Environmental Exposures and Child Health: What we Might Learn in the 21st Century from the National Children’s Study?

In utero and early life environmental exposure programming may be critical to the onset of many diseases and dysfunctions in adulthood (Barker, 2007; Heindel, 2006), such as an increased risk of hypertension, cardiovascular disease (Palinski et al. 2007), diabetes (Armitage et al. 2008), and breast cancer (Xue and Michels, 2007). Some in utero and early life environmental exposures have demonstrated unequivocal harmful effects to children, such as thalidomide Whereas other in utero and early life environmental exposures have come under scrutiny without consensus as to the degree of infl uence on child or adult health, such as exposure to pesticides (Eskenazi et al. 1999), polybrominated biphenyls (PCBs) (Guo et al. 1995), nitrates (Mueller et al. 2004), bisphenol A (vom Saal and Hughes, 2005), and phytoestrogens (Damgaard et al. 2002). Several factors converge to make susceptibility to adverse effects of environmental exposures of particular importance during the developmental periods of the fetus and child. These include host vulnerability during organogenesis and neuronal development; lower exposure thresholds and metabolic capacity of children relative to adults; behavioral factors that may increase children's ingestion of environmental toxins (Goldman et al. 2004); and inhalation of harmful air pollutants (Bates, 1995). Furthermore, during fetal and infant development, vulnerability to some exposures is increased during critical windows (Selevan et al. 2000). Attempts to tease out the timing of exposure associated with health outcomes are challenging. Unfortunately, our understanding of the importance of common environmental exposures occurring in utero and early life with regard to infl uence on child and adult health has been slow. For example, one misconception that took considerable time to alter was the belief that the fetus was protected from exposures—the placenta barrier misconception (Welshons et al. 2003). With this paradigm shift, we now realize that the fetus may face signifi cant environmental exposures and in some cases a biomagnifi cation of exposure (Ask et al. 2002; Hanrahan et al. 2004). Further, bioaccumulation of some chemicals, such as persistent organic pollutants (POPs) in children are higher than in their parents (Thundiyil et al. 2007; Trapp et al. 2008). This has lead to an active research area investigating epigenetic changes occurring from in utero exposures which may affect child or adult health (Dolinoy et al. 2007). Much has been learned about an environmental stressor of the Dutch winter famine of 1944–1945 and specifi c long-term consequences of this deprivation on fetuses (Ravelli et al. 1998; …