ArticleThe journal of allergy and clinical immunology. Global2025
Atopic dermatitis and tobacco smoke exposure during childhood and adolescence.
Article in The journal of allergy and clinical immunology. Global, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Early-Life Secondhand Smoke Exposure and Development of Atopic Dermatitis up to Adulthood.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026Article
- Interactive Effects of Genetic Susceptibility and Early-Life Tobacco Smoke Exposure on the Asthma-Eczema Complex Phenotype in Children: 6-Year Follow-Up Case-Control Study.International journal of molecular sciences · 2025Article
- Safety and Effectiveness of Upadacitinib in Patients with Moderate-to-Severe Atopic Dermatitis Who Smoke: a 2-Year Real-Life Multicenter Study.American journal of clinical dermatology · 2025Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Tobacco smoke may affect atopic dermatitis (AD) because of its known effects on humoral and cellular immunity, but prior studies lack data on disease severity and biomarkers over time. Objective: We investigated the association between passive and active tobacco smoke exposure (TSE) during childhood and adolescence and the activity and severity of AD. Methods: A birth cohort of 10,521 individuals was followed through adolescence as part of the Avon Longitudinal Study of Parents and Children. We used mixed-effect models to determine the risk of AD (based on repeated assessments) with passive smoke exposure during childhood, active TSE during adolescence, and using a serum biomarker of tobacco exposure (cotinine) at 3 time points. Results: After adjusting for confounding factors, there was no evidence of a relationship between passive TSE and concurrent AD activity in childhood (adjusted odds ratio, 0.95; 95% confidence interval, 0.83, 1.07) or of an increased risk between active smoking and AD activity in adolescence (adjusted odds ratio, 0.57; 95% confidence interval, 0.44, 0.75). Secondary analyses demonstrated no dose-response relationship and no increased severity of AD with passive or active TSE. Furthermore, we found no increased risk of AD with a cumulative measure of passive TSE across childhood (adjusted relative risk ratio, 0.98; 95% confidence interval, 0.96, 1.00). Conclusion: Neither active nor passive TSE was associated with AD during childhood and adolescence.
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