Industrial Teratogens
Arsenic
Arsenic is released into the environment through copper, zinc and lead smelters, as well as chemical and glass manufacturers. It has been shown that arsenic is able to cross the placenta and enter the fetus. The total amount of metal accumulating in the fetus increases with gestational age, supporting theories of placental transfer.
Arsenic is know to produce a variety of congenital malformations in laboratory animals, yet there are no documented cases in humans. These malformations are dependant upon the dose concentration and the timing during development.
Cadmium
Only low levels of cadmium are found in the human fetus or new born. It has been hypothesized that placental production of metallothionein may restrict placental transfer of maternal cadmium levels to the fetus, thereby inhibiting cadmium's toxic effects.
Lead
Lead has been studied as an occupational hazard for over 1,000 years. It is necessary to study the effects of lead on reproduction because: 800,000 people, in the U.S. alone, work with lead each year occupationally; it is found most everywhere in the natural environment; it is a cumulative poison; and often the warning signs of lead poisoning are silent. Since the late 1970Õs and early 1980Õs, legislation has been passed to ban lead based paint in the home and to reduce lead content in auto exhaust.
Lead is able to cross the placenta as early as the 12th-14th week of gestation. Cord blood concentrations of lead are generally equivalent to that of the mother, or just a bit lower. Lead is not easily excreted, so it will continue to accumulate in fetal tissues throughout gestation, mostly accumulating in fetal brain. Fetal exposure to lead is most often through maternal ingestion of food and beverages containing the metal.
In the past few decades, scientific research has been able to link fetal exposure to lead with premature birth, decreased birth weight, decreased postnatal growth, increased rates of still births/miscarrages, neurological alterations and an increase in minor malformations. A dose response relationship has been found in two studies; an increase in fetal lead concentration in the blood is proportionate to an increase in minor congenital abnormalities.
Reproductive studies in battery workers have shown that lead is associated with human sterility, abnormal sperm motility and morphology and decreased testicular function. It may also be responsible for chromosomal abnormalities and neonatal deaths.
Lead significantly impairs the timing of cell-cell connections during neurological development as well as alters neuronal migration. The fetal brain is not very well protected from toxicants during development as the endothelial cells in the capillaries of the blood-brain barrier are still immature. They are less resistant to the passage of lead as compared to the capillaries of an adult brain.
Mercury
Methyl mercury is extremely toxic to humans. Mercury in all forms is able to cross the placenta, after which it accumulates in fetal tissues. Fetal levels may be as high as twice that of the mother. Well documented studies of fetal exposure are those of Congenital Minamata Disease and of fetal exposure in Iraq. Congenital Minamata Disease is discussed in great detail in our Agricultural section of this web page.
The mechanism of action of mercuryÕs teratogenicity has been studied in great depth. Increasingly high levels of mercury result in altered neuronal migration and organization of nuclei in the brain. Mercury is also able to directly bind and alter the conformation of DNA and RNA.
References:
- Harada, M., Teratogen Update: Environmentally Induced Birth Defect Risks, ed. J.L. Sever and R.L. Brent. 1986, New York: Alan R. Liss, Inc.
- Klaassen, C. D. (ed.), Casarett and DoullÕs Toxicology. 5th ed. 1996, New York: McGraw-Hill.
- Schardein, J., Chemically Induced Birth Defects. 2nd ed. 1993, New York: Marcel Dekker, Inc.
- Warkany, J., Congenital Malformations. 1971, Chicago: Year Book Medical Publishers.
- Weiss, B. and R.A. Doherty, Teratogen Update: Environmentally Induced birth Defect Risks, ed. J.L. Sever and R.L. Brent. 1986, New York: Alan R. Liss, Inc.
