Session: Aerosol and Health: Biological Effects and Health Impact of Aerosols
Session Chair: Dr. Hendryk Czech, Dr. Ralf Zimmermann
Assessing exhaust effects with human lung cells - advantages and limitations
Prof. Dr. Barbara Rothen-Rutishauser, Université de Fribourg
While internal combustion engines offer great benefits, they are also the source of highly potent air pollutants that cause major environmental and health problems. Many studies clearly show the link between air pollution and a wide variety of human respiratory and systemic health complications [1, 2]. Because combustion-derived exhaust is a complex mixture made of solid, condensed (or liquid), and gaseous fractions, many attempts are ongoing to describe the biological mechanisms and adverse effects on the respiratory system associated with the specific emission fractions. The aim of this presentation is to provide an overview of the state-of the art in this area of research, focusing on the available in vitro lung models to study respiratory toxicity and effects such as oxidative stress, genotoxicity, and inflammatory responses . In addition, air-liquid interface exposure systems are presented that allow exposure of emission exhaust directly to the cell surface . The combination of predictive in vitro lung models and air-liquid exhaust exposures has proven to be a suitable tool for rapid and reliable investigations of complete exhaust toxicity as well as the effects of particulate fraction, i.e. filtered exhaust [5, 6]. Such efforts provide important results for new and improved emission technologies in the early stages of product development and will also help to correlate the exposure source and specific emission fractions with the adverse immune effects observed in humans.
23-Jun-2022 15:00 (20 Minutes) ICM/Hall 4b
In vitro and in vivo effects of combustion emission aerosols
Prof. Dr. Pasi Jalava, University of Eastern Finland
23-Jun-2022 15:20 (20 Minutes) ICM/Hall 4b
Air-liquid interface cell exposure studies on the toxicity of ultrafine particles
Dr. Sebastiano Di Bucchianico, Helmholtz Zentrum München
Ultrafine particles (UFPs) refers to airborne particulate matter of nanoscale size with an aerodynamic diameter of 100 nm or less. UFPs are potential mediators of adverse health effects of air pollution raising concern in the public health community. Due to their size UFPs can reach the most distal lung regions and translocate to extrapulmonary sites potentially leading to different biological responses compared to larger particles. The high surface-tovolume ratio of UFPs increases their capacity to adsorb substantial amounts of chemicals, including toxic organic compounds, which play an important role in their toxicological effects. However, collecting sufficient mass of UFPs for toxicological studies is challenging and exposing cells to resuspended particles is not representative of physiological conditions [1,2]. Hence, there is a need for standardized approaches to investigate features of UFPs associated with their toxicity at the Air-Liquid Interface. Furthermore, a number of in vivo studies have demonstrated that DNA damage can be the result of particles interactions with one lung cell type causing downstream secondary genotoxicity in another. This effect is mainly due to cell-to-cell interplay instead of being caused by aerosols via direct or indirect mechanisms of actions, referred as primary genotoxicity. Traditional in vitro genetic toxicology studies allow for the evaluation of particles elicited primary genotoxicity, and are unable to depict secondary genotoxicity typically observed in vivo. In this presentation, in vitro co-culture systems for the assessment of secondary genotoxic mechanisms resulting after aerosol exposures at the Air-Liquid Interface will be introduced and the role of UFPs chemical identity discussed. For instance, UFPs with similar elemental carbon core and size, but different organic content, were used to explore the importance of UFPs chemical identity in driving UFPs toxicity and a test system was developed combining an Air-Liquid Interface cell exposure system with a miniature combustion aerosol standard generator (miniCAST) which enables highly controlled generation of model soot particles with varying chemical composition.
23-Jun-2022 15:40 (20 Minutes) ICM/Hall 4b
Mechanisms of combustion particle toxicity: role of polycyclic aromatic hydrocarbons and the aryl hydrocarbon receptor
Prof. Dr. Johan Ovrevik, Norwegian Institute of Public Health
Air pollution is the leading environmental risk factor for disease and premature death, worldwide. The main impact has been attributed to ambient particulate matter, first and foremost the so-called fine fraction of particles less than 2.5 microns in aerodynamic diameter (PM2.5). Current legislation of ambient PM is based on mass, treating all PM sources as equally harmful. However, there is a growing consensus that particle chemistry is important for the biological and toxicological effects of ambient air particulate matter (PM), and that some sources are more hazardous than others. Understanding what components and characteristics of outdoor air PM are the key driver of adverse health effects, may enable more targeted and efficient policies to improve air quality and promote health and wellbeing. Polycyclic aromatic hydrocarbons (PAHs) have long been considered central to the carcinogenic effects of combustion PM. Emerging evidence suggests their involvement in also non-malignant lung and cardiovascular effects. The aryl hydrocarbon receptor (AhR), a main sensor of aromatic xenobiotics, likely plays a central role in these processes. This talk will discuss the mechanisms of PAH-induced effects and the involvement of AhR in lung cells and vascular endothelial cells, with particular focus on the regulation of inflammatory mediators.
23-Jun-2022 16:00 (20 Minutes) ICM/Hall 4b
Developments in health risk assessment due to PM2.5 exposure by the European Environment Agency
Dr. Cristina Guerreiro, NILU
The EEA estimates that 307,000 premature deaths were attributable to exposure to for fine particulate matter (PM2.5) in the current EU-27 in 2019; that represents a decrease by 33% compared to 2005 . Following the publication of the 2021 WHO Air Quality Guidelines (AQG), we assessed the impact of the new concentration-response functions (CRFs) on the estimations of the health outcomes. In addition, we assessed the potential health benefits for the European citizens of attaining the 2021 and 2005 WHO AQG, as calculated by the European Environment Agency . The number of premature deaths (PD) and years of life lost (YLL) were estimated for PM2.5 based on the CRFs previously recommended by WHO , and the CRFs indicated by the latest WHO’s recommendations . PD and YLL were estimated per grid cell, then aggregated to country-level by combining population and demographic data per country, age, and sex with gridded concentrations. The results based on 2019 data show that implementing up-to-date recommendations on CRF will reduce in 26 % the PD and YLL related to PM2.5 exposure. The benefit analysis estimations assume that all grid-cells across Europe with annual mean concentrations in 2019 above the WHO AQG of PM2.5 will be in attainment with the WHO AQGs. Compared to the PM2.5 exposure levels in Europe in 2019 and using the CRFs previously recommended by WHO , the estimated health benefit of attaining the 2021 WHO AQG is a reduction in PD and YLL of 58%, while the benefit of attaining the 2005 WHO AQG for PM2.5 is estimated to be a reduction of 21%.
23-Jun-2022 16:20 (20 Minutes) ICM/Hall 4b
Using burden of disease methods to quantify health impacts of air pollution
Prof. Dr. Otto Hänninen, GDCh
Air pollution has been confirmed asaleading environmental health risk factor globally . Contrasting toxicological risk assessment of chemicals, majority of air pollution studies have benefitted from studying large human populations in real world settings. There are no existing safety margins for air pollutionandhealth-based guidelines are widely exceeded .Burden of disease (BoD) methods, introduced three decades ago,combinedifferent types of diseases and premature mortality into a comparable quantified burden. This is achieved by (i) estimating the years of life lost (YLL) due to premature mortality; (ii) accounting for the duration of diseases; and (iii) assigning disability weights (DW) to them. Various diseases and death are then summed as disability adjusted lifeyears (DALY)to quantify the health losses. Epidemiological evidence is directly applied using population attributable fraction approach , even though there is a lot activity and remaining work to do in exposure-response relationships. Some of these issues will be discussed in this presentation.Current global estimates suggest 6M annual deaths due to air pollution with average loss of life of 28 years. In Europecorresponding values are 0.4M deaths and 19.8 years/death .Air pollution originates from wide range of sources including industries, power production, agriculture, domestic heating, transportation systems through air and transcontinental shipping to local street traffic, besides natural phenomena such as sandstorms, forest fires, volcanos etc.with large chemical and aerosol physical differencesin the atmospheric composition. Ongoing work aims at developing methods to account for these in the future burden of disease estimates.Acknowledgements. This work is partof EU grant no. 955390(ULTRHAS).
23-Jun-2022 16:40 (20 Minutes) ICM/Hall 4b