TUBE - Transport derived Ultrafines and the Brain Effects

Black carbon (BC) is a component of ambient particulate matter which originates from incomplete combustion emissions. BC is regarded as an important short-lived climate forcer, and a significant public health hazard. These two concerns have made BC a focus in aerosol science. Even though, the toxicity of BC particles is well recognized, the mechanism of toxicity for BC as a part of the total gas and particle emission mixture from combustion is still largely unknown and studies concerning it are scarce. In the present study, using a novel thermophoresis-based air-liquid interface (ALI) in vitro exposure system, we studied the toxicity of combustion-generated aerosols containing high levels of BC, diluted to atmospheric levels (1 to 10 μg/m³). Applying multiple different aerosol treatments, we simulated different sources and atmospheric aging processes, and utilizing several toxicological endpoints, we thoroughly examined emission toxicity. Our results revealed that an organic coating on the BC particles increased the toxicity, which was seen as larger genotoxicity and immunosuppression. Furthermore, aging of the aerosol also increased its toxicity. A deeper statistical analysis of the results supported our initial conclusions and additionally revealed that toxicity increased with decreasing particle size. These findings regarding BC toxicity can be applied to support policies and technologies to reduce the most hazardous compositions of BC emissions. Additionally, our study showed that the thermophoretic ALI system is both a suitable and useful tool for toxicological studies of emission aerosols.

The adverse effects of air pollutants on the respiratory and cardiovascular systems are unquestionable. However, in recent years, indications of effects beyond these organ systems have become more evident. Traffic-related air pollution has been linked with neurological diseases, exacerbated cognitive dysfunction, and Alzheimer’s disease. However, the exact air pollutant compositions and exposure scenarios leading to these adverse health effects are not known. Although several components of air pollution may be at play, recent experimental studies point to a key role of ultrafine particles (UFPs). While the importance of UFPs has been recognized, almost nothing is known about the smallest fraction of UFPs, and only >23 nm emissions are regulated in the EU. Moreover, the role of the semivolatile fraction of the emissions has been neglected. The Transport-Derived Ultrafines and the Brain Effects (TUBE) project will increase knowledge on harmful ultrafine air pollutants, as well as semivolatile compounds related to adverse health effects. By including all the major current combustion and emission control technologies, the TUBE project aims to provide new information on the adverse health effects of current traffic, as well as information for decision makers to develop more effective emission legislation. Most importantly, the TUBE project will include adverse health effects beyond the respiratory system; TUBE will assess how air pollution affects the brain and how air pollution particles might be removed from the brain. The purpose of this report is to describe the TUBE project, its background, and its goals.

Every second we inhale a danger in the air; many particles in the atmosphere can influence our lives. Outdoor air pollution, especially particulate matter is the largest environmental risk factor and has been associated with many cardiovascular and lung diseases. Importantly, air pollution has recently been discovered to also impact the brain. Here, we review the effects of air pollution on glial cells of the brain, astrocytes and microglia, and the tightly controlled interplay between these cell types. We focus on how traffic related air pollutants which include both gaseous and particulate emissions and their secondary products influence the intercellular communication of microglia and astrocytes. Finally, we place these air pollution and glial interactions in a larger context by discussing their impact on neurodegeneration.