Fetal vulnerability

Pregnancy vomiting is prone to occur in the first trimester thus pharmacotherapy would coincide with the period of maximal fetal vulnerability to chemical injury. Accordingly, antiemetics (antihistamines, or neuroleptics if required) should be used only when continuous vomiting threatens to disturb electrolyte and water balance to a degree that places the fetus at risk. 

As stated above, one substantial difference between the Faroe and the Seychelles populations relates to their PCB exposure. Whereas PCB concentrations in the Seychelles population are among the lowest observed anywhere in the world, the portion of the Faroe population that eats whale blubber accumulates unusually high PCB body burdens. Although it is conceivable that PCB exposure in the Faroe Islands might enhance fetal vulnerability to Hg, that hypothesis is speculative at present experimental animal studies would be needed to test its plausibility. The possibihty of effect modification by PCB exposure was exantined in regression analyses that, in addition to confoundeis, also included the Hg and PCB exposure variables and their product (Hg x... 

And the exposure is often unknown to mothers who, like Claire, drink while unaware that they are pregnant. That unawareness, coupled with high fetal vulnerability to ethyl alcohol, is one reason the substance is so insidious. Its often celebrated place in the public mind only exacerbates the problem. 

Essentially all antipsychotic medications pass through the placenta. The use of these drugs requires critical attention to the timing of the exposure, the dose and duration of use, and fetal susceptibility. When possible, discontinuing antipsychotics for the first trimester is the safest option, as weeks 6 to 10 are the most vulnerable period for organ formation. 

Further research on the relationship between paternal lead exposure and fetal/infant development should be conducted. Additional information on relationships between nutritional deficits and vulnerability of the fetus and child to lead would be valuable. 

Vulnerability of developing brain Relative effects of growth restriction during the fetal and suckling periods on behavior and brain composition of adult rats, J. Nutrition, 103 (1973) 1327-1338. 

Coe CL, Kemnitz JW, Scneider ML. Vulnerability of placental antibody transfer and fetal complement synthesis to disturbance of the pregnant monkey. J Med Primatol 1993 22 294-300. 

Fetal injury can occur in early pregnancy (fetal alcohol syndrome). It may be due to the metabolite, acetaldehyde, and so acute (binge) consumption is more hazardous than similar total intake on a daily basis. The vulnerable period of pregnancy is at 4-10 weeks. Because of this, prevention cannot be reliably achieved after diagnosis of pregnancy (usually 3-8 weeks). 

Figure 9-5 The sensitivity of the conceptus to a theoretical teratogen during rat gestation (modified from 161). The most susceptible window is organogenesis with low levels of vulnerability at the time of implantation and the period of functional maturation. Superimposed are the approximations of when the developmental landmarks that are represented in the four in vitro tests occur. The chick embryo neural retina model (CENR) represents events around GD 10-13. The mouse embryonic stem cell test (EST) corresponds roughly to the period of GD 6-10 in the rat, near the peak of sensitivity. Whole embryo culture (WEC) recapitulates the window at the peak of sensitivity, between GD 9-11 or GD 10-12 depending upon the window within which the culture is conducted. Rabbit cultures are also done between GD 10-12. Represented by the single ( ) and double asterisk ( ), respectively, are the initiation and termination of the dosing period in regulatory compliant preclinical embryo/fetal toxicity studies. Thus, the zebrafish is the only model that permits exposure to test article during this important period.

The critical organ for MeHg toxicity is the brain. Both adult and fetal brains are vulnerable. For elemental Hg, the critical organs are the brain and kidney. Both MeHg and elemental Hg are converted to mercuric Hg in the brain, where it is trapped. The biological mechanisms for removing mercuric Hg from the brain are limited. The critical organ for mercuric Hg toxicity is the kidney, where it accumulates. 

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