Fetal development environmental impact

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. 

And this is very relevant for the way we think about fetal development. The more complex the process that reads out genetic information stored in the genome, the more complex is the vulnerability of that process to environmental impact. 

We know that in the mature brain, neurotransmitters are released by nerve cell endings and act at synapses to mediate the interaction between nerve cells. There s now evidence that during the development of the prenatal brain, neurons can release transmitters before any connections are made, and that such released transmitters, acting as trophic factors, guide the formation of connections.17 Any environmental impact or mutation that affects the synthesis or release of neurotransmitters can be expected to have an effect on the development of the fetal brain. For example, during fetal development in Down syndrome, reductions apparently occur in the levels of various neurotransmitters. This may be one mechanism for the impaired brain development characteristic of this syndrome.18... 

During fetal development, there are critical periods of vulnerability to environmental impacts, the critical periods occurring at various times in different tissues. Cells rapidly dividing to form tissues and organs are at greatest risk, and it s reasonable that fetal programming is more likely to occur in such tissues. 

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. 

The factors are diverse, ranging from caffeine consumption during pregnancy to maternal age at conception. The environmental agents with potential adverse impacts on fetal development for which there is the strongest evidence are all culture-dependent tobacco smoke, alcohol (ethanol), cocaine, and combustion-engine carbon monoxide.4 In this book I focus only on factors for which there is evidence known to me. What the factors all have in common is that all have heavy cultural... 

Meanwhile, what is needed is an understanding of neurological and psychiatric realities. Every fetal environmental impact discussed in this book that we know produces changes in the developing brain and consequent cognitive and emotional deficits has the potential to be related to childhood and adult violence and criminal behavior. 

The major problem concerning the impact of environmental neurotoxins on fetal brain development is not the absence of evidence but the absence of research on the many new chemicals in our midst. Regardless, the evidence that we do have tells us that simplistic genetic-determinist arguments about IQ are dubious. 

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