Prenatal Cocaine Exposure Related to Cortisol Stress Reactivity in 11-Year-Old Children

Received 6 November 2009; received in revised form 15 January 2010; accepted 19 February 2010. published online 19 April 2010.

Objective

Determine the association between prenatal cocaine exposure and postnatal environmental adversity on salivary cortisol stress reactivity in school-aged children.

Study design

Subjects included 743 11-year-old children (n = 320 cocaine-exposed; 423 comparison) followed since birth in a longitudinal prospective multisite study. Saliva samples were collected to measure cortisol at baseline and after a standardized procedure to induce psychological stress. Children were divided into those who showed an increase in cortisol from baseline to post stress and those who showed a decrease or blunted cortisol response. Covariates measured included site, birthweight, maternal pre and postnatal use of alcohol, tobacco or marijuana, social class, changes in caretakers, maternal depression and psychological symptoms, domestic and community violence, child abuse, and quality of the home.

Results

With adjustment for confounding variables, cortisol reactivity to stress was more likely to be blunted in children with prenatal cocaine exposure. Children exposed to cocaine and who experienced domestic violence showed the strongest effects.

Conclusions

The combination of prenatal cocaine exposure and an adverse postnatal environment could downregulate the hypothalamic-pituitary-adrenal axis resulting in the blunted cortisol response to stress possibly increasing risk for later psychopathology and adult disease.

BDI, Beck Depression Inventory, BSI, Brief Symptom Inventory, CD, Conduct disorder, HOME, Home Observation Measurement of the Environment, HPA, Hypothalamic-pituitary-adrenal axis, MLS, Maternal Lifestyle Study, NET, Norepinephrine transporter, ODD, Oppositional defiant disorder, SES, Socioeconomic status

a Department of Pediatrics, Brown Center for the Study of Children at Risk, Warren Alpert Medical School of Brown University, Women & Infants Hospital of Rhode Island, Providence, RI

b Department of Pediatrics, Warren Alpert Medical School of Brown University, Providence, RI

c Department of Psychiatry and Human Behavior, Warren Alpert Medical School of Brown University, Providence, RI

d Department of Pediatrics, Wayne State University, Detroit, MI

e Department of Pediatrics, University of Kentucky Hospital, Lexington, KY

f Department of Pediatrics, University of Miami, Miller School of Medicine, Miami, FL

g RTI International, Rockville, MD

h Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD

Reprint requests: Dr Barry M. Lester, Warren Alpert Medical School of Brown University and Women and Infants Hospital of Rhode Island, 101 Dudley Street, Providence, RI 02905.

Supported by the National Institute of Child Health and Human Development (NICHD) Neonatal Research Network and an interinstitute agreement with the National Institute on Drug Abuse (NIDA) through cooperative agreements: U10-DA-024117-01, U10-HD-21385 (S.S.), U10-DA-024128-06, U10-HD-2786 (H.B.), U10-DA-024119-01, U10-HD-27904 (B.L.), and U10-DA-024118-01, U10-HD-21397 (C.B.); and NICHD contract N01-HD-2-3159 (B.L.). The authors declare no conflicts of interest.

PII: S0022-3476(10)00163-0

doi:10.1016/j.jpeds.2010.02.039

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