TY  - BOOK
AB  - Ageing leads to a decline in lung function, with vital parameters like FEV1 and FVC decreasing from 35 years of age, and a sharper drop in FEV1 after 65 years of age. Structural changes include reduced bronchiole density, enlarged alveoli and increased lung rigidity due to collagen build-up. Ageing also impairs the respiratory response to hypoxaemia and hypercapnia, and reduces mucociliary clearance. Cellular hallmarks such as telomere shortening, mitochondrial dysfunction and chronic inflammation contribute to lung ageing. Air pollution, a key risk factor for respiratory diseases like COPD, further exacerbates lung decline, particularly in older adults, due to oxidative stress. Pollutants cause oxidative damage and protein modifications, and may accelerate cellular senescence. While mechanistic insights remain limited, the impact of air pollutants on lung health is clear. Future research should address emerging threats like microplastics and the role of lifestyle and genetic factors, as political efforts to improve air quality continue.
AU  - Staab-Weijnitz, C.*
AU  - Lehmann, M.
C1  - 74785
C2  - 57577
SP  - 259-276
TI  - Environmental exposure and the ageing lung.
JO  - ERS Monog.
VL  - 2025-April
IS  - 107
PY  - 2025
SN  - 2312-508X
ER  - 

TY  - BOOK
AB  - About half of microbiologically cured TB patients experience TB-related persistent respiratory health problems or residual lung pathology, which are summarised under the term post-TB lung disease (PTLD). The development of PTLD is complex and moderated by a multitude of host, pathogen and environmental risk factors. With regards to pathogenesis, two processes are likely to be important: 1) Mycobacterium tuberculosis infection-driven tissue damage, and 2) pathological tissue remodelling following active disease. The PTLD phenotype that is currently best described in the data is obstructive airways disease in adults. Other patterns of PTLD including bronchiectasis, other (non-obstructive) lung function abnormalities, such as low forced vital capacity or impaired diffusion capacity, and patterns of secondary morbidity, such as chronic pulmonary aspergillosis and pulmonary arterial hypertension, are less well described. In the absence of robust, evidence-based management guidelines for PTLD, clinical statements suggest a set of diagnostic and therapeutic “toolboxes” which must be adapted to the local and clinical context of PTLD patients.
AU  - Rachow, A.
C1  - 68859
C2  - 55051
SP  - 191-209
TI  - The challenge of post-tuberculosis lung disease.
JO  - ERS Monog.
VL  - 2023
IS  - 101
PY  - 2023
SN  - 2312-508X
ER  - 

TY  - JOUR
AU  - Cox, M.J.*
AU  - Ege, M.J.*
AU  - von Mutius, E.
C1  - 58979
C2  - 48478
SP  - ix-xi
TI  - Introduction.
JO  - ERS Monog.
VL  - 2019
IS  - 9781849841023
PY  - 2019
SN  - 2312-508X
ER  - 

TY  - BOOK
AB  - We are at the very beginning of understanding the respiratory microbiome and its influence on health and disease; early indications are that this might be profound. Though it builds on decades of research in other fields, including environmental microbiology, clinical microbiology, gut and oral microbiome work, currently we are describing the organisms that are present in different parts of the respiratory tract under different conditions. Few studies have done so longitudinally and the relationship with disease is largely associative, making translation to clinical applications challenging. We are beginning to understand the nature of the challenges and we can draw common problems from the chapters of this Monograph.
AU  - Cox, M.J.*
AU  - Ege, M.J.*
AU  - von Mutius, E.
C1  - 60384
C2  - 49746
SP  - 240-244
TI  - Challenges, impact and the future.
JO  - ERS Monog.
VL  - 2019
IS  - 9781849841023
PY  - 2019
SN  - 2312-508X
ER  -