TY - JOUR
T1 - Maternal interpersonal trauma and cord blood IgE levels in an inner-city cohort
T2 - A life-course perspective
AU - Sternthal, Michelle Judith
AU - Enlow, Michelle Bosquet
AU - Cohen, Sheldon
AU - Canner, Marina Jacobson
AU - Staudenmayer, John
AU - Tsang, Kathy
AU - Wright, Rosalind J.
N1 - Funding Information:
The Asthma Coalition on Community, Environment, and Social Stress study was funded by grants R01ES10932, U01HL072494, and R01HL080674. M. S. is supported by grant T32-ES07069-29 and the Leaves of Grass Foundation .
Funding Information:
Disclosure of potential conflict of interest: M. J. Sternthal and R. J. Wright have received research support from the National Institutes of Health and the Leaves of Grass Foundation. M. B. Enlow has received research support from the National Institute of Mental Health and the Children's Brain Research Foundation. S. Cohen has received research support from the National Institutes of Health and the MacArthur Foundation and consulted for Johnson & Johnson Consumer and Personal Products Worldwide. The rest of the authors have declared that they have no conflict of interest.
PY - 2009/11
Y1 - 2009/11
N2 - 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). Conclusion: 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.
AB - 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). Conclusion: 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.
KW - Interpersonal trauma
KW - cord blood IgE
KW - life course
KW - pregnancy
KW - urban asthma
UR - https://www.scopus.com/pages/publications/71749115992
U2 - 10.1016/j.jaci.2009.07.030
DO - 10.1016/j.jaci.2009.07.030
M3 - Article
C2 - 19748657
AN - SCOPUS:71749115992
SN - 0091-6749
VL - 124
SP - 954
EP - 960
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
IS - 5
ER -