Prenatal impacts

In Part III, we move past the individual costs of prenatal disruptions to address broader social and economic questions that relate to those costs. What, for example, are the effects of ethnic and cultural heritage, geographic location, and socioeconomic status on the prenatal environment The chapter in this part also seeks to answer questions about the relation between prenatal impacts and social behavior such as criminality. 

Meanwhile, the plasticity of the cerebral cortex, its ability to have its connections shaped by experience, is one of its outstanding properties, and understanding its mechanisms makes possible an understanding of what governs the wiring of the brain. It also raises the implication that any prenatal impact that affects plasticity in the fetal brain can seriously wreck the brain development that occurs both before and after birth. 

Indeed, given the complexity of autistic behavior, it s reasonable to assume that more than a single cause might be involved in different individuals genetic factors, prenatal impacts, postnatal toxins, or some combination of these causes. The question before us here is to what degree might the clinical entities called autism spectrum disorder (broad autism) and its severe form (narrow autism) involve prenatal impact on the developing embryo or fetus ... 

Another idea is that prenatal impact on the activity of the neurotransmitter dopamine, including the effects of maternal psychosocial stress, maternal fever, maternal genetics and hormonal status, use of certain medications, and fetal hypoxia, may be involved in the epigenetic etiology of autism.67... 

Neurodevelopmental models of schizophrenia have for the most part emphasized prenatal brain development, focusing on effects that may alter gene expression.15 For example, according to one idea, individuals with schizophrenia inherit genes that cause structural brain deviations that may be compounded by early environmental impact.16 Much of the focus of this hypothesis has been on postnatal impact, such as stress, that changes brain chemistry, but the idea can also accommodate a focus on prenatal impact. 

Certainly, low socioeconomic status increases the prevalence of infection, exposure to toxins, poor nutrition, and many other prenatal impacts that may be involved in fetal brain damage and in the etiology of later mental illness. 

Cognitive performance is brain performance. In general, any prenatal impact that affects the fetal developing brain has the potential to affect childhood and adult cognitive performance. There is no biological reason why this should not be so. 

The clearest refutation of the idea advanced by hereditarian behavior geneticists that the prenatal environment is of only small consequence for childhood and adult IQ is the research on known IQ effects of prenatal exposure to certain neurotoxins. Any argument that this neurotoxic impact is extreme, rare, and therefore irrelevant is unsound. In addition, every known neurotoxic effect confirms the possible prenatal impact of other environmental agents not yet studied, and we do know there are literally hundreds of such neurotoxins already dispersed in the environment.15... 

It s common that children who are poor have higher levels of depression and antisocial behavior.72 This is not a problem unique to America. In Australia, for example, the more often families experience low income, the higher the rate of child behavior problems at age 5.73 Comparable correlations are found nearly everywhere. Prenatal impacts may be one cause. Another cause may be the child s postnatal experience of maternal depression produced by poverty. Owing to social constraints, female children are more likely to remain in poverty than male children. Later, these female children become pregnant and the cycle of impacts begins again. 

Attention deficit hyperactivity disorder (ADHD) produced by various prenatal impacts is another variable highly correlated with childhood violence and adult criminal behavior. ADHD is associated with conduct problems, social maladaptation, and delinquent behavior. In the United States, ADHD boys with conduct problems in school are at increased risk for later criminality.98 This is true not only in America but also in other industrialized countries, for example, in Germany and Sweden.99... 

Environmental exposures to PCBs are significantly lower than those reported in the workplace and are therefore unlikely to cause adverse human health effects in adults. However, it is apparent from the results of several recent studies on children that there was a correlation between in utero exposure to PCBs, eg, cord blood levels, and developmental deficits (65—68) including reduced bkth weight, neonatal behavior anomaUes, and poorer recognition memories. At four years of age, there was stiU a correlation between prenatal PCB exposure levels and short-term memory function (verbal and quantitative). In these studies the children were all exposed to relatively low environmental levels of PCBs. Although these effects may be related to other contaminants, it is clear that this is an area of concern regarding the potential adverse human health impacts of PCBs. 

The team led by Whyatt used regression analysis to assess whether there was a difference in the association between chlorpyrifos exposure and birth outcome before and after the EPA s action in the summer of 2000 which had ended residential use of chlorpyrifos. Prior to 2001, chlorpyrifos clearly had an impact on birth outcome, but after the EPA action taken in June 2000, levels of exposure declined and there was no longer a statistically significant association between insecticide exposure and birth outcome (Whyatt et al., 2004, 2005). This study provides encouraging evidence linking an action driven by the FQPA to a significant reduction in prenatal and infant exposures and risk. 

Richardson GA, Day NL, McGauhey PJ. (1993). The impact of prenatal marijuana and cocaine use on the infant and child. Clin Obstet Gynecol. 36(2) 302-18. 

IMPACT OF DRUGS OF ABUSE ON DEVELOPING BRAIN STUDIES OF PRENATAL EXPOSURE... 

Findings from human studies of the impact of prenatal exposure to cannabis have been inconsistent. Cannabis users tend to have lower-birth weight infants, but the relationship between prenatal cannabis use and prematurity has not been consistent (Lee, 1998). 

B. L. Vogt, R. J. Librizzi and S. Weiner, Prenatal testing referrals of patients calling teratogen information programs impact and income. Teratology, 33(3) (1986) 95C. 

Debes F, Budtz-Jorgensen E, Weihe P, White RF, Grandjean P (2006) Impact of prenatal methylmercury exposure on neurobehavioral function at age 14 years. Neuro-toxicol Teratol, 28(3) 363-375. 

It is also unclear what role the predicted DNA-PK site in dysbindin-1 may have in enabling or mediating its anti-apoptotic effect. As explained earlier (see Section 2.2.3.3.1), DNA-PK, which phosphorylates dysbindin-1 (Oyama et al., 2009), helps repair double-strand DNA breaks and suppresses apoptosis in developing and adult neurons (cf., Chechlacz et al., 2001, Culmsee et al., 2001, Vermuri et al., 2001, and Neema et al., 2005). Anti-apoptotic effects of DNA-PK on prenatal neurons (Vermuri et al., 2001) presumably have a major impact on brain development, especially given that the highest levels of DNA-PK are found in fetal tissue (Oka et al., 2000). It will thus be important to test if DNA-PK phosphorylation of nuclear dysbindin-1 in developing neurons contributes to the survival of those cells. 

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. 

Bandstra ES, Morrow CE, Anthony JC, Churchill SS, Chitwood DC, Steele BW, Ofir AY, Xue L. Intrauterine growth of full-term infants impact of prenatal cocaine exposure. Pediatrics 2001 108(6) 1309-19. 

Kilbride H, Castor C, Hoffman E, Fuger KL. Thirty-six month outcome of prenatal cocaine exposure for term or near-term infants impact of early case management. J Dev Behav Pediatr 2000 21 19-26. 

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