Recreational Teratogens

Two thirds of all infant mortalities are due to alterations in fetal development or development during the first year of life. Often times, recreational drugs significantly reduce fetal and post natal growth and are known to significantly increase infant mortality.

The effect a drug has on the embryo is dependant on the dose of the drug as well as the period of embryonic development in which the fetus encounters the drug. For instance, during week 5 of development, the central nervous system, heart, eyes, limbs and lips are very susceptible to toxicants. This trend continues from week 3 through week 8 of pregnancy. These teratogens usually disrupt fetal development before the mother knows she is pregnant and has a chance to change her lifestyle.

Page Contents: (Click on the Teratogen name or scroll down)

Alcohol (Ethanol)

Ethanol is the causative agent of Fetal Alcohol Syndrome (FAS). FAS is seen in approximately 2 in 1000 live births, depending upon culture and socioeconomic status. For instance, there is an occurrences of FAS in 19.5:1000 live births in American Native Indian culture verses a rate of 1.9:1000 in middle class Caucasian families. FAS does seem to be dose dependant in that greater amounts of alcohol consumed increases the chances of having an FAS child. Fetal Alcohol Syndrome
Alcohol is able to permeate the placenta and enter fetal circulatory system, thereby causing developmental abnormalities. Ethanol impairs placental blood flow to the fetus by constricting blood vessels: inducing hypoxia and fetal malnutrition. FAS was formally defined in 1970 as containing a combination of the malformations seen below:


Growth deficiencies
Maxillary hypoplasia
Decreased philtrum size
Microphthalmia
Microcephally
Narrow upper lip
Cardiovascular disorders
Short palpebral fissures
Low nose bridge
Small brain size

There are many proposed mechanisms of action for ethanol such as altered neural crest cell migration/increased neural crest cell death or general cell death by superoxide radial lysis of cells.



Tobacco

Thirty percent of pregnant women smoke an average of 9.5 cigarettes per day. Maternally inhaled nicotine can be detected in fetal lung, trachea, kidney, adrenal glands and intestines. Women who smoke during pregnancy are 80% more likely to have a spontaneous abortion as compared to a non smoker.

Nicotine restricts uterine blood vessels and restricts blood flow to the fetus resulting in chronic hypoxia and malnutrition leading to birth defects. On average, offspring of smoking women weigh 170-200 g less at birth as compared to a non smokerŐs child. There is a dose dependence in that the childŐs weight decreases in proportion to number of cigarettes smoked by the mother. There is also a reduction in overall fetal length, reduced head circumference, intrauterine growth retardation as well as behavioral alterations after birth. Other possible malformation (which are still controversial) are cleft lip and palate, cardiac malformations and anencephaly. Smoking during pregnancy increases the risk for premature delivery, abruptio placentae, placenta previa and perinatal mortality.



Cocaine

Cocaine is an anesthetic and vasoconstrictor. An estimated 45% of urban pregnancies and 6% of suburban pregnancies involve cocaine exposure. Approximately 375,000 children are born each year to mothers who use cocaine during pregnancy.
cocaine structure Exposed fetuses often have intrauterine growth retardation, microcephaly, cerebral infarction, urogenital anomalies, an increased risk of sudden infant death syndrome as well as neuronal and behavioral abnormalities. These pregnancies are at risk for premature labor, spontaneous abortion, increased perinatal mortality and fetal death.
Cocaine is thought to induce birth defects by disrupting the vasculature in the placenta thereby inducing intrauterine hypoxia and malnutrition.


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