Moderate Prenatal Alcohol Exposure and Cognitive Status of Children at Age 10 Jennifer A. Willford, Sharon L. Leech, and Nancy L. Day Background: The effects of prenatal alcohol exposure (PAE) on measures of intelligence have been well documented in children with fetal alcohol syndrome. However, deficits in general intellec- tual ability in children with low to moderate PAE are less well understood. The objective of this study was to assess the association between moderate PAE and cognitive ability in children at age 10 controlling for other prenatal and birth factors, maternal and child psychosocial factors, and envi- ronmental characteristics. Methods: Data were collected as part of the Maternal Health Practices and Child Development Project, a prospective study of prenatal substance use with 636 mother–child pairs. Women were as- sessed during each trimester of pregnancy and with their children at birth; 8 and 18 months; and 3, 6, and 10 years. Each phase included an evaluation of growth, development, cognitive, and psycholog- ical functioning. At age 10, cognitive ability was assessed using the composite score and verbal, ab- stract/visual, quantitative, and short-term memory area scores of the Stanford–Binet Intelligence Test, fourth edition. Maternal intellectual ability, maternal prenatal and current drug use, maternal and child psychosocial characteristics, demographics, and home environment were included in the analysis. Results: A significant relation was found between alcohol exposure during the first and second trimesters and the composite score of the Stanford–Binet for African American children at age 10. Significant relations were also found for the verbal, abstract/visual, and quantitative subscales. Additional predictors of IQ at age 10 included mother’s IQ, home environment, and child’s report of depression. Conclusions: There is a significant association between PAE and cognitive ability at age 10 among African American offspring. There was no relation between PAE and scores on the Stanford–Binet scales among the Caucasian offspring. Key Words: Prenatal Alcohol Exposure, Intelligence, Cognitive, Child. D EFICITS IN COGNITIVE ability and underlying dysfunction in the central nervous system (CNS) are necessary elements in the diagnosis of fetal alcohol syndrome (FAS). Low IQ is one of the most frequently reported CNS deficits. In people with FAS, the IQ deficits are stable with maturation (Steinhausen et al., 1994; Streiss- guth et al., 1991) and are noted for both verbal and perfor- mance IQ (Mattson and Riley 1998; Mattson et al., 1997). The level of IQ deficits among those with light to moderate prenatal alcohol exposure (PAE), however, has not been studied extensively, particularly not among older children. Researchers have reported IQ deficits in people who have PAE but who do not meet the criteria for FAS. Testa et al. (2003) performed a meta-analysis to evaluate the effects of PAE on children at 1 year of age. When they combined published data, weighting the results toward the studies with larger sample sizes, they found that PAE had a significant effect on the Mental Development Index of the Bayley Scales of Infant Development and that these effects were significant at levels of less than 1 drink per day. Among 7.5-year-old children, Streissguth et al. (1990) reported that IQ deficits were associated with PAE meas- ured in mid-pregnancy. They calculated an effect size of 6.7 points for 2 or more drinks per day on the full-scale IQ as measured by the Wechsler Intelligence Scale for Chil- dren (Wechsler, 1991). In addition, the effect of PAE was exacerbated by lower paternal education and more chil- dren in the household, 2 measures of socioeconomic status. In a recent report, however, Jacobson et al. (2004) found that among 7.5-year-old children, PAE did not affect the Full Scale IQ, although among those offspring whose mothers were older, they found a 2.9-point decrease in the Full Scale IQ. Mothers with a positive screen on the Michigan Alcohol Screening Test also had children with lower IQs, although presumably, these would represent From the Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania (JAW, NLD); and the University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania (SLL). Received for publication May 24, 2005; accepted February 3, 2006. This work is supported by the National Institute of Alcoholism and Alcohol Abuse (AA06666, NLD, P.I.; AA013981 JAW, P.I.) and National Institute on Drug Abuse (DA03874, NLD, P.I.). Reprint requests: Jennifer A. Willford, PhD, Western Psychiatric Institute & Clinic, University of Pittsburgh, 3811 O’Hara Street, Pittsburgh, PA 15213; Fax: 412-246-6875; E-mail: willford@epid. wpic.pitt.edu Copyright r 2006 by the Research Society on Alcoholism. DOI: 10.1111/j.1530-0277.2006.00119.x Alcohol Clin Exp Res, Vol 30, No 6, 2006: pp 1051–1059 1051 ALCOHOLISM:CLINICAL AND EXPERIMENTAL RESEARCH Vol. 30, No. 6 June 2006