Maternal Smoking during Pregnancy and Early Childhood and Development of Asthma and Rhinoconjunctivitis - a MeDALL Project

Abstract

Background: The role of tobacco smoke exposure in the development and persistence of asthma and rhinoconjunctivitis through childhood into adolescence is unclear.

Objectives: We assessed the associations of parental smoking from fetal life through adolescence with asthma and rhinoconjunctivitis during childhood and adolescence.

Methods: We analyzed data for 10,860 participants of five European birth cohort studies from the Mechanisms of the Development of Allergy (MeDALL) consortium. Parental smoking habits and health outcomes (early transient, persistent, and adolescent-onset asthma and rhinoconjunctivitis) were based on questionnaires covering the period from pregnancy to 14-16 y of age. Data were combined and analyzed using a one-stage and two-stage individual participant data meta-analysis.

Results: Overall, any maternal smoking during pregnancy tended to be associated with an increased odds of prevalent asthma [adjusted odds ratio (aOR)=1.19 (95% CI: 0.98, 1.43)], but not prevalent rhinoconjunctivitis [aOR=1.05 (95% CI: 0.90, 1.22)], during childhood and adolescence. In analyses with phenotypes related to age of onset and persistence of disease, any maternal smoking during pregnancy was associated with early transient asthma [aOR=1.79 (95% CI: 1.14, 2.83)]. Maternal smoking of ≥10 cigarettes/day during pregnancy was associated with persistent asthma [aOR=1.66 (95% CI: 1.29, 2.15)] and persistent rhinoconjunctivitis [aOR=1.55 (95% CI, 1.09, 2.20)]. Tobacco smoke exposure during fetal life, infancy, childhood, and adolescence was not associated with adolescent-onset asthma or rhinoconjunctivitis.

Conclusions: Findings from this combined analysis of five European birth cohorts strengthen evidence linking early exposure to tobacco smoke with asthma during childhood and adolescence. Children with high early-life exposure were more likely than unexposed children to have early transient and persistent asthma and persistent rhinoconjunctivitis. https://doi.org/10.1289/EHP2738.

Figure 1.

Prevalence of asthma and rhinoconjunctivitis in five European birth cohorts. Note: BAMSE, Children, Allergy, Milieu, Stockholm, Epidemiology; GINIplus, German Infant Nutritional Intervention; LISAplus, Influences of Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood; MAS, Multicentre Allergy Study; PIAMA, Prevention and Incidence of Asthma and Mite Allergy.

Figure 2.

Associations between maternal smoking during pregnancy ($N=\mathrm{9,052}$) or any secondhand smoke (SHS) during infancy ($N=\mathrm{7,970}$) and prevalence of asthma up to 14–16 y of age in five European birth cohorts. Cohort-specific odds ratios (ORs) and 95% confidence intervals (CIs) were obtained by generalized estimating equation models. Adjusted for sex, parental education level, parental allergy, older siblings, breastfeeding, study center, intervention arm, and early day-care attendance. Combined OR and 95% CI were derived from cohort-specific OR and 95% CI using a random effects model. Note: BAMSE, Children, Allergy, Milieu, Stockholm, Epidemiology; GINIplus, German Infant Nutritional Intervention; LISA, Influences of Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood; MAS, Multicentre Allergy Study; PIAMA, Prevention and Incidence of Asthma and Mite Allergy.

Figure 2.

Associations between maternal smoking during pregnancy ($N=\mathrm{9,052}$) or any secondhand smoke (SHS) during infancy ($N=\mathrm{7,970}$) and prevalence of asthma up to 14–16 y of age in five European birth cohorts. Cohort-specific odds ratios (ORs) and 95% confidence intervals (CIs) were obtained by generalized estimating equation models. Adjusted for sex, parental education level, parental allergy, older siblings, breastfeeding, study center, intervention arm, and early day-care attendance. Combined OR and 95% CI were derived from cohort-specific OR and 95% CI using a random effects model. Note: BAMSE, Children, Allergy, Milieu, Stockholm, Epidemiology; GINIplus, German Infant Nutritional Intervention; LISA, Influences of Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood; MAS, Multicentre Allergy Study; PIAMA, Prevention and Incidence of Asthma and Mite Allergy.

Figure 3.

Associations between maternal smoking during pregnancy ($N=\mathrm{9,016}$) or any secondhand smoke (SHS) during infancy ($N=\mathrm{7,932}$) and prevalence of rhinoconjunctivitis up to 14 y of age in five European birth cohorts. Cohort-specific odds ratios (ORs) and 95% confidence intervals (CIs) were obtained by generalized estimating equation models. Adjusted for sex, parental education level, parental allergy, older siblings, breastfeeding, study center, intervention arm, and early day-care attendance. Combined OR and 95% CI were derived from cohort-specific OR and 95% CI using a random effects model. Note: BAMSE, Children, Allergy, Milieu, Stockholm, Epidemiology; GINIplus, German Infant Nutritional Intervention; LISA, Influences of Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood; MAS, Multicentre Allergy Study; PIAMA, Prevention and Incidence of Asthma and Mite Allergy.

Figure 3.

Associations between maternal smoking during pregnancy ($N=\mathrm{9,016}$) or any secondhand smoke (SHS) during infancy ($N=\mathrm{7,932}$) and prevalence of rhinoconjunctivitis up to 14 y of age in five European birth cohorts. Cohort-specific odds ratios (ORs) and 95% confidence intervals (CIs) were obtained by generalized estimating equation models. Adjusted for sex, parental education level, parental allergy, older siblings, breastfeeding, study center, intervention arm, and early day-care attendance. Combined OR and 95% CI were derived from cohort-specific OR and 95% CI using a random effects model. Note: BAMSE, Children, Allergy, Milieu, Stockholm, Epidemiology; GINIplus, German Infant Nutritional Intervention; LISA, Influences of Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood; MAS, Multicentre Allergy Study; PIAMA, Prevention and Incidence of Asthma and Mite Allergy.

Figure 4.

Maternal smoking during pregnancy and the development of early transient, persistent, and adolescent-onset disease phenotypes (asthma $N=\mathrm{7,210}$ and rhinoconjunctivitis $N=\mathrm{6,991}$). Odds ratios (ORs) and 95% confidence intervals (CIs) were obtained by logistic regression and were adjusted for sex, parental education, parental allergy, secondhand smoke (SHS) during infancy, older siblings, breastfeeding, study center, intervention arm, and early day-care attendance.

Figure 5.

Secondhand smoke (SHS) exposure in childhood in relation to adolescent-onset asthma and rhinoconjunctivitis. Odds ratios (ORs) and 95% confidence intervals (CIs) were obtained by logistic regression and were adjusted for sex, parental education, parental allergy, older siblings, breastfeeding, study center, intervention arm, day-care attendance, and maternal smoking during pregnancy.