title: Maternal interpersonal trauma and cord blood IgE levels in an inner-city cohort: a life-course perspective.
abstract: BACKGROUND
  Prenatal stress affects immunocompetence in offspring, although the underlying mechanisms are not well understood.
  
  
  OBJECTIVE
  We sought to examine associations between maternal lifetime interpersonal trauma (IPT) and cord blood total IgE levels in a sample of urban newborns (n = 478).
  
  
  METHODS
  Maternal IPT during childhood and adolescence (birth to 17 years), adulthood (18 years to index pregnancy), and the index pregnancy were ascertained by using the Revised Conflict Tactics Scale at 28.4 +/- 7.9 weeks' gestation. Cord blood IgE levels were derived by using a fluoroenzyme immunoassay. We examined effects of maternal IPT on increased cord blood IgE levels (upper quartile, 1.08 IU/mL) by using logistic regression, adjusting for confounders and mediating variables.
  
  
  RESULTS
  Maternal trauma was categorized as unexposed (n = 285 [60%]), early (childhood and/or teenage years only, n = 107 [22%]), late (adulthood and/or index pregnancy only, n = 29 [6%]), and chronic (early and late, n = 57 [12%]) exposure. Relative to no IPT, early (odds ratio [OR], 1.78; 95% CI, 1.05-3.00) and chronic maternal IPT (OR, 2.25; 95% CI, 1.19-4.24) were independently associated with increased IgE levels in unadjusted analyses. When adjusting for standard controls, including maternal age and race, season of birth, child's sex, and childhood and current socioeconomic status, early effects became nonsignificant (OR, 1.48; 95% CI, 0.85-2.58). Chronic exposure remained significant in fully adjusted models, including standard controls, current negative life events, allergen exposure, and potential pathway variables (maternal atopy, prenatal smoking, and birth weight; OR, 2.18; 95% CI, 1.06-4.50).
  
  
  CONCLUSIONS
  These data link chronic trauma over the mother's life course with increased IgE levels in infants at birth. Research examining associations between maternal trauma and indicators of offspring's atopic risk might be particularly relevant in inner-city high-risk populations.
authors.affiliation: Department of Environmental and Occupational Medicine and Epidemiology, Harvard School of Public Health, Boston, Mass 02215, USA. msternth@hsph.harvard.edu
authors.forename: Michelle Judith
authors.initials: MJ
authors.lastname: Sternthal
authors.forename: Michelle Bosquet
authors.initials: MB
authors.lastname: Enlow
authors.forename: Sheldon
authors.initials: S
authors.lastname: Cohen
authors.forename: Marina Jacobson
authors.initials: MJ
authors.lastname: Canner
authors.forename: John
authors.initials: J
authors.lastname: Staudenmayer
authors.forename: Kathy
authors.initials: K
authors.lastname: Tsang
authors.forename: Rosalind J
authors.initials: RJ
authors.lastname: Wright
mesh_terms: D000293:Adolescent; D000328:Adult; D000485:Allergens / Q000276:immunology; D002908:Chronic Disease; D015331:Cohort Studies; D005260:Female; D005312:Fetal Blood / Q000276:immunology*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D007231:Infant, Newborn; D016015:Logistic Models; D008297:Male; D033261:Maternal-Fetal Relations; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood / Q000276:immunology*; D013315:Stress, Psychological / Q000097:blood / Q000276:immunology*
chemical_list: D000485:Allergens; D007073:Immunoglobulin E