2024 International Symposium on Respiratory Medicine

Environment and Airway Diseases

Invited Speaker

Marc Chadeau-Hyam

Professor of Computational Epidemiology and Biostatistics, School of Public Health, Imperial College, London

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Professor Chadeau-Hyam has gained expertise over the last 15 years in devising, applying and adapting computationally efficient methods to analyse and integrate complex and high-dimensional data. As an active member of the European exposome initiative, he has developed inegrative approaches to explore the stressor- triggered molecular mechanisms involved in the determination of individual risk profiles. In 2021, Professor Chadeau-Hyam joined the REACT team, where he provided statististical oversight. His team currently includes ~15 members with a unique diversity of profiles, including medical, biological, and statistical backgrounds, all collaborating for the in-depth analysis of large-scale data from mega-sized and/or deeply phenotypes cohort studies.

Brief content of the topic

The Exposome concept has been developed as a necessary complement to the genome to better understand the determinants of health and of the risk of chronic diseases. The external exposome combines a large range of external factors potentially impacting human health from conception onwards. These external exposures (i) are heterogeneous in nature, scale, and variability, (ii) feature complex correlation patterns and (iii) may operate as mixtures. The internal exposome can be defined as the way these exposures are embodied and its exploration relies on the screening and integration of high-resolution molecular data. The isolated exploration of an omic profile offers the possibility to capture stressor-induced biological/biochemical alterations, potentially impacting individual risk profiles, but this may only yield a fractional picture of the complex molecular events involved, therefore limiting our understanding of the effective mechanisms mediating the effect of the exposome. Taking examples from real-world exposome projects we will illustrate the use of statistical and machine learning techniques to accommodate co-occurring exposures contributing to population stratification, explore the links between these and health outcomes, and investigate the (multi)-omic response to these sets of exposures.

Chun-Hwa Wang

Attending Physician, Lin-Kuo Chang Gung Memorial Hospital

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Brief content of the topic

There is increasing evidence and concern about the relationship between asthma and environmental factors. Polycyclic aromatic hydrocarbons (PAHs) are the main constituents of particulate matter air pollutants (PM10 and PM2.5) and are traffic-related air pollutants that are related to the amount of diesel exhaust particulates (DEP) produced. Previous studies have shown these substances enhance the production of pro-allergen cytokines and IgE and worsen the severity of asthma by increasing Th2 and Th17 cytokines. Moreover, these air pollutants may stimulate airway epithelial cells, and secretion of epithelial injury cytokines affects the classification and differentiation of innate lymphocytes, thereby regulating the onset of asthma, control of asthma and airway remodeling. 

Our study found that the annual decline in FVC (n=83, r=-0.760, p<0.0001), FEV1 (r=-0.641, p<0.0001) and FEV1 predicted value (r=-0.678, p<0.0001) was inversely correlated to the yearly exposure of PAH concentration. There was highly correlation between the annual decline in FVC, FEV1 and FEV1 predicted value and exposure of annual concentration of PAH in asthmatics living in high air pollution area, but not in the group of asthmatics living in moderate to low air pollution area. Circulating ILC2 and ILC3 cells in peripheral blood of asthmatic patients who were living in high air pollution areas were higher than those in asthmatic patients living in moderate to low air pollution. The RORrt involved in the regulation of IL-17A and GATA-3 associated with Th2 differentiation were significantly higher in asthmatic patients living in high air pollution areas. The gene expression of Th1 and Th2 cytokines in PBMC derived from asthmatic patients living in high air pollution area was significantly higher than those in the low air pollution area. Among high air pollution area, the asthmatics that were atopic to HDM had a higher level of ILC2 cells compared to those without atopic to mite. 

The level of T-BET and GATA-3 was significantly higher in PBMC exposed to mite or mite+BaP, even in asthmatics with or without atopic to HDM. The regulation of FOXP3 expression in Treg cells which occurs through the concerted action of transcription factors and extensive epigenetic control mechanisms was also significantly increased in PBMC exposed to mite or mite + BaP, while asthmatics was either atopic or non-atopic to HDM. However, the level of RORt in PBMC did not show any difference in asthmatics with either atopic or non-atopic to HDM. The mite and air pollution involved in the regulation of IL-17A and GATA-3 associated with Th2 differentiation may contribute to the yearly lung function decline in asthmatic patients with atopic to mite and living in high air pollution areas.

Hsiao-Chi Chuang

Professor, School of Respiratory Therapy, College of Medicine, Taipei Medical University

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The overall aim of research is to understand comprehensively how specific factors, such as aerosol-contained free radicals, regulate cell signalling and protein and lipid metabolites during health and disease in the lung environment. In particular, I am elucidating the pathways leading from the interaction of such reactive oxygen species (ROS), through the intracellular signalling cascades, to the apoptotic activities. Specifically, my research interests are:

Brief content of the topic

Climate change has the potential to amplify air pollution and modify the physicochemical attributes of particulate matter, including its size, dispersion, and chemical makeup. These modifications critically affect particle deposition in the lungs, leading to pronounced respiratory implications. As such, climate change can significantly influence lung particle deposition by altering the nature of airborne particulates, heightening the risk of respiratory disease onset.

The intertwined effects of climate change and air pollution pose pressing global health dilemmas, especially concerning respiratory ailments. Projected increases in the frequency and severity of extreme weather events due to climate change can further escalate air pollution. Furthermore, anticipated economic growth and population surges in many regions globally will likely augment air pollution levels, intensifying respiratory disease burdens. Vulnerable groups, such as children, the elderly, and those with existing respiratory conditions, are particularly at risk.

Compounding these challenges, the adverse consequences include heightened inflammation, increased oxidative stress, and compromised lung immune functions. Therefore, it's paramount that public health initiatives address and mitigate the respiratory repercussions of both climate change and air pollution

Kai-Jen Chuang

Professor of department of Public Health, School of medicine, College of medicine, Taipei Medical University

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Brief content of the topic

Taiwan’s employed population is 11.45 million, accounting for nearly half of Taiwan’s total population. The population in the manufacturing and service industries is approximately 8.06 million. Workers in Taiwan's manufacturing industry are easily exposed to dust and metal fumes, while workers in the service industry are easily exposed to cooking aerosol and volatile organic chemicals.Exposure to these air pollutants will significantly increase workers' risk for future cardiovascular and pulmonary diseases. Therefore, this series of studies discusses the association between occupational exposure to air pollution and cardiopulmonary biological markers, and discusses how to effectively intervene to improve air quality in occupational places or reduce air pollution exposure.