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. 2018 Apr 12;126(4):047005.
doi: 10.1289/EHP2738.

Maternal Smoking During Pregnancy and Early Childhood and Development of Asthma and Rhinoconjunctivitis - A MeDALL Project

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Free PMC article

Maternal Smoking During Pregnancy and Early Childhood and Development of Asthma and Rhinoconjunctivitis - A MeDALL Project

Jesse D Thacher et al. Environ Health Perspect. .
Free PMC article

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.

Figures

Bar graph plotting percentage (y-axis) of asthma across prevalence of asthma in those aged 4 to 6 years, 8 to 10 years, and 14 to 16 years, and prevalence of rhinoconjunctivitis in those aged 4 to 6 years, 8 to 10 years, and 14 to 16 years (x-axis) in five cohorts, namely, BAMSE, GINIplus, LISAplus, MAS, and PIAMA.
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.
Figures 2A, 2B, 2C, and 2D are forest plots indicating the odds ratio with 95 percent confidence intervals and percentage weight for the maternal smoking during pregnancy and overall risk of asthma-crude models (Overall, I-squared = 34.7 percent, p equals 0.190), maternal smoking during pregnancy and overall risk of asthma-adjusted models (Overall, I-squared = 8.1 percent, p equals 0.361), secondhand smoke exposure during infancy and overall risk of asthma-crude models (Overall, I-squared = 0.0 percent, p equals 0.816), and secondhand smoke exposure during infancy and overall risk of asthma-adjusted models (Overall, I-squared = 0.0 percent, p equals 0.877), respectively, observed in five cohorts, namely, BAMSE, GINIplus, LISAplus, MAS, and PIAMA.
Figure 2.
Associations between maternal smoking during pregnancy (N=9,052) or any secondhand smoke (SHS) during infancy (N=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.
Figures 2A, 2B, 2C, and 2D are forest plots indicating the odds ratio with 95 percent confidence intervals and percentage weight for the maternal smoking during pregnancy and overall risk of asthma-crude models (Overall, I-squared = 34.7 percent, p equals 0.190), maternal smoking during pregnancy and overall risk of asthma-adjusted models (Overall, I-squared = 8.1 percent, p equals 0.361), secondhand smoke exposure during infancy and overall risk of asthma-crude models (Overall, I-squared = 0.0 percent, p equals 0.816), and secondhand smoke exposure during infancy and overall risk of asthma-adjusted models (Overall, I-squared = 0.0 percent, p equals 0.877), respectively, observed in five cohorts, namely, BAMSE, GINIplus, LISAplus, MAS, and PIAMA.
Figure 2.
Associations between maternal smoking during pregnancy (N=9,052) or any secondhand smoke (SHS) during infancy (N=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.
Figures 3A, 3B, 3C, and 3D are forest plots indicating the odds ratio with 95 percent confidence intervals and percentage weight for the maternal smoking during pregnancy and overall risk of rhinoconjunctivitis-crude models (Overall, I-squared = 0.0 percent, p equals 0.591), maternal smoking during pregnancy and overall risk of rhinoconjunctivitis-adjusted models (Overall, I-squared = 0.0 percent, p equals 0.450), secondhand smoke exposure during infancy C asthma rhinoconjunctivitis-crude models (Overall, I-squared = 0.0 percent, p equals 0.510), and secondhand smoke exposure during infancy and overall risk of rhinoconjunctivitis-adjusted models (Overall, I-squared = 0.0 percent, p equals 0.437), respectively, observed in five cohorts, namely, BAMSE, GINIplus, LISAplus, MAS, and PIAMA.
Figure 3.
Associations between maternal smoking during pregnancy (N=9,016) or any secondhand smoke (SHS) during infancy (N=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.
Figures 3A, 3B, 3C, and 3D are forest plots indicating the odds ratio with 95 percent confidence intervals and percentage weight for the maternal smoking during pregnancy and overall risk of rhinoconjunctivitis-crude models (Overall, I-squared = 0.0 percent, p equals 0.591), maternal smoking during pregnancy and overall risk of rhinoconjunctivitis-adjusted models (Overall, I-squared = 0.0 percent, p equals 0.450), secondhand smoke exposure during infancy C asthma rhinoconjunctivitis-crude models (Overall, I-squared = 0.0 percent, p equals 0.510), and secondhand smoke exposure during infancy and overall risk of rhinoconjunctivitis-adjusted models (Overall, I-squared = 0.0 percent, p equals 0.437), respectively, observed in five cohorts, namely, BAMSE, GINIplus, LISAplus, MAS, and PIAMA.
Figure 3.
Associations between maternal smoking during pregnancy (N=9,016) or any secondhand smoke (SHS) during infancy (N=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.
Graph plotting odds ratio with 95 percent confidence intervals (y-axis) across early transient, persistent, and adolescent-onset phenotypes (x-axis) for asthma and rhinoconjunctivitis.
Figure 4.
Maternal smoking during pregnancy and the development of early transient, persistent, and adolescent-onset disease phenotypes (asthma N=7,210 and rhinoconjunctivitis N=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.
Graph plotting odds ratio with 95 percent confidence intervals (y-axis) obtained for children aged 1 to 2 years, 4 to 6 years, 8 to 10 years, and 14 to 16 years (x-axis) to examine the association of SHS exposure with asthma and rhinoconjunctivitis.
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.

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