Fetal impacts

I look at many possible causes of fetal damage in this book, but give particular emphasis to man-made environmental toxins, be they chemical pollutants in our air, water, and land, or substances in the consumer marketplace, legal and otherwise. The effects of these toxins are often connected to more than one type of fetal damage. Prenatal exposure to lead, for example, is connected to postnatal occurrences of lower IQ, ADHD, and schizophrenia, usually in different individuals. Prenatal exposure to tobacco smoke, as another example, is connected to a host of effects with adverse postnatal consequences as well. The effects of both sorts of toxins can also be related to other fetal impacts, which in turn are often connected to important social... 

Among academics, a debate continues about whether psychiatric disorders are caused by poverty (causation) or whether individuals with those disorders are socially and psychologically maladapted and therefore poor as a consequence (selection).66 It seems to me this debate is ridiculous, since given the fetal-impact-poverty cycle, both causation and selection must occur. 

What seems certain to me is that accepting things as they are is a defeat of the human spirit. But I don t think such defeat is necessary. I m optimistic about what mankind can and will do to eliminate preventable fetal impacts that damage the brains and bodies of generations of children. It s a tractable problem, much of it man-made. 

This material is hazardous through inhalation, skin absorption, penetration through broken skin, ingestion, and produces local skin/eye impacts. It is known to mimic estrogen in the body (hyperestrogenism). In animals, it has caused feminization of male animals and interfered with conception, ovulation, and fetal development in female animals. Specific signs and symptoms of acute high-dose exposure to zearalenone have not been established or have not been published. 

However, combining different phases of the reproductive cycle into a single study design increases the risk of an adverse event compromising the evaluation of subsequent stages, e.g., any impact on fertility of the male or female could result in too few litters for the embryo-fetal development evaluation. Under such circumstances, a separate embryo-fetal development study would have to be scheduled with the associated added cost and use of animals. Further, a separate embryo-fetal development study is recommended if the test item is poorly tolerated with repeated dosing in order to limit the duration of the administration period. 

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. 

Undemutrition during fetal and early life impacts upon the development of the immune organs and appears to diminish cellular immunity and increase the risk of atopic disorders during childhood (Langley-Evans and Carrington 2006). The references confirm that many food components have a beneficial impact on various elements of the immune system. Proteins, some fats, vitamins (A, B6, E, and folic acid), macro- and microelements (zinc, iron, selenium, and copper), and certain bacteria (probiotic bacteria), for example, have a considerable effect on the immune system. 

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. 

It is possible to perform a one-generation reproduction test (Table XVI) which would assess the impact of all ST and LT toxic effects on mating, fertility, fetal toxicity, dominant lethal mutagenesis, teratogenesis, gestational and post-natal effects on survival, growth, lactation, etc., in a period of four to five months. 

Two observations suggest near normal function for rcel cells. First, loss of Rcelp minimally impacts hematopoiesis in otherwise normal tissue [46]. Second, adoptive transfer of murine rcel fetal liver cells rescues hematopoiesis in lethally irradiated mice. Moreover, tissue-specific loss of Rcelp in liver also results in otherwise healthy mice, as judged histologically and biochemically (i.e., transaminase activity) [11]. These... 

Any xenobiotic associated with adverse effects on development of male or female reproductive function can be classified as a reproductive toxicant (Evans, 2007 Rogers and Kavlock, 2008). Even chemicals adversely affecting animal well-being have a potential negative impact on development and reproductive function. This chapter will attempt to focus on toxicants which are available for or could arise from military and terrorist activities and specific mechanisms of actions which have a direct effect upon the male and/or female reproductive tract or which target normal embryonic and/or fetal growth and maturation (Evans, 2007). 

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