Fetal development disruptions/disruptive effects

HCH also penetrates the placenta barrier [A96, A101]. Complications during pregnancy occurred 1.5 times more frequently in the 213 women whose blood contained HCH than in the 89 women with no signs of this insecticide (78.3% and 58.4% respectively). It is especially significant that twice as many women with HCH in their blood spontaneously miscarried during the first trimester as those without HCH (7.5% and 3.4% respectively). Causal factors included disruptions in prenatal fetal development, and disruptions in women s hormonal systems under the effect of HCH [A96]. Postpartum complications in women who had HCH in their blood were 2.5... 

Many chemicals cause a decrease in brain size during fetal development. Changes in brain size can be caused in various ways. A decreased brain weight may be a consequence of general undernutrition caused by effects on placental functioning. Examples of other possible mechanisms are inhibition of cell multiplication or cell growth, increased cell death, disrupted trophic effects induced by changes in cell maturation and neurochemistry. 

Recently, Harrison and Sharp and Irvine summarized the hypothesis and status of evidence implicating endocrine disruption and their adverse impacts on human health (Sharp and Skakkebaek, 1993 Harrison, 2001 Sharp and Irvine, 2004). They outlined that exposure of the fetal/ developing male to environmental pollutants resulted in hypospadias, cryptorchidism, prostrate cancer, testicular cancer, a global decrease in sperm counts, and decreased male reproductive capacity. Detrimental effects in women include breast cancer, cystic ovaries, and endometriosis. 

Prenatal development is subject to a variety of environmental impacts that can divert, disrupt, and stop development altogether. The effects may not be observable at birth, but many of them affect later cognitive performance and emotional stability that may remain subclinical and may never be considered as deriving from the fetal period. 

In some animals, consumption of a phytoestrogen-rich diet can cause temporary infertility and reproductive system disorders (Irvine, 1999). In humans, lower testosterone levels and a decline in human semen quality over the past century have been luiked to increased exposure to environmental endocrine disrupters (EDCs) (Sharpe and Skakkebaek, 1993). Furthermore, cases of sexual impotence have been reported in males exposed to synthetic estrogens in the pharmaceutical industry (Mattison et al., 1990). If this might be the case, the fetal-prepubertal period and Sertoli cell development would be of critical importance (Sharpe and Skakkebaek, 1993). However, an adverse effect of phytoestrogens on male fertility has yet to be proven. Recent work (Mitchell et al., 2001) addressing this point led to the conclusion that up to 40 mg/day of isoflavones over a two-month period had no effects on gonadotrophin and... 

In 42 methadone-maintained women methadone had profound effects on fetal neurobehavioral functioning, implying a disruption of or threat to fetal neural development (45). At peak concentrations the fetuses had slower heart rates, less heart rate variability, fewer heart rate accelerations, reduced duration of movements, reduced motor activity, and a lower degree of coupling between... 

The adverse effects of ethanol are not limited to the metabolism of ethanol itself. Vitamin A (retinol) is converted into retinoic acid, an important signal molecule for growth and development in vertebrates, by the same dehydrogenases that metabolize ethanol. Consequently, this activation does not take place in the presence of ethanol, which acts as a competitive inhibitor. Moreover, the MEOS system induced by ethanol inactivates retinoic acid. These disruptions in the retinoic acid signaling pathway are believed to be responsible, at least in part, for fetal alcohol syndrome as well as the development of a variety of cancers. 

Fetal brain development is a vast subject, the focus of hundreds of research laboratories and clinical groups around the world. In this chapter I highlight some of this research to illustrate how the fetal environment can interact with brain development and to identify broadly the points at which that development is most vulnerable to environmental effects that may alter it in some way, whether divergently or disruptively. 

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