Covington Chandice Y, Nordstrom-Klee Beth, Ager Joel, Sokol Robert, Delaney-Black Virginia
School of Nursing, University of California at Los Angeles, Los Angeles, CA 90095, USA.
Neurotoxicol Teratol. 2002 Jul-Aug;24(4):489-96. doi: 10.1016/s0892-0362(02)00233-7.
Prenatal exposure to cocaine, alcohol, and cigarettes has been linked to decreased birth weight and length. Unclear, however, is whether growth deficits persist into childhood. Women who were pregnant, African-American, not HIV-positive, and who delivered singleton infants were extensively screened throughout pregnancy for cocaine, alcohol, cigarette, and other illicit drug use. Of the approximately 1100 eligible subjects, 665 families were located at a 7-year postbirth follow-up and 540 participated. After appropriate control for potential confounders and prenatal exposures, prenatal exposure to cocaine, alcohol, and cigarettes each independently predicted birth weight and length. At age 7, prenatal cocaine exposure was significantly related to height deficits after accounting for other prenatal exposures and significant confounders. Children at age 7 exposed to cocaine in utero were up to 1 in. shorter and twice as likely to fall below the 10th percentile in height as the control children after accounting for other significant confounders including other prenatal exposures. Maternal age moderated the relation between prenatal exposures and child growth. Children born to women over 30 and exposed to cocaine were up to 2 in. shorter and four times more likely to have clinically significant height deficits at age 7. Children of older women and exposed to moderate-to-high levels of alcohol prenatally were up to 14 lb lighter and five times more likely to fall below the 10th percentile in weight. Similar growth restriction was not associated with prenatal exposures for children born to younger mothers. These outcomes add to the growing body of literature detailing long-term effects of prenatal drug exposure, suggesting differential effects for cocaine and alcohol, and indicating that maternal age may moderate these effects. Mechanisms for growth restriction and failure of catch-up under conditions of prenatal exposures are presented, suggesting further study of these developmental outcomes.
产前接触可卡因、酒精和香烟与出生体重和身长降低有关。然而,生长缺陷是否会持续到儿童期尚不清楚。对怀孕、非裔美国、非艾滋病毒阳性且分娩单胎婴儿的妇女在整个孕期进行了广泛筛查,以检测她们是否使用可卡因、酒精、香烟及其他非法药物。在大约1100名符合条件的受试者中,665个家庭在产后7年随访时被找到,540个家庭参与了研究。在对潜在混杂因素和产前暴露进行适当控制后,产前接触可卡因、酒精和香烟各自独立预测了出生体重和身长。在7岁时,在考虑了其他产前暴露和显著混杂因素后,产前接触可卡因与身高缺陷显著相关。在考虑了包括其他产前暴露在内的其他显著混杂因素后,子宫内接触可卡因的7岁儿童比对照儿童矮多达1英寸,身高低于第10百分位数的可能性是对照儿童的两倍。母亲年龄调节了产前暴露与儿童生长之间的关系。30岁以上且接触可卡因的妇女所生的孩子在7岁时矮多达2英寸,临床上出现显著身高缺陷的可能性是四倍。年龄较大的妇女所生且产前接触中度至高度酒精的孩子体重轻多达14磅,体重低于第10百分位数的可能性是五倍。年轻母亲所生孩子的生长受限与产前暴露无关。这些结果增加了越来越多详细描述产前药物暴露长期影响的文献,表明可卡因和酒精的影响存在差异,并表明母亲年龄可能调节这些影响。文中提出了产前暴露情况下生长受限和追赶失败的机制,建议对这些发育结果进行进一步研究。