D1.155 - Clinical, Functional and Inflammatory Characteristics of Young Adults with Bronchial Asthma Using Conventional Cigarettes, Electronic Nicotine Delivery Systems and Heated Tobacco Products

Bronchial asthma remains a major medical and social problem, and up to one fifth of patients continue to smoke despite having a chronic respiratory disease.[1] The rapid growth of electronic nicotine delivery systems (ENDS) and heated tobacco products (HTPs), especially among young adults, has created a new group of asthma patients exposed to multiple nicotine and tobacco products, while evidence on their impact on asthma control and airway inflammation is limited. To evaluate the impact of different smoking devices (conventional cigarettes, ENDS, HTPs and their combinations) on asthma control, lung function, quality of life and inflammatory profile in young adults with BA

An open observational study was conducted in a specialized allergy department and included patients aged 18–45 years with physician-diagnosed BA for at least 12 months.Asthma control (Asthma Control Test, ACT), asthma-related quality of life (AQLQ), spirometry (FEV₁ before bronchodilation), fractional exhaled nitric oxide (FeNO) and blood biomarkers (eosinophils, neutrophils, eosinophil cationic protein [ECP], periostin, thymic stromal lymphopoietin [TSLP], interleukin‑13 [IL‑13]) were assessed using standardized protocols. Patients were classified as non-smokers or smokers (conventional cigarettes, ENDS, HTPs, waterpipe, single or multiple use)

A total of 153 patients were enrolled (149 men, 4 women; mean age 22.14±3.09 years); 59 were non-smokers and 94 were smokers, 56.4% of whom were multi-users of different devices.Compared with non-smokers, smokers had poorer asthma control (ACT 16.2±3.8 vs 18.9±3.6; mean difference −2.7 points, p<0.001) and lower AQLQ scores (4.48±1.12 vs 5.31±0.89; mean difference −0.83, p<0.001).[1] Baseline FEV₁ was lower in smokers (83.9±15.2% vs 88.4±13.8% predicted; difference −4.5%, p<0.05), and values <80% and <70% predicted were 1.65 and 1.87 times more frequent, respectively. A shift in inflammatory phenotype was observed in smokers, with lower ECP (−18.3%, p<0.05) and a trend towards lower blood eosinophils (−10.3%), alongside higher neutrophil counts (+14.3%, p<0.01).Periostin and TSLP levels were significantly higher in smokers (+31.0% and +73.5%, respectively; both p<0.05), while IL‑13 and total IgE did not differ between groups.Subgroup analysis revealed no statistically significant differences between conventional cigarettes, ENDS, HTPs and their combinations regarding ACT, AQLQ, FEV₁ or biomarker profiles (p>0.05).

In young adults with BA, all studied smoking devices—including ENDS and HTPs—are associated with similarly adverse effects on asthma control, lung function and quality of life, and with a shift towards a less eosinophilic and more neutrophilic inflammatory pattern with elevated epithelial alarmins periostin and TSLP.Alternative nicotine delivery methods cannot be considered safe options for asthma patients and should be explicitly targeted in smoking-cessation counselling and phenotype-oriented management strategies.