Introduction
The adverse health effects of smoking have been recognised since the 1950s, while the harmful impact of passive smoking on children has been documented since 1974 [1]. Tobacco smoke contains more than 4,000 chemical compounds, many of which are associated with systemic toxicity [2]. Smoking is a well-established risk factor for a wide range of diseases, including cardiovascular disorders and malignancies [3]. Passive smoking refers to involuntary exposure to environmental tobacco smoke, and many adverse effects associated with active smoking may also occur following passive exposure [4]. In paediatric populations, secondhand smoke exposure has been associated with an increased risk of otitis media, respiratory infections, and early mortality [5].
Despite ongoing tobacco control strategies, both tobacco use and secondhand smoke exposure remain prevalent in Türkiye [6]. According to the World Health Organization’s 2019 Global Tobacco Epidemic Report, tobacco consumption continues to be widespread, particularly among men [7]. Globally, a considerable proportion of children are still exposed to environmental tobacco smoke, representing a persistent public health concern [8]. A study in adolescents demonstrated reduced pulmonary function in individuals exposed to passive smoking, suggesting that the amount of exposure may be more important than the type of exposure [9]. Tobacco use remains one of the leading causes of preventable morbidity and mortality worldwide [10].
Atopic dermatitis is a chronic, relapsing, pruritic inflammatory skin disorder. Alterations in inflammatory biomarkers have been described in affected children [11]. Its prevalence has increased in parallel with industrialization, and environmental factors, together with genetic predisposition and nutritional influences, are considered important contributors to disease pathogenesis [12–14].
Although previous studies suggest a relationship between tobacco smoke exposure and the development of atopic dermatitis, evidence focusing specifically on non-allergic atopic dermatitis in early childhood is limited. The present study was designed to evaluate the association between early-life passive tobacco smoke exposure and disease severity. By highlighting the dermatological consequences of environmental tobacco expo-sure, this study aims to contribute to preventive strategies and increased public awareness.
Material and methods
Study design and setting
This single-centre, prospective observational study with a cross-sectional design was conducted between February and April 2025 at a tertiary paediatric allergy outpatient clinic. Children aged 0–24 months with a clinical diagnosis of non-allergic atopic dermatitis were consecutively enrolled and classified according to the presence of passive tobacco smoke exposure.
Participants and eligibility criteria
The study population consisted of children aged 0–24 months diagnosed with non-allergic atopic dermatitis. The diagnosis of atopic dermatitis was established based on clinical criteria. Non-allergic atopic dermatitis was defined as atopic dermatitis without evidence of sensitization to the food or inhalant allergens assessed during routine clinical evaluation.
To determine eligibility for the study, allergy test results obtained during routine clinical follow-up were reviewed. Allergen sensitization was assessed in all 104 participants. Serum allergen-specific IgE levels were measured using the ImmunoCAP system (Thermo Fisher Scientific, Uppsala, Sweden). A specific IgE level of ≥ 0.35 kU/l was considered positive.
Skin prick tests were performed, when clinically indicated as part of routine clinical evaluation, using the relevant food and/or inhalant allergens. Histamine (10 mg/ml) and saline were used as the positive and negative controls, respectively. A wheal diameter of ≥ 3 mm, in the absence of a reaction or dermographism to the negative control, was considered positive.
Children with sensitization to at least one allergen, as demonstrated by a positive skin prick test and/or serum-specific IgE result, were not included in the study. No additional skin prick tests or serum-specific IgE measurements were performed specifically for research purposes.
Environmental exposures were assessed through structured interviews with parents using the study questionnaire. Written informed consent was obtained from all parents or legal guardians before enrolment.
Inclusion criteria: 1) Age between 0 and 24 months, 2) Clinical diagnosis of non-allergic atopic dermatitis, 3) Complete questionnaire data, 4) Written informed consent.
Exclusion criteria: (1) evidence of food or inhalant sensitization identified during routine clinical evaluation; (2) the presence of another chronic dermatological disease, such as seborrhoeic dermatitis or irritant contact dermatitis; and (3) household pets, intensive chemical exposure, or detergent exposure.
Data collection tools and variables
“Smoking Parent” questionnaire
A structured questionnaire entitled “Smoking Parent” was developed based on World Health Organization tobacco control recommendations, international epidemiological data, and paediatric allergy literature. Although not previously standardized, its content and face validity were assessed by an expert panel consisting of three paediatric allergists and one public health specialist. Item wording was revised in line with the panel’s recommendations to ensure clarity and conceptual consistency.
The questionnaire included four sections: Sociode-mographic characteristics, Parental smoking behaviour and prenatal and postnatal tobacco smoke exposure, Child’s environmental exposures, Clinical characteristics and treatment patterns.
Smoking in the child’s environment indicated the presence of smoking in the immediate environment, whereas daily passive smoke exposure duration included exposure occurring in any setting.
Assessment of atopic dermatitis severity
Disease severity was evaluated using the SCORAD (Scoring Atopic Dermatitis) index, which assesses lesion extent, intensity, and subjective symptoms. Scores were classified as mild (< 25), moderate (25–50), or severe (> 50).
SCORAD assessments were performed by trained paediatric allergy specialists during routine clinical evaluation, before the exposure questionnaire was completed by the parents.
Outcome measures
The primary outcome was the association between passive tobacco smoke exposure and disease severity, measured using the SCORAD score.
Secondary outcomes included associations between SCORAD score and maternal active smoking during pregnancy, prenatal passive smoke exposure and its duration, paternal active and passive smoking and paternal passive-exposure duration, postnatal household smoking, and smoking in the child’s environmen.
Sample selection
Given the exploratory nature of the study, no formal sample size calculation was performed. All eligible participants meeting the inclusion criteria during the study period were consecutively enrolled, resulting in a final sample of 104 children.
Statistical analysis
Statistical analyses were performed using IBM SPSS Statistics version 22.0. Continuous variables were expressed as mean ± standard deviation or median (minimum–maximum), as appropriate, while categorical variables were presented as frequencies and percentages.
Normality was assessed using histograms, probability plots, and Kolmogorov–Smirnov or Shapiro–Wilk tests. Two-group comparisons were performed using independent-samples t-tests or Mann–Whitney U tests. Categorical variables were analysed using χ2 or Fisher’s exact tests. Comparisons involving three or more groups were conducted using one-way ANOVA or appropriate non-parametric tests.
All analyses were performed using the full study population (n = 104). A p-value < 0.05 was considered statistically significant.
Results
A total of 104 children were included, of whom 62 (59.6%) were male and 42 (40.4%) were female. The age distribution was 0–6 months in 37 (35.6%), 7–12 months in 35 (33.7%), 13–18 months in 22 (21.2%), and 19–24 months in 10 (9.6%). Most participants were born at term (37–42 weeks; n = 94, 90.4%), while 9 (8.7%) were preterm and 1 (1.0%) was post-term.
Birth weight was most commonly between 2501 and 3500 g (n = 71, 68.3%), followed by ≥ 3501 g (n = 21, 20.2%), 1501–2500 g (n = 11, 10.6%), and ≤ 1500 g (n = 1, 1.0%) (Table 1). No additional comorbidities were identified. A family history of allergy was present in 47 (45.2%) children.
Table 1
Demographic and birth characteristics of the study population (n = 104)
At least 1 parent was an active smoker in 52 families (50.0%). Maternal active smoking during pregnancy was reported in 9 (8.7%) cases, while prenatal passive smoke exposure was identified in 42 (40.4%) children. Most mothers reported either no exposure (59.6%) or exposure for 1–2 h daily (27.9%). Among fathers, 48 (46.2%) were active smokers and 63 (60.6%) reported passive smoking exposure.
Postnatal household smoking was present in 23 (22.1%) families, whereas smoking in the child’s environment was reported in 10 (9.6%) cases. Daily passive exposure was not reported in the majority of participants (84.6%).
Disease severity was classified as mild in 49 (47.1%) children, moderate in 31 (29.8%), and severe in 24 (23.1%). All participants had non-allergic atopic dermatitis, with disease onset most frequently between 1 and 6 months of age (63.5%). The most common clinical findings were isolated erythema (33.7%) and erythema accompanied by dryness and pruritus (23.1%). Emollients alone were used in 57 children (54.8%), while 18 children (17.3%) received emollients combined with topical corticosteroids. Overall, 79 children (76.0%) received an emollient either alone or in combination with another treatment, whereas 7 children (6.7%) received no treatment (Table 2).
Table 2
Clinical and environmental characteristics of the study population
The mean SCORAD score was 22.53 ±17.33. Skewness (0.592) and kurtosis (–1.012) indicated an approximately normal distribution.
Children with smoking parents had significantly higher SCORAD scores than those with non-smoking parents (33.42 ±15.04 vs. 11.64 ±11.78, p < 0.001). Maternal active smoking during pregnancy was not significantly associated with disease severity (p = 0.220). SCORAD scores differed significantly across prenatal passive smoke exposure-duration categories, increasing from 19.42 ±17.56 among children with no prenatal exposure to 24.73 ±15.77, 28.49 ±18.03, and 38.74 ±11.83 among those exposed for 1–2, 2–4, and > 4 h/day, respectively (p = 0.048). Paternal active smoking and paternal passive smoke exposure-duration categories were also significantly associated with SCORAD scores (p < 0.001 for both). Prenatal passive smoke exposure was associated with significantly higher SCORAD scores (27.11 ±16.12 vs. 19.42 ±17.56, p = 0.026).
Postnatal household smoking was also associated with higher SCORAD scores (33.06 ±16.23 vs. 19.54 ±16.54, p = 0.001), whereas smoking in the child’s environment did not reach statistical significance (32.44 ±15.60 vs. 21.47 ±17.25, p = 0.057) (Table 3).
Table 3
Association between smoking exposure and SCORAD scores
Discussion
Both genetic predisposition and environmental exposures are known to play important roles in the pathogenesis of atopic dermatitis. Previous studies have shown that children with atopic dermatitis are more frequently exposed to tobacco smoke during both prenatal and postnatal periods compared with healthy controls [15]. Exposure during early life, particularly during critical phases of immune maturation and skin barrier development, may influence both disease onset and progression.
The interaction between genetic susceptibility and environmental tobacco exposure has also been implicated in shaping asthma–eczema phenotypes in childhood [16, 17]. In the birth cohort study by Wang et al., passive tobacco smoke exposure was evaluated between 6 months and 3 years of age [17]. In contrast, the present study focused on an earlier developmental period (0–2 years), providing additional insight into early-life exposure. The predominance of male participants observed in both studies may suggest increased susceptibility to environmental factors in early childhood.
The high prevalence of parental smoking and both prenatal and postnatal exposure indicates a substantial environmental burden. In addition, more than half of the patients had moderate-to-severe disease, and disease onset most commonly occurred within the first 6 months of life, supporting the role of early environmental factors.
Consistent with previous reports [17, 18], household smoking during pregnancy and early childhood was common. The evaluation of exposure duration and frequency enabled comparisons of SCORAD scores across exposure categories, supporting the biological plausibility of the observed associations.
Although most patients were primarily managed with emollients, the presence of untreated cases may reflect gaps in parental awareness and disease management.
Previous studies have reported higher SCORAD scores in children exposed to passive smoking [19]. In agreement with these findings, our results demonstrated significantly increased disease severity in children with smoking parents. This suggests that tobacco exposure may influence the clinical severity of atopic dermatitis.
Meta-analyses indicate that prenatal passive smoke exposure, rather than maternal active smoking, is associated with an increased risk of atopic dermatitis [20]. Similarly, in our study, prenatal passive exposure was significantly associated with higher SCORAD scores, whereas maternal active smoking was not. These findings highlight the importance of protecting pregnant women from environmental tobacco smoke.
Paternal smoking and paternal passive smoke exposure were also associated with increased disease severity. A graded increase was observed across prenatal passive smoke exposure categories; however, no strictly monotonic pattern was observed across categories of paternal exposure duration. The study by Miyahara et al. focused on respiratory outcomes [21], whereas evidence regarding dermatological consequences remains limited. Environmental tobacco smoke has nevertheless been associated with childhood atopic dermatitis [22]. Our findings extend this evidence by demonstrating a significant association between paternal smoking and disease severity.
In a recent cross-sectional study by Günal et al., mixed allergic phenotypes were common among children with food allergy, with a high prevalence of concomitant atopic dermatitis [23]. Although our cohort included only children with non-allergic atopic dermatitis, the findings suggest that passive tobacco smoke exposure may aggravate skin barrier dysfunction and immune activation. Larger prospective studies are needed to further clarify these relationships.
Overall, the findings of this study indicate that environmental tobacco smoke is an important and potentially modifiable factor influencing disease severity in early childhood atopic dermatitis. Smoking cessation and the maintenance of smoke-free home environments should be considered integral components of management.
This study has several limitations. The single-centre design and relatively small sample size may limit generalizability. Tobacco smoke exposure was assessed using parental self-report, which may introduce recall and reporting bias.
Although participants with household pets, intensive chemical exposure, or detergent exposure were excluded, residual confounding from other environmental exposures cannot be entirely ruled out. In addition, sensitization was assessed as part of routine clinical care rather than by a uniform allergen panel, so subclinical sensitization may have gone undetected in some children. Multivariable analysis was not performed; therefore, the reported associations are unadjusted and residual confounding cannot be excluded.
Multiple comparisons were performed without formal adjustment, which may increase the risk of type I error. In addition, no formal sample size calculation was performed. Finally, the cross-sectional design precludes definitive causal inference.
Conclusions
Passive tobacco smoke exposure, particularly paternal smoking and postnatal household exposure, is associated with increased disease severity in children aged 0–2 years with non-allergic atopic dermatitis. SCORAD scores increased across prenatal passive smoke exposure-duration categories; however, the small subgroup sizes and absence of a formal trend analysis warrant cautious interpretation.
These findings highlight the importance of early preventive strategies and family-based smoking cessation interventions. Further large-scale and longitudinal studies are required to evaluate long-term outcomes and interactions with allergic sensitization.
