Prenatal exposure to alcohol

Barr, H. M., Streissguth, A. P., Darby, B. L., Sampson, P. D., Prenatal exposure to alcohol, caffeine, tobacco, and aspirin Effects on fine and gross motor performance in 4-year-old children. Developmental-Psychology 26(3), 339-348, 1990. 

Although estimates vary, FAS occurs in one to three of every 1,000 live births (USDHHS, 1990). As you think about these statistics, remember that there is great individual variability in the effects on the fetus of prenatal exposure to alcohol. In this regard, the rate of occurrence of FAS is much lower than the rate of women who use alcohol while they are pregnant. Furthcrmt)re, rates of FAS vary with the population... 

Everybody wants to know the safe level of drinking during pregnancy. As our brief discussion of FAS suggests, no simple answer is available. Actually, it is best to think of FAS as the most severe result of a continuum of effects of prenatal exposure to alcohol (Rasmussen, 2005). Subtle behavioral or cognitive cfVects may be observed on the other end of the continuum. Each abnormal outcome may have its own yardstick of amount of alcohol exposure and timing of exposure (Jacob.son et al., 1993 USDHHS, 1990). 

Prenatal exposure to alcohol is also a predictor of alcohol abuse later in life.33 Moderate consumption of alcohol by a mother during pregnancy is associated with increased responses of infants to the odor of alcohol even if the infants show no signs of FASD. 

Each year in America, the national consumption of alcohol by women of child-bearing age adds approximately 100,000 more mentally retarded children to the population. How many more children not diagnosed as mentally retarded are affected by prenatal exposure to alcohol We know only that this exposure is related to atypical brain development, neuropsychological deficits, academic difficulties, emotional dysfunction, and social dysfunction.39 Is this constellation of problems acceptable collateral damage of the alcoholic beverages industry ... 

Wass, T.S., Simmons, R.W., Thomas, J.D., and RBey, E.P. (2002). Timing accuracy and variability in children with prenatal exposure to alcohol. Alcoholism Clin. Exp. Res. 26 1887-1896. 

Mattson SM, Riley EP. 1995. Prenatal exposure to alcohol. What the images reveal. Alcohol Health Res World 19 273-278. 

Prenatal exposure to ethanol results in a spectrum of abnormalities including, at one extreme, fetal alcohol syndrome, which includes growth retardation, facial anomalies, mental retardation, and microencephaly. Children with less severe prenatal exposures often lack the characteristic facial features of fetal alcohol syndrome, but suffer from a similar pattern of cognitive deficits (Berman and Hannigan, 2000). Mild exposures are associated with variable deficits in motor development and functional delays (Levitt, 1998). 

The societal and medical costs of alcohol abuse are staggering. It is estimated that about 30% of all people admitted to hospitals have coexisting alcohol problems. Once in the hospital, people with chronic alcoholism generally have poorer outcomes. In addition, each year thousands of children are born in the United States with morphologic and functional defects resulting from prenatal exposure to ethanol. Despite the investment of many resources and much basic research, alcoholism remains a common chronic disease that is difficult to treat. 

The impact of prenatal exposure to cocaine on fetal growth and fetal head circumference has been studied in 476 African-American neonates, including 253 full-term infants prenatally exposed to cocaine (with or without alcohol, tobacco, or marijuana) and 223 non-cocaine exposed infants (147 drug-free, 76 exposed to alcohol, tobacco, or marijuana) (300). The cocaine-associated deficit in fetal growth was 0.63 standard deviations and for gestational age 0.33 standard deviations. There were also cocaine-associated deficits in birth weight and length, but no evidence of a disproportionate effect on head circumference. 

Beyond the genetic factors, the causes of ADHD are unknown and very few studies have examined the relationship between ADHD and exposures to environmental chemicals. It is known, however, that maternal prenatal exposures to lead, alcohol, tobacco smoke, and marijuana are known to result in the birth of children with high incidences of ADHDJ14-17 ft has also been established that exposure to excessive quantities of phenylalanine either prenatally in utero, as a result of the mother having phenylketonuria (PKU) and fetus not having PKU, or postnatally where the child has PKU, results in the development of ADHD hyperactive and behavioral... 

Since speech and language acquisition develop relatively late in children, separating prenatal and postnatal effects on their development is often impossible. Known factors include the general social effects of poverty combined with fetal alcohol spectrum disorder, producing deficits in children in language performance.28 Other factors common in a poverty environment and known to affect language performance are prenatal exposure to cocaine and tobacco.29... 

Miller MW (1992) Effects of prenatal exposure to ethanol on cell proliferation and neuronal migration. In Miller MW (ed) Development of the Central Nervous System Effects of Alcohol and Opiates, Wiley-Liss, New York, pp 47-69. 

Environmental risk factors include prenatal exposure to drugs such as alcohol and nicotine, obstetric complications, head injury, and psychosocial adversity (Biederman and Faraone, 2005 Romano et al., 2006). Prenatal exposure to ethanol affects mainly dopaminergic transmission and causes hyperactivity (Gibson et al., 2000). Rats exposed to ethanol prenatally show attention deficits that are similar to those of children with fetal alcohol syndrome and ADHD (Hausknecht et al., 2005). 

A distinct relation between parental occupational exposure and childhood cancer was shown for solvents and paints. High parental exposure resulted in higher incidences of childhood cancers. In the same study, however, generally more cancers were found as a result of parental use of alcohol and tobacco smoke. Childhood leukemia and nervous system cancers, in particular, are the types suspected to be caused by parental exposure to paints and solvents. Kishi et al. described an elevated risk for acute lymphatic leukemia in children of mothers with prenatal exposures to benzene and to paints. In former studies with small numbers of children these tendencies could also be shown, mainly in male painters whose children showed a higher incidence of childhood leukemia and brain tumors. 18.3.4.2.4 Respiratory effects... 

The behavioral effects of prenatal cocaine exposure at age 5 years have been studied in 140 children exposed to cocaine, 61 exposed to alcohol, tobacco, and/or marijuana, and 120 not exposed to any drugs (290). They were evaluated with the Achenbach Child Behavior Checklist. There was no association between behavior and intrauterine cocaine exposure. However, the current behavioral health of the mother, including recent drug use and psychological functioning, did affect the child s internalizing and externalizing behavior. 

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