Prenatal and postnatal maternal stress and wheeze in urban children: effect of maternal sensitization

Abstract

Rationale: Critical periods for programming early wheeze risk may include pregnancy and infancy. Effects of timing remain poorly understood.

Objectives: Associations among prenatal and postnatal maternal stress and children's wheeze were prospectively examined in 653 families. Effect modification by maternal sensitization was also examined.

Methods: Stress was indexed by a maternal negative life events (NLEs) score (range, 0-9) ascertained during pregnancy and between 1 and 2 years postpartum. Mothers reported child wheeze every 3 months up to age 2 years. Relationships of prenatal and postnatal maternal NLEs with repeated wheeze (≥2 episodes) were examined using logistic regression adjusting for covariates. Penalized splines were implemented to explore possible nonlinear associations. We also examined the interaction between prenatal stress and maternal sensitization indexed by allergen-specific IgE from maternal prenatal serum.

Measurements and main results: Adjusted models considering prenatal or postnatal NLEs alone both showed an exposure-response relationship between higher stress and child wheeze. When considering prenatal and postnatal stress concurrently, only children of mothers with high stress in both periods were significantly more likely to wheeze (adjusted odds ratio, 3.04; 95% confidence interval, 1.67-5.53) than children of mothers reporting low stress in both periods. Associations between high prenatal stress and wheeze were significant in children born to nonsensitized mothers (any IgE <0.35 kU/L) but not in the sensitized group (P for interaction = 0.03).

Conclusions: Although children have heightened sensitivity to maternal stress in utero and in early childhood, those with higher stress in both periods were particularly at risk for wheeze. The prenatal maternal immune milieu modified effects.

Figure 1.

Exposure-response relationships between maternal negative life events (NLEs) and children’s repeated wheeze. Penalized spline curves demonstrating the relationship of (A) prenatal maternal NLEs and (B) postnatal maternal NLEs in separate models with children’s repeated wheeze by age 2 years are shown. Solid line depicts the penalized spline curve; dotted lines indicate the 95% confidence bounds. Models were adjusted for child’s sex; season of birth; maternal race; maternal education; maternal atopy; prenatal traffic-related air pollution (black carbon); household cockroach allergen; and the neighborhood disadvantage index.

Figure 2.

Relationships of combined levels of prenatal and postnatal maternal stress with children’s repeated wheeze. Odds ratios (ORs) and 95% confidence intervals for repeated wheeze comparing each combination of prenatal–postnatal stress. High stress is indicated by a negative life events score greater than or equal to 3, and low stress is indicated by a negative life events score of 0–2. Logistic regression models were adjusted for child’s sex; season of birth; maternal race; maternal education; maternal prenatal and postnatal smoking; maternal atopy; prenatal traffic-related air pollution (black carbon); household cockroach allergen; and the neighborhood disadvantage index.

Figure 3.

Associations between prenatal maternal negative life events (NLEs) and children’s repeated wheeze, stratified by maternal sensitization. Odds ratios (ORs) and 95% confidence intervals for repeated wheeze comparing high prenatal NLEs (≥3) with low prenatal NLEs (0–2) groups, stratified by maternal sensitization (defined by any IgE level ≥0.35 kU/L). Models were adjusted for child’s sex; season of birth; maternal race; maternal education; prenatal traffic-related air pollution (black carbon); household cockroach allergen; and the neighborhood disadvantage index.