Symposium speakers: Stramatoula Tsrikika (Greece), Guy Brusselle (Belgium), Aslı Görek Dilektaşlı (Turkey), Marko Idzko (Austria).
Long term consequences of short term decisions
The youth tobacco epidemic is a major public health threat and adolescent smoking cessation has many unique challenges, some addressed in a presentation by Stramatoula Tsrikika. Rising youth tobacco use, influenced by social media, peer pressure, and industry tactics, is further complicated by experimentation with e-liquids and fancy modifiable devices, often without considering long-term health risks. Addressing this issue requires collaboration among policymakers, healthcare professionals, educators, and communities.
Key actions include raising awareness of smoking risks through evidence-based interventions and fostering supportive environments for reducing tobacco use. Together, these efforts aim to protect adolescents from the harmful effects of smoking.
Inflammatory pathways triggered by smoking
Moving on to the second talk, Guy Brusseles delved into the cellular mechanisms associated with smoking in asthma. He discussed the potential inflammatory pathways underlying asthma immunopathology in adults with a smoking history. Cigarette smoke, rich in reactive oxygen species, activates airway epithelial cells, triggering the production of proinflammatory mediators and resulting in distinct inflammatory phenotypes. Both type 2-high and type 2-low inflammatory phenotypes are observed in smoking asthmatics, with smoking linked to neutrophilic inflammation driven by type 1 and type 17 pathways. Looking more in detail at the innate lymphoid cells (ILCs) that are activated by alarmins such as TSLP, IL-25 and IL-33, Brusselles showed data demonstrating that IL-33 expression is decreased in bronchial mucosa of current smokers. This may have important relevance for future treatment choices following the ongoing development of new biologics.
Airway restructuring, leading to airway limitation
Smoking also induces structural changes in the airways, such as goblet cell hyperplasia and squamous metaplasia, and in the lung parenchyma, including the destruction of alveolar attachments. In a study by Verleden and colleagues examining small airways disease in smokers with pre-COPD, they observed a significant loss of alveolar attachments compared to healthy controls. This finding is important as the parenchymal destruction is contributing to airflow limitation together with airway inflammation and remodelling.
Sustained smoking worsens COPD outcome
The third speaker, Aslı Görek Dilektaşlı, talked about smoking before and after COPD diagnosis. Dilektaşlı showed that smoking after a COPD diagnosis can lead to an accelerated decline in lung function and an increase in symptom burden. The frequency of exacerbations of COPD (ECOPD) may either increase or decrease, but the progression of emphysema and air trapping is likely to worsen. This progression is associated with a higher risk of hospitalizations and mortality. Additionally, continued smoking may alter how patients respond to pharmacotherapy, potentially reducing the effectiveness of treatments.
Plenty of reasons to continue to offer support for smoking cessation
On the other hand, benefits of quitting smoking for individuals with COPD include improved respiratory symptoms, better lung function, slower disease progression and reduced airway inflammation. Moreover, quitting smoking lowers the risk of complications and mortality. In conclusion, research strongly support that smoking cessation is the most effective way to prevent and slow progression of COPD, and it reduces both mortality and morbidity. Hence, healthcare providers should actively support smoking cessation and encourage patients to quit smoking for better lung health outcomes.
Impact of smoking on treatment response
Finally, Marko Idzko highlighted recent findings on how smoking affects the response to biological treatments and corticosteroid unresponsiveness in asthmatic smokers. Idzko discussed how smoking interferes with glucocorticoid receptor (GR) signalling in asthmatic patients by downregulating the expression of the receptor. He further provided evidence that inhaled corticosteroids (ICS) have reduced efficacy in smokers with severe asthma, including patients with COPD. While guidelines recommend quitting smoking before starting biologic therapies, smokers have been excluded from randomized controlled trials. New real-world data suggest that smokers may have a reduced response to biological treatments. Idzko showed data demonstrating that biologics remain effective for treating severe asthma, in patients suffering on severe asthma and COPD, as well as in patients suffering on severe COPD and eosinophilic asthma (both allergic and non-allergic). In conclusion, asthma patients should avoid smoking or quit to improve the effectiveness of their treatment.
Ingvild Bjellmo Johnsen
Medical Advisor Respiratory, Chiesi Nordic
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ID 9992-10-09.2024