Prenatal and Postnatal Maternal Stress and Wheeze in Urban Children

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 ¼ 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.Keywords: negative life events; stress; pregnancy; maternal sensitization; childhood wheeze Childhood wheezing illnesses account for significant morbidity and health care use (1). Recurrent wheeze may be a precedent of asthma and reduced lung function (2). An important step in identifying children at risk for costly respiratory disorders is characterizing risk factors and mechanisms that lead to and maintain early predisposition.Although the spectrum of wheeze phenotypes is complex and mechanisms of early environmental influences are incompletely understood (3, 4), aberrant proinflammatory states are central determinants (5, 6). Glucocorticoid action and sympathovagal balance are important in regulating immune function and airway response in early development (7,8). Thus, environmental factors, such as psychosocial stressors, that influence the programming of regulatory systems involved in these processes (i.e., hypothalamic-pituitary-adrenal [HPA] axis, autonomic nervous system, immune function) may be particularly relevant.Evidence links psychosocial stress to wheeze, asthma, and airway hyperesponsiveness (9). Animal studies suggest effects begin prenatally. Prenatal stress increases allergen-induced ...

Early origins of inflammation: An examination of prenatal and childhood social adversity in a prospective cohort study

“…Our findings align with the results of prior studies showing that adverse exposures during the prenatal period and early infancy have effects independent of subsequent adversity, in samples of children (Mathilda Chiu et al, 2012), adolescents (Bosch et al, 2012), and adults (Entringer et al, 2011; Entringer et al, 2008a; Entringer et al, 2008b; Ziol-Guest et al, 2009). Some of this work suggests that gestation or early childhood is a “sensitive period” for the effects on social adversity on later health.…”

“…Inflammation is a common pathway to multiple diseases (Bosch et al, 2012; Mathilda Chiu et al, 2012; Ziol-Guest et al, 2009), and the acute phase reactant C-reactive protein (CRP) functions as a marker of systemic inflammation (Ridker et al, 2002). CRP is mainly produced in the liver (Libby et al, 2002), and rises in response to inflammatory cytokines that that are typically modulated by infection or injury (Ridker et al, 2002).…”

Prenatal Stress, Prematurity, and Asthma

“…Prenatal stress has been associated with asthma or wheeze (a key symptom of asthma) in several studies [7, 32–38]. Similar to prematurity, factors or exposures that may confound or modify the putative effects of prenatal stress on asthma include socioeconomic status and access to health care [39], in utero environmental tobacco smoke [39], intensity of stressful exposures or perceived maternal stress[36], maternal obesity [33], maternal race or ethnicity[39], air pollution[40], and parental history of asthma or allergies [32, 41].…”

“…There is conflicting or insufficient evidence of a critical “time window” for detrimental effects of maternal stress during pregnancy [33, 35, 37], an interaction between prenatal stress and the neonate’s sex[36], or the relative independent contributions of pre- and post-natal stress [32, 33, 35] to the pathogenesis of childhood asthma. Because a significant proportion of children who experience wheeze before age 4 years have transient wheeze but no asthma, a key limitation of most (but not all[34]) published studies is the relatively short duration of follow-up after birth, which precludes a confident diagnosis of asthma.…”

Prenatal and postnatal stress and asthma in children: Temporal- and sex-specific associations

“…A growing number of prospective epidemiological studies demonstrate associations between increased prenatal maternal stress and early asthma phenotypes(1–5). While the magnitude of the association varies across studies, likely due to differences in study design, timing of exposure, and differences in the stress measure used, a recent meta-analysis substantiated a significant relationship between prenatal stress and childhood asthma(6).…”