The Comprehensive Systematic Review of Association of Environmental Tobacco Smoke Exposure with the Incidence of Childhood Eczema

The Comprehensive Systematic Review of Association of Environmental Tobacco Smoke Exposure with the Incidence of Childhood Eczema

Authors

  • Febryana Ramadhani General Practitioner, Atma Jaya General Hospital, Indonesia / Faculty of Medicine, University of Prima Indonesia
  • Ayub Quisa Military Doctor - Unit 71 of the Indonesian Special Forces Command / Graduate of Faculty Medicine, Sebelas Maret University, Indonesia
  • Danny Gunawan Department of Dermatovenereology, Atma Jaya General Hospital, Indonesia / Faculty of Medicine, Atma Jaya Catholic University, Indonesia

Keywords:

Environmental tobacco smoke, childhood eczema, atopic dermatitis, secondhand smoke, IgE sensitization, dose-response

Abstract

Background: Environmental tobacco smoke (ETS) is a pervasive indoor pollutant, yet its association with childhood eczema remains debated due to heterogeneous findings.

Methods: This systematic review synthesized 80 studies examining ETS exposure (prenatal/postnatal, questionnaire/biomarker-assessed) and childhood eczema (0–18 years), focusing on IgE-sensitized (atopic) versus non-atopic eczema. Primary outcomes were odds ratios (ORs), relative risks (RRs), and hazard ratios (HRs) with 95% confidence intervals.

Results: Passive smoke increased atopic dermatitis (AD) risk (OR 1.18; 95%CI 1.01–1.38) (1). Postnatal parental smoking during infancy was significantly associated with AD up to age 24 years (OR 1.25–1.39 for IgE-associated AD) (2). Prenatal maternal smoking with concurrent postnatal exposure yielded the strongest atopic eczema risk at age 4 (OR 2.14; 1.33–3.46) (3). Dose-response gradients were significant: maternal smoking ≥11 cigarettes/day gave RR 1.60 for AD by age 5.5 years (4). Both parents smoking increased total allergy risk (OR 4.72 versus 3.97 for one parent) (5). The critical novel finding: ETS specifically increased IgE-sensitized (atopic) eczema (OR 1.82 for prenatal; 1.62 for postnatal) but showed no association with non-atopic eczema (OR ~1.00) (2,3). Null or inverse findings (e.g., OR 0.46 for high maternal cotinine + vitamin D) (9) were explained by failure to distinguish atopic subtypes, short follow-up, or confounding by nutritional status.

Discussion: The weight of evidence supports a significant positive, dose-dependent association between postnatal household ETS exposure and atopic (IgE-mediated) childhood eczema, persisting into young adulthood. The atopic/non-atopic distinction is the primary explanatory mechanism for prior heterogeneity.

Conclusion: ETS is a modifiable risk factor specifically for IgE-associated childhood eczema. Future studies must stratify eczema by atopic status and use biomarker-validated ETS measurement.

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Published

2026-06-01