutations and cancer, particles potent to cause DNA damage can be regarded as more likely to have an effect on cancer development. The genotoxicity of particles may due to oxidizing substances including transition metals, DNA-reactive polyaromatic compounds as well as the insoluble particle core (Knaapen et al., 2002, Karlsson et al., 2004).

Due to lack of data regarding how particles from different sources contribute to effects on human health, particles are often handled as a uniform pollutant. Usually particulate matter (PM) is divided into different size fractions; the respirable particles with an aerodynamic diameter of less than 10 μm (PM10) consist of a coarse fraction of PM with an aerodynamic diameter of 2.5–10 μm, a fine fraction with particles less than 2.5 μm (PM2.5), and ultrafine particles with a diameter less than 0.1 μm (PM0.1), also known as nanoparticles. The PM fractions seem to possess different qualities in their ability to induce pathophysiological conditions. Generally, the fine fraction is thought to have more long term health effects whereas the coarse fraction is associated with short term health effects, but the picture is not clear and the literature describing morbidity and mortality in response to exposure of a certain PM fraction varies between areas where studies have been performed (Brunekreef and Forsberg, 2005).

Instead of focusing on the different size fractions of particles, a more source-specific approach may be more relevant, which requires studies focused on how particles from different sources differ in toxicity. The concentration of particles in the air at a given location is depending on contributions from long-range transport and local sources. In Sweden, two of the most important local sources are suspension of road dust, mainly due to the use of studded tires and sanding of roads in winter, and particles generated from wood combustion (Forsberg et al., 2005). So far, not much is known regarding the effects of tire–road wear particles. A Finnish study suggests that re-suspended road dust has less effect on respiratory health in asthmatics compared to combustion-related PM (Penttinen et al., 2001). However, an in vitro study from Finland showed that spring-time PM10, which is mostly derived from re-suspension of road dust, induced inflammatory cytokines more than winter-time PM10, mostly derived from long-range transport and local combustion sources (Salonen et al., 2004).

The aim of this study was to investigate and compare the genotoxicity and the ability to induce inflammatory mediators of particles from wood and pellets combustion, from tire–road wear and collected from an urban street and a subway station. The comet assay was used to assess genotoxicity after exposure of the human lung cell line A549. Inflammatory effects were measured as induction of IL-6, IL-8 and TNF-α after exposure of human macrophages.

Section snippets

Particle samples

The different PM-samples and how they were collected are described in short in Table 1. This study relied on particles collected by different investigators for different purposes and the same collection procedure was unfortunately not possible to obtain for the particle samples. Wear particles originating from the road–tire interface were generated by the Swedish National Road and Transport Research Institute (VTI) Road Simulator. Sampling in the simulator hall makes it possible to sample pure

Emissions of particles and organic compounds during residential burning of wood and pellets

The PM from wood and pellets combustion used in this study was sampled from the chimneys of one-family houses. The emission of particles and organic compounds differed substantially depending on the wood boiler and pellets burner used. Combustion in the old-type wood boiler led to over 4-times higher emissions of particles compared to the modern boiler and 8-times higher emissions compared to the pellet burner (Table 2). The difference between the different combustions were even more obvious

Discussion

The aim of this study was to compare different types of particles generated through human activity regarding their genotoxic and inflammatory evoking potential. The results show that all types of particles used in our experiments could pose a health risk, although there were variations among their ability to induce cytokine secretion and DNA damage.

Even though particles are recognized as causing a health risk and several health effects have been observed in epidemiological studies, it is not

Acknowledgements

We thank Christer Johansson at the City of Stockholm Environment and Health Administration, Mats Gustafsson at the Swedish National Road and Transport Research Institute and Linda Johansson from SP Swedish National Testing and Research Institute for providing the particles. This study was financially supported by the Swedish Environmental Protection Agency. The authors of this paper are partners of the EU Network of Excellence, Environmental Cancer Risk, Nutrition and Individual Susceptibility

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