Читать книгу Handbook of Clinical Gender Medicine - Группа авторов - Страница 44

It is now common understanding that prenatal life is no safe haven for the fetus and that the environment in which the pregnant mother lives has a direct impact on the development of the fetus. In effect, there is no other time throughout the life span of an individual where it is so intimately exposed to the environment. Whatever affects the pregnant mother may well affect her growing embryo and fetus, in many cases in a greatly amplified manner. The impact of exogenous toxins on the developing fetus is dependent on qualitative and quantitative factors and also on when they occur during the development of the fetus. First trimester exposure will generally have teratogenic effects while second and third trimester exposure will more often be expressed in growth restriction and organ failure.

Environmental toxins are abundant. Whyatt et al. [2] examined the home use of pesticides (mostly against cockroaches) in a cohort of 314 pregnant women from an urban minority group. More than 85% reported the use of pesticides in their home and all had detectable blood levels of at least three pesticides, which are known neurotoxins for the developing fetus and may cause permanent brain damage that may even be transmitted to subsequent generations. Alcohol is a good example of how the intrauterine environment may be affected by exogenous toxins resulting in an enormous negative impact on the fetus and embryo. Up to 1% of US live births are affected by fetal alcohol spectrum disorders (FASD), which is defined by any impairment related to fetal exposure to alcohol, and 0.05-0.5% of live births are affected by the devastating results of fetal alcohol syndrome [3]. It is estimated that alcohol consumption during pregnancy is responsible for more cases of mental retardation in the USA than all other known causes combined, including chromosomal aberrations [3]. Unfortunately, there is virtually no threshold for alcohol toxicity, and postconceptional alcohol consumption by the pregnant woman, i.e. before she even knows about her pregnancy, may be as hazardous to the fetus or even more so than throughout pregnancy. Tobacco is another example: maternal smoking affects the developing fetus directly and causes reduced placental perfusion, lower birth weight, and a whole spectrum of adverse outcomes in the fetus and newborn and in later life. Xiao et al. [4] showed in a rat model that intrauterine exposure to nicotine increases the blood pressure response to angiotensin II in adult offspring. This phenomenon is gender specific as it could be demonstrated in male rats but not in female rats. Prenatal exposure to tobacco also increases the prevalence of cognitive and auditory processing deficits in the adult offspring, probably based on thinning of the cerebral cortex, and is more commonly observed in female adolescents than in males. Some other adverse effects also seem to be sex specific. Jacobsen et al. [5] evaluated 181 male and female smokers and nonsmokers with or without prenatal exposure to maternal smoking. Individuals exposed prenatally to nicotine showed a reduction of cortical cholinergic markers on which attentional function is highly dependent. Reductions in auditory and visual attention were greatest among females who were exposed prenatally to nicotine and who were smokers themselves. Intrauterine exposure to nicotine in males was associated with marked deficits in auditory attention.